{"status":"ok","message-type":"work-list","message-version":"1.0.0","message":{"facets":{},"total-results":13039,"items":[{"indexed":{"date-parts":[[2026,1,8]],"date-time":"2026-01-08T07:51:15Z","timestamp":1767858675935,"version":"3.49.0"},"reference-count":43,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2005,5]]},"abstract":"<jats:p>Notch signaling pathway genes are required for nephrogenesis, raising the possibility that Notch effector Hairy-related genes should also control nephron formation. We performed in situ hybridization of Hairy transcription factors with segment-specific lectins and\/or antibodies during early nephrogenesis to identify their possible roles in segment identity of the nephron. We found that among all of Notch downstream Hairy genes, only Hes1, Hes5, Hey1, and HeyL were expressed in a segment-specific manner in early nephrons and their expression pattern changed dynamically during metanephric development. Based on these patterns of expression, it was possible to propose a pairwise association of specific ligand and receptor and to suggest that the effector of this association is one of the Hairy transcription factors. We found that Hes5 is specifically expressed in the anlage of the loop of Henle, suggesting that it might be involved in the determination of its cell identity. We also examined the morphological appearance of kidneys from mice where the Hes1 or Hes5 genes were deleted and found that at least at the gross morphological level, there was little difference from wild-type kidneys. Because Hairy genes associate with other transcription factors to exert their effect, it is necessary to examine a more complete array of genetic deletions before a conclusion can be reached regarding their role in kidney development. These studies provide the basis for the future development of strategies to examine the role of individual effector molecules in the determination of the differentiation pattern of the nephron.<\/jats:p>","DOI":"10.1152\/ajprenal.00369.2004","type":"journal-article","created":{"date-parts":[[2005,4,8]],"date-time":"2005-04-08T21:18:29Z","timestamp":1112995109000},"page":"F939-F952","source":"Crossref","is-referenced-by-count":95,"title":["Segmental expression of Notch and Hairy genes in nephrogenesis"],"prefix":"10.1152","volume":"288","author":[{"given":"Linghong","family":"Chen","sequence":"first","affiliation":[]},{"given":"Qais","family":"Al-Awqati","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-199210000-00008"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00164.x"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1126\/science.284.5415.770"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1101\/gad.9.21.2609"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200105000-00021"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.1.F50"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1038\/74307"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1023\/B:JOMG.0000037159.63644.81"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1242\/dev.00697"},{"key":"R10","doi-asserted-by":"crossref","unstructured":"ConlonRA, Reaume AG, and Rossant J.Notch1 is required for the coordinate segmentation of somites.Development121: 1533\u20131545, 1995.","DOI":"10.1242\/dev.121.5.1533"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1006\/dbio.2002.0756"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1101\/gad.13.21.2801"},{"key":"R13","unstructured":"EganSE, St-Pierre B, and Leow CC.Notch receptors, partners and regulators: from conserved domains to powerful functions.Curr Top Microbiol Immunol228: 273\u2013324, 1998."},{"key":"R14","unstructured":"EkblomP.Renal development. In:The Kidney: Physiology and Pathophysiology(2nd edition), edited by Seldin DW and Giebisch G. New York: Raven, 1992, p. 475\u2013501."},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1521-1878(199804)20:4<298::AID-BIES6>3.0.CO;2-M"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1101\/gad.291004"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1006\/scdb.1998.0260"},{"key":"R18","doi-asserted-by":"crossref","unstructured":"HamadaY, Kadokawa Y, Okabe M, Ikawa M, Coleman JR, and Tsujimoto Y.Mutation in ankyrin repeats of the mouse Notch2 gene induces early embryonic lethality.Development126: 3415\u20133424, 1999.","DOI":"10.1242\/dev.126.15.3415"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1101\/gad.10.12.1467"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(86)90353-3"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1101\/gad.9.24.3136"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.10208"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.21.17.6080-6089.2001"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1101\/gad.12.7.1046"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1038\/383707a0"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1101\/gad.12.15.2269"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1177\/35.1.3794309"},{"key":"R28","doi-asserted-by":"crossref","unstructured":"LeimeisterC, Dale K, Fischer A, Klamt B, de Angelis MH, Radtke F, McGrew MJ, Pourquie O, and Gesssler M.Oscillating Expression of c-Hey2 in the presomitic mesoderm suggests that the segmentation clock may use combinatiorial signaling through multiple interacting bHLH factors.Development227: 91\u2013103, 2000.","DOI":"10.1006\/dbio.2000.9884"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1016\/S0925-4773(99)00080-5"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1016\/S1567-133X(03)00114-5"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1016\/S0925-4773(00)00459-7"},{"key":"R32","doi-asserted-by":"crossref","unstructured":"McCrightB, Gao X, Shen L, Lozier J, Lan Y, Maguire M, Herzlinger D, Weinmaster G, Jiang R, and Gridley T.Defects in development of the kidney, heart and eye vasculature in mice homozygous for a hypomorphic Notch2 mutation.Development128: 491\u2013502, 2001.","DOI":"10.1242\/dev.128.4.491"},{"key":"R33","doi-asserted-by":"crossref","unstructured":"MendelsohnC, Batourina E, Fung S, Gilbert T, and Dodd J.Stromal cells mediate retinoid-dependent functions essential for renal development.Development126: 1139\u20131148, 1999.","DOI":"10.1242\/dev.126.6.1139"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1016\/S1084-9521(03)00023-5"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1006\/dbio.1999.9454"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1007\/BF00315754"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1038\/ng0797-235"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1016\/j.modgep.2004.04.007"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1038\/19091"},{"key":"R40","unstructured":"TisherCCand Madsen KM.Anatomy of the kidney. In:The Kidney(5th ed.), edited by Brenner BM and Rector FC, Jr. Philadelphia, PA: Saunders, 1996, p. 3\u201371."},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1242\/dev.00682"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/8.5.723"},{"key":"R43","doi-asserted-by":"crossref","unstructured":"ZhengJL, Shou JY, Guillemot F, Kageyama R, and Gao WQ.Hes1 is a negative regulator of inner ear hair cell differentiation.Development127: 4551\u20134560, 2000.","DOI":"10.1242\/dev.127.21.4551"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00369.2004","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,7,8]],"date-time":"2021-07-08T04:46:48Z","timestamp":1625719608000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00369.2004"}},"issued":{"date-parts":[[2005,5]]},"references-count":43,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2005,5]]}},"alternative-id":["10.1152\/ajprenal.00369.2004"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00369.2004","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2005,5]]}},{"indexed":{"date-parts":[[2026,1,8]],"date-time":"2026-01-08T08:43:27Z","timestamp":1767861807730,"version":"3.49.0"},"reference-count":54,"publisher":"American Physiological Society","issue":"1","funder":[{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health","doi-asserted-by":"publisher","award":["R01-HL-128189"],"award-info":[{"award-number":["R01-HL-128189"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2026,1,1]]},"abstract":"<jats:p>\n                    Protein phosphatase 2A (PP2A) B55\u03b1 is required for angiotensin type 2 receptor (AT\n                    <jats:sub>2<\/jats:sub>\n                    R) natriuretic signaling and AT\n                    <jats:sub>2<\/jats:sub>\n                    R intracellular trafficking in renal proximal tubule cells (RPTCs). RPTC PP2A B55\u03b1 is thus a key AT\n                    <jats:sub>2<\/jats:sub>\n                    R signaling intermediate and potential therapeutic target to promote sodium excretion in hypertensive individuals. This study introduces knocking down B55\u03b1 in vivo specifically in RPTCs using renal interstitial infusion of siRNA as a novel and unique approach to investigate physiological protein function in the kidney.\n                  <\/jats:p>","DOI":"10.1152\/ajprenal.00256.2025","type":"journal-article","created":{"date-parts":[[2025,12,18]],"date-time":"2025-12-18T01:10:07Z","timestamp":1766020207000},"page":"F102-F117","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Protein phosphatase 2A subunit B55 alpha is required for angiotensin type 2 receptor elicited natriuresis"],"prefix":"10.1152","volume":"330","author":[{"given":"John J.","family":"Gildea","sequence":"first","affiliation":[{"name":"University of Virginia School of Medicine","place":["United States"]}]},{"given":"Jie","family":"Li","sequence":"additional","affiliation":[{"name":"University of Virginia School of Medicine","place":["United States"]}]},{"given":"Nancy L.","family":"Howell","sequence":"additional","affiliation":[{"name":"University of Virginia School of Medicine","place":["United States"]}]},{"given":"Brandon A.","family":"Kemp","sequence":"additional","affiliation":[{"name":"University of Virginia School of Medicine","place":["United States"]}]},{"given":"Mark R.","family":"Conaway","sequence":"additional","affiliation":[{"name":"University of Virginia School of Medicine","place":["United States"]}]},{"given":"David L.","family":"Brautigan","sequence":"additional","affiliation":[{"name":"University of Virginia School of Medicine","place":["United States"]}]},{"given":"Robert M.","family":"Carey","sequence":"additional","affiliation":[{"name":"University of Virginia School of Medicine","place":["United States"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3089-7766","authenticated-orcid":false,"given":"Susanna R.","family":"Keller","sequence":"additional","affiliation":[{"name":"University of Virginia School of Medicine","place":["United States"]}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0605545103"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2011.03.001"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.3390\/ijms23042317"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1124\/pharmrev.120.000281"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.115.304110"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.116.308384"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000254833.85106.4d"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.107.103242"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.112.191403"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.111.184788"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.119.12705"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1146\/annurev-biochem-062917-012332"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1016\/j.canlet.2013.02.036"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.121.319519"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1016\/0006-291x(89)92189-x"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1161\/JAHA.119.012016"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.112.194175"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.C200198200"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1021\/bi961669e"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.119.316193"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00002.2015"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.V261122"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1586\/epr.10.10"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1007\/82_2013_334"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1038\/hr.2012.13"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1111\/tra.12839"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.22.13503"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.3390\/cells5030034"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1007\/BF00215889"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1007\/s004410050817"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.3389\/fphar.2020.01179"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-018-21040-6"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1038\/s41586-023-06870-3"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1126\/sciadv.adp5491"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.2654-19.2020"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1038\/s41388-021-02068-x"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.201606033"},{"key":"B38","unstructured":"Cell Signaling Technology. PhosphoSitePlus (Online). www.phosphosite.org\/proteinAction.action?id=16454&showAllSites=true [2024 Jun]."},{"key":"B39","unstructured":"Zhou J. CST Curation Set: 12496 (Online). 2011. www.phosphosite.org\/siteAction.action?id=23084414 [2024 Jun]."},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1042\/CS20220236"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1210\/mend.11.9.9975"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M313333200"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M707166200"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.11.8.2657"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2018050522"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1093\/function\/zqac046"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.E22-11-0510"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1992.366"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.E17-04-0211"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.3389\/fphys.2022.991705"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.3389\/fcell.2020.00358"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1142\/S179398441241005X"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.3389\/fphys.2022.861659"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2020.03.038"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00256.2025","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,1,7]],"date-time":"2026-01-07T14:18:20Z","timestamp":1767795500000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00256.2025"}},"issued":{"date-parts":[[2026,1,1]]},"references-count":54,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2026,1,1]]}},"alternative-id":["10.1152\/ajprenal.00256.2025"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00256.2025","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2026,1,1]]},"assertion":[{"value":"2025-07-01","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2025-07-28","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2025-12-15","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2026-01-07","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,1,10]],"date-time":"2026-01-10T01:41:04Z","timestamp":1768009264443,"version":"3.49.0"},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1996,1,1]]},"abstract":"<jats:p> The proximal tubule contains the target for nitric oxide (NO), soluble guanylate cyclase, and has the capacity for NO production. Inhibition of renal NO synthesis reduces fractional excretion of lithium, suggesting an inhibitory effect of NO on proximal tubule Na+ transport. The present studies determined direct effects of donors of NO in rabbit proximal tubule. In both freshly isolated proximal tubule segments and in primary cultures of proximal tubule cells, sodium nitroprusside (SNP) and S-nitroso-N-acetylpenicillamine (SNAP) caused dose-dependent increases in guanosine 3',5'-cyclic monophosphate (cGMP). SNAP was more potent than SNP in stimulating cGMP; this was associated with an enhanced production of nitrite, the stable end-product of NO. In rabbit proximal tubule cells, SNP or SNAP (10(-3) M) significantly inhibited the activity of the apical Na+\/H+ exchanger, determined by assay of amiloride-sensitive 22Na+ uptake (% inhibition: SNP, 34.90 +\/- 5.52%, P &lt; 0.001; SNAP, 30.77 +\/- 8.20%, P &lt; 0.002). To determine the role of cGMP in mediating these effects, proximal tubule cells were incubated with the membrane-permeable analogue, 8-bromoguanosine 3',5'-cyclic monophosphate (8-BrcGMP). Na+\/H+ exchange was significantly inhibited by 8-BrcGMP (10(3)M) (% inhibition: 32.40 +\/- 9.06%: P &lt; 0.05). The inhibitor of soluble guanylate cyclase, LY-83583, caused partial inhibition of SNP-stimulated cGMP generation and partly blocked the inhibitory effect of SNP on Na+\/H+ exchange. Protein kinase A (PKA) activity was not stimulated by SNP, indicating that potential cross-activation of PKA by cGMP did not mediate the effects of NO donors. These data indicate that NO stimulates soluble guanylate cyclase in rabbit proximal tubule and causes inhibition of Na-\/H+ exchange. This is at least partly mediated by generation of cGMP. We conclude that NO is an important autocrine or paracrine factor directly regulating Na+ transport in the proximal tubule. <\/jats:p>","DOI":"10.1152\/ajprenal.1996.270.1.f106","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T07:01:46Z","timestamp":1514012506000},"page":"F106-F115","source":"Crossref","is-referenced-by-count":42,"title":["Nitric oxide stimulates guanylate cyclase and regulates sodium transport in rabbit proximal tubule"],"prefix":"10.1152","volume":"270","author":[{"given":"A.","family":"Roczniak","sequence":"first","affiliation":[{"name":"Department of Medicine, University of Ottawa, Ontario, Canada."}]},{"given":"K. D.","family":"Burns","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Ottawa, Ontario, Canada."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1996.270.1.F106","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:09:14Z","timestamp":1567973354000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1996.270.1.F106"}},"issued":{"date-parts":[[1996,1,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1996,1,1]]}},"alternative-id":["10.1152\/ajprenal.1996.270.1.F106"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1996.270.1.f106","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1996,1,1]]}},{"indexed":{"date-parts":[[2026,1,10]],"date-time":"2026-01-10T09:46:20Z","timestamp":1768038380830,"version":"3.49.0"},"reference-count":61,"publisher":"American Physiological Society","issue":"6","funder":[{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health","doi-asserted-by":"publisher","award":["R01DH091185"],"award-info":[{"award-number":["R01DH091185"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["R01DK125015"],"award-info":[{"award-number":["R01DK125015"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["R01DK121758"],"award-info":[{"award-number":["R01DK121758"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["R01DK090242"],"award-info":[{"award-number":["R01DK090242"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["R01DK131811"],"award-info":[{"award-number":["R01DK131811"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100010554","name":"Pitt | Clinical and Translational Science Institute, University of Pittsburgh","doi-asserted-by":"publisher","award":["PINCH"],"award-info":[{"award-number":["PINCH"]}],"id":[{"id":"10.13039\/100010554","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2023,12,1]]},"abstract":"<jats:p> The incidence of end-stage renal disease (ESRD) has been increasing worldwide. Its treatment involves renal replacement therapy, either by dialyses or renal transplantation from a living or deceased donor. Although the initial mortality rates for patients on dialysis are comparable with kidney transplant recipients, the quality of life and long-term prognosis are greatly improved in transplanted patients. However, there is a large gap between availability and need for donor kidneys. This has led to the increase in the use of expanded kidney donor criteria. Allograft dysfunction immediately after transplant sets it up for many complications, such as acute rejection and shorter allograft survival. Delayed graft function (DGF) is one of the immediate posttransplant insults to the kidney allograft, which is increasing in prevalence due to efforts to maximize the available donor pool for kidneys and use of expanded kidney donor criteria. In this review, we discuss the risk factors for DGF, its implications for long-term allograft survival, animal models of DGF, and the therapeutic options currently under evaluation for prevention and management of DGF. <\/jats:p>","DOI":"10.1152\/ajprenal.00146.2023","type":"journal-article","created":{"date-parts":[[2023,10,19]],"date-time":"2023-10-19T08:00:25Z","timestamp":1697702425000},"page":"F817-F825","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":7,"title":["Delayed graft function post renal transplantation: a review on animal models and therapeutics"],"prefix":"10.1152","volume":"325","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4933-3426","authenticated-orcid":false,"given":"Anne C. S.","family":"Barbosa","sequence":"first","affiliation":[{"name":"Division of Nephrology, Department of Pediatrics, University of Pittsburgh, UPMC Children\u2019s Hospital, Pittsburgh, Pennsylvania, United States"}]},{"given":"Lillian G.","family":"Mauroner","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Pediatrics, University of Pittsburgh, UPMC Children\u2019s Hospital, Pittsburgh, Pennsylvania, United States"}]},{"given":"Juhi","family":"Kumar","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Pediatrics, University of Pittsburgh, UPMC Children\u2019s Hospital, Pittsburgh, Pennsylvania, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1908-4809","authenticated-orcid":false,"given":"Sunder","family":"Sims-Lucas","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Pediatrics, University of Pittsburgh, UPMC Children\u2019s Hospital, Pittsburgh, Pennsylvania, United States"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1159\/000520466"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1007\/s11255-020-02687-5"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1159\/000491558"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfn158"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0129279"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00064.2015"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/j.transproceed.2013.02.145"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1177\/0963689719872699"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.3390\/jcm12123871"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2014.18"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1177\/0391560321993540"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-6143.2010.03179.x"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1186\/s12882-020-02181-1"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1111\/ajt.13817"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-6143.2006.01597.x"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1111\/ctr.13520"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1111\/ctr.14779"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfn667"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2015.190"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1111\/ctr.13190"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009040412"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1136\/bmjopen-2021-059631"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1111\/ajt.16574"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.5555\/uri:pii:0039606065901248"},{"key":"B25","first-page":"721","volume":"5","author":"Skoskiewicz M","year":"1973","journal-title":"Transplant Proc"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/j.athoracsur.2005.08.074"},{"key":"B27","first-page":"287","volume":"9","author":"Ge F","year":"2011","journal-title":"Exp Clin Transplant"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1111\/tri.12129"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.26717\/BJSTR.2019.14.002617"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2020.07.033"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1101\/cshperspect.a015503"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1126\/science.abo7935"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2019080767"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2019020163"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2020050717"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1124\/mol.117.111146"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa1501969"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119632"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119457"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1172\/JCI84712"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0115709"},{"key":"B42","first-page":"1061","volume":"285","author":"Hauet T","year":"1998","journal-title":"J Pharmacol Exp Ther"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1097\/00007890-199710150-00025"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.V111138"},{"key":"B45","first-page":"23","volume":"286","author":"Elimadi A","year":"1998","journal-title":"J Pharmacol Exp Ther"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0701755"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1093\/ejcts\/ezx053"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007111267"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1111\/ajt.14262"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1172\/JCI83000"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-020-04588-2"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1097\/TP.0000000000000960"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2016.03.034"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1096\/fj.11-195396"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1111\/ajt.12447"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1097\/TP.0000000000002218"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.3389\/ti.2022.10139"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1159\/000500550"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1136\/bmj.m3734"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2020071106"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1111\/ajt.14767"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00146.2023","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,11,27]],"date-time":"2023-11-27T14:20:10Z","timestamp":1701094810000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00146.2023"}},"issued":{"date-parts":[[2023,12,1]]},"references-count":61,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2023,12,1]]}},"alternative-id":["10.1152\/ajprenal.00146.2023"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00146.2023","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2023,12,1]]},"assertion":[{"value":"2023-05-31","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2023-10-11","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2023-10-11","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2023-11-27","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,1,10]],"date-time":"2026-01-10T03:44:17Z","timestamp":1768016657349,"version":"3.49.0"},"reference-count":46,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2011,11]]},"abstract":"<jats:p> Metabolic syndrome (MetS) is associated with glomerular hyperfiltration and is a risk factor for chronic kidney disease, but the underlying mechanisms are poorly defined. This study tested the hypothesis that increased glomerular filtration rate (GFR) in early MetS is associated with renal adiposity and microvascular proliferation. Twelve MetS-prone Ossabaw pigs were randomized to 10 wk of a standard (lean, n = 6) or atherogenic (MetS, n = 6) diet. Kidney hemodynamics and function, perirenal fat volume, and tubular dynamics were assessed in vivo by multidetector computed tomography (CT) and blood oxygen level-dependent (BOLD)-MRI. Microvascular architecture was assessed ex vivo with micro-CT. Candidate injury mechanisms were evaluated in kidney tissue by Western blotting and histology. Basal GFR, renal blood flow, and renal cortical perfusion and volume were elevated in the MetS group. Perirenal and kidney tissue fat, proximal-nephron intratubular fluid concentration, and endothelial nitric oxide synthase expression were increased in MetS. GFR levels correlated with tissue triglyceride levels. Elevated spatial density of 20- to 40-\u03bcm cortical microvessels was accompanied by mild oxidative stress, inflammation, and with proximal tubular vacuolization. Medullary size and perfusion were relatively preserved, and BOLD-MRI showed intact medullary tubular response to furosemide. Increased GFR in early MetS is associated with renal adiposity and microvascular proliferation, which involve mainly the renal cortex and precede significant activation of oxidative stress and inflammation. Renal adiposity and proliferative microvessels may represent novel therapeutic targets for preserving renal function in early MetS. <\/jats:p>","DOI":"10.1152\/ajprenal.00333.2011","type":"journal-article","created":{"date-parts":[[2011,7,20]],"date-time":"2011-07-20T22:24:52Z","timestamp":1311200692000},"page":"F1078-F1087","source":"Crossref","is-referenced-by-count":91,"title":["Increased glomerular filtration rate in early metabolic syndrome is associated with renal adiposity and microvascular proliferation"],"prefix":"10.1152","volume":"301","author":[{"given":"Zilun","family":"Li","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, Division of Nephrology and Hypertension,"},{"name":"Division of Vascular Surgery, First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China"}]},{"given":"John R.","family":"Woollard","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Division of Nephrology and Hypertension,"}]},{"given":"Shenming","family":"Wang","sequence":"additional","affiliation":[{"name":"Division of Vascular Surgery, First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China"}]},{"given":"Michael J.","family":"Korsmo","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Division of Nephrology and Hypertension,"}]},{"given":"Behzad","family":"Ebrahimi","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Division of Nephrology and Hypertension,"}]},{"given":"Joseph P.","family":"Grande","sequence":"additional","affiliation":[{"name":"Department of Laboratory Medicine and Pathology, and"}]},{"given":"Stephen C.","family":"Textor","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Division of Nephrology and Hypertension,"}]},{"given":"Amir","family":"Lerman","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota; and"}]},{"given":"Lilach O.","family":"Lerman","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Division of Nephrology and Hypertension,"},{"name":"Division of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota; and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/S1043-2760(00)00301-5"},{"key":"B2","doi-asserted-by":"crossref","first-page":"1640","DOI":"10.1161\/CIRCULATIONAHA.109.192644","volume":"120","author":"Alberti K","year":"2009","journal-title":"Circulation"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1159\/000095329"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.77.10.6007"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.107.093989"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000167121.14254.a0"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000184250.37607.da"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000027105.02327.48"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1161\/01.ATV.0000077477.40824.52"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000089880.32275.7C"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000117774.83396.E9"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.49.7.1258"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1001\/jama.298.17.2038"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1148\/radiol.2432060655"},{"key":"B15","first-page":"35","volume":"56","author":"Dyson MC","year":"2006","journal-title":"Comp Med"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2010.142"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.1982.tb25720.x"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1001\/jama.287.3.356"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00628.2006"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1615\/CritRevEukarGeneExpr.v18.i3.30"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1007\/s10654-009-9382-3"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1161\/ATVBAHA.107.151092"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M500801200"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-009-1364-x"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007010089"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfq522"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1161\/ATVBAHA.109.201475"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00468.2010"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2010.526"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ijo.0802858"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.108.124149"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1161\/ATVBAHA.110.210070"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1161\/ATVBAHA.107.143081"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.162349799"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00503.2010"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1038\/ncpneph0565"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002160"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00159.2010"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000051700.07403.27"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2362.2005.01497.x"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.04071206"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1097\/RLI.0b013e3181f0213f"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.90677.2008"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1161\/01.ATV.0000142443.52606.81"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1161\/01.ATV.0000227469.40826.01"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000125742.65841.8B"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00333.2011","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:13:09Z","timestamp":1567973589000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00333.2011"}},"issued":{"date-parts":[[2011,11]]},"references-count":46,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2011,11]]}},"alternative-id":["10.1152\/ajprenal.00333.2011"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00333.2011","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2011,11]]}},{"indexed":{"date-parts":[[2026,1,21]],"date-time":"2026-01-21T10:35:23Z","timestamp":1768991723616,"version":"3.49.0"},"reference-count":55,"publisher":"American Physiological Society","issue":"1","funder":[{"name":"University of Toronto Connaught Fund"},{"DOI":"10.13039\/501100000024","name":"Gouvernement du Canada | Canadian Institutes of Health Research (Instituts de recherche en sant\u00e9 du Canada)","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100000024","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Canadian Foundation for Innovation (CFI)"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2019,7,1]]},"abstract":"<jats:p>Although percutaneous tibial nerve stimulation is considered a clinically effective therapy for treating overactive bladder, the mechanism by which overactive bladder symptoms are suppressed remains unclear. The goal of the present study was to better understand the role of specific neural inputs (i.e., fiber types) on the bladder-inhibitory effects of tibial nerve stimulation (TNS). In 24 urethane-anesthetized rats, a continuous suprapubic saline infusion model was used to achieve repeated filling and emptying of the bladder. A total of 4 TNS trials (pulse frequency:\u20095 Hz) were applied in randomized order, where each trial used different amplitude settings: 1) no stimulation (control), 2) A\u03b2-fiber activation, 3) A\u03b4-fiber activation, and 4) C-fiber activation. Each stimulation trial was 30 min in duration, with an intertrial washout period of 60\u221290 min. Our findings showed that TNS evoked statistically significant changes in bladder function (e.g., bladder capacity, residual volume, voiding efficiency, and basal pressure) only at stimulation amplitudes that electrically recruited unmyelinated C-fibers. In a subset of experiments, TNS also resulted in transient episodes of overflow incontinence. It is noted that changes in bladder function occurred only during the poststimulation period. The bladder-inhibitory effects of TNS in a continuous bladder filling model suggests that electrical recruitment of unmyelinated C-fibers has important functional significance. The implications of these findings in percutaneous tibial nerve stimulation therapy should be further investigated.<\/jats:p>","DOI":"10.1152\/ajprenal.00502.2018","type":"journal-article","created":{"date-parts":[[2019,5,29]],"date-time":"2019-05-29T19:01:41Z","timestamp":1559156501000},"page":"F163-F171","source":"Crossref","is-referenced-by-count":20,"title":["Recruitment of unmyelinated C-fibers mediates the bladder-inhibitory effects of tibial nerve stimulation in a continuous-fill anesthetized rat model"],"prefix":"10.1152","volume":"317","author":[{"given":"Jason P.","family":"Paquette","sequence":"first","affiliation":[{"name":"Institute of Biomaterials and Biomedical Engineering, University of Toronto, Toronto, Ontario, Canada"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8079-5074","authenticated-orcid":false,"given":"Paul B.","family":"Yoo","sequence":"additional","affiliation":[{"name":"Institute of Biomaterials and Biomedical Engineering, University of Toronto, Toronto, Ontario, Canada"},{"name":"Department of Electrical and Computer Engineering, University of Toronto, Toronto, Ontario, Canada"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuroscience.2009.03.058"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1983.244.1.R106"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/j.eururo.2012.04.037"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1111\/iju.13033"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/j.ucl.2004.09.007"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00516.2015"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1002\/nau.22556"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1016\/j.medengphy.2018.01.004"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/j.juro.2010.06.113"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/j.eururo.2006.07.024"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(05)66469-5"},{"key":"B12","volume-title":"Anatomy of the Rat","author":"Greene EC","year":"1955"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1097\/01.ju.0000092069.00376.5c"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.14814\/phy2.13001"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1002\/nau.20593"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00212.2014"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00059.2014"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1002\/nau.23577"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/j.juro.2009.08.160"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/0160-5402(86)90064-1"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1007\/BF00165805"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(91)91495-M"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00572.2012"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1002\/phy2.205"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1966.sp007980"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/j.juro.2007.10.030"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1002\/nau.23323"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1016\/j.neures.2009.01.016"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1007\/s12576-016-0468-x"},{"key":"B30","unstructured":"Paquette JP, Yoo PB. Changes in bladder capacity and voiding efficiency estimated during continuous-fill cystometry in anesthetized rats that are provided with tibial nerve stimulation. Program No. 508.09. 2017 Neuroscience Meeting Planner [Online]. Washington, DC: Society for Neuroscience, 2017."},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1002\/nau.22266"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1016\/j.juro.2009.12.036"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1016\/j.juro.2012.11.175"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1016\/0165-1838(80)90019-3"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1016\/0165-1838(83)90088-7"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1002\/ar.1092150111"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1016\/j.neures.2013.03.011"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1002\/nau.20850"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1007\/s11934-012-0274-9"},{"key":"B40","doi-asserted-by":"crossref","first-page":"203","DOI":"10.33549\/physiolres.932248","volume":"61","author":"Steffens H","year":"2012","journal-title":"Physiol Res"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2010.202614"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00343.2012"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1002\/nau.22506"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1016\/j.juro.2011.04.023"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00609.2011"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00526.2010"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(05)65863-6"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1109\/TBME.1981.324719"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1111\/j.1464-410X.2006.06055.x"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1016\/j.expneurol.2004.11.003"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(90)91590-D"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1986.251.6.R1177"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1152\/jn.1981.46.5.1056"},{"key":"B54","first-page":"77","volume":"110","author":"Yoshiyama M","year":"1993","journal-title":"J Pharmacol Exp Ther"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00107.2012"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00502.2018","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2020,12,16]],"date-time":"2020-12-16T03:48:06Z","timestamp":1608090486000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00502.2018"}},"issued":{"date-parts":[[2019,7,1]]},"references-count":55,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2019,7,1]]}},"alternative-id":["10.1152\/ajprenal.00502.2018"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00502.2018","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2019,7,1]]}},{"indexed":{"date-parts":[[2026,1,21]],"date-time":"2026-01-21T05:34:37Z","timestamp":1768973677577,"version":"3.49.0"},"reference-count":31,"publisher":"American Physiological Society","issue":"5","funder":[{"DOI":"10.13039\/100017618","name":"HHS | NIH | NIDDK | Division of Diabetes, Endocrinology, and Metabolic Diseases","doi-asserted-by":"publisher","award":["DK096418"],"award-info":[{"award-number":["DK096418"]}],"id":[{"id":"10.13039\/100017618","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2025,5,1]]},"abstract":"<jats:p> Our findings identify a reliable timepoint at which female mice subjected to unilateral ischemia-reperfusion consistently develop CKD changes relative to much shorter duration in male mice. We provide a novel model to study the AKI-CKD transition in female mice. <\/jats:p>","DOI":"10.1152\/ajprenal.00280.2024","type":"journal-article","created":{"date-parts":[[2025,3,25]],"date-time":"2025-03-25T21:01:49Z","timestamp":1742936509000},"page":"F684-F690","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":2,"title":["Prolonged unilateral renal ischemia-reperfusion as a model for acute to chronic kidney injury in female mice"],"prefix":"10.1152","volume":"328","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9163-6087","authenticated-orcid":false,"given":"Kaitlynn","family":"Stowers","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/01hcyya48","id-type":"ROR","asserted-by":"publisher"}],"name":"University of Cincinnati","place":["United States"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7717-6248","authenticated-orcid":false,"given":"Valeria","family":"Rudman-Melnick","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/01hcyya48","id-type":"ROR","asserted-by":"publisher"}],"name":"University of Cincinnati","place":["United States"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7130-689X","authenticated-orcid":false,"given":"Qing","family":"Ma","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/01hcyya48","id-type":"ROR","asserted-by":"publisher"}],"name":"University of Cincinnati","place":["United States"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7847-8552","authenticated-orcid":false,"given":"Prasad","family":"Devarajan","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/01hcyya48","id-type":"ROR","asserted-by":"publisher"}],"name":"University of Cincinnati","place":["United States"]}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00305.2019"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00590.2019"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.3349\/ymj.2023.0306"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/s41572-021-00284-z"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1093\/ckj\/sfaa177"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2016.05.005"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.34067\/KID.0000000000000321"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/s41392-023-01379-7"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0152153"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00199.2018"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1159\/000363726"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00431.2011"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2015.10.015"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-024-80930-0"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.3389\/fcell.2022.869069"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.2005477117"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1038\/s41584-019-0322-7"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1038\/s41419-023-05969-9"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2016.05.008"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2002.kid590.x"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/j.cardiores.2005.05.005"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.3892\/mmr.2014.2089"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00099.2020"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2024.08.034"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1038\/s41581-023-00757-2"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-021-04701-x"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2010.141"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1186\/s12929-020-0623-9"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.3389\/fphys.2019.00153"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2021081150"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00049.2017"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00280.2024","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,4,17]],"date-time":"2025-04-17T12:54:58Z","timestamp":1744894498000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00280.2024"}},"issued":{"date-parts":[[2025,5,1]]},"references-count":31,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2025,5,1]]}},"alternative-id":["10.1152\/ajprenal.00280.2024"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00280.2024","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2025,5,1]]},"assertion":[{"value":"2024-09-30","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2024-10-22","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2025-03-14","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2025-04-17","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,1,21]],"date-time":"2026-01-21T01:39:22Z","timestamp":1768959562406,"version":"3.49.0"},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1991,5,1]]},"abstract":"<jats:p> Patients with diffuse, proliferative lupus nephritis (DPLN) were subjected to differential solute clearances (n = 22) and serial renal biopsy (n = 11) before and again after 6-12 mo of immunosuppressive therapy. Glomerular sieving of dextrans of graded size was analyzed with a heteroporous membrane model. This revealed active DPLN to be associated with 1) a reduction of overall pore density accompanied by a 53% depression of glomerular filtration rate (GFR), and 2) appearance of a subset of large, nondiscriminatory pores, which accounted for the observed nephrotic level of proteinuria. Morphometric analysis of biopsy tissue provided evidence of reduced filtration surface area due to global or segmental occlusion of capillary loops in glomerular tufts. Activity of DPLN resolved posttreatment. A computed increase in pore density was associated with a 24% increment in GFR; a marked reduction in the fraction of shuntlike pores was accompanied by a parallel reduction of proteinuria into a subnephrotic range. Repeat biopsy revealed diminished glomerular cellularity, fewer immune deposits, and an ensuing increase in the fraction of tuft area occupied by patent loops. Epithelial filtration slit frequency also increased. Neither functional nor structural recovery was complete, however. Residual pore density approximated only 23-35% of that in healthy controls, and corresponding shuntlike pores were threefold more prominent. We conclude that severe DPLN is only partially reversible by current modalities of treatment and that the ensuing residual injury is far more severe than suggested by conventional tests of renal function. <\/jats:p>","DOI":"10.1152\/ajprenal.1991.260.5.f717","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T18:33:48Z","timestamp":1513967628000},"page":"F717-F727","source":"Crossref","is-referenced-by-count":2,"title":["Extent of glomerular injury in active and resolving lupus nephritis: a theoretical analysis"],"prefix":"10.1152","volume":"260","author":[{"given":"B. D.","family":"Myers","sequence":"first","affiliation":[{"name":"Department of Medicine, Stanford University Medical Center, California94305."}]},{"given":"A.","family":"Chagnac","sequence":"additional","affiliation":[{"name":"Department of Medicine, Stanford University Medical Center, California94305."}]},{"given":"H.","family":"Golbetz","sequence":"additional","affiliation":[{"name":"Department of Medicine, Stanford University Medical Center, California94305."}]},{"given":"L.","family":"Newton","sequence":"additional","affiliation":[{"name":"Department of Medicine, Stanford University Medical Center, California94305."}]},{"given":"S.","family":"Strober","sequence":"additional","affiliation":[{"name":"Department of Medicine, Stanford University Medical Center, California94305."}]},{"given":"R. K.","family":"Sibley","sequence":"additional","affiliation":[{"name":"Department of Medicine, Stanford University Medical Center, California94305."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1991.260.5.F717","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:24:01Z","timestamp":1567956241000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1991.260.5.F717"}},"issued":{"date-parts":[[1991,5,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1991,5,1]]}},"alternative-id":["10.1152\/ajprenal.1991.260.5.F717"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1991.260.5.f717","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1991,5,1]]}},{"indexed":{"date-parts":[[2026,1,18]],"date-time":"2026-01-18T21:15:16Z","timestamp":1768770916400,"version":"3.49.0"},"reference-count":33,"publisher":"American Physiological Society","issue":"8","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,4,15]]},"abstract":"<jats:p>Acute kidney injury (AKI) is a common clinical problem that still lacks effective treatment. Phosphodiesterase-5 (PDE5) inhibitors possess anti-apoptotic and anti-oxidant properties, making it a promising therapy for ischemia-reperfusion (I\/R) injury of various organs. The present study evaluated the early nephroprotective effects of Tadalafil, a PDE5 inhibitor, in an experimental model of renal I\/R. Sprague-Dawley rats were divided into two groups: vehicle-treated I\/R ( n = 10), and Tadalafil (10 mg\/kg po)-treated I\/R group ( n = 11). After removal of the right kidney and collection of two baseline urine samples, the left renal artery was clamped for 45 min followed by reperfusion for 60, 120, 180, and 240 min. Functional and histological parameters of the kidneys from the various groups were determined. In the vehicle-treated I\/R group, glomerular filtration rate was significantly reduced compared with that in normal kidneys. In addition, the ischemic kidney showed remarkable cast formation, necrosis, and congestion, a consistent pattern of acute tubular necrosis. Furthermore, urinary excretion of NGAL and KIM-1, two novel biomarkers of kidney injury, substantially increased following I\/R insult. In contrast, Tadalafil treatment resulted in a significant improvement in kidney function and amelioration of the adverse histological alterations of the ischemic kidney. Noteworthy, the urinary excretion of NGAL and KIM-1 markedly decreased in the Tadalafil-treated I\/R group. These findings demonstrate that Tadalafil possesses early nephroprotective effects in rat kidneys subjected to I\/R insult. This approach may suggest a prophylactic therapy for patients with ischemic AKI.<\/jats:p>","DOI":"10.1152\/ajprenal.00649.2012","type":"journal-article","created":{"date-parts":[[2013,1,31]],"date-time":"2013-01-31T01:15:54Z","timestamp":1359594954000},"page":"F1099-F1104","source":"Crossref","is-referenced-by-count":39,"title":["Phosphodiesterase-5 inhibition attenuates early renal ischemia-reperfusion-induced acute kidney injury: assessment by quantitative measurement of urinary NGAL and KIM-1"],"prefix":"10.1152","volume":"304","author":[{"given":"Rima","family":"Sohotnik","sequence":"first","affiliation":[{"name":"Department of Nephrology and Hypertension, Carmel Medical Center, Haifa, Israel;"}]},{"given":"Omri","family":"Nativ","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, Rappaport Faculty of Medicine, Technion, Haifa, Israel;"}]},{"given":"Abeer","family":"Abbasi","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, Rappaport Faculty of Medicine, Technion, Haifa, Israel;"},{"name":"Department of Urology, Bnai Zion Hospital, Haifa, Israel;"}]},{"given":"Hoda","family":"Awad","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, Rappaport Faculty of Medicine, Technion, Haifa, Israel;"}]},{"given":"Victor","family":"Frajewicki","sequence":"additional","affiliation":[{"name":"Department of Nephrology and Hypertension, Carmel Medical Center, Haifa, Israel;"}]},{"given":"Bishara","family":"Bishara","sequence":"additional","affiliation":[{"name":"Department of Surgery, Rambam Medical Center, Haifa, Israel;"}]},{"given":"Igor","family":"Sukhotnik","sequence":"additional","affiliation":[{"name":"Department of Pediatric Surgery, Bnai Zion Hospital, Haifa, Israel;"}]},{"given":"Zaher","family":"Armaly","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Anglican Hospital, Nazareth, Israel;"}]},{"given":"Doron","family":"Aronson","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Rambam Medical Center, Haifa, Israel; and"}]},{"given":"Samuel N.","family":"Heyman","sequence":"additional","affiliation":[{"name":"Department of Medicine, Hadassah Hebrew University Hospital, Mt. Scopus, Jerusalem, Israel;"}]},{"given":"Ofer","family":"Nativ","sequence":"additional","affiliation":[{"name":"Department of Urology, Bnai Zion Hospital, Haifa, Israel;"}]},{"given":"Zaid","family":"Abassi","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, Rappaport Faculty of Medicine, Technion, Haifa, Israel;"},{"name":"Research Unit, Rambam Medical Center, Haifa, Israel"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/j.lfs.2012.02.002"},{"key":"B2","doi-asserted-by":"crossref","first-page":"965","DOI":"10.1681\/ASN.V115965","volume":"11","author":"Agarwal A","year":"2000","journal-title":"J Am Soc Nephrol"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1172\/JCI45161"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1007\/s00210-007-0183-5"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004090740"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90609.2008"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1093\/ckj\/sfs008"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1797.2010.01317.x"},{"key":"B9","first-page":"6274","volume":"19","author":"Faddegon S","year":"2012","journal-title":"Can J Urol"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1159\/000321927"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2009.347"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.7.4135"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1016\/S0167-5273(02)00189-4"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/j.jss.2007.12.752"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1097\/01.ccx.0000144939.24897.71"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(05)70238-5"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/j.tox.2008.12.017"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1590\/S0102-86502010000600006"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00077.2007"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000088027.54400.C6"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(05)74811-X"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1985.101"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00324.2002"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1016\/j.acthis.2009.02.005"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1016\/j.athoracsur.2011.07.002"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1093\/cvr\/cvp170"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/j.eururo.2004.10.002"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ijir.3901577"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1172\/JCI200422353"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ijir.3901497"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1159\/000060075"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfi177"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.pharmtox.48.113006.094615"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00649.2012","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,2,7]],"date-time":"2022-02-07T01:39:15Z","timestamp":1644197955000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00649.2012"}},"issued":{"date-parts":[[2013,4,15]]},"references-count":33,"journal-issue":{"issue":"8","published-print":{"date-parts":[[2013,4,15]]}},"alternative-id":["10.1152\/ajprenal.00649.2012"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00649.2012","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2013,4,15]]}},{"indexed":{"date-parts":[[2026,1,19]],"date-time":"2026-01-19T07:02:51Z","timestamp":1768806171806,"version":"3.49.0"},"reference-count":28,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2020,11,1]]},"abstract":"<jats:p> To investigate the mechanism of renal ischemia-reperfusion injury (IRI) via regulation of N<jats:sup>6<\/jats:sup>-methyl-adenosine (m6A) and relevant genes, IRI was induced in Sprague-Dawley rats, and urine and serum creatinine levels and tissue structure changes were observed. m6A and methyltransferase-like 3 (METTL3) protein levels were assessed via dot-blot and Western blot analyses, respectively. The hypoxia\/reoxygenation (H\/R) cell model was constructed using NRK-52E cells, and METTL3 protein levels were assessed. METTL3 was inhibited to observe its impact on NRK-52E cell apoptosis and m6A expression in H\/R processes. Methylated RNA immunoprecipitation (MeRIP) sequencing was conducted followed by MeRIP-quantitative RT-PCR and quantitative RT-PCR validation. Our results indicated that urine and serum creatinine levels increased and that renal injury and cell apoptosis were both observed in the IRI model. In additon, m6A expression increased in the IRI model, and METTL3 protein levels significantly increased in the IRI and H\/R models. When METTL3 was inhibited, m6A levels were accordingly decreased and cell apoptosis was suppressed in the H\/R in vitro model. Based on MeRIP sequencing, transcription factor activating enhancer binding protein 2\u03b1 ( tfap2a), cytochrome P-450 1B1 ( cyp1b1), and forkhead box D1 ( foxd1) were significantly differentially expressed, as was m6A, which is involved in the negative regulation of cell proliferation and kidney development. We confirmed that foxd1 mRNA and its methylation levels contributed to IRI and H\/R. <\/jats:p>","DOI":"10.1152\/ajprenal.00222.2020","type":"journal-article","created":{"date-parts":[[2020,9,21]],"date-time":"2020-09-21T10:50:42Z","timestamp":1600685442000},"page":"F839-F847","source":"Crossref","is-referenced-by-count":37,"title":["METTL3 contributes to renal ischemia-reperfusion injury by regulating Foxd1 methylation"],"prefix":"10.1152","volume":"319","author":[{"given":"Fanhang","family":"Meng","sequence":"first","affiliation":[{"name":"Department of Organ Transplantation, Zhujiang Hospital, Southern Medical University, Guangzhou, China"},{"name":"Department of Organ Transplantation, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China"}]},{"given":"Yongguang","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Organ Transplantation, Zhujiang Hospital, Southern Medical University, Guangzhou, China"}]},{"given":"Qiuyuan","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Organ Transplantation, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China"}]},{"given":"Qing","family":"Ma","sequence":"additional","affiliation":[{"name":"Department of Organ Transplantation, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China"}]},{"given":"Shijie","family":"Gu","sequence":"additional","affiliation":[{"name":"Department of Organ Transplantation, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China"}]},{"given":"Ruiwen","family":"Cui","sequence":"additional","affiliation":[{"name":"Department of Organ Transplantation, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China"}]},{"given":"Ronghua","family":"Cao","sequence":"additional","affiliation":[{"name":"Department of Organ Transplantation, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China"}]},{"given":"Ming","family":"Zhao","sequence":"additional","affiliation":[{"name":"Department of Organ Transplantation, Zhujiang Hospital, Southern Medical University, Guangzhou, China"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbamcr.2019.118553"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(11)61454-2"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1155\/2014\/431524"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1186\/s12864-016-2913-x"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.71.10.3971"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1007\/s12011-015-0515-0"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1038\/nchembio.482"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1186\/gb4143"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/j.tig.2012.11.003"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(17)31630-6"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1242\/dev.01604"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/j.jgg.2013.10.002"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1038\/nchembio.1432"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1038\/nrm3785"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1016\/j.tibs.2012.12.006"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMe1715190"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1158\/1078-0432.CCR-03-0166"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1158\/1940-6207.CAPR-13-0271"},{"key":"B19","first-page":"87","volume":"128","author":"Sirotkovi\u0107-Skerlev M","year":"2006","journal-title":"Lijec Vjesn"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.3892\/mmr.2016.5535"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1002\/dvdy.20119"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/s41590-018-0275-z"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.3892\/etm.2019.7689"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1002\/jcb.29258"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1016\/j.molcel.2012.10.015"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1097\/01.tp.0000250769.86623.a3"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1038\/s41586-018-0749-z"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1007\/s11010-013-1799-z"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00222.2020","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2020,11,3]],"date-time":"2020-11-03T18:45:03Z","timestamp":1604429103000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00222.2020"}},"issued":{"date-parts":[[2020,11,1]]},"references-count":28,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2020,11,1]]}},"alternative-id":["10.1152\/ajprenal.00222.2020"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00222.2020","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2020,11,1]]}},{"indexed":{"date-parts":[[2026,1,18]],"date-time":"2026-01-18T22:24:52Z","timestamp":1768775092677,"version":"3.49.0"},"reference-count":33,"publisher":"American Physiological Society","issue":"4","funder":[{"DOI":"10.13039\/501100002702","name":"Aalborg University","doi-asserted-by":"crossref","award":["1"],"award-info":[{"award-number":["1"]}],"id":[{"id":"10.13039\/501100002702","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2017,4,1]]},"abstract":"<jats:p>The textbook account of whole body acid-base balance in terms of endogenous acid production, renal net acid excretion, and gastrointestinal alkali absorption, which is the only comprehensive model around, has never been applied in clinical practice or been formally validated. To improve understanding of acid-base modeling, we managed to write up this conventional model as an expression solely on urine chemistry. Renal net acid excretion and endogenous acid production were already formulated in terms of urine chemistry, and we could from the literature also see gastrointestinal alkali absorption in terms of urine excretions. With a few assumptions it was possible to see that this expression of net acid balance was arithmetically identical to minus urine charge, whereby under the development of acidosis, urine was predicted to acquire a net negative charge. The literature already mentions unexplained negative urine charges so we scrutinized a series of seminal papers and confirmed empirically the theoretical prediction that observed urine charge did acquire negative charge as acidosis developed. Hence, we can conclude that the conventional model is problematic since it predicts what is physiologically impossible. Therefore, we need a new model for whole body acid-base balance, which does not have impossible implications. Furthermore, new experimental studies are needed to account for charge imbalance in urine under development of acidosis.<\/jats:p>","DOI":"10.1152\/ajprenal.00560.2016","type":"journal-article","created":{"date-parts":[[2016,12,29]],"date-time":"2016-12-29T02:10:17Z","timestamp":1482977417000},"page":"F647-F653","source":"Crossref","is-referenced-by-count":11,"title":["Whole body acid-base modeling revisited"],"prefix":"10.1152","volume":"312","author":[{"given":"Troels","family":"Ring","sequence":"first","affiliation":[{"name":"Department of Nephrology, Aalborg University Hospital, Aalborg, Denmark; and"},{"name":"Department of Health and Science Technology, Faculty of Medicine, Aalborg University, Aalborg, Denmark"}]},{"given":"S\u00f8ren","family":"Nielsen","sequence":"additional","affiliation":[{"name":"Department of Health and Science Technology, Faculty of Medicine, Aalborg University, Aalborg, Denmark"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2016.04.023"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/B978-0-12-381462-3.00052-5"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1172\/JCI105371"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.334"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00154.2015"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/B978-1-4160-6193-9.10016-8"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-014-1669-x"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1172\/JCI105163"},{"key":"B9","doi-asserted-by":"crossref","first-page":"403","DOI":"10.1016\/S0021-9258(18)91456-0","volume":"9","author":"Henderson LJ","year":"1911","journal-title":"J Biol Chem"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1021\/ed067p501"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1610954113"},{"key":"B12","doi-asserted-by":"crossref","first-page":"349","DOI":"10.1016\/S0065-3101(22)00697-1","volume":"25","author":"Kildeberg P","year":"1978","journal-title":"Adv Pediatr"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.253.1.F199"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1172\/JCI104001"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1172\/JCI105164"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00115.2003"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1172\/JCI105466"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1989.280"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1159\/000186509"},{"key":"B21","first-page":"328","volume":"3","author":"Oh MS","year":"1992","journal-title":"J Am Soc Nephrol"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/B978-1-4377-0974-2.00014-2"},{"key":"B23","doi-asserted-by":"crossref","first-page":"239","DOI":"10.1152\/ajplegacy.1945.144.2.239","volume":"144","author":"Pitts RF","year":"1945","journal-title":"Am J Physiol"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1172\/JCI104353"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1172\/JCI104384"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0162872"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/0034-5687(80)90002-X"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1021\/ed071p117"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1172\/JCI104354"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/0002-9343(78)90227-9"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2015.87"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1172\/JCI105370"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.79"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1986.250.2.F181"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00560.2016","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,6,21]],"date-time":"2024-06-21T13:33:01Z","timestamp":1718976781000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00560.2016"}},"issued":{"date-parts":[[2017,4,1]]},"references-count":33,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2017,4,1]]}},"alternative-id":["10.1152\/ajprenal.00560.2016"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00560.2016","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2017,4,1]]}},{"indexed":{"date-parts":[[2026,1,6]],"date-time":"2026-01-06T13:07:16Z","timestamp":1767704836656},"reference-count":35,"publisher":"American Physiological Society","issue":"8","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2014,10,15]]},"abstract":"<jats:p>Osmotic water transport across the peritoneal membrane is applied during peritoneal dialysis to remove the excess water accumulated in patients with end-stage renal disease. The discovery of aquaporin water channels and the generation of transgenic animals have stressed the need for novel and accurate methods to unravel molecular mechanisms of water permeability in vivo. Here, we describe the use of fluorescently labeled albumin as a reliable indicator of osmotic water transport across the peritoneal membrane in a well-established mouse model of peritoneal dialysis. After detailed evaluation of intraperitoneal tracer mass kinetics, the technique was validated against direct volumetry, considered as the gold standard. The pH-insensitive dye Alexa Fluor 555-albumin was applied to quantify osmotic water transport across the mouse peritoneal membrane resulting from modulating dialysate osmolality and genetic silencing of the water channel aquaporin-1 (AQP1). Quantification of osmotic water transport using Alexa Fluor 555-albumin closely correlated with direct volumetry and with estimations based on radioiodinated (<jats:sup>125<\/jats:sup>I) serum albumin (RISA). The low intraperitoneal pressure probably accounts for the negligible disappearance of the tracer from the peritoneal cavity in this model. Taken together, these data demonstrate the appropriateness of pH-insensitive Alexa Fluor 555-albumin as a practical and reliable intraperitoneal volume tracer to quantify osmotic water transport in vivo.<\/jats:p>","DOI":"10.1152\/ajprenal.00098.2014","type":"journal-article","created":{"date-parts":[[2014,8,7]],"date-time":"2014-08-07T03:38:25Z","timestamp":1407382705000},"page":"F981-F989","source":"Crossref","is-referenced-by-count":18,"title":["Quantification of osmotic water transport in vivo using fluorescent albumin"],"prefix":"10.1152","volume":"307","author":[{"given":"Johann","family":"Morelle","sequence":"first","affiliation":[{"name":"Division and Laboratory of Nephrology, Cliniques Universitaires Saint-Luc, Universit\u00e9 Catholique de Louvain Medical School, Brussels, Belgium;"}]},{"given":"Amadou","family":"Sow","sequence":"additional","affiliation":[{"name":"Division and Laboratory of Nephrology, Cliniques Universitaires Saint-Luc, Universit\u00e9 Catholique de Louvain Medical School, Brussels, Belgium;"}]},{"given":"Didier","family":"Vertommen","sequence":"additional","affiliation":[{"name":"de Duve Institute, Universit\u00e9 Catholique de Louvain Medical School, Brussels, Belgium;"}]},{"given":"Fran\u00e7ois","family":"Jamar","sequence":"additional","affiliation":[{"name":"Department of Nuclear Medicine, Cliniques Universitaires Saint-Luc, Universit\u00e9 Catholique de Louvain Medical School, Brussels, Belgium;"}]},{"given":"Bengt","family":"Rippe","sequence":"additional","affiliation":[{"name":"Department of Nephrology, University Hospital of Lund, Lund, Sweden; and"}]},{"given":"Olivier","family":"Devuyst","sequence":"additional","affiliation":[{"name":"Division and Laboratory of Nephrology, Cliniques Universitaires Saint-Luc, Universit\u00e9 Catholique de Louvain Medical School, Brussels, Belgium;"},{"name":"Institute of Physiology, Zurich Center for Integrative Human Physiology, University of Zurich, Zurich, Switzerland"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1002\/anie.200460804"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1177\/002215540305101214"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000092146.67909.E2"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00038.2009"},{"key":"B5","first-page":"421","volume":"111","author":"De Paepe M","year":"1988","journal-title":"J Lab Clin Med"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1998.275.1.H234"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009070694"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.01068.2011"},{"key":"B9","doi-asserted-by":"crossref","first-page":"122","DOI":"10.1681\/ASN.V22122","volume":"2","author":"Flessner MF","year":"1991","journal-title":"J Am Soc Nephrol"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1983.244.1.H89"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/jappl.1994.76.1.485"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.08804.x"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.00729.2007"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2010.199588"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.8.4296"},{"key":"B16","doi-asserted-by":"crossref","first-page":"155","DOI":"10.1177\/089686088900900303","volume":"9","author":"Mactier RA","year":"1989","journal-title":"Perit Dial Int"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1159\/000170042"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00304.x"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000285"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-007-0402-4"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1177\/002215549904700910"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfl497"},{"key":"B23","doi-asserted-by":"crossref","first-page":"317","DOI":"10.1177\/089686080602600307","volume":"26","author":"Rippe B","year":"2006","journal-title":"Perit Dial Int"},{"key":"B24","doi-asserted-by":"crossref","first-page":"S32","DOI":"10.1177\/089686080902902S05","volume":"29","author":"Rippe B","year":"2009","journal-title":"Perit Dial Int"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1097\/00000539-200112000-00031"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfl368"},{"key":"B27","doi-asserted-by":"crossref","first-page":"316","DOI":"10.1177\/089686080202200304","volume":"22","author":"Van Biesen W","year":"2002","journal-title":"Perit Dial Int"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1007\/s002320001009"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1146\/annurev-med-043010-193843"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1999.276.1.C76"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2012080869"},{"key":"B32","doi-asserted-by":"crossref","first-page":"118","DOI":"10.1177\/089686089501500206","volume":"15","author":"Zakaria ER","year":"1995","journal-title":"Perit Dial Int"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1159\/000170209"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1996.270.5.H1549"},{"key":"B35","doi-asserted-by":"crossref","first-page":"497","DOI":"10.1177\/089686089801800507","volume":"18","author":"Zhu Q","year":"1998","journal-title":"Perit Dial Int"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00098.2014","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,4,13]],"date-time":"2022-04-13T21:14:39Z","timestamp":1649884479000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00098.2014"}},"issued":{"date-parts":[[2014,10,15]]},"references-count":35,"journal-issue":{"issue":"8","published-print":{"date-parts":[[2014,10,15]]}},"alternative-id":["10.1152\/ajprenal.00098.2014"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00098.2014","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2014,10,15]]}},{"indexed":{"date-parts":[[2026,1,6]],"date-time":"2026-01-06T13:18:37Z","timestamp":1767705517186},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1993,12,1]]},"abstract":"<jats:p> Endogenous adenosine, secreted locally by the kidney during tissue hypoxia, induces heterogeneous renal hemodynamic responses. We investigated the cortical and outer medullary blood flow responses to intrarenal infusions of adenosine and adenosine A1- and A2-receptor agonists in anesthetized rats. These agents were infused into the renal interstitium through chronically implanted capsules, and blood flow was measured by laser-Doppler probes. Short (1 min, 0.05 ml) intrarenal infusions of adenosine (0.5 mumol) lowered cortical blood flow to 27 +\/- 10% of baseline (n = 7, P &lt; 0.0005). Medullary blood flow response was biphasic, i.e., a transient decrease in flow to 52 +\/- 8% of baseline (n = 17, P &lt; 0.0001) followed by a more-sustained increase in flow to 135 +\/- 6% (n = 17, P &lt; 0.0001). N6-cyclopentyladenosine, an adenosine receptor A1 agonist, reduced both cortical and medullary blood flow to 59 +\/- 4% (n = 10, P &lt; 0.0001) and 38 +\/- 5% (n = 11, P &lt; 0.0001) of baseline, respectively. By contrast, 2-[p- (carboxyethyl)phenethylamino]-5'-N-ethycarboxamidoadenosine (CGS-21680C), an adenosine receptor A2 agonist, increased dramatically the medullary blood flow to 184 +\/- 15% of baseline (n = 12, P &lt; 0.0005), without major changes in cortical flow. We conclude that intrarenal adenosine reduces cortical blood flow and predominantly increases medullary flow via A1 and A2 receptors, respectively. These hemodynamic responses could play a role in protection of the outer medulla from hypoxia. <\/jats:p>","DOI":"10.1152\/ajprenal.1993.265.6.f802","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T06:20:49Z","timestamp":1514010049000},"page":"F802-F806","source":"Crossref","is-referenced-by-count":24,"title":["Disparate effects of adenosine A1- and A2-receptor agonists on intrarenal blood flow"],"prefix":"10.1152","volume":"265","author":[{"given":"Y.","family":"Agmon","sequence":"first","affiliation":[{"name":"Department of Medicine, Hadassah University Hospital, Jerusalem,Israel."}]},{"given":"D.","family":"Dinour","sequence":"additional","affiliation":[{"name":"Department of Medicine, Hadassah University Hospital, Jerusalem,Israel."}]},{"given":"M.","family":"Brezis","sequence":"additional","affiliation":[{"name":"Department of Medicine, Hadassah University Hospital, Jerusalem,Israel."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1993.265.6.F802","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:34:29Z","timestamp":1567960469000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1993.265.6.F802"}},"issued":{"date-parts":[[1993,12,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1993,12,1]]}},"alternative-id":["10.1152\/ajprenal.1993.265.6.F802"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1993.265.6.f802","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1993,12,1]]}},{"indexed":{"date-parts":[[2026,1,23]],"date-time":"2026-01-23T21:27:41Z","timestamp":1769203661571,"version":"3.49.0"},"reference-count":16,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2002,7,1]]},"abstract":"<jats:p> Recent evidence suggested that Na can be stored in an osmotically inactive form. We investigated whether osmotically inactive Na storage is reduced in a rat model of salt-sensitive (SS) hypertension. SS and salt-resistant (SR) Dahl-Rapp rats as well as Sprague-Dawley (SD) rats were fed a high (8%)- or low (0.1%)-NaCl diet for 4 wk ( n = 10\/group). Mean arterial pressure (MAP) was measured at the end of the experiment. Wet and dry weights, water content, total body Na (TBS), and bone Na content were measured by dessication and dry ashing. MAP was higher in both Dahl strains than in SD rats. In SS rats, 8% NaCl led to Na accumulation, water retention, and hypertension due to impaired renal Na excretion. There was no dietary-induced Na retention in SR and SD rats. TBS was variable; nevertheless, TBS was significantly correlated with body water and MAP in all strains. However, the extent of Na-associated volume and MAP increases was strain specific. Osmotically inactive Na in SD rats was threefold higher than in SS and SR rats. Both SS and SR Dahl rat strains displayed reduced osmotically inactive Na storage capacity compared with SD controls. A predisposition to fluid accumulation and high blood pressure results from this alteration. Additional factors, including impaired renal Na excretion, probably contribute to hypertension in SS rats. Our results draw attention to the role of osmotically inactive Na storage. <\/jats:p>","DOI":"10.1152\/ajprenal.00323.2001","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T15:32:35Z","timestamp":1425396755000},"page":"F134-F141","source":"Crossref","is-referenced-by-count":112,"title":["Reduced osmotically inactive Na storage capacity  and hypertension in the Dahl model"],"prefix":"10.1152","volume":"283","author":[{"given":"Jens","family":"Titze","sequence":"first","affiliation":[{"name":"Department of Nephrology, Friedrich-Alexander-University Erlangen-N\u00fcrnberg, D-91054 Erlangen;"}]},{"given":"Holger","family":"Krause","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Friedrich-Alexander-University Erlangen-N\u00fcrnberg, D-91054 Erlangen;"}]},{"given":"Hermann","family":"Hecht","sequence":"additional","affiliation":[{"name":"Department of Chemistry and Physics, Federal Center for Meat Research, D-95326 Kulmbach; and Departments of"}]},{"given":"Peter","family":"Dietsch","sequence":"additional","affiliation":[{"name":"Biochemistry and"}]},{"given":"J\u00f6rn","family":"Rittweger","sequence":"additional","affiliation":[{"name":"Physiology, Free University of Berlin, D-14195 Berlin, Germany"}]},{"given":"Rainer","family":"Lang","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Friedrich-Alexander-University Erlangen-N\u00fcrnberg, D-91054 Erlangen;"}]},{"given":"Karl A.","family":"Kirsch","sequence":"additional","affiliation":[{"name":"Physiology, Free University of Berlin, D-14195 Berlin, Germany"}]},{"given":"Karl F.","family":"Hilgers","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Friedrich-Alexander-University Erlangen-N\u00fcrnberg, D-91054 Erlangen;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.3181\/00379727-123-31473"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.3181\/00379727-125-32135"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1172\/JCI102959"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1172\/JCI103168"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.40.4.94"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(69)91554-2"},{"key":"B7","first-page":"377","volume":"44","author":"Dobesova Z","year":"1995","journal-title":"Physiol Res"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.4.F585"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/jappl.1972.33.5.688"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.15.4.436"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1999.277.5.R1392"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.2000.80.1.135"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.3181\/00379727-122-31298"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1988.120"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-199715080-00008"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1046\/j.1440-1681.2000.03250.x"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00323.2001","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:09:56Z","timestamp":1567966196000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00323.2001"}},"issued":{"date-parts":[[2002,7,1]]},"references-count":16,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2002,7,1]]}},"alternative-id":["10.1152\/ajprenal.00323.2001"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00323.2001","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2002,7,1]]}},{"indexed":{"date-parts":[[2026,3,5]],"date-time":"2026-03-05T02:17:52Z","timestamp":1772677072367,"version":"3.50.1"},"reference-count":66,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2011,4]]},"abstract":"<jats:p>Podocytes are considered terminally differentiated cells in the mature kidney under normal conditions. In the face of injury, podocytes may proceed along several possible pathways, including dedifferentiation and proliferation, persistent cell cycle arrest, hypertrophy, apoptosis, or necrosis. There is mounting evidence that transdifferentiation into a dysregulated phenotype may also be a potential cell fate. We have previously reported that the transcript of SM22\u03b1, an actin-binding protein considered one of the earliest markers of smooth muscle differentiation, is upregulated nearly 70-fold in glomeruli of rats with passive Heymann nephritis (PHN). In contrast, the SM22\u03b1 transcript is absent in normal adult rat glomeruli. The purpose of this study was to define SM22\u03b1's expression during kidney development and its role in glomerular diseases characterized by podocyte injury and proteinuria. During glomerulogenesis and podocyte differentiation, SM22\u03b1 was expressed in glomeruli. This expression disappeared with glomerular maturation. Along with SM22\u03b1 induction in PHN, confirmed at both mRNA and protein levels, SM22\u03b1 was also induced across a broad range of proteinuric diseases, including experimental animal models (puromycin aminonucleoside nephropathy, adriamycin nephropathy, passive nephrotoxic nephritis, and diet-induced obesity) and human diseases (collapsing glomerulopathy, diabetic nephropathy, classic focal segmental glomerulosclerosis, IgA nephropathy, minimal-change disease, membranous nephropathy, and membranoproliferative glomerulonephritis). Crescentic glomerulonephritis was induced in SM22\u03b1 +\/+ and SM22\u03b1 \u2212\/\u2212 mice by intraperitoneal injection of sheep anti-rabbit glomeruli antibody 12.5 mg\/20 g body wt \u00d7 2 doses ( n = 12\u201315\/group), with mice euthanized at 7 and 14 days. Compared with SM22\u03b1 \u2212\/\u2212 mice, SM22\u03b1 +\/+ mice demonstrated worse disease by histopathological parameters. In addition, there was greater apoptosis (cleaved caspase-3 immunostaining), fewer podocytes (Wilms' tumor-1 immunostaining), and less proliferation (Ki-67 immunostaining) in diseased SM22\u03b1 +\/+ mice. Furthermore, there was decreased activation of Erk1\/2 in diseased SM22\u03b1 +\/+ mice. We conclude that the de novo expression of SM22\u03b1 in glomerular epithelial cells affects the course of crescentic glomerulonephritis.<\/jats:p>","DOI":"10.1152\/ajprenal.00187.2010","type":"journal-article","created":{"date-parts":[[2011,2,3]],"date-time":"2011-02-03T04:49:24Z","timestamp":1296708564000},"page":"F1026-F1042","source":"Crossref","is-referenced-by-count":30,"title":["Role of smooth muscle protein SM22\u03b1 in glomerular epithelial cell injury"],"prefix":"10.1152","volume":"300","author":[{"given":"Caroline B.","family":"Marshall","sequence":"first","affiliation":[{"name":"Divisions of 1Nephrology and"}]},{"given":"Ron D.","family":"Krofft","sequence":"additional","affiliation":[{"name":"Divisions of 1Nephrology and"}]},{"given":"Mary J.","family":"Blonski","sequence":"additional","affiliation":[{"name":"Divisions of 1Nephrology and"}]},{"given":"Jolanta","family":"Kowalewska","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Washington, Seattle, Washington; and"}]},{"given":"Christine M.","family":"Logar","sequence":"additional","affiliation":[{"name":"Divisions of 1Nephrology and"}]},{"given":"Jeffrey W.","family":"Pippin","sequence":"additional","affiliation":[{"name":"Divisions of 1Nephrology and"}]},{"given":"Francis","family":"Kim","sequence":"additional","affiliation":[{"name":"Cardiology, Department of Medicine, and"}]},{"given":"Robert","family":"Feil","sequence":"additional","affiliation":[{"name":"Interfakult\u00e4res Institut f\u00fcr Biochemie, Universtit\u00e4t T\u00fcbingen, T\u00fcbingen, Germany"}]},{"given":"Charles E.","family":"Alpers","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Washington, Seattle, Washington; and"}]},{"given":"Stuart J.","family":"Shankland","sequence":"additional","affiliation":[{"name":"Divisions of 1Nephrology and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M006323200"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008070795"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1172\/JCI200523371"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/j.biocel.2008.02.011"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000067651.34743.B0"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000033611.79556.AE"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1172\/JCI37978"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/gkg224"},{"key":"B9","first-page":"223","volume":"138","author":"Coimbra T","year":"1991","journal-title":"Am J Pathol"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.122.1.103"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1161\/ATVBAHA.109.200501"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/S0891-5849(99)00249-X"},{"key":"B13","doi-asserted-by":"crossref","first-page":"413","DOI":"10.1681\/ASN.V123413","volume":"12","author":"Endlich N","year":"2001","journal-title":"J Am Soc Nephrol"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000126417.38728.F6"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1042\/BJ20080320"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/jappl.2000.89.5.1985"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1159\/000064469"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.e02-11-0743"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1006\/excr.1998.3948"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1038\/nrm1682"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/j.lfs.2008.11.017"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1159\/000213505"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.16.10948"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.141.3.805"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1177\/002215540305101203"},{"key":"B26","doi-asserted-by":"crossref","first-page":"175","DOI":"10.1016\/S1016-8478(23)07371-5","volume":"23","author":"Je HD","year":"2007","journal-title":"Mol Cells"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1038\/73456"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.106.142851"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1172\/JCI17988"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1002\/1526-968X(200009)28:1<15::AID-GENE20>3.0.CO;2-C"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1097-0169(1997)38:3<250::AID-CM3>3.0.CO;2-9"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2008.070057"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008121226"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.102.17.2124"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00216.2009"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5001965"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.4161\/cc.8.8.8147"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1210414"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1007\/s001250051447"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfp338"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1159\/000090619"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.139.1.193"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M602703200"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/14.12.2860"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1159\/000103020"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2009.386"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119163"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00020.2002"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90421.2008"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000190604.90049.71"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00205.x"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1021\/pr900705r"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008070709"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006010089"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00559.2007"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1126\/science.1145209"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)81112-5"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.121.5.1065"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M110086200"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-291X(05)81449-4"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1016\/j.mad.2004.09.023"},{"key":"B62","first-page":"372","volume":"144","author":"Verbeek MM","year":"1994","journal-title":"Am J Pathol"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005010055"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1042\/bj20030796"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1210\/me.2006-0104"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.2001.21.4.1336-1344.2001"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00187.2010","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,4,3]],"date-time":"2024-04-03T20:06:20Z","timestamp":1712174780000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00187.2010"}},"issued":{"date-parts":[[2011,4]]},"references-count":66,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2011,4]]}},"alternative-id":["10.1152\/ajprenal.00187.2010"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00187.2010","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2011,4]]}},{"indexed":{"date-parts":[[2026,3,5]],"date-time":"2026-03-05T03:22:49Z","timestamp":1772680969225,"version":"3.50.1"},"reference-count":81,"publisher":"American Physiological Society","issue":"2","funder":[{"name":"NIH","award":["P30 AG013280"],"award-info":[{"award-number":["P30 AG013280"]}]},{"name":"NIH","award":["RO1 HL101186"],"award-info":[{"award-number":["RO1 HL101186"]}]},{"name":"NIH","award":["R24 DK094768-01"],"award-info":[{"award-number":["R24 DK094768-01"]}]},{"name":"NIH","award":["R01 DK093493-02"],"award-info":[{"award-number":["R01 DK093493-02"]}]},{"name":"NIH","award":["5 R01 DK 056799-12"],"award-info":[{"award-number":["5 R01 DK 056799-12"]}]},{"name":"NIH","award":["R01 DK097598-01A1"],"award-info":[{"award-number":["R01 DK097598-01A1"]}]},{"name":"NIH","award":["RO1 AG038550"],"award-info":[{"award-number":["RO1 AG038550"]}]},{"name":"NIH","award":["5 R01 DK 056799-10"],"award-info":[{"award-number":["5 R01 DK 056799-10"]}]},{"DOI":"10.13039\/501100001652","name":"Friedrich-Alexander-Universit\u00e4t Erlangen-N\u00fcrnberg (Friedrich Alexander University of Erlangen Nuremberg)","doi-asserted-by":"publisher","award":["EFI-CYDER"],"award-info":[{"award-number":["EFI-CYDER"]}],"id":[{"id":"10.13039\/501100001652","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2015,7,15]]},"abstract":"<jats:p> Kidney aging is accompanied by characteristic changes in the glomerulus, but little is known about the effect of aging on glomerular parietal epithelial cells (PECs), nor if the characteristic glomerular changes in humans and rats also occur in very old mice. Accordingly, a descriptive analysis was undertaken in 27-mo-old C57B6 mice, considered advanced age. PEC density was significantly lower in older mice compared with young mice (aged 3 mo), and the decrease was more pronounced in juxtamedullary glomeruli compared with outer cortical glomeruli. In addition to segmental and global glomerulosclerosis in older mice, staining for matrix proteins collagen type IV and heparan sulfate proteoglycan were markedly increased in Bowman's capsules of older mouse glomeruli, consistent with increased extracellular matrix production by PECs. De novo staining for CD44, a marker of activated and profibrotic PECs, was significantly increased in aged glomeruli. CD44 staining was more pronounced in the juxtamedullary region and colocalized with phosphorylated ERK. Additionally, a subset of aged PECs de novo expressed the epithelial-to-mesenchymal transition markers \u03b1-smooth muscle and vimentin, with no changes in epithelial-to-mesenchymal transition markers E-cadherin and \u03b2-catenin. The mural cell markers neural\/glial antigen 2, PDGF receptor-\u03b2, and CD146 as well as Notch 3 were also substantially increased in aged PECs. These data show that mice can be used to better understand the aging kidney and that PECs undergo substantial changes, especially in juxtamedullary glomeruli, that may participate in the overall decline in glomerular structure and function with advancing age. <\/jats:p>","DOI":"10.1152\/ajprenal.00144.2015","type":"journal-article","created":{"date-parts":[[2015,5,28]],"date-time":"2015-05-28T08:54:22Z","timestamp":1432803262000},"page":"F164-F178","source":"Crossref","is-referenced-by-count":52,"title":["Changes in glomerular parietal epithelial cells in mouse kidneys with advanced age"],"prefix":"10.1152","volume":"309","author":[{"given":"Sebastian S.","family":"Roeder","sequence":"first","affiliation":[{"name":"Division of Nephrology, University of Washington, Seattle, Washington;"},{"name":"Friedrich-Alexander-Universit\u00e4t Erlangen-N\u00fcrnberg (FAU), Erlangen, Germany"}]},{"given":"Ania","family":"Stefanska","sequence":"additional","affiliation":[{"name":"Division of Nephrology, University of Washington, Seattle, Washington;"}]},{"given":"Diana G.","family":"Eng","sequence":"additional","affiliation":[{"name":"Division of Nephrology, University of Washington, Seattle, Washington;"}]},{"given":"Natalya","family":"Kaverina","sequence":"additional","affiliation":[{"name":"Division of Nephrology, University of Washington, Seattle, Washington;"}]},{"given":"Maria W.","family":"Sunseri","sequence":"additional","affiliation":[{"name":"Division of Nephrology, University of Washington, Seattle, Washington;"}]},{"given":"Bairbre A.","family":"McNicholas","sequence":"additional","affiliation":[{"name":"Division of Nephrology, University of Washington, Seattle, Washington;"}]},{"given":"Peter","family":"Rabinovitch","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Washington, Seattle, Washington;"}]},{"given":"Felix B.","family":"Engel","sequence":"additional","affiliation":[{"name":"Department of Nephropathology, Friedrich-Alexander-Universit\u00e4t Erlangen-N\u00fcrnberg (FAU), Erlangen, Germany; and"}]},{"given":"Christoph","family":"Daniel","sequence":"additional","affiliation":[{"name":"Department of Nephropathology, Friedrich-Alexander-Universit\u00e4t Erlangen-N\u00fcrnberg (FAU), Erlangen, Germany; and"}]},{"given":"Kerstin","family":"Amann","sequence":"additional","affiliation":[{"name":"Department of Nephropathology, Friedrich-Alexander-Universit\u00e4t Erlangen-N\u00fcrnberg (FAU), Erlangen, Germany; and"}]},{"given":"Julia","family":"Lichtnekert","sequence":"additional","affiliation":[{"name":"Division of Nephrology, University of Washington, Seattle, Washington;"}]},{"given":"Jeffrey W.","family":"Pippin","sequence":"additional","affiliation":[{"name":"Division of Nephrology, University of Washington, Seattle, Washington;"}]},{"given":"Stuart J.","family":"Shankland","sequence":"additional","affiliation":[{"name":"Division of Nephrology, University of Washington, Seattle, Washington;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfn235"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/0002-9343(86)90718-7"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.267.1.F35"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfg231"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/j.semcdb.2008.02.001"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-013-2686-2"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/j.ajpath.2011.04.003"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1016\/j.arr.2014.02.003"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-61779-815-3_22"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00449.2014"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.05263-11"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfr483"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2011.208"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1053\/ajkd.2003.50007"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1001\/jama.298.17.2038"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1159\/000083890"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1002\/path.4076"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2010.338"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.10571011"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.163"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.28"},{"key":"B22","volume-title":"The Mouse in Biomedical Research: Normative Biology, Husbandry, and Models","author":"Flurkey K","year":"2006"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1186\/1755-1536-4-11"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2012.65"},{"key":"B25","author":"Harrison DE","year":"2015","journal-title":"The Jackson Laboratories. Baseline Life Span Data: Commonly Used JAX Mice and Crosses (Study 1)"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1038\/labinvest.2014.160"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.63.s83.8.x"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.4161\/auto.19821"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1172\/JCI200320530"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2014.06.004"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-146-3-200702060-00006"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2014.218"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2011.300"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1111\/j.1532-5415.1985.tb07117.x"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1002\/path.2111"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00785.x"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1017\/S0952523800005198"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1159\/000328010"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1111\/j.1474-9726.2006.00185.x"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1186\/1471-2369-15-174"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.130.5.1219"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.14670\/HH-11-623"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1002\/ar.1092320205"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2009.386"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00428.2009"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1159\/000357356"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00699.2013"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014070641"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00430.x"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0b013e328362485e"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1038\/4499994"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1159\/000313943"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008070709"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-152-9-201005040-00006"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2003.09.026"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1111\/acel.12008"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2014.1"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002039"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010090970"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1016\/j.ajpath.2014.08.007"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1101\/gad.8.16.1888"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1016\/B978-0-12-391498-9.00008-5"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1100\/2012\/845046"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2013.66"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1111\/j.1582-4934.2009.00937.x"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00614.2011"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.266.6.F942"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.1016\/j.mvr.2012.03.008"},{"key":"B69","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.5.F839"},{"key":"B70","doi-asserted-by":"publisher","DOI":"10.1093\/gerona\/54.11.B492"},{"key":"B71","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2013.48"},{"key":"B72","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013050452"},{"key":"B73","doi-asserted-by":"publisher","DOI":"10.1053\/j.ackd.2010.05.002"},{"key":"B74","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005010055"},{"key":"B75","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2009.07.012"},{"key":"B76","doi-asserted-by":"publisher","DOI":"10.1093\/gerona\/gls157"},{"key":"B77","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005050488"},{"key":"B78","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005111239"},{"key":"B79","doi-asserted-by":"publisher","DOI":"10.1172\/JCI36183"},{"key":"B80","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00516.2011"},{"key":"B81","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00020.2013"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00144.2015","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T21:10:39Z","timestamp":1567977039000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00144.2015"}},"issued":{"date-parts":[[2015,7,15]]},"references-count":81,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2015,7,15]]}},"alternative-id":["10.1152\/ajprenal.00144.2015"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00144.2015","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2015,7,15]]}},{"indexed":{"date-parts":[[2026,3,5]],"date-time":"2026-03-05T03:22:25Z","timestamp":1772680945446,"version":"3.50.1"},"reference-count":126,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2008,11]]},"abstract":"<jats:p>The kidney is faced with unique challenges for oxygen regulation, both because its function requires that perfusion greatly exceeds that required to meet metabolic demand and because vascular control in the kidney is dominated by mechanisms that regulate glomerular filtration and tubular reabsorption. Because tubular sodium reabsorption accounts for most oxygen consumption (V\u0307o<jats:sub>2<\/jats:sub>) in the kidney, renal V\u0307o<jats:sub>2<\/jats:sub>varies with glomerular filtration rate. This provides an intrinsic mechanism to match changes in oxygen delivery due to changes in renal blood flow (RBF) with changes in oxygen demand. Renal V\u0307o<jats:sub>2<\/jats:sub>is low relative to supply of oxygen, but diffusional arterial-to-venous (AV) oxygen shunting provides a mechanism by which oxygen superfluous to metabolic demand can bypass the renal microcirculation. This mechanism prevents development of tissue hyperoxia and subsequent tissue oxidation that would otherwise result from the mismatch between renal V\u0307o<jats:sub>2<\/jats:sub>and RBF. Recent evidence suggests that RBF-dependent changes in AV oxygen shunting may also help maintain stable tissue oxygen tension when RBF changes within the physiological range. However, AV oxygen shunting also renders the kidney susceptible to hypoxia. Given that tissue hypoxia is a hallmark of both acute renal injury and chronic renal disease, understanding the causes of tissue hypoxia is of great clinical importance. The simplistic paradigm of oxygenation depending only on the balance between local perfusion and V\u0307o<jats:sub>2<\/jats:sub>is inadequate to achieve this goal. To fully understand the control of renal oxygenation, we must consider a triad of factors that regulate intrarenal oxygenation: local perfusion, local V\u0307o<jats:sub>2<\/jats:sub>, and AV oxygen shunting.<\/jats:p>","DOI":"10.1152\/ajprenal.90230.2008","type":"journal-article","created":{"date-parts":[[2008,6,13]],"date-time":"2008-06-13T01:03:25Z","timestamp":1213319005000},"page":"F1259-F1270","source":"Crossref","is-referenced-by-count":239,"title":["Intrarenal oxygenation: unique challenges and the biophysical basis of homeostasis"],"prefix":"10.1152","volume":"295","author":[{"given":"Roger G.","family":"Evans","sequence":"first","affiliation":[]},{"given":"Bruce S.","family":"Gardiner","sequence":"additional","affiliation":[]},{"given":"David W.","family":"Smith","sequence":"additional","affiliation":[]},{"given":"Paul M.","family":"O'Connor","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.253.3.F440"},{"key":"R2","unstructured":"Bagshaw SM, Delaney A, Haase M, Ghali WA, Bellomo R.Loop diuretics in the management of acute renal failure: a systematic review meta-analysis.Crit Care Resusc9: 60\u201368, 2007."},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1980.238.1.F50"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002312"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00169.2002"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1016\/0026-2862(72)90036-2"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2002.025270"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200401000-00010"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000079785.13922.F6"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115316"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.267.6.F1063"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199503093321006"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00665.2000"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1007\/s10439-006-9236-z"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00115.2005"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1979.236.5.F423"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00224.2002"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1113\/expphysiol.2003.026740"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00926.2007"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00222.2006"},{"key":"R21","doi-asserted-by":"crossref","unstructured":"Dole VP, Emerson KJ, Phillips RA, Hamilton P, Van Slyke DD.The renal extraction of oxygen in experimental shock.Am J Physiol145: 261\u2013269 1946.","DOI":"10.1152\/ajplegacy.1946.145.3.337"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-4419-8997-0_6"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.2001.00927.x"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1989.261"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1097\/01.hjh.0000133744.85490.9d"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200501000-00003"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.2005.04202.x"},{"key":"R28","doi-asserted-by":"crossref","unstructured":"Fine LG, Bandyopadhay D, Norman JT.Is there a common mechanism for the progression of different types of renal diseases other than proteinuria? Towards the unifying theme of chronic hypoxia.Kidney Int Suppl75: S22\u2013S26, 2000.","DOI":"10.1046\/j.1523-1755.57.s75.12.x"},{"key":"R29","unstructured":"Fine LG, Orphanides C, Norman JT.Progressive renal disease: the chronic hypoxia hypothesis.Kidney Int Suppl65: S74\u2013S78, 1998."},{"key":"R30","doi-asserted-by":"crossref","unstructured":"Flemming B, Seeliger E, Wronski T, Steer K, Arenz N, Persson PB.Oxygen and renal hemodynamics in the conscious rat.J Am Soc Nephrol11: 18\u201324, 2000.","DOI":"10.1681\/ASN.V11118"},{"key":"R31","unstructured":"Fourman J, Moffat DB.The Blood Vessels of the Kidney. Oxford, UK: Blackwell Scientific, 1971."},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1007\/BF00315846"},{"key":"R33","doi-asserted-by":"crossref","unstructured":"Freeman BA, Crapo JD.Hyperoxia increases oxygen radical production in rat lungs and lung mitochondria.J Biol Chem256: 10986\u201310992, 1981.","DOI":"10.1016\/S0021-9258(19)68544-3"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1993.264.2.R428"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00077.2007"},{"key":"R36","unstructured":"Gullans SR, Hebert SC.Metabolic basis of ion transport. In:Brenner and Rector's The Kidney(5th ed.), edited by Brenner BM. Philadelphia, PA: WB Saunders, 1996, p. 211\u2013246."},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1097\/01.CCM.0000171531.06133.B0"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.00100106"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1159\/000170341"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfh570"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000418"},{"key":"R42","doi-asserted-by":"crossref","unstructured":"Hoy WE, Kondalsamy-Chennakesavan S, Scheppingen J, Sharma S, Katz I.A chronic disease outreach program for Aboriginal communities.Kidney Int Suppl: S76\u2013S82, 2005.","DOI":"10.1111\/j.1523-1755.2005.09814.x"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1109\/JPROC.2006.871767"},{"key":"R44","doi-asserted-by":"crossref","unstructured":"Hwang S, Bohman R, Navas P, Norman JT, Bradley T, Fine LG.Hypertrophy of renal mitochondria.J Am Soc Nephrol1: 822\u2013827, 1990.","DOI":"10.1681\/ASN.V15822"},{"key":"R45","doi-asserted-by":"crossref","unstructured":"Ji Y, Liu J.Vasculature based model for characterizing oxygen transport in skin tissues\u2013analogy to the Weinbaum-Jiji bioheat equation.Heat Mass Trans40: 627\u2013637, 2004.","DOI":"10.1007\/s00231-003-0443-y"},{"key":"R46","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.00385.2005"},{"key":"R47","doi-asserted-by":"crossref","unstructured":"Kang DH, Hughes J, Mazzali M, Schreiner GF, Johnson RJ.Impaired angiogenesis in the remnant kidney model. II. Vascular endothelial growth factor administration reduces renal fibrosis and stabilizes renal function.J Am Soc Nephrol12: 1448\u20131457, 2001.","DOI":"10.1681\/ASN.V1271448"},{"key":"R48","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000034910.58454.FD"},{"key":"R49","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000013783.63773.8F"},{"key":"R50","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00474.x"},{"key":"R51","doi-asserted-by":"publisher","DOI":"10.1016\/S0730-725X(02)00534-9"},{"key":"R52","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1939.sp003759"},{"key":"R53","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1961.tb02147.x"},{"key":"R54","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.2001.280.1.R62"},{"key":"R55","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.00348.2006"},{"key":"R56","doi-asserted-by":"publisher","DOI":"10.1159\/000114203"},{"key":"R57","doi-asserted-by":"crossref","unstructured":"Levy MN.Effect of variations of blood flow on renal oxygen extraction.Am J Physiol199: 13\u201318, 1960.","DOI":"10.1152\/ajplegacy.1960.199.1.13"},{"key":"R58","doi-asserted-by":"crossref","unstructured":"Levy MN.Influence of variations in blood flow and of dinitrophenol on renal oxygen consumption.Am J Physiol196: 937\u2013942, 1959.","DOI":"10.1152\/ajplegacy.1959.196.4.937"},{"key":"R59","doi-asserted-by":"crossref","unstructured":"Levy MN, Imperial ES.Oxygen shunting in renal cortical and medullary capillaries.Am J Physiol200: 159\u2013162, 1961.","DOI":"10.1152\/ajplegacy.1961.200.1.159"},{"key":"R60","doi-asserted-by":"crossref","unstructured":"Levy MN, Sauceda G.Diffusion of oxygen from arterial to venous segments of renal capillaires.Am J Physiol196: 1336\u20131339, 1959.","DOI":"10.1152\/ajplegacy.1959.196.6.1336"},{"key":"R61","doi-asserted-by":"crossref","unstructured":"Levy SE, Blalock A.The effects of unilateral nephrectomy on the renal blood flow and oxygen consumption of unanesthetized dogs.Am J Physiol122: 609\u2013613, 1938.","DOI":"10.1152\/ajplegacy.1938.122.3.609"},{"key":"R62","doi-asserted-by":"crossref","unstructured":"Levy SE, Light RA, Blalock A.The blood flow and oxygen consumption of the kidney in experimental hypertension.Am J Physiol122: 38\u201342, 1938.","DOI":"10.1152\/ajplegacy.1938.122.1.38"},{"key":"R63","doi-asserted-by":"publisher","DOI":"10.1002\/jmri.20260"},{"key":"R64","doi-asserted-by":"crossref","unstructured":"Li N, Yi F, Spurrier JL, Bobrowitz CA, Zou AP.Production of superoxide through NADH oxidase in thick ascending limb of Henle's loop in rat kidney.Am J Physiol Renal Physiol282: F1111\u2013F1119, 2002.","DOI":"10.1152\/ajprenal.00218.2001"},{"key":"R65","unstructured":"Liss P.Effects of contrast media on renal microcirculation and oxygen tension.Anexperimental study in the rat.Acta Radiol Suppl409: 1\u201329, 1997."},{"key":"R66","doi-asserted-by":"publisher","DOI":"10.1258\/rsmacta.44.1.111"},{"key":"R67","doi-asserted-by":"publisher","DOI":"10.1007\/s004240050455"},{"key":"R68","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.33.4.1013"},{"key":"R69","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.49"},{"key":"R70","unstructured":"Maddox DA, Brenner BM.Glomerular ultrafiltration. In:Brenner & Rector's The Kidney(5th ed.), edited by Brenner BM. Philadelphia, PA: W.B. Saunders, 1996, p. 286\u2013333."},{"key":"R71","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00461.x"},{"key":"R72","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000125614.35046.10"},{"key":"R73","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000128047.13396.48"},{"key":"R74","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00321.2002"},{"key":"R75","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000092792.97122.E0"},{"key":"R76","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000079042.13465.1A"},{"key":"R77","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2006.06.001"},{"key":"R78","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1996.76.2.425"},{"key":"R79","unstructured":"Nelimarkka O.Renal oxygen and lactate metabolism in hemorrhagic shock.Anexperimental study.Acta Chir Scand Suppl518: 1\u201344, 1984."},{"key":"R80","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00814.2005"},{"key":"R81","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.2006.04476.x"},{"key":"R82","doi-asserted-by":"publisher","DOI":"10.1159\/000071289"},{"key":"R83","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.2006.04475.x"},{"key":"R84","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.2006.04391.x"},{"key":"R85","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00275.2005"},{"key":"R86","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00334.2001"},{"key":"R87","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2728(74)90176-5"},{"key":"R88","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1990.70.3.885"},{"key":"R89","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.2006.04473.x"},{"key":"R90","doi-asserted-by":"publisher","DOI":"10.1007\/s00125-003-1155-z"},{"key":"R91","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.107.097832"},{"key":"R92","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00166.2007"},{"key":"R93","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00540.2006"},{"key":"R94","doi-asserted-by":"publisher","DOI":"10.3109\/10739689509146755"},{"key":"R95","doi-asserted-by":"publisher","DOI":"10.1080\/10739680590895064"},{"key":"R96","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006080895"},{"key":"R97","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00140.x"},{"key":"R98","doi-asserted-by":"publisher","DOI":"10.1007\/BF00584854"},{"key":"R99","doi-asserted-by":"publisher","DOI":"10.3109\/08860229209106636"},{"key":"R100","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00159.x"},{"key":"R101","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.2006.04472.x"},{"key":"R102","unstructured":"Schieppati A, Remuzzi G.Chronic renal diseases as a public health problem: epidemiology, social, and economic implications.Kidney Int Suppl: S7\u2013S10, 2005."},{"key":"R103","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.259.6.F910"},{"key":"R104","doi-asserted-by":"crossref","unstructured":"Sharan M, Popel AS.A mathematical model of countercurrent exchange of oxygen between paired arterioles and venules.Math Biosci90: 17\u201334, 1988.","DOI":"10.1016\/0025-5564(88)90022-3"},{"key":"R105","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00830.2004"},{"key":"R106","doi-asserted-by":"publisher","DOI":"10.1191\/0267659105pf780oa"},{"key":"R107","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1993.265.2.H537"},{"key":"R108","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.2006.04474.x"},{"key":"R109","doi-asserted-by":"publisher","DOI":"10.1093\/gerona\/61.8.795"},{"key":"R110","doi-asserted-by":"publisher","DOI":"10.1007\/s11538-006-9102-z"},{"key":"R111","unstructured":"Thomas SE, Anderson S, Gordon KL, Oyama TT, Shankland SJ, Johnson RJ.Tubulointerstitial disease in aging: evidence for underlying peritubular capillary damage, a potential role for renal ischemia.J Am Soc Nephrol9: 231\u2013242, 1998."},{"key":"R112","doi-asserted-by":"publisher","DOI":"10.1109\/JPROC.2006.871770"},{"key":"R113","doi-asserted-by":"crossref","unstructured":"Torelli G, Milla E, Faelli A, Costantini S.Energy requirement for sodium reabsorption in the in vivo rabbit kidney.Am J Physiol211: 576\u2013580, 1966.","DOI":"10.1152\/ajplegacy.1966.211.3.576"},{"key":"R114","doi-asserted-by":"publisher","DOI":"10.1097\/01.mnh.0000196147.65330.a3"},{"key":"R115","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00034.2002"},{"key":"R116","doi-asserted-by":"publisher","DOI":"10.1001\/jama.294.7.813"},{"key":"R117","doi-asserted-by":"crossref","unstructured":"Van Slyke DD, Rhoads CP, Hiller A, Alving AS.Relationships between urea excretion, renal blood flow, renal oxygen consumption, and diuresis. The mechanism of urea excretion.Am J Physiol109: 336\u2013374, 1934.","DOI":"10.1152\/ajplegacy.1934.109.2.336"},{"key":"R118","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.00182.2004"},{"key":"R119","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.2006.04478.x"},{"key":"R120","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00483.x"},{"key":"R121","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00626.2004"},{"key":"R122","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000052945.84627.8F"},{"key":"R123","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.00099.2006"},{"key":"R124","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00250.2005"},{"key":"R125","doi-asserted-by":"publisher","DOI":"10.1016\/0306-3623(90)91037-R"},{"key":"R126","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00074.2002"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.90230.2008","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,9,12]],"date-time":"2021-09-12T03:40:35Z","timestamp":1631418035000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.90230.2008"}},"issued":{"date-parts":[[2008,11]]},"references-count":126,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2008,11]]}},"alternative-id":["10.1152\/ajprenal.90230.2008"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.90230.2008","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2008,11]]}},{"indexed":{"date-parts":[[2026,3,5]],"date-time":"2026-03-05T05:22:33Z","timestamp":1772688153547,"version":"3.50.1"},"reference-count":36,"publisher":"American Physiological Society","issue":"1","funder":[{"DOI":"10.13039\/100015502","name":"Dialysis Clinics","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100015502","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100017618","name":"HHS | NIH | NIDDK | Division of Diabetes, Endocrinology, and Metabolic Diseases","doi-asserted-by":"publisher","award":["P30DK074038"],"award-info":[{"award-number":["P30DK074038"]}],"id":[{"id":"10.13039\/100017618","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000738","name":"U.S. Department of Veterans Affairs","doi-asserted-by":"publisher","award":["I01 BX000820"],"award-info":[{"award-number":["I01 BX000820"]}],"id":[{"id":"10.13039\/100000738","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000738","name":"U.S. Department of Veterans Affairs","doi-asserted-by":"publisher","award":["I01CX002391"],"award-info":[{"award-number":["I01CX002391"]}],"id":[{"id":"10.13039\/100000738","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2024,7,1]]},"abstract":"<jats:p> Mitochondria are centrally involved in acute kidney injury (AKI). Here, we show that cilia-deficient renal tubule cells both in vitro in cell culture and in vivo in mice are primed for injury with mitochondrial defects and aberrant tryptophan metabolism. These data suggest therapeutic strategies such as enhancing ciliogenesis or improving mitochondrial function to protect patients at risk for AKI. <\/jats:p>","DOI":"10.1152\/ajprenal.00225.2023","type":"journal-article","created":{"date-parts":[[2024,5,9]],"date-time":"2024-05-09T08:01:26Z","timestamp":1715241686000},"page":"F61-F76","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":4,"title":["Cilia-deficient renal tubule cells are primed for injury with mitochondrial defects and aberrant tryptophan metabolism"],"prefix":"10.1152","volume":"327","author":[{"given":"Xiaofeng","family":"Zuo","sequence":"first","affiliation":[{"name":"Department of Medicine, Medical University of South Carolina, Charleston, South Carolina, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8340-9017","authenticated-orcid":false,"given":"Brennan","family":"Winkler","sequence":"additional","affiliation":[{"name":"Department of Medicine, Medical University of South Carolina, Charleston, South Carolina, United States"}]},{"given":"Kasey","family":"Lerner","sequence":"additional","affiliation":[{"name":"Department of Medicine, Medical University of South Carolina, Charleston, South Carolina, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4832-4170","authenticated-orcid":false,"given":"Daria V.","family":"Ilatovskaya","sequence":"additional","affiliation":[{"name":"Department of Physiology, Medical College of Georgia, Augusta University, Augusta, Georgia, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9938-7203","authenticated-orcid":false,"given":"Aleksandra S.","family":"Zamaro","sequence":"additional","affiliation":[{"name":"Department of Physiology, Medical College of Georgia, Augusta University, Augusta, Georgia, United States"}]},{"given":"Yujing","family":"Dang","sequence":"additional","affiliation":[{"name":"Department of Medicine, Medical University of South Carolina, Charleston, South Carolina, United States"}]},{"given":"Yanhui","family":"Su","sequence":"additional","affiliation":[{"name":"Department of Medicine, Medical University of South Carolina, Charleston, South Carolina, United States"}]},{"given":"Peifeng","family":"Deng","sequence":"additional","affiliation":[{"name":"Department of Medicine, Medical University of South Carolina, Charleston, South Carolina, United States"}]},{"given":"Wayne","family":"Fitzgibbon","sequence":"additional","affiliation":[{"name":"Department of Medicine, Medical University of South Carolina, Charleston, South Carolina, United States"}]},{"given":"Jessica","family":"Hartman","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, South Carolina, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1617-5919","authenticated-orcid":false,"given":"Kwon Moo","family":"Park","sequence":"additional","affiliation":[{"name":"Department of Anatomy, School of Medicine, Kyungpook National University, Daegu, Republic of Korea"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7787-8503","authenticated-orcid":false,"given":"Joshua H.","family":"Lipschutz","sequence":"additional","affiliation":[{"name":"Department of Medicine, Medical University of South Carolina, Charleston, South Carolina, United States"},{"name":"Department of Medicine, Ralph H. Johnson Veterans Affairs Health Care System, Charleston, South Carolina, United States"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(80)90128-2"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/s0896-6273(00)80251-2"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pgen.1001361"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M117.795674"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.e08-07-0772"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.RA118.006527"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.151.3.709"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00596.2009"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00427.2012"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1038\/srep22281"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1038\/nature17184"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.11.12.4259"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1155\/2019\/6201764"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1186\/s12917-017-1281-3"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1126\/science.1219855"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1038\/nm.3092"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1177\/1178646917691938"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0129346"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1310653110"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1038\/s41591-018-0138-z"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/j.celrep.2019.01.041"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2018.10.022"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1177\/1178646917694600"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.3109\/13813455.2011.623705"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1038\/478192a"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00673.2020"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00672.2020"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1016\/s0074-7696(03)31002-2"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00011.2015"},{"key":"B30","first-page":"314","volume":"107","author":"Yoder BK","year":"1995","journal-title":"Proc Assoc Am Physicians"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1038\/ng.2715"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2020.05.049"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2015.01.030"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-021-84609-8"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.02560317"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1172\/jci.insight.154773"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00225.2023","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,6,20]],"date-time":"2024-06-20T17:04:56Z","timestamp":1718903096000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00225.2023"}},"issued":{"date-parts":[[2024,7,1]]},"references-count":36,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2024,7,1]]}},"alternative-id":["10.1152\/ajprenal.00225.2023"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00225.2023","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2024,7,1]]},"assertion":[{"value":"2023-08-01","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2024-04-11","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2024-04-24","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2024-06-20","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,3,5]],"date-time":"2026-03-05T05:20:36Z","timestamp":1772688036582,"version":"3.50.1"},"reference-count":50,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2014,3,15]]},"abstract":"<jats:p> Basement membrane abnormalities have often been observed in kidney cysts of polycystic kidney disease (PKD) patients and animal models. There is an abnormal deposition of extracellular matrix molecules, including laminin-\u03b1<jats:sub>3<\/jats:sub>,\u03b2<jats:sub>3<\/jats:sub>,\u03b3<jats:sub>2<\/jats:sub> (laminin-332), in human autosomal dominant PKD (ADPKD). Knockdown of PKD1 paralogs in zebrafish leads to dysregulated synthesis of the extracellular matrix, suggesting that altered basement membrane assembly may be a primary defect in ADPKD. In this study, we demonstrate that laminin-332 is aberrantly expressed in cysts and precystic tubules of human autosomal recessive PKD (ARPKD) kidneys as well as in the kidneys of PCK rats, an orthologous ARPKD model. There was aberrant expression of laminin-\u03b3<jats:sub>2<\/jats:sub> as early as postnatal day 2 and elevated laminin-332 protein in postnatal day 30, coinciding with the formation and early growth of renal cysts in PCK rat kidneys. We also show that a kidney cell line derived from Oak Ridge polycystic kidney mice, another model of ARPKD, exhibited abnormal lumen-deficient and multilumen structures in Matrigel culture. These cells had increased proliferation rates and altered expression levels of laminin-332 compared with their rescued counterparts. A function-blocking polyclonal antibody to laminin-332 significantly inhibited their abnormal proliferation rates and rescued their aberrant phenotype in Matrigel culture. Furthermore, abnormal laminin-332 expression in cysts originating from collecting ducts and proximal tubules as well as in precystic tubules was observed in a human end-stage ADPKD kidney. Our results suggest that abnormal expression of laminin-332 contributes to the aberrant proliferation of cyst epithelial cells and cyst growth in genetic forms of PKD. <\/jats:p>","DOI":"10.1152\/ajprenal.00104.2013","type":"journal-article","created":{"date-parts":[[2013,12,27]],"date-time":"2013-12-27T01:59:03Z","timestamp":1388109543000},"page":"F640-F654","source":"Crossref","is-referenced-by-count":16,"title":["Aberrant expression of laminin-332 promotes cell proliferation and cyst growth in ARPKD"],"prefix":"10.1152","volume":"306","author":[{"given":"Soundarapandian","family":"Vijayakumar","sequence":"first","affiliation":[{"name":"Department of Pediatrics, University of Rochester Medical Center, Rochester, New York;"},{"name":"Department of Pharmacology and Physiology, University of Rochester Medical Center, Rochester, New York;"}]},{"given":"Suparna","family":"Dang","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, University of Rochester Medical Center, Rochester, New York;"}]},{"given":"M. Peter","family":"Marinkovich","sequence":"additional","affiliation":[{"name":"Program in Epithelial Biology, Stanford University School of Medicine, Stanford, California;"},{"name":"Dermatology Service, Veterans Affairs Palo Alto Health Care System, Palo Alto, California;"}]},{"given":"Zelmira","family":"Lazarova","sequence":"additional","affiliation":[{"name":"Department of Dermatology, Medical College of Wisconsin, Milwaukee, Wisconsin;"}]},{"given":"Bradley","family":"Yoder","sequence":"additional","affiliation":[{"name":"Department of Cell, Development and Integrative Biology, The University of Alabama at Birmingham, Birmingham, Alabama;"}]},{"given":"Vicente E.","family":"Torres","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota;"}]},{"given":"Darren P.","family":"Wallace","sequence":"additional","affiliation":[{"name":"The Kidney Institute, Department of Medicine, University of Kansas Medical Center, Kansas City, Kansas"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.3109\/15419069409004431"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1747.1999.00546.x"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1158\/1541-7786.MCR-08-0148"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1980.43"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbadis.2011.03.003"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1210\/jc.2013-2994"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1101\/gad.1689908"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1053\/j.gastro.2005.09.055"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2011.109"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.E11-08-0718"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00195.2003"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1038\/ng1701"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M606151200"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)63539-0"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0035546"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1538\/expanim.49.51"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1002\/dvdy.22278"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1186\/bcr3203"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00473.x"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/j.jaad.2004.06.004"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118942"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/nmeth1015"},{"key":"B23","first-page":"98A","volume":"25","author":"Lepage M","year":"2011","journal-title":"Can J Gastroenterol"},{"key":"B24","first-page":"1","volume":"10","author":"Liu Y","year":"2009","journal-title":"Cell Biol"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.E05-11-1070"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1242\/dmm.003194"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00785.x"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.137.3.685"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.E10-06-0523"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1126\/science.8191288"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009060603"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00339.2005"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1016\/S0960-8966(99)00033-4"},{"key":"B34","author":"Rasband WS","year":"2014","journal-title":"ImageJ"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00243.2011"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-0714.2010.00936.x"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.253"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005121298"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00038.2010"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2009.128"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1016\/j.biocel.2007.07.015"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1016\/j.matbio.2010.10.005"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1038\/ng833"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.26.8.2877-2886.2006"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra022161"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1986.194"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.433"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00273.2001"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1093\/carcin\/bgm281"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.6.F1037"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00104.2013","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T00:05:20Z","timestamp":1567987520000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00104.2013"}},"issued":{"date-parts":[[2014,3,15]]},"references-count":50,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2014,3,15]]}},"alternative-id":["10.1152\/ajprenal.00104.2013"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00104.2013","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2014,3,15]]}},{"indexed":{"date-parts":[[2026,2,28]],"date-time":"2026-02-28T19:00:02Z","timestamp":1772305202002,"version":"3.50.1"},"reference-count":43,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2005,2]]},"abstract":"<jats:p> The protective factor of female gender appears to be lost in diabetes; the incidence of diabetes and its complications, including diabetic nephropathy, are equal in women and men. This study examined the effects of estrogen deficiency by ovariectomy (OVX) and replacement with 17\u03b2-estradiol (OVX+E<jats:sub>2<\/jats:sub>) on renal function and pathology in the nondiabetic (ND) and streptozotocin (STZ)-induced diabetic (D) rat kidneys for 12 wk. Diabetes was associated with an increase in urine albumin excretion (UAE; ND, 0.39 \u00b1 0.03; D, 5.9 \u00b1 0.8 mg\/day; P &lt; 0.001), decrease in creatinine clearance (CrCl; ND, 0.69 \u00b1 0.03; D, 0.43 \u00b1 0.09 mg\u00b7min<jats:sup>\u22121<\/jats:sup>\u00b7100 g body wt<jats:sup>\u22121<\/jats:sup>; P &lt; 0.05), increase in the index of glomerulosclerosis [GSI; ND, 0.01 \u00b1 0.01; D, 0.15 \u00b1 0.04 arbitrary units (AU); P &lt; 0.01], tubulointerstitial fibrosis (TIFI; ND, 0.04 \u00b1 0.04; D, 0.68 \u00b1 0.2 AU; P &lt; 0.01), and transforming growth factor-\u03b2 (TGF-\u03b2) protein expression (ND, 0.61 \u00b1 0.02; D, 1.25 \u00b1 0.07 AU; P &lt; 0.01). In the D group, the severity of these changes was augmented with OVX (UAE, 8.1 \u00b1 0.6 mg\/day; CrCl, 0.40 \u00b1 0.04 mg\u00b7min<jats:sup>\u22121<\/jats:sup>\u00b7100 g body wt<jats:sup>\u22121<\/jats:sup>; GSI, 0.29 \u00b1 0.04 AU; TIFI, 0.90 \u00b1 0.06 AU; TGF-\u03b2, 1.26 \u00b1 0.10 AU), whereas E<jats:sub>2<\/jats:sub> replacement attenuated these changes (UAE, 6.3 \u00b1 0.8 mg\/day; CrCl, 0.66 \u00b1 0.03 mg\u00b7min<jats:sup>\u22121<\/jats:sup>\u00b7100 g body wt<jats:sup>\u22121<\/jats:sup>; GSI, 0.06 \u00b1 0.02 AU; TIFI, 0.36 \u00b1 0.08 AU; TGF-\u03b2, 0.57 \u00b1 0.08 AU). We conclude that E<jats:sub>2<\/jats:sub> deficiency increases the severity of renal disease in a diabetic animal model and that E<jats:sub>2<\/jats:sub> replacement is renoprotective by attenuating the decline in renal function and pathology associated with diabetes. <\/jats:p>","DOI":"10.1152\/ajprenal.00195.2004","type":"journal-article","created":{"date-parts":[[2004,9,29]],"date-time":"2004-09-29T01:38:12Z","timestamp":1096421892000},"page":"F399-F405","source":"Crossref","is-referenced-by-count":132,"title":["17\u03b2-Estradiol replacement improves renal function and pathology associated with diabetic nephropathy"],"prefix":"10.1152","volume":"288","author":[{"given":"Richard W.","family":"Mankhey","sequence":"first","affiliation":[]},{"given":"Faizah","family":"Bhatti","sequence":"additional","affiliation":[]},{"given":"Christine","family":"Maric","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ijo.0801806"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1007\/s11883-004-0032-7"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1001\/jama.291.14.1701"},{"key":"R3A","unstructured":"Animal models of diabetic complications consortium. Validation of mouse models of diabetic nephropathy. http:\/\/www.amdcc.org\/."},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/18.1.54"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1001\/archinte.164.9.934"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1053\/S0270-9295(03)00132-3"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.2337\/diab.34.7.634"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1161\/hy0202.103297"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1016\/S0008-6363(01)00527-2"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1001\/archinte.1916.00080130010002"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)64277-0"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.2105\/AJPH.87.3.443"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1159\/000169073"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00721.x"},{"key":"R17","unstructured":"Goldfarb S and Ziyadeh F. TGF-\u03b2: a crucial component of the pathogenesis of diabetic nephropathy. Trans Am Clin Climatol Assoc 112: 27\u201332, 2001."},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000105993.63023.D8"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1016\/j.jacc.2003.11.024"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.2337\/diacare.21.4.518"},{"key":"R21","doi-asserted-by":"crossref","unstructured":"Jacobsen P, Rossing K, Tarnow L, Rossing P, Mallet C, Poirier O, Cambien F, and Parving HH. Progression of diabetic nephropathy in normotensive type 1 diabetic patients. Kidney Int Suppl 71: S101\u2013S105, 1999.","DOI":"10.1046\/j.1523-1755.1999.07125.x"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)63155-0"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.00367.2002"},{"key":"R24","unstructured":"Maric C, Enright C, Bhatti F, Mankhey RW, and Sandberg K. 17\u03b2 Estradiol attenuates ANG II-induced cell proliferation and ECM synthesis in renal interstitial fibroblasts (Abstract). Exp Biology 2003."},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000128219.65330.EA"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M105316200"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00679.x"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.2.F309"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.6.F875"},{"key":"R30","unstructured":"Potier M, Elliot SJ, Tack I, Lenz O, Striker GE, Striker LJ, and Karl M. Expression and regulation of estrogen receptors in mesangial cells: influence on matrix metalloproteinase-9. J Am Soc Nephrol 12: 241\u2013251, 2001."},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.med.53.082901.103904"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1055\/s-2007-1014683"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1136\/bmj.316.7130.504"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1987.262"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00376.x"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1210\/endo-96-1-219"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1177\/000331970305400402"},{"key":"R38","unstructured":"Strippoli GF, Di Paolo S, Cincione R, Di Palma AM, Teutonico A, Grandaliano G, Schena FP, and Gesualdo L. Clinical and therapeutic aspects of diabetic nephropathy. J Nephrol 16: 487\u2013499, 2003."},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-0528.2000.tb10406.x"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1159\/000065442"},{"key":"R41","unstructured":"Van Goor H, Fidler V, Weening JJ, and Grond J. Determinants of focal and segmental glomerulosclerosis in the rat after renal ablation. Evidence for involvement of macrophages and lipids. Lab Invest 64: 754\u2013765, 1991."},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00590.x"},{"key":"R42A","doi-asserted-by":"publisher","DOI":"10.1001\/jama.290.16.2159"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.2337\/diacare.25.3.500"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00195.2004","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T21:48:51Z","timestamp":1567979331000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00195.2004"}},"issued":{"date-parts":[[2005,2]]},"references-count":43,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2005,2]]}},"alternative-id":["10.1152\/ajprenal.00195.2004"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00195.2004","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2005,2]]}},{"indexed":{"date-parts":[[2026,3,1]],"date-time":"2026-03-01T17:33:42Z","timestamp":1772386422211,"version":"3.50.1"},"reference-count":35,"publisher":"American Physiological Society","issue":"1","funder":[{"DOI":"10.13039\/100000738","name":"U.S. Department of Veterans Affairs","doi-asserted-by":"publisher","award":["IK2BX003839"],"award-info":[{"award-number":["IK2BX003839"]}],"id":[{"id":"10.13039\/100000738","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2022,1,1]]},"abstract":"<jats:p> 15-Lipoxygenase (15-LO) has both pro- and anti-inflammatory functions in leukocytes, and its role in kidney injury and repair is unexplored. Our study showed that 15-LO worsens inflammation and fibrosis in a rodent model of chronic kidney disease using genetic and pharmacological manipulation. Silencing 15-LO promotes an increase in M2c-like wound-healing macrophages in the kidney and alters kidney metabolism globally, protecting against anaerobic glycolysis after injury. <\/jats:p>","DOI":"10.1152\/ajprenal.00214.2021","type":"journal-article","created":{"date-parts":[[2021,12,6]],"date-time":"2021-12-06T11:16:28Z","timestamp":1638789388000},"page":"F105-F119","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":15,"title":["15-Lipoxygenase worsens renal fibrosis, inflammation, and metabolism in a murine model of ureteral obstruction"],"prefix":"10.1152","volume":"322","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4824-1922","authenticated-orcid":true,"given":"John R.","family":"Montford","sequence":"first","affiliation":[{"name":"Rocky Mountain Regional Veterans Affairs Medical Center, Aurora, Colorado"},{"name":"Division of Nephrology and Hypertension, Department of Medicine, University of Colorado, Aurora, Colorado"}]},{"given":"Colin","family":"Bauer","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Medicine, University of Colorado, Aurora, Colorado"}]},{"given":"Jeremy","family":"Rahkola","sequence":"additional","affiliation":[{"name":"Rocky Mountain Regional Veterans Affairs Medical Center, Aurora, Colorado"}]},{"given":"Julie A.","family":"Reisz","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Genetics, University of Colorado, Aurora, Colorado"}]},{"given":"Deanna","family":"Floyd","sequence":"additional","affiliation":[{"name":"Rocky Mountain Regional Veterans Affairs Medical Center, Aurora, Colorado"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2420-2358","authenticated-orcid":true,"given":"Katharina","family":"Hopp","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Medicine, University of Colorado, Aurora, Colorado"},{"name":"Consortium for Fibrosis Research and Translation, University of Colorado, Aurora, Colorado"}]},{"given":"Danielle E.","family":"Soranno","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Medicine, University of Colorado, Aurora, Colorado"},{"name":"Consortium for Fibrosis Research and Translation, University of Colorado, Aurora, Colorado"},{"name":"Pediatric Nephrology, Department of Pediatrics, University of Colorado, Aurora, Colorado"}]},{"given":"Jelena","family":"Klawitter","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Medicine, University of Colorado, Aurora, Colorado"}]},{"given":"Mary C. M.","family":"Weiser-Evans","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Medicine, University of Colorado, Aurora, Colorado"},{"name":"Consortium for Fibrosis Research and Translation, University of Colorado, Aurora, Colorado"},{"name":"Department of Pharmacology, University of Colorado, Aurora, Colorado"}]},{"given":"Raphael","family":"Nemenoff","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Medicine, University of Colorado, Aurora, Colorado"},{"name":"Consortium for Fibrosis Research and Translation, University of Colorado, Aurora, Colorado"},{"name":"Department of Pharmacology, University of Colorado, Aurora, Colorado"}]},{"given":"Sarah","family":"Faubel","sequence":"additional","affiliation":[{"name":"Rocky Mountain Regional Veterans Affairs Medical Center, Aurora, Colorado"},{"name":"Division of Nephrology and Hypertension, Department of Medicine, University of Colorado, Aurora, Colorado"}]},{"given":"Seth B.","family":"Furgeson","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Medicine, University of Colorado, Aurora, Colorado"},{"name":"Consortium for Fibrosis Research and Translation, University of Colorado, Aurora, Colorado"},{"name":"Denver Health, Denver, Colorado"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1038\/s41581-019-0110-2"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.0901473"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014111138"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)62950-1"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000131272.06958.DE"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-014-3023-0"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0143961"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2013.135"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.3389\/fphar.2019.00719"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-019-39007-6"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1016\/S0021-9258(18)34018-3"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1007\/s10157-021-02021-y"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbalip.2019.07.009"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007080939"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbalip.2016.07.014"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/j.gene.2015.07.073"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/j.mam.2017.03.001"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00262.2018"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2016.06.030"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1002\/rcm.7834"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-4939-9236-2_2"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1002\/0471250953.bi1411s37"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1002\/cpbi.11"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1194\/jlr.M082362"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1007\/s10555-018-9738-9"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/S0021-9150(97)00204-9"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/j.prostaglandins.2009.09.006"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1089\/ars.2015.6372"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/j.yjmcc.2018.03.004"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1111\/apha.13317"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1159\/000431214"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1189\/jlb.3HI0515-189R"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.1402149"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2015020177"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1021\/acscentsci.7b00589"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00214.2021","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,1,6]],"date-time":"2022-01-06T18:23:30Z","timestamp":1641493410000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00214.2021"}},"issued":{"date-parts":[[2022,1,1]]},"references-count":35,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2022,1,1]]}},"alternative-id":["10.1152\/ajprenal.00214.2021"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00214.2021","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2022,1,1]]},"assertion":[{"value":"2021-06-02","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2021-12-01","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2022-01-06","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,3,5]],"date-time":"2026-03-05T09:33:10Z","timestamp":1772703190958,"version":"3.50.1"},"reference-count":31,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2004,2]]},"abstract":"<jats:p>Plasma membrane Ca<jats:sup>2+<\/jats:sup>-ATPases (PMCAs) are a ubiquitous system for the expulsion of Ca<jats:sup>2+<\/jats:sup>from eukaryotic cells. In tight monolayers of polarized Madin-Darby canine kidney (MDCK) cells representing a distal kidney tubule model, PMCAs are responsible for about one-third of the vectorial Ca<jats:sup>2+<\/jats:sup>transport under resting conditions, with the remainder being provided by the Na<jats:sup>+<\/jats:sup>\/Ca<jats:sup>2+<\/jats:sup>exchanger. Vitamin D<jats:sub>3<\/jats:sub>(VitD) is known to increase PMCA expression and activity in Ca<jats:sup>2+<\/jats:sup>-transporting tissues such as the intestine, as well as in osteoblasts and Madin-Darby bovine kidney epithelial cells. We found that VitD upregulated the expression of the PMCAs (mainly PMCA4b) in MDCK cell lysates at the RNA and protein level in a time- and dose-dependent manner. Interestingly, VitD caused a decrease of the PMCAs in the apical plasma membrane fraction and a concomitant increase of the pumps in the basolateral membrane. Functional studies demonstrated that transcellular<jats:sup>45<\/jats:sup>Ca<jats:sup>2+<\/jats:sup>flux from the apical-to-basolateral compartment was significantly enhanced by VitD. These findings demonstrate that VitD is a positive regulator of the PMCAs in MDCK epithelial cells. The correlation of decreased apical\/increased basolateral expression of the PMCAs with an increase in transcellular Ca<jats:sup>2+<\/jats:sup>flux from the apical (urine) toward the basolateral (blood) compartment indicates the physiological relevance of VitD function in kidney tubular Ca<jats:sup>2+<\/jats:sup>reabsorption.<\/jats:p>","DOI":"10.1152\/ajprenal.00076.2003","type":"journal-article","created":{"date-parts":[[2004,1,31]],"date-time":"2004-01-31T01:13:21Z","timestamp":1075511601000},"page":"F363-F369","source":"Crossref","is-referenced-by-count":49,"title":["Vitamin D<sub>3<\/sub>upregulates plasma membrane Ca<sup>2+<\/sup>-ATPase expression and potentiates apico-basal Ca<sup>2+<\/sup>flux in MDCK cells"],"prefix":"10.1152","volume":"286","author":[{"given":"Sertac N.","family":"Kip","sequence":"first","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota 55905"}]},{"given":"Emanuel E.","family":"Strehler","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota 55905"}]}],"member":"24","reference":[{"key":"REF1","doi-asserted-by":"publisher","DOI":"10.1054\/tice.2000.0135"},{"key":"REF2","unstructured":"Ausubel FM, Brent R, Kingston RE, Moore DD, Seidman JG, Smith JA, and Struhl K.Current Protocols in Molecular Biology. New York: Wiley, 1998."},{"key":"REF3","doi-asserted-by":"crossref","unstructured":"Bindels RJM.Calcium handling by the mammalian kidney.J Exp Biol184: 89-104, 1993.","DOI":"10.1242\/jeb.184.1.89"},{"key":"REF4","doi-asserted-by":"publisher","DOI":"10.1042\/bj3160353"},{"key":"REF5","doi-asserted-by":"publisher","DOI":"10.1210\/edrv-10-1-3"},{"key":"REF6","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.38.23741"},{"key":"REF7","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1995.75.3.429"},{"key":"REF8","doi-asserted-by":"publisher","DOI":"10.1006\/abbi.2000.1908"},{"key":"REF9","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.3.1667"},{"key":"REF10","doi-asserted-by":"crossref","unstructured":"Handler JS.Use of cultured epithelia to study transport and its regulation.J Exp Biol106: 55-69, 1983.","DOI":"10.1242\/jeb.106.1.55"},{"key":"REF11","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.93.2.269"},{"key":"REF12","doi-asserted-by":"publisher","DOI":"10.1096\/fj.02-0225com"},{"key":"REF13","doi-asserted-by":"crossref","unstructured":"Hoenderop JGJ, Muller D, van der Kemp AWCM, Hartog A, Suzuki M, Ishibashi K, Imai M, Sweep F, Willems PHGM, van Os CH, and Bindels RJM.Calcitriol controls the epithelial calcium channel in kidney.J Am Soc Nephrol12: 1342-1349, 2001.","DOI":"10.1681\/ASN.V1271342"},{"key":"REF14","doi-asserted-by":"publisher","DOI":"10.1016\/S1570-9639(02)00438-7"},{"key":"REF15","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.13.8375"},{"key":"REF16","doi-asserted-by":"crossref","unstructured":"Hoenderop JGJ, Willems PHGM, and Bindels RJM.Toward a comprehensive molecular model of active calcium reabsorption.Am J Physiol Renal Physiol278: F352-F360, 2000.","DOI":"10.1152\/ajprenal.2000.278.3.F352"},{"key":"REF17","doi-asserted-by":"publisher","DOI":"10.1126\/science.2849209"},{"key":"REF18","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.1041390113"},{"key":"REF19","doi-asserted-by":"crossref","unstructured":"Kip SNand Strehler EE.Characterization of PMCA isoforms and their contribution to transcellular Ca2+flux in MDCK cells.Am J Physiol Renal Physiol284: F122-F132, 2003.","DOI":"10.1152\/ajprenal.00161.2002"},{"key":"REF20","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199803053381004"},{"key":"REF21","doi-asserted-by":"publisher","DOI":"10.1016\/S0143-4160(97)90051-8"},{"key":"REF22","unstructured":"Lowe KE, Maiyar AC, and Norman AW.Vitamin D-mediated gene expression.Crit Rev Eukaryot Gene Expr2: 65-109, 1992."},{"key":"REF23","doi-asserted-by":"crossref","unstructured":"Magyar CE, White KE, Rojas R, Apodaca G, and Friedman PA.Plasma membrane Ca2+-ATPase and NCX1 Na+\/Ca2+exchanger expression in distal convoluted tubule cells.Am J Physiol Renal Physiol283: F29-F40, 2002.","DOI":"10.1152\/ajprenal.00252.2000"},{"key":"REF24","doi-asserted-by":"publisher","DOI":"10.1016\/0076-6879(90)92092-R"},{"key":"REF25","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.98.3.991"},{"key":"REF26","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.73.4.1212"},{"key":"REF27","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.81.3.635"},{"key":"REF28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1979.237.1.F1"},{"key":"REF29","doi-asserted-by":"publisher","DOI":"10.1006\/abio.1997.2431"},{"key":"REF30","doi-asserted-by":"publisher","DOI":"10.1021\/bi00047a007"},{"key":"REF31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.5.F985"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00076.2003","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,6,14]],"date-time":"2021-06-14T05:34:47Z","timestamp":1623648887000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00076.2003"}},"issued":{"date-parts":[[2004,2]]},"references-count":31,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2004,2]]}},"alternative-id":["10.1152\/ajprenal.00076.2003"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00076.2003","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2004,2]]}},{"indexed":{"date-parts":[[2026,2,28]],"date-time":"2026-02-28T13:49:54Z","timestamp":1772286594000,"version":"3.50.1"},"reference-count":33,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2006,3]]},"abstract":"<jats:p> The aim of the current study was to determine whether renal medullary oxygenation is independent of the level of cortical blood flow by testing responses to stimuli that selectively reduce blood flow in either the cortex or medulla. In anesthetized rabbits, renal arterial infusion of [Phe<jats:sup>2<\/jats:sup>,Ile<jats:sup>3<\/jats:sup>,Orn<jats:sup>8<\/jats:sup>]-vasopressin selectively reduced medullary perfusion and Po<jats:sub>2<\/jats:sub> (\u221254 \u00b1 24 and \u221250 \u00b1 10%, respectively) but did not significantly affect cortical perfusion or tissue oxygenation. In contrast, stimulation of the renal nerves resulted in renal cortical ischemia with reductions in total renal blood flow (\u221276 \u00b1 3% at 4 Hz), cortical perfusion (\u221257 \u00b1 17%), and cortical Po<jats:sub>2<\/jats:sub> (\u221244 \u00b1 12%). Medullary tissue Po<jats:sub>2<\/jats:sub> was reduced by \u221270 \u00b1 5% at 4 Hz, despite medullary perfusion being unaffected and distal tubular sodium reabsorption being reduced (by \u221283.3 \u00b1 1.2% from baseline). In anesthetized rats, in which renal perfusion pressure was maintained with an aortic constrictor, intravenous infusion of ANG II (0.5\u20135 \u03bcg\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7min<jats:sup>\u22121<\/jats:sup>) dose dependently reduced cortical perfusion (up to \u221265 \u00b1 3%; P &lt; 0.001) and cortical Po<jats:sub>2<\/jats:sub> (up to \u221257 \u00b1 4%; P &lt; 0.05). However, medullary perfusion was only significantly reduced at the highest dose (5 \u03bcg\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7min<jats:sup>\u22121<\/jats:sup>; by 29 \u00b1 6%). Medullary perfusion was not reduced by 1 \u03bcg\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7min<jats:sup>\u22121<\/jats:sup> ANG II, but medullary Po<jats:sub>2<\/jats:sub> was significantly reduced (\u221212 \u00b1 4%). Thus, although cortical and medullary blood flow may be independently regulated, medullary oxygenation may be compromised during moderate to severe cortical ischemia even when medullary blood flow is maintained. <\/jats:p>","DOI":"10.1152\/ajprenal.00275.2005","type":"journal-article","created":{"date-parts":[[2005,10,11]],"date-time":"2005-10-11T23:23:56Z","timestamp":1129073036000},"page":"F688-F694","source":"Crossref","is-referenced-by-count":78,"title":["Renal medullary tissue oxygenation is dependent on both cortical and medullary blood flow"],"prefix":"10.1152","volume":"290","author":[{"given":"Paul M.","family":"O'Connor","sequence":"first","affiliation":[]},{"given":"Michelle M.","family":"Kett","sequence":"additional","affiliation":[]},{"given":"Warwick P.","family":"Anderson","sequence":"additional","affiliation":[]},{"given":"Roger G.","family":"Evans","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200401000-00010"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-4684-4895-5_23"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000083341.64034.00"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0706036"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00061.2002"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1097\/01.hjh.0000133744.85490.9d"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-201x.2000.00741.x"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1996.270.6.R1257"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1996.271.3.R647"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00151.2002"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1986.250.6.R960"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1172\/JCI113612"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1990.258.1.H229"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.2000.279.3.R907"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.2001.280.1.R62"},{"key":"R16","doi-asserted-by":"crossref","unstructured":"Levy MN and Imperial ES. Oxygen shunting in renal cortical and medullary capillaries. Am J Physiol 200: 159\u2013162, 1961.","DOI":"10.1152\/ajplegacy.1961.200.1.159"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.49"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.1997.tb01807.x"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.1998.tb02179.x"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1998.274.5.R1283"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1990.70.3.885"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1007\/s00125-003-1155-z"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1996.270.3.R630"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.3.F653"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1097\/00005344-200208000-00006"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1016\/0002-9343(82)90181-4"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.259.6.F910"},{"key":"R28","doi-asserted-by":"crossref","unstructured":"Strauss J, Beran AV, Brown CT, and Katurich N. Renal oxygenation under \u201cnormal\u201d conditions. Am J Physiol 215: 1482\u20131487, 1968.","DOI":"10.1152\/ajplegacy.1968.215.6.1482"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.1996.tb15995.x"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00034.2002"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00483.x"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00729.x"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00074.2002"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00275.2005","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:16:16Z","timestamp":1567970176000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00275.2005"}},"issued":{"date-parts":[[2006,3]]},"references-count":33,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2006,3]]}},"alternative-id":["10.1152\/ajprenal.00275.2005"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00275.2005","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2006,3]]}},{"indexed":{"date-parts":[[2026,3,4]],"date-time":"2026-03-04T05:32:14Z","timestamp":1772602334093,"version":"3.50.1"},"reference-count":54,"publisher":"American Physiological Society","issue":"9","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2012,11,1]]},"abstract":"<jats:p> Aberrant melanocortin signaling has been implicated in the pathogenesis of wasting in chronic kidney disease (CKD). Previously, we demonstrated that agouti-related peptide (AgRP), a melenocortin-4 receptor antagonist, reduced CKD-associated cachexia in CKD mice. Our previous studies with AgRP utilized dual energy X-ray (DXA) densitometry to assess the body composition in mice (Cheung W, Kuo HJ, Markison S, Chen C, Foster AC, Marks DL, Mak RH. J Am Soc Nephrol 18: 2517\u20132524, 2007; Cheung W, Yu PX, Little BM, Cone RD, Marks DL, Mak RH. J Clin Invest 115: 1659\u20131665, 2005). DXA is unable to differentiate water content in mice, and fluid retention in CKD may lead to an overestimate of lean mass. In this study, we employed quantitative magnetic resonance technique to evaluate body composition change following central administration of AgRP in a CKD mouse model. AgRP treatment improved energy expenditure, total body mass, fat mass, and lean body mass in CKD mouse. We also investigated the effect of CKD-associated cachexia on the signaling pathways leading to wasting in skeletal muscle, as well as whether these changes can be ameliorated by central administration of AgRP. AgRP treatment caused an overall decrease in proinflammatory cytokines, which may be one important mechanism of its effects. Muscle wasting in CKD may be due to the activation of proteolytic pathways as well as inhibition of myogenesis and muscle regeneration processes. Our results suggest that these aberrant pathological pathways leading to muscle wasting in CKD mice were ameliorated by central administration of AgRP. <\/jats:p>","DOI":"10.1152\/ajprenal.00341.2012","type":"journal-article","created":{"date-parts":[[2012,8,24]],"date-time":"2012-08-24T00:54:44Z","timestamp":1345769684000},"page":"F1315-F1324","source":"Crossref","is-referenced-by-count":40,"title":["Melanocortin antagonism ameliorates muscle wasting and inflammation in chronic kidney disease"],"prefix":"10.1152","volume":"303","author":[{"given":"Wai W.","family":"Cheung","sequence":"first","affiliation":[{"name":"Pediatric Nephrology, University of California, San Diego, California"}]},{"given":"Robert H.","family":"Mak","sequence":"additional","affiliation":[{"name":"Pediatric Nephrology, University of California, San Diego, California"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0604893104"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5001969"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004100842"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2362.2010.02347.x"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.02602"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1038\/nrm3118"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00019.2003"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006091024"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-009-1427-z"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1172\/JCI22521"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.150"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1089\/hum.2010.057"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.2012.02423.x"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2003.042374"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-010-0919-9"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.2010.05809.x"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.01026.2004"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1194\/jlr.R200014-JLR200"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1194\/jlr.M005744"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00579.2003"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1038\/oby.2004.200"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0004973"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1210\/en.2010-1135"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0b013e3282f02204"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1016\/j.ghir.2007.07.009"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-011-1765-5"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1007\/s13539-011-0019-5"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5001622"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00192.2009"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200207056"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.20757"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2004.12.007"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1038\/oby.2009.471"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.00734.2009"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-002-0981-z"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.21"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-007-0594-z"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1017\/S0007114507252675"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-006-0235-y"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(04)00400-3"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1189\/jlb.0506356"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.50.2.248"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1007\/s00216-003-2224-3"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1038\/oby.2004.20"},{"key":"B45","first-page":"14","volume":"27","author":"Tsuchida K","year":"2008","journal-title":"Acta Myol"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1093\/ajcn\/82.4.801"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1210\/en.2006-0251"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1096\/fj.04-2421fje"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.3945\/ajcn.2010.28608B"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2012.84"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008060628"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1096\/fj.10-176917"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2009.090275"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1301\/00296640260085949"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00341.2012","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T23:42:18Z","timestamp":1567986138000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00341.2012"}},"issued":{"date-parts":[[2012,11,1]]},"references-count":54,"journal-issue":{"issue":"9","published-print":{"date-parts":[[2012,11,1]]}},"alternative-id":["10.1152\/ajprenal.00341.2012"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00341.2012","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2012,11,1]]}},{"indexed":{"date-parts":[[2026,3,5]],"date-time":"2026-03-05T14:20:10Z","timestamp":1772720410707,"version":"3.50.1"},"reference-count":29,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2017,9,1]]},"abstract":"<jats:p>We examined bladder and urethral sphincter activity in mice with or without spinal cord injury (SCI) after C-fiber afferent desensitization induced by capsaicin pretreatment and changes in electrophysiological properties of mouse bladder afferent neurons 4 wk after SCI. Female C57BL\/6N mice were divided into four groups: 1) spinal intact (SI)-control, 2) SI-capsaicin pretreatment (Cap), 3) SCI-control, and 4) SCI-Cap groups. Continuous cystometry and external urethral sphincter (EUS)-electromyogram (EMG) were conducted under an awake condition. In the Cap groups, capsaicin (25, 50, or 100 mg\/kg) was injected subcutaneously 4 days before the experiments. In the SI-Cap group, 100 mg\/kg capsaicin pretreatment significantly increased bladder capacity and decreased the silent period duration of EUS\/EMG compared with the SI-control group. In the SCI-Cap group, 50 and 100 mg\/kg capsaicin pretreatment decreased the number of nonvoiding contractions (NVCs) and the duration of reduced EUS activity during voiding, respectively, compared with the SCI-control group. In SCI mice, hexamethonium, a ganglionic blocker, almost completely blocked NVCs, suggesting that they are of neurogenic origin. Patch-clamp recordings in capsaicin-sensitive bladder afferent neurons from SCI mice showed hyperexcitability, which was evidenced by decreased spike thresholds and increased firing rate compared with SI mice. These results indicate that capsaicin-sensitive C-fiber afferent pathways, which become hyperexcitable after SCI, can modulate bladder and urethral sphincter activity in awake SI and SCI mice. Detrusor overactivity as shown by NVCs in SCI mice is significantly but partially dependent on capsaicin-sensitive C-fiber afferents, whereas the EUS relaxation during voiding is enhanced by capsaicin-sensitive C-fiber bladder afferents in SI and SCI mice.<\/jats:p>","DOI":"10.1152\/ajprenal.00097.2017","type":"journal-article","created":{"date-parts":[[2017,6,22]],"date-time":"2017-06-22T00:30:32Z","timestamp":1498091432000},"page":"F796-F804","source":"Crossref","is-referenced-by-count":40,"title":["The role of capsaicin-sensitive C-fiber afferent pathways in the control of micturition in spinal-intact and spinal cord-injured mice"],"prefix":"10.1152","volume":"313","author":[{"given":"Katsumi","family":"Kadekawa","sequence":"first","affiliation":[{"name":"Department of Urology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania;"},{"name":"Southern Knights\u2019 Laboratory, Okinawa, Japan;"},{"name":"Okinawa Kyodo Hospital, Okinawa, Japan;"}]},{"given":"Tsuyoshi","family":"Majima","sequence":"additional","affiliation":[{"name":"Department of Urology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania;"},{"name":"Department of Urology, Nagoya University Graduate School of Medicine, Nagoya, Japan; and"}]},{"given":"Takahiro","family":"Shimizu","sequence":"additional","affiliation":[{"name":"Department of Urology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania;"}]},{"given":"Naoki","family":"Wada","sequence":"additional","affiliation":[{"name":"Department of Urology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania;"}]},{"given":"William C.","family":"de Groat","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Cell Biology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania;"}]},{"given":"Anthony J.","family":"Kanai","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania;"}]},{"given":"Momokazu","family":"Goto","sequence":"additional","affiliation":[{"name":"Department of Urology, Nagoya University Graduate School of Medicine, Nagoya, Japan; and"}]},{"given":"Mitsuharu","family":"Yoshiyama","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Cell Biology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania;"},{"name":"Department of Urology, University of Yamanashi Graduate School of Medical Science, Chuo, Japan"}]},{"given":"Kimio","family":"Sugaya","sequence":"additional","affiliation":[{"name":"Southern Knights\u2019 Laboratory, Okinawa, Japan;"}]},{"given":"Naoki","family":"Yoshimura","sequence":"additional","affiliation":[{"name":"Department of Urology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania;"},{"name":"Department of Pharmacology and Cell Biology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1002\/nau.21108"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/nn902"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/j.juro.2012.11.049"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1993.265.1.R132"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(95)00212-9"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1999.277.3.R786"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/j.expneurol.2004.02.014"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1016\/0165-1838(90)90105-R"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/S0079-6123(05)52005-3"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(01)62606-5"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00142.2006"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.3389\/fphys.2014.00387"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1007\/s00192-011-1403-6"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.1984.tb16534.x"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1016\/j.eururo.2012.03.031"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/j.lfs.2013.03.021"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00450.2015"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(87)90263-0"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/0165-1838(90)90256-I"},{"key":"B20","doi-asserted-by":"crossref","first-page":"729","DOI":"10.1016\/S0022-3565(24)38194-7","volume":"289","author":"Matsuda H","year":"1999","journal-title":"J Pharmacol Exp Ther"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/j.juro.2008.10.139"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1097\/01.ju.0000088340.26588.74"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1016\/0306-4522(83)90223-3"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00508.2011"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1016\/j.juro.2013.07.058"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.1997.269bh.x"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/S0306-4522(97)00376-X"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.3023-06.2006"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00016.2015"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00097.2017","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,6,19]],"date-time":"2025-06-19T22:18:20Z","timestamp":1750371500000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00097.2017"}},"issued":{"date-parts":[[2017,9,1]]},"references-count":29,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2017,9,1]]}},"alternative-id":["10.1152\/ajprenal.00097.2017"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00097.2017","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2017,9,1]]}},{"indexed":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T11:48:24Z","timestamp":1772192904550,"version":"3.50.1"},"reference-count":27,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2003,6,1]]},"abstract":"<jats:p> The degree to which loss of the NHE3 Na<jats:sup>+<\/jats:sup>\/H<jats:sup>+<\/jats:sup> exchanger in the kidney contributes to impaired Na<jats:sup>+<\/jats:sup>-fluid volume homeostasis in NHE3-deficient ( Nhe3 <jats:sup>\u2212\/\u2212<\/jats:sup>) mice is unclear because of the coexisting intestinal absorptive defect. To more accurately assess the renal effects of NHE3 ablation, we developed a mouse with transgenic expression of rat NHE3 in the intestine and crossed it with Nhe3 <jats:sup>\u2212\/\u2212<\/jats:sup> mice. Transgenic Nhe3 <jats:sup>\u2212\/\u2212<\/jats:sup> (tg Nhe3 <jats:sup>\u2212\/\u2212<\/jats:sup>) mice tolerated dietary NaCl depletion better than nontransgenic knockouts and showed no evidence of renal salt wasting. Unlike nontransgenic Nhe3 <jats:sup>\u2212\/\u2212<\/jats:sup> mice, tg Nhe3 <jats:sup>\u2212\/\u2212<\/jats:sup> mice tolerated a 5% NaCl diet. When fed a 5% NaCl diet, tg Nhe3 <jats:sup>\u2212\/\u2212<\/jats:sup> mice had lower serum aldosterone than tg Nhe3 <jats:sup>\u2212\/\u2212<\/jats:sup> mice on a 1% NaCl diet, indicating improved extracellular fluid volume status. Na<jats:sup>+<\/jats:sup>-loaded tg Nhe3 <jats:sup>\u2212\/\u2212<\/jats:sup> mice had sharply increased urinary Na<jats:sup>+<\/jats:sup> excretion, reflective of increased absorption of Na<jats:sup>+<\/jats:sup> in the small intestine; nevertheless, they remained hypotensive, and renal studies showed a reduction in glomerular filtration rate (GFR) similar to that observed in nontransgenic Nhe3 <jats:sup>\u2212\/\u2212<\/jats:sup> mice. These data show that reduced GFR, rather than being secondary to systemic hypovolemia, is a major renal compensatory mechanism for the loss of NHE3 and indicate that loss of NHE3 in the kidney alters the set point for Na<jats:sup>+<\/jats:sup>-fluid volume homeostasis. <\/jats:p>","DOI":"10.1152\/ajprenal.00418.2002","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:38:08Z","timestamp":1425415088000},"page":"F1190-F1198","source":"Crossref","is-referenced-by-count":55,"title":["Renal function in NHE3-deficient mice with transgenic  rescue of small intestinal absorptive defect"],"prefix":"10.1152","volume":"284","author":[{"given":"Alison L.","family":"Woo","sequence":"first","affiliation":[{"name":"Departments of Molecular Genetics, Biochemistry, and Microbiology and"}]},{"given":"William T.","family":"Noonan","sequence":"additional","affiliation":[{"name":"Molecular and Cellular Physiology, The University of Cincinnati College of Medicine, Cincinnati, Ohio 45267-0524; and"}]},{"given":"Patrick J.","family":"Schultheis","sequence":"additional","affiliation":[{"name":"Department of Biological Sciences, Northern Kentucky University, Highland Heights, Kentucky 41099"}]},{"given":"Jonathan C.","family":"Neumann","sequence":"additional","affiliation":[{"name":"Departments of Molecular Genetics, Biochemistry, and Microbiology and"}]},{"given":"Patrice A.","family":"Manning","sequence":"additional","affiliation":[{"name":"Departments of Molecular Genetics, Biochemistry, and Microbiology and"}]},{"given":"John N.","family":"Lorenz","sequence":"additional","affiliation":[{"name":"Molecular and Cellular Physiology, The University of Cincinnati College of Medicine, Cincinnati, Ohio 45267-0524; and"}]},{"given":"Gary E.","family":"Shull","sequence":"additional","affiliation":[{"name":"Departments of Molecular Genetics, Biochemistry, and Microbiology and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.404"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI3971"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.265.5.F736"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.2001.0359k.x"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.00297.2001"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.94.21.11710"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1172\/JCI112716"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.281.4.F718"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.2001.281.6.G1385"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M205627200"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.1.F172"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.3.F447"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M008548200"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.4.1727"},{"key":"B15","first-page":"412","volume":"17","author":"Navar LG","year":"1997","journal-title":"Semin Nephrol"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/S0955-0674(02)00353-8"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M102901200"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.4.1732"},{"key":"B19","first-page":"1565","volume":"10","author":"Rosivall L.","year":"1995","journal-title":"Nephrol Dial Transplant"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1172\/JCI1249"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1038\/969"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.44.29150"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.090091297"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.2.F298"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1974.61"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1007\/PL00005899"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1126\/science.7527588"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00418.2002","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T22:27:09Z","timestamp":1567981629000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00418.2002"}},"issued":{"date-parts":[[2003,6,1]]},"references-count":27,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2003,6,1]]}},"alternative-id":["10.1152\/ajprenal.00418.2002"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00418.2002","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2003,6,1]]}},{"indexed":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T08:39:50Z","timestamp":1772181590054,"version":"3.50.1"},"reference-count":47,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2006,10]]},"abstract":"<jats:p>Podocytes are exposed to mechanical forces arising from glomerular capillary pressure and filtration. It has been shown that stretch affects podocyte biology in vitro and plays a significant role in the development of glomerulosclerosis in vivo. However, whether podocytes are sensitive to fluid shear stress is completely unknown. In the present study, we therefore exposed cells of a recently generated conditionally immortalized mouse podocyte cell line to defined fluid shear stress in a flow chamber, mimicking flow of the glomerular ultrafiltrate over the surface of podocytes in Bowman's space. Shear stress above 0.25 dyne\/cm<jats:sup>2<\/jats:sup>resulted in dramatic loss of podocytes but not of proximal tubular epithelial cells (LLC-PK<jats:sub>1<\/jats:sub>cells) after 20 h. At 0.015\u20130.25 dyne\/cm<jats:sup>2<\/jats:sup>, lamellipodia formation in podocytes was enhanced and the actin nucleation protein cortactin was redistributed to the cell margins. Shear stress further diminished stress fibers and the presence of vinculin in focal adhesions. Linear zonula occludens-1 distribution at cell-cell contacts remained unaffected at low shear stress. At 0.25 dyne\/cm<jats:sup>2<\/jats:sup>, the monolayer was broken up and remaining cell-cell contacts were reinforced by F-actin and \u03b1-actinin. Because the cytoskeletal changes induced by shear stress suggested the involvement of tyrosine kinases (TKs), we tested several TK inhibitors that were all without effect on podocyte number under static conditions. At 0.25 dyne\/cm<jats:sup>2<\/jats:sup>, however, the TK inhibitors genistein and AG 82 were associated with marked podocyte loss. Our data demonstrate that podocytes are highly sensitive to fluid shear stress. Shear stress induces a reorganization of the actin cytoskeleton and activates specific tyrosine kinases that are required to withstand fluid shear stress.<\/jats:p>","DOI":"10.1152\/ajprenal.00196.2005","type":"journal-article","created":{"date-parts":[[2006,5,10]],"date-time":"2006-05-10T03:36:35Z","timestamp":1147232195000},"page":"F856-F865","source":"Crossref","is-referenced-by-count":130,"title":["Podocytes are sensitive to fluid shear stress in vitro"],"prefix":"10.1152","volume":"291","author":[{"given":"Colin","family":"Friedrich","sequence":"first","affiliation":[]},{"given":"Nicole","family":"Endlich","sequence":"additional","affiliation":[]},{"given":"Wilhelm","family":"Kriz","sequence":"additional","affiliation":[]},{"given":"Karlhans","family":"Endlich","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0703355"},{"key":"R2","doi-asserted-by":"crossref","unstructured":"Akiyama T, Ishida J, Nakagawa S, Ogawara H, Watanabe S, Itoh N, Shibuya M, and Fukami Y.Genistein, a specific inhibitor of tyrosine-specific protein kinases.J Biol Chem262: 5592\u20135595, 1987.","DOI":"10.1016\/S0021-9258(18)45614-1"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1096-9896(199711)183:3<272::AID-PATH914>3.0.CO;2-U"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200201000-00011"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.29.6.1296"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1995.75.3.519"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000060201.41923.88"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.122.3.729"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0405179101"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00362.x"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1172\/JCI111349"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejcb.2005.09.006"},{"key":"R13","doi-asserted-by":"crossref","unstructured":"Endlich N, Kress KR, Reiser J, Uttenweiler D, Kriz W, Mundel P, and Endlich K.Podocytes respond to mechanical stress in vitro.J Am Soc Nephrol12: 413\u2013422, 2001.","DOI":"10.1681\/ASN.V123413"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1096\/fj.02-0125fje"},{"key":"R15","doi-asserted-by":"crossref","unstructured":"Essig M, Terzi F, Burtin M, and Friedlander G.Mechanical strains induced by tubular flow affect the phenotype of proximal tubular cells.Am J Physiol Renal Physiol281: F751\u2013F762, 2001.","DOI":"10.1152\/ajprenal.2001.281.4.F751"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1126\/science.8066447"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.150.3.627"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1159\/000046097"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1159\/000013302"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1007\/BF02621134"},{"key":"R21","doi-asserted-by":"crossref","unstructured":"Kaksonen M, Peng HB, and Rauvala H.Association of cortactin with dynamic actin in lamellipodia and on endosomal vesicles.J Cell Sci113: 4421\u20134426, 2000.","DOI":"10.1242\/jcs.113.24.4421"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1007\/BF02522869"},{"key":"R23","doi-asserted-by":"crossref","unstructured":"Kretzler M, Koeppen-Hagemann I, and Kriz W.Podocyte damage is a critical step in the development of glomerulosclerosis in the uninephrectomised-desoxycorticosterone hypertensive rat.Virchows Arch425: 181\u2013193, 1994.","DOI":"10.1007\/BF00230355"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000070073.79690.57"},{"key":"R25","doi-asserted-by":"crossref","unstructured":"Kriz W, Hosser H, Hahnel B, Simons JL, and Provoost AP.Development of vascular pole-associated glomerulosclerosis in the Fawn-hooded rat.J Am Soc Nephrol9: 381\u2013396, 1998.","DOI":"10.1681\/ASN.V93381"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.E02-08-0466"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00848.x"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00067.2003"},{"key":"R29","unstructured":"Martineau LC, McVeigh LI, Jasmin BJ, and Kennedy CR.p38 MAP kinase mediates mechanically induced COX-2 and PG EP4 receptor expression in podocytes: implications for the actin cytoskeleton.Am J Physiol Renal Physiol286: F693\u2013F701, 2004."},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.2000.278.2.H339"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1172\/JCI12609"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/15.9.1379"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)63209-9"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00102.x"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00217.x"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00066.x"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1159\/000081555"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00711.x"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1007\/s004240100589"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.2174\/1570161033386745"},{"key":"R41","unstructured":"Simons JL, Provoost AP, Anderson S, Troy JL, Rennke HG, Sandstrom DJ, and Brenner BM.Pathogenesis of glomerular injury in the fawn-hooded rat: early glomerular capillary hypertension predicts glomerular sclerosis.J Am Soc Nephrol3: 1775\u20131782, 1993."},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1204208"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1016\/S1534-5807(03)00297-1"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1016\/S0962-8924(00)89101-1"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1038\/nature02543"},{"key":"R46","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00404.2002"},{"key":"R47","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1996.271.2.C635"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00196.2005","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,7,27]],"date-time":"2021-07-27T01:56:04Z","timestamp":1627350964000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00196.2005"}},"issued":{"date-parts":[[2006,10]]},"references-count":47,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2006,10]]}},"alternative-id":["10.1152\/ajprenal.00196.2005"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00196.2005","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2006,10]]}},{"indexed":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T03:49:37Z","timestamp":1772164177859,"version":"3.50.1"},"reference-count":35,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2012,7,1]]},"abstract":"<jats:p>\n                    Regulation of water and urea transport in the inner medullary collecting duct is essential for urine concentration. Aquaporin (AQP)2 water channels and urea transporter (UT)-A1 are inserted into the apical membrane upon phosphorylation of the channels to allow the transcellular movement of water and urea. Since ANG II activates PKC in many cell types, we tested the hypothesis that ANG II-induced regulation of water and urea transport is mediated by PKC. Osmotic minipumps delivered ANG II to wild-type (WT) or PKC-\u03b1\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice for 7 days. Inner medullas were harvested, and protein abundance was determined by immunoblot. ANG II increased systolic blood pressure to a similar degree in WT and PKC-\u03b1\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice. ANG II had no effect on the urine output of WT mice but increased that of PKC-\u03b1\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice. In accordance with observed differences in urine output, AQP2 abundance was unchanged in ANG II-treated WT animals but was decreased in PKC-\u03b1\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice. No change in membrane accumulation was seen. Phosphorylation of the cAMP-induced transcription factor CREB was decreased in PKC-\u03b1\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice in response to ANG II with no change in overall CREB abndance. ANG II did not alter the abundance of UT-A1 protein in WT or PKC-\u03b1\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice. Phosphorylation and overall abundance of tonicity-responsive enhancer-binding protein, a transcription factor that regulates UT-A1, were also unaltered by ANG II in either group. We conclude that PKC-\u03b1 protects against ANG II-induced decreases in urine concentrating ability by maintaining AQP2 levels through CREB phosphorylation.\n                  <\/jats:p>","DOI":"10.1152\/ajprenal.00098.2012","type":"journal-article","created":{"date-parts":[[2012,4,5]],"date-time":"2012-04-05T00:32:39Z","timestamp":1333585959000},"page":"F37-F44","source":"Crossref","is-referenced-by-count":20,"title":["Lack of protein kinase C-\u03b1 leads to impaired urine concentrating ability and decreased aquaporin-2 in angiotensin II-induced hypertension"],"prefix":"10.1152","volume":"303","author":[{"given":"Tiffany L.","family":"Thai","sequence":"first","affiliation":[{"name":"Renal Division, School of Medicine, Emory University, Atlanta, Georgia"}]},{"given":"Mitsi A.","family":"Blount","sequence":"additional","affiliation":[{"name":"Renal Division, School of Medicine, Emory University, Atlanta, Georgia"}]},{"given":"Janet D.","family":"Klein","sequence":"additional","affiliation":[{"name":"Renal Division, School of Medicine, Emory University, Atlanta, Georgia"}]},{"given":"Jeff M.","family":"Sands","sequence":"additional","affiliation":[{"name":"Renal Division, School of Medicine, Emory University, Atlanta, Georgia"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90228.2008"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00197.2007"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00424.2009"},{"key":"B4","doi-asserted-by":"crossref","first-page":"1658","DOI":"10.1681\/ASN.V8111658","volume":"8","author":"Bouby N","year":"1997","journal-title":"J Am Soc Nephrol"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1038\/nm1000"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/S1097-2765(03)00134-5"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005010031"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00053.2006"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1998.78.3.583"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1096\/fj.09-146985"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1996.270.6.C1695"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/j.cellsig.2004.05.001"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.5.F835"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00682.2009"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00664.2011"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00173.2006"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.272.1.F3"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M407224200"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00090.2006"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00469.2010"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2009.134"},{"key":"B22","doi-asserted-by":"crossref","first-page":"861","DOI":"10.1681\/ASN.V86861","volume":"8","author":"Matsumura Y","year":"1997","journal-title":"J Am Soc Nephrol"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.1996.tb02821.x"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.90.24.11663"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1007\/s00232-002-1053-1"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-003-1124-x"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.biochem.68.1.821"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1590\/S0100-879X2002000900001"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbamem.2006.06.001"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M207525200"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00168.2010"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00322.2010"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1038\/sj.emboj.7601734"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00274.2003"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.272.4.F443"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00098.2012","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,1,12]],"date-time":"2022-01-12T01:27:52Z","timestamp":1641950872000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00098.2012"}},"issued":{"date-parts":[[2012,7,1]]},"references-count":35,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2012,7,1]]}},"alternative-id":["10.1152\/ajprenal.00098.2012"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00098.2012","relation":{"has-review":[{"id-type":"doi","id":"10.3410\/f.717247956.792502907","asserted-by":"object"}]},"ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2012,7,1]]}},{"indexed":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T03:50:05Z","timestamp":1772164205175,"version":"3.50.1"},"reference-count":46,"publisher":"American Physiological Society","issue":"9","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,11,1]]},"abstract":"<jats:p>\n                    Deletions of claudin-2 (Cldn2) and aquaporin1 (AQP1) reduce proximal fluid reabsorption (PFR) by about 30% and 50%, respectively. Experiments were done to replicate these observations and to determine in AQP1\/claudin-2 double knockout mice (DKO) if the effects of deletions of these established water pores are additive. PFR was determined in inactin\/ketamine-anesthetized mice by free-flow micropuncture using single-nephron I\n                    <jats:sup>125<\/jats:sup>\n                    -iothalamate (io) clearance. Animal means of PFR [% of glomerular filtration rate (GFR)] derived from TF\/P\n                    <jats:sub>iothalamate<\/jats:sub>\n                    ratios in 12 mice in each of four groups [wild type (WT), Cldn2\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    , AQP1\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    , and DKO) were 45.8 \u00b1 0.85 (51 tubules), 35.4 \u00b1 1 (54 tubules; P &lt; 0.01 vs. WT), 36.8 \u00b1 1 (63 tubules; P &lt; 0.05 vs. WT), and 33.9 \u00b1 1.4 (69 tubules; P &lt; 0.01 vs. WT). Kidney and single-nephron GFRs (SNGFR) were significantly reduced in all mutant strains. The direct relationship between PFR and SNGFR was maintained in mutant mice, but the slope of this relationship was reduced in the absence of Cldn2 and\/or AQP1. Transtubular osmotic pressure differences were not different between WT and Cldn2\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice, but markedly increased in DKO. In conclusion, the deletion of Cldn2, AQP1, or of both Cldn2 and AQP1 reduces PFR by 22.7%, 19.6%, and 26%, respectively. Our data are consistent with an up to 25% paracellular contribution to PFR. The reduced osmotic water permeability caused by absence of AQP1 augments luminal hypotonicity. Aided by a fall in filtered load, the capacity of non-AQP1-dependent transcellular reabsorption is sufficient to maintain PFR without AQP1 and claudin-2 at 75% of control.\n                  <\/jats:p>","DOI":"10.1152\/ajprenal.00342.2013","type":"journal-article","created":{"date-parts":[[2013,9,18]],"date-time":"2013-09-18T23:59:03Z","timestamp":1379548743000},"page":"F1352-F1364","source":"Crossref","is-referenced-by-count":61,"title":["Fluid reabsorption in proximal convoluted tubules of mice with gene deletions of claudin-2 and\/or aquaporin1"],"prefix":"10.1152","volume":"305","author":[{"given":"Jurgen","family":"Schnermann","sequence":"first","affiliation":[{"name":"Kidney Disease Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland"}]},{"given":"Yuning","family":"Huang","sequence":"additional","affiliation":[{"name":"Kidney Disease Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland"}]},{"given":"Diane","family":"Mizel","sequence":"additional","affiliation":[{"name":"Kidney Disease Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.00165"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1978.234.4.F349"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1984.247.1.F130"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1983.245.3.F279"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1986.250.4.F680"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1007\/BF00583732"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.0021.2001"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1980.60.2.510"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.68.2.127"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00025.2009"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1995.268.5.C1077"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1007\/BF00586045"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.141.7.1539"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.153.2.263"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1984.246.2.F167"},{"key":"B16","doi-asserted-by":"crossref","first-page":"1819","DOI":"10.1002\/cphy.c110045","volume":"2","author":"Gunzel D","year":"2012","journal-title":"Comprehensive Physiol"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2011.03.001"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1126\/science.1279809"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00297.2004"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-201X.2004.01318.x"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-004-1330-1"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0608384104"},{"key":"B23","first-page":"121","volume-title":"Aquaporins","author":"Knepper MA","year":"2001"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1994.266.5.R1544"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.93.23.13367"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.3.F447"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.8.4296"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1007\/s00232-013-9530-2"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1985.249.1.F12"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0912901107"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.120.2.371"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1023\/B:NERE.0000010430.23137.be"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1982.tb06945.x"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1987.253.1.R8"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1985.249.1.F124"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1097\/00006231-200106000-00003"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.060665"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1007\/s004240000258"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.16.9660"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbamem.2005.01.008"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1172\/JCI109229"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.6.F1030"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1007\/BF00582545"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.39.22907"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00581.2004"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1007\/BF00232587"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00342.2013","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,3,6]],"date-time":"2022-03-06T06:48:12Z","timestamp":1646549292000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00342.2013"}},"issued":{"date-parts":[[2013,11,1]]},"references-count":46,"journal-issue":{"issue":"9","published-print":{"date-parts":[[2013,11,1]]}},"alternative-id":["10.1152\/ajprenal.00342.2013"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00342.2013","relation":{"has-review":[{"id-type":"doi","id":"10.3410\/f.718114263.793537186","asserted-by":"object"}]},"ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2013,11,1]]}},{"indexed":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T03:50:14Z","timestamp":1772164214162,"version":"3.50.1"},"reference-count":59,"publisher":"American Physiological Society","issue":"1","funder":[{"DOI":"10.13039\/100000054","name":"HHS | NIH | National Cancer Institute","doi-asserted-by":"publisher","award":["P30-CA068485"],"award-info":[{"award-number":["P30-CA068485"]}],"id":[{"id":"10.13039\/100000054","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["K08-DK106472"],"award-info":[{"award-number":["K08-DK106472"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["R01-DK101791"],"award-info":[{"award-number":["R01-DK101791"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["R01-DK81646"],"award-info":[{"award-number":["R01-DK81646"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["P30-DK020593"],"award-info":[{"award-number":["P30-DK020593"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["U24-DK059637"],"award-info":[{"award-number":["U24-DK059637"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["P30-DK114809"],"award-info":[{"award-number":["P30-DK114809"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2022,7,1]]},"abstract":"<jats:p>Disruption of the blood-urine barrier can result in acute or chronic inflammatory bladder injury. Here, we demonstrate that pharmacological inhibition of hypoxia-inducible factor (HIF)-prolyl hydroxylation prevented bladder injury and protected from urinary dysfunction in a mouse model of cyclophosphamide-induced disruption of the blood-urine barrier. Our study highlights a potential role for HIF-activating small-molecule compounds in the prevention or therapy of bladder injury and urinary dysfunction and provides a rationale for future clinical studies.<\/jats:p>","DOI":"10.1152\/ajprenal.00344.2021","type":"journal-article","created":{"date-parts":[[2022,5,2]],"date-time":"2022-05-02T07:46:38Z","timestamp":1651477598000},"page":"F81-F91","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":3,"title":["Inhibition of hypoxia-inducible factor-prolyl hydroxylation protects from cyclophosphamide-induced bladder injury and urinary dysfunction"],"prefix":"10.1152","volume":"323","author":[{"given":"Douglass B.","family":"Clayton","sequence":"first","affiliation":[{"name":"Division of Pediatric Urology, Department of Urology, Vanderbilt University Medical Center, Nashville, Tennessee"}]},{"given":"Ching Man Carmen","family":"Tong","sequence":"additional","affiliation":[{"name":"Division of Pediatric Urology, Department of Urology, Vanderbilt University Medical Center, Nashville, Tennessee"}]},{"given":"Belinda","family":"Li","sequence":"additional","affiliation":[{"name":"Division of Pediatric Urology, Department of Urology, Vanderbilt University Medical Center, Nashville, Tennessee"}]},{"given":"Abby S.","family":"Taylor","sequence":"additional","affiliation":[{"name":"Division of Pediatric Urology, Department of Urology, Vanderbilt University Medical Center, Nashville, Tennessee"}]},{"given":"Shuvro","family":"De","sequence":"additional","affiliation":[{"name":"Division of Pediatric Urology, Department of Urology, Vanderbilt University Medical Center, Nashville, Tennessee"}]},{"given":"Matthew D.","family":"Mason","sequence":"additional","affiliation":[{"name":"Division of Pediatric Urology, Department of Urology, Vanderbilt University Medical Center, Nashville, Tennessee"}]},{"given":"Anne G.","family":"Dudley","sequence":"additional","affiliation":[{"name":"Division of Pediatric Urology, Department of Urology, Vanderbilt University Medical Center, Nashville, Tennessee"}]},{"given":"Olena","family":"Davidoff","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee"},{"name":"Medical and Research Services, Department of Veterans Affairs Hospital, Tennessee Valley Healthcare System, Nashville, Tennessee"}]},{"given":"Hanako","family":"Kobayashi","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee"},{"name":"Medical and Research Services, Department of Veterans Affairs Hospital, Tennessee Valley Healthcare System, Nashville, Tennessee"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7051-8994","authenticated-orcid":true,"given":"Volker H.","family":"Haase","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee"},{"name":"Medical and Research Services, Department of Veterans Affairs Hospital, Tennessee Valley Healthcare System, Nashville, Tennessee"},{"name":"Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1097\/01.ju.0000152092.03931.9a"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1097\/01.ju.0000155595.98120.8e"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1097\/01.ju.0000155596.98780.82"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/j.urology.2016.07.030"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/j.urology.2015.11.001"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/j.juro.2013.02.026"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-021-92756-1"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1097\/JIM.0000000000000218"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1038\/nrd4422"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1146\/annurev-pharmtox-010818-021637"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1172\/JCI21086"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1146\/annurev-physiol-021909-135922"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1038\/nchembio0308-152"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/j.molcel.2008.04.009"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1038\/nm.2507"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00224.2015"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/j.mam.2016.01.001"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1038\/nrm1366"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1126\/science.1059796"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1172\/JCI30117"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1053\/j.gastro.2007.10.012"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1126\/scitranslmed.3008523"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1039\/c7sc02103h"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1002\/cmdc.201700783"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1016\/j.kisu.2020.12.002"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00350.2018"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00245.2018"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.151.5.961"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2017.06.015"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1089\/neu.2013.2888"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1016\/j.jchromb.2013.07.004"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1124\/dmd.118.083766"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.4314\/ejhs.v28i6.5"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(01)00507-4"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1016\/0006-2952(79)90222-3"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1111\/j.1464-410X.2007.06773.x"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00297.2013"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1016\/j.devcel.2013.07.017"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.3389\/fnsys.2018.00009"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00083.2019"},{"key":"B41","first-page":"113","volume":"48","author":"Juszczak K","year":"2007","journal-title":"Folia Med Cracov"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-018-38274-z"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1096\/fj.201701415R"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0111838"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1016\/j.urology.2012.07.019"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1016\/j.juro.2015.08.001"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00240.2017"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1053\/j.gastro.2010.06.068"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1038\/mi.2013.29"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1152\/ajplung.00250.2011"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1007\/s10565-006-0078-0"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.082370"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1084\/jem.193.9.1027"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1172\/JCI84433"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1111\/febs.13578"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00202.2014"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00139.2013"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1523005113"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2016.02.006"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00344.2021","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,6,21]],"date-time":"2022-06-21T11:57:42Z","timestamp":1655812662000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00344.2021"}},"issued":{"date-parts":[[2022,7,1]]},"references-count":59,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2022,7,1]]}},"alternative-id":["10.1152\/ajprenal.00344.2021"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00344.2021","relation":{"has-review":[{"id-type":"doi","id":"10.3410\/f.742103411.793594191","asserted-by":"object"}]},"ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2022,7,1]]},"assertion":[{"value":"2021-09-16","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2022-04-25","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2022-04-25","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2022-06-21","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T03:50:23Z","timestamp":1772164223419,"version":"3.50.1"},"reference-count":55,"publisher":"American Physiological Society","issue":"8","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,10,15]]},"abstract":"<jats:p>\n                    Epithelial cells are continuously exposed to mechanical forces including shear stress and stretch, although the effect these forces have on tight junction (TJ) organization and function are poorly understood. Umbrella cells form the outermost layer of the stratified uroepithelium and undergo large cell shape and surface area changes during the bladder cycle. Here we investigated the effects of bladder filling and voiding on the umbrella cell TJ. We found that bladder filling promoted a significant increase in the length of the TJ ring, which was quickly reversed within 5 min of voiding. Interestingly, when isolated uroepithelial tissue was mounted in Ussing chambers and exposed to physiological stretch, we observed a 10-fold drop in both transepithelial electrical resistance (TER) and the umbrella cell junctional resistance. The effects of stretch on TER were reversible and dependent on the applied force. Furthermore, the integrity of the umbrella cell TJ was maintained in the stretched uroepithelium, as suggested by the limited permeability of biotin, fluorescein, and ruthenium red. Finally, we found that depletion of extracellular Ca\n                    <jats:sup>2+<\/jats:sup>\n                    by EGTA completely disrupted the TER of unstretched, but not of stretched uroepithelium. Taken together, our studies indicate that the umbrella cell TJ undergoes major structural and functional reorganization during the bladder cycle. The impact of these changes on bladder function is discussed.\n                  <\/jats:p>","DOI":"10.1152\/ajprenal.00282.2013","type":"journal-article","created":{"date-parts":[[2013,7,25]],"date-time":"2013-07-25T10:54:06Z","timestamp":1374749646000},"page":"F1158-F1168","source":"Crossref","is-referenced-by-count":58,"title":["Bladder filling and voiding affect umbrella cell tight junction organization and function"],"prefix":"10.1152","volume":"305","author":[{"given":"Marcelo D.","family":"Carattino","sequence":"first","affiliation":[{"name":"Department of Medicine Renal-Electrolyte Division, University of Pittsburgh, Pittsburgh, Pennsylvania; and"},{"name":"Department of Cell Biology, University of Pittsburgh, Pittsburgh, Pennsylvania"}]},{"given":"H. Sandeep","family":"Prakasam","sequence":"additional","affiliation":[{"name":"Department of Medicine Renal-Electrolyte Division, University of Pittsburgh, Pittsburgh, Pennsylvania; and"}]},{"given":"Wily G.","family":"Ruiz","sequence":"additional","affiliation":[{"name":"Department of Medicine Renal-Electrolyte Division, University of Pittsburgh, Pittsburgh, Pennsylvania; and"}]},{"given":"Dennis R.","family":"Clayton","sequence":"additional","affiliation":[{"name":"Department of Medicine Renal-Electrolyte Division, University of Pittsburgh, Pittsburgh, Pennsylvania; and"}]},{"given":"Meredith","family":"McGuire","sequence":"additional","affiliation":[{"name":"Department of Medicine Renal-Electrolyte Division, University of Pittsburgh, Pittsburgh, Pennsylvania; and"}]},{"given":"Luciana I.","family":"Gallo","sequence":"additional","affiliation":[{"name":"Department of Medicine Renal-Electrolyte Division, University of Pittsburgh, Pittsburgh, Pennsylvania; and"}]},{"given":"Gerard","family":"Apodaca","sequence":"additional","affiliation":[{"name":"Department of Medicine Renal-Electrolyte Division, University of Pittsburgh, Pittsburgh, Pennsylvania; and"},{"name":"Department of Cell Biology, University of Pittsburgh, Pittsburgh, Pennsylvania"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00341.2003"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1101\/cshperspect.a002584"},{"key":"B2a","doi-asserted-by":"publisher","DOI":"10.1016\/S0090-4295(01)01026-3"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1096\/fj.04-3260com"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00341.2002"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1165\/ajrcmb.25.5.4486"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.2436350100"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.143.2.391"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.147.4.891"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1990.259.6.C978"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-185X.1975.tb01057.x"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.22590"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.266.5.F775"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00327.2009"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.E12-08-0568"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0805636105"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1038\/emboj.2010.91"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/j.jmb.2007.09.040"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.2012.06555.x"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1007\/s00018-012-0949-x"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1038\/297685a0"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1007\/978-94-009-1495-7_5"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.6.F867"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1007\/BF01869689"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1007\/BF01868646"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.87.3.736"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.02-02-0029"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.00972"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1007\/BF00219766"},{"key":"B30","doi-asserted-by":"crossref","first-page":"227","DOI":"10.1007\/BF00225533","volume":"186","author":"Metz J","year":"1978","journal-title":"Cell Tissue Res"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M406906200"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.145.3.579"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200302070"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.56.3.797"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.96.3.606"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1007\/s11626-008-9116-y"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1007\/s00232-001-0182-2"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.22.1.173"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.E04-12-1089"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1146\/annurev-physiol-012110-142150"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200711165"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M109.000521"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.01-09-0435"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.E05-03-0193"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1152\/physiol.00027.2004"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00138.2006"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.20676"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00403.2002"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1016\/S1046-2023(03)00027-6"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1165\/ajrcmb.22.2.3938"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(82)90339-7"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.200810154"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.E08-04-0439"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00025.2006"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.E11-09-0823"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00282.2013","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:56:07Z","timestamp":1567972567000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00282.2013"}},"issued":{"date-parts":[[2013,10,15]]},"references-count":55,"journal-issue":{"issue":"8","published-print":{"date-parts":[[2013,10,15]]}},"alternative-id":["10.1152\/ajprenal.00282.2013"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00282.2013","relation":{"has-review":[{"id-type":"doi","id":"10.3410\/f.718047205.793488741","asserted-by":"object"}]},"ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2013,10,15]]}},{"indexed":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T03:50:23Z","timestamp":1772164223553,"version":"3.50.1"},"reference-count":37,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2010,3]]},"abstract":"<jats:p>It is unknown whether generalized vascular dysfunction precedes the development of kidney disease. Therefore, we studied myogenic constriction and endothelium-mediated dilatory responses in two inbred Fawn-Hooded (FH) rat strains, one of which spontaneously develops hypertension, proteinuria, and glomerulosclerosis (FHH), whereas the other (FHL) does not. Small renal, mesenteric resistance arteries and thoracic aorta isolated from FH rats before (7 wk old) and after the development of mild proteinuria (12 wks old) were mounted in perfused and isometric set-ups, respectively. Myogenic response, endothelium-dependent relaxation, and the contribution of endothelium-mediated dilatory compounds were studied using their respective inhibitors. Myogenic reactivity was assessed constructing pressure-diameter curves in the presence and absence of calcium. At the age of 7 wk, renal arteries isolated from kidneys of FHH rats developed significantly lower myogenic tone compared with FHL, most likely because of excessive cyclo-oxygenase 1-mediated production of constrictive prostaglandins. Consequently, young FHH demonstrated reduced maximal myogenic tone (22 \u00b1 4.8 vs. 10.8 \u00b1 2.0%, P = 0.03) and the peak myogenic index (\u22126.9 \u00b1 4.8 vs. 0.6 \u00b1 0.8%\/mmHg, P = 0.07 for FHL vs. FHH, respectively). Active myogenic curves obtained in mesenteric arteries isolated from 7-wk-old rats did not differ between either strain, demonstrating a similar level of systemic myogenic tone in FHL and FHH rats. Therefore, before any renal end-organ damage is present, myogenic response seems selectively impaired in renal vasculature of FHH rats. Aortic reactivity did not differ between FHL and FHH at the time points studied. The present study shows that vascular dysfunction in both small renal and systemic arteries precedes renal end-organ damage in a spontaneous model of hypertension-associated renal damage. These early vascular changes might be potentially involved in the increased susceptibility of FHH rats to renal injury.<\/jats:p>","DOI":"10.1152\/ajprenal.00289.2009","type":"journal-article","created":{"date-parts":[[2009,12,9]],"date-time":"2009-12-09T21:37:43Z","timestamp":1260394663000},"page":"F625-F633","source":"Crossref","is-referenced-by-count":29,"title":["Renal vascular dysfunction precedes the development of renal damage in the hypertensive Fawn-Hooded rat"],"prefix":"10.1152","volume":"298","author":[{"given":"Peter","family":"Ochodnick\u00fd","sequence":"first","affiliation":[{"name":"Faculty of Pharmacy, Department of Pharmacology and Toxicology, Comenius University Bratislava, Bratislava, Slovakia;"}]},{"given":"Robert H.","family":"Henning","sequence":"additional","affiliation":[{"name":"Department of Clinical Pharmacology, University Medical Center Groningen and Groningen Institute for Drug Exploration, University of Groningen, Groningen; and"}]},{"given":"Hendrik J.","family":"Buikema","sequence":"additional","affiliation":[{"name":"Department of Clinical Pharmacology, University Medical Center Groningen and Groningen Institute for Drug Exploration, University of Groningen, Groningen; and"}]},{"given":"Dick","family":"de Zeeuw","sequence":"additional","affiliation":[{"name":"Department of Clinical Pharmacology, University Medical Center Groningen and Groningen Institute for Drug Exploration, University of Groningen, Groningen; and"}]},{"given":"Abraham P.","family":"Provoost","sequence":"additional","affiliation":[{"name":"Department of Pediatric Surgery, Erasmus Medical Center, Rotterdam, The Netherlands"}]},{"given":"Richard P. E.","family":"van Dokkum","sequence":"additional","affiliation":[{"name":"Department of Clinical Pharmacology, University Medical Center Groningen and Groningen Institute for Drug Exploration, University of Groningen, Groningen; and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1042\/cs0970037"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.19.6.795"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1999.79.2.387"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1007\/BF00285287"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1999.276.1.R189"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000145895.62896.98"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/S0895-7061(97)00163-5"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1999.276.3.R855"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1038\/24388"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1097\/00005344-199204002-00053"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000036865.22253.D4"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00431.x"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.19.4.326"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-198907000-00003"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1159\/000187098"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00331.x"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00159.2004"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00335.2005"},{"key":"B19","first-page":"96","volume":"13","author":"Morris ST","year":"2000","journal-title":"J Nephrol"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfn483"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005121322"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.54.7.2206"},{"key":"B23","first-page":"S2","volume":"45","author":"Provoost AP","year":"1994","journal-title":"Kidney Int Suppl"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1161\/hy1201.096817"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000019756.88731.83"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1097\/00005344-199611000-00014"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.287"},{"key":"B28","doi-asserted-by":"crossref","first-page":"1775","DOI":"10.1681\/ASN.V3111775","volume":"3","author":"Simons JL","year":"1993","journal-title":"J Am Soc Nephrol"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.2337\/diab.44.5.561"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0706042"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1016\/S0033-0620(96)80003-X"},{"key":"B32","doi-asserted-by":"crossref","first-page":"71","DOI":"10.1681\/ASN.V11171","volume":"11","author":"Veelken R","year":"2000","journal-title":"J Am Soc Nephrol"},{"key":"B33","doi-asserted-by":"crossref","first-page":"249","DOI":"10.1681\/ASN.V82249","volume":"8","author":"Verseput GH","year":"1997","journal-title":"J Am Soc Nephrol"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1097\/01.hjh.0000249699.04113.36"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00036.x"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.4.F706"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000047651.45322.16"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00289.2009","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,10,15]],"date-time":"2021-10-15T17:16:31Z","timestamp":1634318191000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00289.2009"}},"issued":{"date-parts":[[2010,3]]},"references-count":37,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2010,3]]}},"alternative-id":["10.1152\/ajprenal.00289.2009"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00289.2009","relation":{"has-review":[{"id-type":"doi","id":"10.3410\/f.1355959.827057","asserted-by":"object"}]},"ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2010,3]]}},{"indexed":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T03:50:23Z","timestamp":1772164223935,"version":"3.50.1"},"reference-count":37,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2010,12]]},"abstract":"<jats:p>\n                    Salt reabsorption by the loop of Henle controls NaCl handling and blood pressure regulation. Increased oxidative stress stimulates NaCl transport in one specific segment of the loop of Henle called the thick ascending limb (TAL). The isoprostane 8-iso-prostaglandin-F2\u03b1 (8-iso-PGF2\u03b1) is one of the most abundant nonenzymatic lipid oxidation products and has been implicated in the development of hypertension. However, it is not known whether 8-iso-PGF2\u03b1 regulates transport or the mechanisms involved. Because protein kinase A (PKA) stimulates NaCl transport in several nephron segments, we hypothesized that 8-iso-PGF2\u03b1 increases NaCl transport in the cortical TAL (cTAL) via a PKA-dependent mechanism. We examined the effect of luminal 8-iso-PGF2\u03b1 on NaCl transport by measuring chloride absorption ( J\n                    <jats:sub>Cl<\/jats:sub>\n                    ) in isolated microperfused cTALs. Adding 8-iso-PGF2\u03b1 to the lumen increased J\n                    <jats:sub>Cl<\/jats:sub>\n                    by 54% (from 288.7 \u00b1 30.6 to 446.5 \u00b1 44.3 pmol\u00b7min\n                    <jats:sup>\u22121<\/jats:sup>\n                    \u00b7mm\n                    <jats:sup>\u22121<\/jats:sup>\n                    ; P &lt; 0.01), while adding it to the bath enhanced J\n                    <jats:sub>Cl<\/jats:sub>\n                    by 35% (from 236.3 \u00b1 35.3 to 319.2 \u00b1 39.8 pmol\u00b7min\n                    <jats:sup>\u22121<\/jats:sup>\n                    \u00b7mm\n                    <jats:sup>\u22121<\/jats:sup>\n                    ; P &lt; 0.05). This stimulation was blocked by Na-K-2Cl cotransporter inhibition. Next, we tested the role of cAMP. Basal cAMP in the cTAL was 18.6 \u00b1 1.6 fmol\u00b7min\n                    <jats:sup>\u22121<\/jats:sup>\n                    \u00b7mm\n                    <jats:sup>\u22121<\/jats:sup>\n                    , and 8-iso-PGF2\u03b1 raised it to 35.1 \u00b1 1.4 fmol\u00b7min\n                    <jats:sup>\u22121<\/jats:sup>\n                    \u00b7mm\n                    <jats:sup>\u22121<\/jats:sup>\n                    , an increase of 94% ( P &lt; 0.01). Because cAMP stimulates PKA, we measured J\n                    <jats:sub>Cl<\/jats:sub>\n                    using the PKA-selective inhibitor H89. In the presence of H89 (10 \u03bcM), 8-iso-PGF2\u03b1 failed to increase transport regardless of whether it was added to the lumen (216.1 \u00b1 16.7 vs. 209.7 \u00b1 23.8 pmol\u00b7min\n                    <jats:sup>\u22121<\/jats:sup>\n                    \u00b7mm\n                    <jats:sup>\u22121<\/jats:sup>\n                    ; NS) or the bath (150.4 \u00b1 32.9 vs. 127.1 \u00b1 28.6 pmol\u00b7min\n                    <jats:sup>\u22121<\/jats:sup>\n                    \u00b7mm\n                    <jats:sup>\u22121<\/jats:sup>\n                    ; NS). We concluded that 8-iso-PGF2\u03b1 stimulates cAMP and increases Cl transport in cTALs via a PKA-dependent mechanism.\n                  <\/jats:p>","DOI":"10.1152\/ajprenal.00225.2010","type":"journal-article","created":{"date-parts":[[2010,9,22]],"date-time":"2010-09-22T21:05:14Z","timestamp":1285189514000},"page":"F1396-F1400","source":"Crossref","is-referenced-by-count":8,"title":["8-iso-prostaglandin-F2\u03b1 stimulates chloride transport in thick ascending limbs: role of cAMP and protein kinase A"],"prefix":"10.1152","volume":"299","author":[{"given":"Pablo D.","family":"Cabral","sequence":"first","affiliation":[{"name":"Hypertension and Vascular Research Division, Department of Internal Medicine, Henry Ford Hospital, Detroit, Michigan;"}]},{"given":"Guillermo B.","family":"Silva","sequence":"additional","affiliation":[{"name":"Department of Renal Physiology, J. Robert Cade Foundation CONICET, Cordoba;"},{"name":"Department of Renal Physiology and Hypertension, Mons. Carlos V. Cruvellier Foundation, San Juan, Argentina; and"}]},{"given":"Sandra T.","family":"Baigorria","sequence":"additional","affiliation":[{"name":"Department of Renal Physiology, J. Robert Cade Foundation CONICET, Cordoba;"}]},{"given":"Luis A.","family":"Juncos","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics and Division of Nephrology, Department of Medicine, University of Mississippi Medical Center, Jackson, Mississippi"}]},{"given":"Luis I.","family":"Juncos","sequence":"additional","affiliation":[{"name":"Department of Renal Physiology, J. Robert Cade Foundation CONICET, Cordoba;"}]},{"given":"N\u00e9stor H.","family":"Garc\u00eda","sequence":"additional","affiliation":[{"name":"Department of Renal Physiology, J. Robert Cade Foundation CONICET, Cordoba;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1996.271.2.C455"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90446.2008"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1996.1404"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1089\/ars.2005.7.236"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1038\/348637a0"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1982.198"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M109.037135"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1977.232.4.F383"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1999.277.5.R1476"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00239.x"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.34.3.508"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1985.65.3.760"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.34.4.983"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00543.2009"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00447.2005"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/j.bcp.2008.03.014"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.1993.tb55605.x"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.37.2.541"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00346.2001"},{"key":"B20","doi-asserted-by":"crossref","first-page":"4317","DOI":"10.1016\/S0021-9258(17)41781-9","volume":"269","author":"Morrow JD","year":"1994","journal-title":"J Biol Chem"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.38.3.655"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00248.2005"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.3.F359"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118745"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.35.1.476"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.34.20617"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/S0005-2760(96)00162-2"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.33.1.424"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.259.3.F408"},{"key":"B30","author":"Silva GB","year":"2006","journal-title":"J Am Soc Nephrol"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.108.120212"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00472.2009"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000236646.83354.51"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00021.2003"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00269.2004"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115790"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000136395.06810.cf"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00225.2010","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,11,10]],"date-time":"2021-11-10T08:02:37Z","timestamp":1636531357000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00225.2010"}},"issued":{"date-parts":[[2010,12]]},"references-count":37,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2010,12]]}},"alternative-id":["10.1152\/ajprenal.00225.2010"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00225.2010","relation":{"has-review":[{"id-type":"doi","id":"10.3410\/f.7084956.7308055","asserted-by":"object"}]},"ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2010,12]]}},{"indexed":{"date-parts":[[2026,2,25]],"date-time":"2026-02-25T12:06:16Z","timestamp":1772021176829,"version":"3.50.1"},"reference-count":38,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2002,5,1]]},"abstract":"<jats:p>The role of nitric oxide (NO) and prostaglandins (PG) in modifying renal hemodynamics was examined in clipped and nonclipped kidneys of unilateral renal artery stenosis. Chronic unilateral renal ischemia was established by 4-wk-clipping the left renal artery of canine kidneys, and renal interstitial nitrate+nitrite and PGE<jats:sub>2<\/jats:sub>contents were evaluated by the microdialysis technique. Unilateral renal artery stenosis caused 45 \u00b1 1 and 73 \u00b1 1% decrements in renal plasma flow (RPF) in moderately and severely clipped kidneys and 21 \u00b1 3% decrements in nonclipped kidneys with severe stenosis. Renal nitrate+nitrite decreased in moderately (\u221231 \u00b1 1%) and severely clipped kidneys (\u221263 \u00b1 4%). N<jats:sup>\u03c9<\/jats:sup>-nitro-l-arginine methyl ester reduced RPF (\u221256 \u00b1 3%) and glomerular filtration rate (GFR; \u221254 \u00b1 3%) in moderately clipped kidneys, whereas this inhibitory effect was abolished in severely clipped kidneys. In contrast, renal PGE<jats:sub>2<\/jats:sub>contents increased modestly in moderate clipping and were markedly elevated in severely clipped kidneys (from 111 \u00b1 7 to 377 \u00b1 22 pg\/ml); sulpyrine impaired renal hemodynamics only in severely clipped kidneys. In contralateral nonclipped kidneys, although renal PGE<jats:sub>2<\/jats:sub>was not increased, sulpyrine reduced RPF (\u221232 \u00b1 1%) and GFR (\u221233 \u00b1 3%) in severe stenosis. Collectively, NO plays a substantial role in maintaining renal hemodynamics both under basal condition and in moderate renal artery stenosis, whereas the contributory role shifts from NO to PG as renal artery stenosis progresses. Furthermore, because intrarenal angiotensin II is reported to increase in nonclipped kidneys, unilateral severe ischemia may render the nonclipped kidney susceptible to PG inhibition.<\/jats:p>","DOI":"10.1152\/ajprenal.00012.2001","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:35:05Z","timestamp":1425414905000},"page":"F859-F865","source":"Crossref","is-referenced-by-count":13,"title":["Stenosis-dependent role of nitric oxide and prostaglandins in chronic renal ischemia"],"prefix":"10.1152","volume":"282","author":[{"given":"Hirobumi","family":"Tokuyama","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, School of Medicine, Keio University, Tokyo 160-8582, Japan"}]},{"given":"Koichi","family":"Hayashi","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, School of Medicine, Keio University, Tokyo 160-8582, Japan"}]},{"given":"Hiroto","family":"Matsuda","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, School of Medicine, Keio University, Tokyo 160-8582, Japan"}]},{"given":"Eiji","family":"Kubota","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, School of Medicine, Keio University, Tokyo 160-8582, Japan"}]},{"given":"Masanori","family":"Honda","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, School of Medicine, Keio University, Tokyo 160-8582, Japan"}]},{"given":"Ken","family":"Okubo","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, School of Medicine, Keio University, Tokyo 160-8582, Japan"}]},{"given":"Yuri","family":"Ozawa","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, School of Medicine, Keio University, Tokyo 160-8582, Japan"}]},{"given":"Takao","family":"Saruta","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, School of Medicine, Keio University, Tokyo 160-8582, Japan"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117421"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.267.1.F174"},{"key":"B3","doi-asserted-by":"crossref","first-page":"875","DOI":"10.1681\/ASN.V16875","volume":"1","author":"Baylis C","year":"1990","journal-title":"J Am Soc Nephrol"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.262.6.F943"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.98.18.1842"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.5.F797"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.33.6.1470"},{"key":"B8","first-page":"2","volume":"16","author":"Greco BA","year":"1996","journal-title":"Semin Nephrol"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.31.1.201"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1982.243.6.F553"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00791.x"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.17.5.707"},{"key":"B13","doi-asserted-by":"crossref","first-page":"2272","DOI":"10.1681\/ASN.V10112272","volume":"10","author":"Matsuda H","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-199512000-00006"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1994.267.6.H2245"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.25.4.796"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118681"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1007\/BF00227908"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/0304-3940(94)90073-6"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1378\/chest.111.2_Supplement.46S"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1983.245.2.F131"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1016\/0090-6980(80)90144-6"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-199715120-00001"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.36.6.81"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.40.1.35"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.11.6.724"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-199601000-00013"},{"key":"B29","first-page":"721","volume":"91","author":"Shimamoto K","year":"1978","journal-title":"J Lab Clin Med"},{"key":"B30","first-page":"212","volume":"19","author":"Shintani F","year":"1994","journal-title":"J Psychiatry Neurosci"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.31.2.649"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.20.5.643"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.25.5.1021"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1984.247.6.F975"},{"key":"B35","first-page":"S98","volume":"18","author":"Tokuyama H","year":"2000","journal-title":"J Hypertens"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1016\/0140-6736(92)90865-Z"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.34.1.96"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.29.4.1025"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.31.1.271"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00012.2001","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,5,1]],"date-time":"2022-05-01T09:34:31Z","timestamp":1651397671000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00012.2001"}},"issued":{"date-parts":[[2002,5,1]]},"references-count":38,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2002,5,1]]}},"alternative-id":["10.1152\/ajprenal.00012.2001"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00012.2001","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2002,5,1]]}},{"indexed":{"date-parts":[[2026,2,25]],"date-time":"2026-02-25T09:22:43Z","timestamp":1772011363524,"version":"3.50.1"},"reference-count":41,"publisher":"American Physiological Society","issue":"3","funder":[{"name":"Conacyt Mexico","award":["188712"],"award-info":[{"award-number":["188712"]}]},{"name":"DGAPA-UNAM","award":["IN207716"],"award-info":[{"award-number":["IN207716"]}]},{"name":"NIDDK, NIH","award":["DK051496-15"],"award-info":[{"award-number":["DK051496-15"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2018,9,1]]},"abstract":"<jats:p>Familial hyperkalemic hypertension (FHHt) can be mainly attributed to increased activity of the renal Na<jats:sup>+<\/jats:sup>:Cl<jats:sup>\u2212<\/jats:sup>cotransporter (NCC), which is caused by altered expression and regulation of the with-no-lysine (K) 1 (WNK1) or WNK4 kinases. The WNK1 gene gives rise to a kidney-specific isoform that lacks the kinase domain (KS-WNK1), the expression of which occurs primarily in the distal convoluted tubule. The role played by KS-WNK1 in the modulation of the WNK\/STE20-proline-alanine rich kinase (SPAK)\/NCC pathway remains elusive. In the present study, we assessed the effect of human KS-WNK1 on NCC activity and on the WNK4-SPAK pathway. Microinjection of oocytes with human KS-WNK1 cRNA induces remarkable activation and phosphorylation of SPAK and NCC. The effect of KS-WNK1 was abrogated by eliminating a WNK-WNK-interacting domain and by a specific WNK inhibitor, WNK463, indicating that the activation of SPAK\/NCC by KS-WNK1 is due to interaction with another WNK kinase. Under control conditions in oocytes, the activating serine 335 of the WNK4 T loop is not phosphorylated. In contrast, this serine becomes phosphorylated when the intracellular chloride concentration ([Cl<jats:sup>\u2212<\/jats:sup>]<jats:sub>i<\/jats:sub>) is reduced or when KS-WNK1 is coexpressed with WNK4. KS-WNK1-mediated activation of WNK4 is not due to a decrease of the [Cl<jats:sup>\u2212<\/jats:sup>]<jats:sub>i<\/jats:sub>. Coimmunoprecipitation analysis revealed that KS-WNK1 and WNK4 interact with each other and that WNK4 becomes autophosphorylated at serine 335 when it is associated with KS-WNK1. Together, these observations suggest that WNK4 becomes active in the presence of KS-WNK1, despite a constant [Cl<jats:sup>\u2212<\/jats:sup>]<jats:sub>i<\/jats:sub>.<\/jats:p>","DOI":"10.1152\/ajprenal.00145.2018","type":"journal-article","created":{"date-parts":[[2018,5,31]],"date-time":"2018-05-31T16:13:51Z","timestamp":1527783231000},"page":"F734-F745","source":"Crossref","is-referenced-by-count":52,"title":["Kidney-specific WNK1 isoform (KS-WNK1) is a potent activator of WNK4 and NCC"],"prefix":"10.1152","volume":"315","author":[{"given":"Eduardo R.","family":"Argaiz","sequence":"first","affiliation":[{"name":"Molecular Physiology Unit, Instituto de Investigaciones Biom\u00e9dicas, Universidad Nacional Aut\u00f3noma de M\u00e9xico, Tlalpan, Mexico City, Mexico"},{"name":"Department of Nephrology and Mineral Metabolism, Instituto Nacional de Ciencias M\u00e9dicas y Nutrici\u00f3n Salvador Zubir\u00e1n, Tlalpan Mexico City, Mexico"},{"name":"Tecnol\u00f3gico de Monterrey, Escuela de Medicina y Ciencias de la Salud, Monterrey, Nuevo Le\u00f3n, Mexico"}]},{"given":"Maria","family":"Chavez-Canales","sequence":"additional","affiliation":[{"name":"INSERM UMRS1155, University Pierre and Marie Curie, Faculty of Medicine, Paris, France"},{"name":"Translational Medicine Unit, Instituto de Investigaciones Biom\u00e9dicas, Universidad Nacional Aut\u00f3noma de M\u00e9xico and Instituto Nacional de Cardiolog\u00eda Ignacio Ch\u00e1vez, Tlalpan, M\u00e9xico City, Mexico"}]},{"given":"Mauricio","family":"Ostrosky-Frid","sequence":"additional","affiliation":[{"name":"Department of Nephrology and Mineral Metabolism, Instituto Nacional de Ciencias M\u00e9dicas y Nutrici\u00f3n Salvador Zubir\u00e1n, Tlalpan Mexico City, Mexico"},{"name":"PECEM, Facultad de Medicina, Universidad Nacional Aut\u00f3noma de M\u00e9xico, Coyoacan, Mexico City, Mexico"}]},{"given":"Alejandro","family":"Rodr\u00edguez-Gama","sequence":"additional","affiliation":[{"name":"Molecular Physiology Unit, Instituto de Investigaciones Biom\u00e9dicas, Universidad Nacional Aut\u00f3noma de M\u00e9xico, Tlalpan, Mexico City, Mexico"}]},{"given":"Norma","family":"V\u00e1zquez","sequence":"additional","affiliation":[{"name":"Molecular Physiology Unit, Instituto de Investigaciones Biom\u00e9dicas, Universidad Nacional Aut\u00f3noma de M\u00e9xico, Tlalpan, Mexico City, Mexico"},{"name":"Department of Nephrology and Mineral Metabolism, Instituto Nacional de Ciencias M\u00e9dicas y Nutrici\u00f3n Salvador Zubir\u00e1n, Tlalpan Mexico City, Mexico"}]},{"given":"Xochiquetzal","family":"Gonzalez-Rodriguez","sequence":"additional","affiliation":[{"name":"Departamento de Qu\u00edmica Anal\u00edtica, Facultad de Qu\u00edmica, Universidad Nacional Aut\u00f3noma de M\u00e9xico, Coyoacan, Mexico City, Mexico"}]},{"given":"Jesus","family":"Garcia-Valdes","sequence":"additional","affiliation":[{"name":"Departamento de Qu\u00edmica Anal\u00edtica, Facultad de Qu\u00edmica, Universidad Nacional Aut\u00f3noma de M\u00e9xico, Coyoacan, Mexico City, Mexico"}]},{"given":"Juliette","family":"Hadchouel","sequence":"additional","affiliation":[{"name":"INSERM UMRS1155, University Pierre and Marie Curie, Faculty of Medicine, Paris, France"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2915-265X","authenticated-orcid":false,"given":"David","family":"Ellison","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Medicine, Oregon Health and Science University, Portland, Oregon"},{"name":"Veterans Affairs Portland Health Care System, Portland, Oregon"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4378-9043","authenticated-orcid":false,"given":"Gerardo","family":"Gamba","sequence":"additional","affiliation":[{"name":"Molecular Physiology Unit, Instituto de Investigaciones Biom\u00e9dicas, Universidad Nacional Aut\u00f3noma de M\u00e9xico, Tlalpan, Mexico City, Mexico"},{"name":"Department of Nephrology and Mineral Metabolism, Instituto Nacional de Ciencias M\u00e9dicas y Nutrici\u00f3n Salvador Zubir\u00e1n, Tlalpan Mexico City, Mexico"},{"name":"Tecnol\u00f3gico de Monterrey, Escuela de Medicina y Ciencias de la Salud, Monterrey, Nuevo Le\u00f3n, Mexico"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014050470"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00065.2015"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.E17-08-0529"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00255.2013"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1200947109"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1007\/s00232-009-9165-5"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.114.04036"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.451"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.23.24.9208-9221.2003"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2015070751"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00508.2012"},{"key":"B12","doi-asserted-by":"crossref","first-page":"17713","DOI":"10.1016\/S0021-9258(17)32499-7","volume":"269","author":"Gamba G","year":"1994","journal-title":"J Biol Chem"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2016090948"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1146\/annurev-physiol-021115-105431"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1006128107"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00187.2006"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1038\/ng1877"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(01)00241-0"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/ddq525"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M404671200"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000089830.97681.3B"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1042\/BJ20121903"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M603773200"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1126\/scisignal.2005050"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.025312"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90396.2008"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1304592110"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00280.2005"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2015.289"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2014.12.006"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1042\/BJ20111879"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0037751"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1304230110"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1042\/BJ20051180"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1042\/BJ20060220"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1016\/j.celrep.2013.02.024"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1126\/science.1062844"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.242735399"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1016\/j.febslet.2013.04.032"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1038\/nchembio.2168"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2007.03.009"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00145.2018","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,24]],"date-time":"2022-08-24T20:41:20Z","timestamp":1661373680000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00145.2018"}},"issued":{"date-parts":[[2018,9,1]]},"references-count":41,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2018,9,1]]}},"alternative-id":["10.1152\/ajprenal.00145.2018"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00145.2018","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2018,9,1]]}},{"indexed":{"date-parts":[[2026,2,25]],"date-time":"2026-02-25T18:01:40Z","timestamp":1772042500740,"version":"3.50.1"},"reference-count":37,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2004,9]]},"abstract":"<jats:p>PGE<jats:sub>2<\/jats:sub>is a potent stimulator of renin release. So far, the contribution of each of the four PGE<jats:sub>2<\/jats:sub>receptor subtypes (EP<jats:sub>1<\/jats:sub>\u2013EP<jats:sub>4<\/jats:sub>) in the regulation of renin release has not been characterized. Therefore, we investigated the effects PGE<jats:sub>2<\/jats:sub>on renin secretion rates (RSR) from isolated, perfused kidneys of EP<jats:sub>1<\/jats:sub>\u2212\/\u2212, EP<jats:sub>2<\/jats:sub>\u2212\/\u2212, EP<jats:sub>3<\/jats:sub>\u2212\/\u2212, EP<jats:sub>4<\/jats:sub>\u2212\/\u2212, and wild-type mice. PGE<jats:sub>2<\/jats:sub>concentration dependently stimulated RSR from kidneys of all four knockout strains with a threshold concentration of 1 nM in EP<jats:sub>1<\/jats:sub>\u2212\/\u2212, EP<jats:sub>2<\/jats:sub>\u2212\/\u2212, EP<jats:sub>3<\/jats:sub>\u2212\/\u2212, and wild-type mice, whereas the threshold concentration was shifted to 10 nM in EP<jats:sub>4<\/jats:sub>\u2212\/\u2212 mice. Moreover, the maximum stimulation of RSR by PGE<jats:sub>2<\/jats:sub>at 1 \u03bcM was significantly reduced in EP<jats:sub>4<\/jats:sub>\u2212\/\u2212 (12.8-fold of control) and EP<jats:sub>2<\/jats:sub>\u2212\/\u2212 (15.9-fold) compared with wild-type (20.7-fold), EP<jats:sub>1<\/jats:sub>\u2212\/\u2212 (23.8-fold), and EP<jats:sub>3<\/jats:sub>\u2212\/\u2212 (20.1-fold). In contrast, stimulation of RSR by either the loop diuretic bumetanide or the \u03b2-adrenoceptor agonist isoproterenol was similar in all strains. PGE<jats:sub>2<\/jats:sub>exerted a dual effect on renal vascular tone, inducing vasodilatation at low concentrations (1 nmol\/) and vasoconstriction at higher concentrations (100 nmol\/) in kidneys of wild-type mice. In kidneys of EP<jats:sub>2<\/jats:sub>\u2212\/\u2212 as well as EP<jats:sub>4<\/jats:sub>\u2212\/\u2212 mice, vasodilatation at low PGE<jats:sub>2<\/jats:sub>concentrations was prevented, whereas vasoconstriction at higher concentrations was augmented. In contrast, the vasodilatatory component was pronounced in kidneys of EP<jats:sub>1<\/jats:sub>and EP<jats:sub>3<\/jats:sub>knockout mice, whereas in both genotypes the vasoconstriction at higher PGE<jats:sub>2<\/jats:sub>concentrations was markedly blunted. Our data provide evidence that PGE<jats:sub>2<\/jats:sub>stimulates renin release via activation of EP<jats:sub>2<\/jats:sub>and EP<jats:sub>4<\/jats:sub>receptors, whereas EP<jats:sub>1<\/jats:sub>and EP<jats:sub>3<\/jats:sub>receptors appear to be without functional relevance in juxtaglomerular cells. In contrast, all four receptor subtypes are involved in the control of renal vascular tone, EP<jats:sub>1<\/jats:sub>and EP<jats:sub>3<\/jats:sub>receptors increasing, and EP<jats:sub>2<\/jats:sub>as well as EP<jats:sub>4<\/jats:sub>receptors, decreasing it.<\/jats:p>","DOI":"10.1152\/ajprenal.00072.2004","type":"journal-article","created":{"date-parts":[[2004,5,4]],"date-time":"2004-05-04T00:19:03Z","timestamp":1083629943000},"page":"F427-F433","source":"Crossref","is-referenced-by-count":94,"title":["Stimulation of renin release by prostaglandin E<sub>2<\/sub>is mediated by EP<sub>2<\/sub>and EP<sub>4<\/sub>receptors in mouse kidneys"],"prefix":"10.1152","volume":"287","author":[{"given":"Frank","family":"Schweda","sequence":"first","affiliation":[]},{"given":"J\u00fcrgen","family":"Klar","sequence":"additional","affiliation":[]},{"given":"Shuh","family":"Narumiya","sequence":"additional","affiliation":[]},{"given":"Rolf M.","family":"N\u00fcsing","sequence":"additional","affiliation":[]},{"given":"Armin","family":"Kurtz","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.2001.280.1.H327"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1038\/259244a0"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.1.F12"},{"key":"R4","doi-asserted-by":"crossref","unstructured":"Castrop H, Schweda F, Schumacher K, Wolf K, and Kurtz A.Role of renocortical cyclooxygenase-2 for renal vascular resistance and macula densa control of renin secretion.J Am Soc Nephrol12: 867\u2013874, 2001.","DOI":"10.1681\/ASN.V125867"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.00081.2002"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.3.F449"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1210\/endo-106-5-1400"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.44.6.796"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1990.70.4.1067"},{"key":"R10","unstructured":"Hackenthal E, Schwertschlag U, and Seyberth HW.Prostaglandins and renin release studies in the isolated perfused rat kidney.Prog Biochem Pharmacol17: 98\u2013107, 1980."},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117620"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.26.1.137"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.1984.247.3.E343"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.18.10501"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00351.2001"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1989.102"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.3.F659"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00988.x"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1016\/0262-1746(85)90075-7"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1172\/JCI200318018"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.4.F755"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.40.1.35"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1016\/S0090-6980(75)80011-6"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.252.4.F717"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00280.2002"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1998.8461"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1172\/JCI6749"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.86.6.663"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1016\/S0960-894X(01)00359-6"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.5.F706"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1038\/26233"},{"key":"R32","doi-asserted-by":"crossref","unstructured":"Vander AJ.Direct effects of prostaglandin on renal function and renin release in anesthetized dog.Am J Physiol214: 218\u2013221, 1968.","DOI":"10.1152\/ajplegacy.1968.214.2.218"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.34.1.96"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1016\/0090-6980(81)90106-4"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.5.F819"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M006218200"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.062053399"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00072.2004","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,6,17]],"date-time":"2021-06-17T07:53:07Z","timestamp":1623916387000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00072.2004"}},"issued":{"date-parts":[[2004,9]]},"references-count":37,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2004,9]]}},"alternative-id":["10.1152\/ajprenal.00072.2004"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00072.2004","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2004,9]]}},{"indexed":{"date-parts":[[2026,2,24]],"date-time":"2026-02-24T02:23:11Z","timestamp":1771899791023,"version":"3.50.1"},"reference-count":32,"publisher":"American Physiological Society","issue":"3","funder":[{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["RO1-DK111380"],"award-info":[{"award-number":["RO1-DK111380"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["KO1-DK103834"],"award-info":[{"award-number":["KO1-DK103834"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["RO3-DK119752"],"award-info":[{"award-number":["RO3-DK119752"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"HHS | NIH | National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["RO1-HL147818"],"award-info":[{"award-number":["RO1-HL147818"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["P30-DK079307"],"award-info":[{"award-number":["P30-DK079307"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2021,3,1]]},"abstract":"<jats:p> We have identified the major aldosterone-dependent cleaved form of the \u03b3ENaC subunit in the kidney as a twice-cleaved peptide. This form appears to be identical in size with a subunit cleaved in vitro by the extracellular protease CAP1 (prostasin). In the absence of reducing agents, it has an overall molecular mass less than that of the intact subunit, consistent with the excision of an inhibitory domain. <\/jats:p>","DOI":"10.1152\/ajprenal.00536.2020","type":"journal-article","created":{"date-parts":[[2021,2,1]],"date-time":"2021-02-01T11:15:31Z","timestamp":1612178131000},"page":"F485-F491","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":24,"title":["Cleavage state of \u03b3ENaC in mouse and rat kidneys"],"prefix":"10.1152","volume":"320","author":[{"given":"Gustavo","family":"Frindt","sequence":"first","affiliation":[{"name":"Department of Physiology and Biophysics, Weill Cornell School of Medicine, New York, New York"}]},{"given":"Shujie","family":"Shi","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2413-5415","authenticated-orcid":false,"given":"Thomas R.","family":"Kleyman","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania"},{"name":"Department of Cell Biology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania"},{"name":"Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania"}]},{"given":"Lawrence G.","family":"Palmer","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, Weill Cornell School of Medicine, New York, New York"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.r800083200"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00418.2019"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.010908.163108"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/39329"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1172\/JCI13229"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00422.2005"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1172\/JCI7840"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1111\/apha.13249"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0000000000000578"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0b013e3283330fb2"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00668.2016"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.200809989"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.201511533"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00323.2010"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00401.2009"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.C400080200"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M610636200"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M115.640763"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M804176200"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.5.2743"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.7554\/eLife.39340"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M611761200"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00609.2019"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M604109200"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00157.2014"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1111\/apha.13060"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00133.2012"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M705664200"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M805676200"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1111\/apha.13286"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1111\/apha.13512"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00031.2008"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00536.2020","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,8,24]],"date-time":"2021-08-24T17:35:33Z","timestamp":1629826533000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00536.2020"}},"issued":{"date-parts":[[2021,3,1]]},"references-count":32,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2021,3,1]]}},"alternative-id":["10.1152\/ajprenal.00536.2020"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00536.2020","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2021,3,1]]},"assertion":[{"value":"2020-10-08","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2021-01-25","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2021-03-12","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,2,21]],"date-time":"2026-02-21T06:53:26Z","timestamp":1771656806848,"version":"3.50.1"},"reference-count":25,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2014,7,15]]},"abstract":"<jats:p>Various animal models have been used in research into bladder dysfunction, and in vivo cystometry is a common method to analyze bladder function in animals. However, it is rather difficult to perform reliably in small animals. Transabdominal bladder ultrasonography combined with cystometry in urethane-anesthetized mice have revealed physical inhibition of bladder wall movement by a bladder catheter conventionally placed in the bladder apex. For reliable evaluation of mouse lower urinary tract function, we established a novel cystometry method in which a catheter was placed in the bladder anterior wall, in combination with bladder ultrasonography. This new method allowed the bladder to be well distended (i.e., larger maximum bladder capacity, lower pressure threshold, higher voided volume, and higher bladder compliance compared with conventional methods), which reflected more spontaneous voiding than conventional cystometry methods. We also demonstrated the usefulness of bladder ultrasonography for analysis of mouse bladder function, especially bladder dynamics, maximum bladder capacity, and post-voiding residual volume. We analyzed bladder functional changes in lipopolysaccharide (LPS)-induced cystitis by combining bladder ultrasonography and this new cystometry method. Bladder ultrasonography revealed a rapid decrease in bladder capacity, and cystometry showed a rapid decrease in voided volume due to intravesical LPS instillation. This new cystometry method also revealed a rapid decrease in bladder compliance caused by LPS instillation, which was not detectable by conventional methods. The combination of ultrasonography and the new cystometry method may become a powerful tool for analysis of mouse bladder function and could contribute to the development of new treatments for bladder dysfunction.<\/jats:p>","DOI":"10.1152\/ajprenal.00043.2014","type":"journal-article","created":{"date-parts":[[2014,5,8]],"date-time":"2014-05-08T01:36:16Z","timestamp":1399512976000},"page":"F234-F241","source":"Crossref","is-referenced-by-count":19,"title":["Combination of bladder ultrasonography and novel cystometry method in mice reveals rapid decrease in bladder capacity and compliance in LPS-induced cystitis"],"prefix":"10.1152","volume":"307","author":[{"given":"Kentaro","family":"Takezawa","sequence":"first","affiliation":[{"name":"Department of Neuroscience and Cell Biology, Osaka University Graduate School of Medicine, Osaka, Japan; and"},{"name":"Department of Urology, Osaka University Graduate School of Medicine, Osaka, Japan"}]},{"given":"Makoto","family":"Kondo","sequence":"additional","affiliation":[{"name":"Department of Neuroscience and Cell Biology, Osaka University Graduate School of Medicine, Osaka, Japan; and"}]},{"given":"Hiroshi","family":"Kiuchi","sequence":"additional","affiliation":[{"name":"Department of Urology, Osaka University Graduate School of Medicine, Osaka, Japan"}]},{"given":"Tetsuji","family":"Soda","sequence":"additional","affiliation":[{"name":"Department of Urology, Osaka University Graduate School of Medicine, Osaka, Japan"}]},{"given":"Tetsuya","family":"Takao","sequence":"additional","affiliation":[{"name":"Department of Urology, Osaka University Graduate School of Medicine, Osaka, Japan"}]},{"given":"Yasushi","family":"Miyagawa","sequence":"additional","affiliation":[{"name":"Department of Urology, Osaka University Graduate School of Medicine, Osaka, Japan"}]},{"given":"Akira","family":"Tsujimura","sequence":"additional","affiliation":[{"name":"Department of Urology, Osaka University Graduate School of Medicine, Osaka, Japan"}]},{"given":"Norio","family":"Nonomura","sequence":"additional","affiliation":[{"name":"Department of Urology, Osaka University Graduate School of Medicine, Osaka, Japan"}]},{"given":"Shoichi","family":"Shimada","sequence":"additional","affiliation":[{"name":"Department of Neuroscience and Cell Biology, Osaka University Graduate School of Medicine, Osaka, Japan; and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1002\/nau.21108"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1002\/nau.20500"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1038\/nn902"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1097\/00005392-199907000-00073"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1111\/j.1442-2042.2012.03216.x"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2005.088435"},{"key":"B7","doi-asserted-by":"crossref","first-page":"3383","DOI":"10.1128\/IAI.57.11.3383-3388.1989","volume":"57","author":"de Man P","year":"1989","journal-title":"Infect Immun"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1016\/S0090-4295(02)01791-0"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1172\/JCI31766"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1097\/01.ju.0000143192.68223.f7"},{"key":"B11","doi-asserted-by":"crossref","first-page":"4","DOI":"10.1002\/nau.20798","volume":"29","author":"Haylen BT","year":"2010","journal-title":"Neurourol Urodyn"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/j.ultrasmedbio.2012.04.012"},{"key":"B13","doi-asserted-by":"crossref","first-page":"3749","DOI":"10.4049\/jimmunol.162.7.3749","volume":"162","author":"Hoshino K","year":"1999","journal-title":"J Immunol"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/j.eururo.2006.09.019"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1007\/s002400000114"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1111\/j.1464-410X.2008.07891.x"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00054.2008"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1007\/s00345-009-0488-8"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.0163.2001"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/j.neulet.2003.12.007"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1371\/journal.ppat.0030060"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1002\/nau.20552"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00695.2009"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.90406.2008"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00574.2012"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00043.2014","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,7,12]],"date-time":"2023-07-12T23:15:01Z","timestamp":1689203701000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00043.2014"}},"issued":{"date-parts":[[2014,7,15]]},"references-count":25,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2014,7,15]]}},"alternative-id":["10.1152\/ajprenal.00043.2014"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00043.2014","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2014,7,15]]}},{"indexed":{"date-parts":[[2026,2,25]],"date-time":"2026-02-25T21:12:40Z","timestamp":1772053960330,"version":"3.50.1"},"reference-count":70,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2005,8]]},"abstract":"<jats:p>Chronic hyperglycemia causes structural alterations of proteins through the Maillard reaction. In diabetes, methylglyoxal (MGO)-induced hydroimidazolones are the predominant modification. In contrast to acute hyperglycemia, mitochondrial respiration is depressed in chronic diabetes. To determine whether MGO-derived protein modifications result in abnormalities in mitochondrial bioenergetics and superoxide formation, proteomics and functional studies were performed in renal cortical mitochondria isolated from rats with 2, 6, and 12 mo of streptozotocin-induced diabetes. MGO-modified proteins belonged to the following two pathways: 1) oxidative phosphorylation and 2) fatty acid \u03b2-oxidation. Two of these proteins were identified as components of respiratory complex III, the major site of superoxide production in health and disease. Mitochondria from rats with diabetes exhibited a diminution of oxidative phosphorylation. A decrease in the respiratory complex III activity was significantly correlated with the quantity of MGO-derived hydroimidazolone present on mitochondrial proteins in both diabetic and control animals. In diabetes, isolated renal mitochondria produced significantly increased quantities of superoxide and showed evidence of oxidative damage. Administration of aminoguanidine improved mitochondrial respiration and complex III activity and decreased oxidative damage to mitochondrial proteins. Therefore, posttranslational modifications of mitochondrial proteins by MGO may represent pathogenic events leading to mitochondria-induced oxidative stress in the kidney in chronic diabetes.<\/jats:p>","DOI":"10.1152\/ajprenal.00415.2004","type":"journal-article","created":{"date-parts":[[2005,4,7]],"date-time":"2005-04-07T00:12:34Z","timestamp":1112832754000},"page":"F420-F430","source":"Crossref","is-referenced-by-count":287,"title":["Glycation of mitochondrial proteins from diabetic rat kidney is associated with excess superoxide formation"],"prefix":"10.1152","volume":"289","author":[{"given":"Mariana G.","family":"Rosca","sequence":"first","affiliation":[]},{"given":"Tiberiu G.","family":"Mustata","sequence":"additional","affiliation":[]},{"given":"Michael T.","family":"Kinter","sequence":"additional","affiliation":[]},{"given":"Aylin M.","family":"Ozdemir","sequence":"additional","affiliation":[]},{"given":"Timothy S.","family":"Kern","sequence":"additional","affiliation":[]},{"given":"Luke I.","family":"Szweda","sequence":"additional","affiliation":[]},{"given":"Michael","family":"Brownlee","sequence":"additional","affiliation":[]},{"given":"Vincent M.","family":"Monnier","sequence":"additional","affiliation":[]},{"given":"Miriam F.","family":"Weiss","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M100550200"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1042\/bj3570593"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1042\/bst0311358"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.biochem.69.1.1005"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1159\/000075627"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.2337\/diab.43.6.836"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1016\/0076-6879(90)86100-A"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1080\/15216540152845984"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1979.59.3.527"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M304854200"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-5793(99)00920-5"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1016\/j.freeradbiomed.2003.08.018"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1046\/j.0022-3042.2001.00737.x"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1002\/j.1460-2075.1996.tb00897.x"},{"key":"R15","unstructured":"Fersht A.Enzyme Structure and Mechanisms. New York:Freeman, 1985."},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1996.271.1.H192"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1096\/fj.02-1102fje"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.47.7.1114"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1196\/annals.1297.057"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1021\/bi981512h"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1021\/bi971958i"},{"key":"R22","unstructured":"Hunte C, Solmaz S, and Lange C.Electron transfer between yeast cytochrome bc1 complex and cytochrome c: a structural analysis (Abstract).Biochem Biophys Acta1555: 21028, 2002."},{"key":"R23","unstructured":"Islam M, Tanaka M, Suzuki H, Torii K, Torii N, Hattori N, and Ozawa T.A complete cDNA sequence for core I protein subunit of human ubiquinol-cytochrome c reductase.Biochem Mol Biol Int32: 797\u2013805, 1994."},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1016\/j.abb.2003.08.017"},{"key":"R25","doi-asserted-by":"crossref","unstructured":"Kaneda K, Iwao J, Sakata N, and Takebayashi S.Correlation between mitochondrial enlargement in renal proximal tubules and microalbuminuria in rats with early streptozotocin- induced diabetes.Acta Pathol Jpn42: 855\u2013860, 1992.","DOI":"10.1111\/j.1440-1827.1992.tb01890.x"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1016\/0145-2126(95)00162-X"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1007\/BF02815119"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1074\/mcp.M300119-MCP200"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.51.10.2944"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.52.10.2603"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1016\/0003-9861(92)90146-N"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-5793(97)01159-9"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000077412.07578.44"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1016\/S0891-5849(96)00428-5"},{"key":"R35","unstructured":"Ledenev A, Konstantinov A, Popova E, and Ruuge E.A simple assay of the superoxide generation rate with Tiron as an EPR-visible radical scavenger.Biochem Int13: 391\u2013396, 1986."},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1016\/j.abb.2003.09.046"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1046\/j.0022-3042.2002.00744.x"},{"key":"R38","doi-asserted-by":"crossref","unstructured":"Lo T, Westwood M, McLellan A, Selwood T, and Thornalley P.Binding and modification of proteins by methylglyoxal under physiological conditions. A kinetic and mechanistic study with N alpha-acetylarginine, N alpha-acetylcysteine, N alpha-acetyl-lysine, and bovine serum albumin.J Biol Chem269: 32299\u201332305, 1994.","DOI":"10.1016\/S0021-9258(18)31635-1"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1002\/1522-2683(20001001)21:16<3427::AID-ELPS3427>3.0.CO;2-L"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1016\/S0003-2697(05)80005-3"},{"key":"R41","doi-asserted-by":"crossref","unstructured":"McLellan A, Thornalley P, Benn J, and Sonksen P.Glyoxalase system in clinical diabetes mellitus and correlation with diabetic complications.Clin Sci (Colch)87: 21\u201329, 1994.","DOI":"10.1042\/cs0870021"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1016\/S0003-9861(03)00166-8"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1006\/abio.2000.4514"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1007\/BF00573477"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM198602133140702"},{"key":"R46","doi-asserted-by":"crossref","unstructured":"Nishi S, Ueno M, Hisaki S, Iimo N, Iguchi S, Oyama Y, Imai N, Arakawa M, and Gejyo F.Ultrastructural characteristics of diabetic nephropathy.Med Electron Microsc33: 65\u201373, 2002.","DOI":"10.1007\/s007950070004"},{"key":"R47","doi-asserted-by":"publisher","DOI":"10.1038\/35008121"},{"key":"R48","doi-asserted-by":"crossref","unstructured":"Nyengaard J, Chang K, Berhorst S, Reiser K, Williamson J, and Tilton R.Discordant effects of guanidines on renal structure and function and on regional vascular dysfunction and collagen changes in diabetic rats.Diabetes46: 94\u2013106, 1997.","DOI":"10.2337\/diabetes.46.1.94"},{"key":"R49","doi-asserted-by":"publisher","DOI":"10.1076\/apab.109.3.241.11592"},{"key":"R50","doi-asserted-by":"publisher","DOI":"10.1021\/bi00002a032"},{"key":"R51","doi-asserted-by":"publisher","DOI":"10.1111\/j.1432-1033.1993.tb17638.x"},{"key":"R52","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118798"},{"key":"R53","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.8.4699"},{"key":"R54","doi-asserted-by":"publisher","DOI":"10.3181\/00379727-182-42323"},{"key":"R55","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00302.2001"},{"key":"R56","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.47.33426"},{"key":"R57","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000077414.59717.74"},{"key":"R58","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-5793(98)01033-3"},{"key":"R59","doi-asserted-by":"publisher","DOI":"10.2337\/diab.40.10.1328"},{"key":"R60","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M207217200"},{"key":"R61","doi-asserted-by":"crossref","unstructured":"Taylor R, Birch-Machin M, Bartlett K, Lowerson S, and Turnbull D.The control of mitochondrial oxidation by complex III in rat muscle and liver mitochondria. Implications for our understanding of mitochondrial cytopathies in man.J Biol Chem269: 3523\u20133528, 1994.","DOI":"10.1016\/S0021-9258(17)41894-1"},{"key":"R62","unstructured":"Thornalley P.Advanced glycation and the development of diabetic complications. Unifying the involvement of glucose, methylglyoxal and oxidative stress.Endocrinol Metab3: 149\u2013166, 1996."},{"key":"R63","doi-asserted-by":"publisher","DOI":"10.1016\/j.abb.2003.08.013"},{"key":"R64","doi-asserted-by":"publisher","DOI":"10.1042\/bj20030763"},{"key":"R65","doi-asserted-by":"crossref","unstructured":"Trumpower B.A concerted, alternating sites mechanism of ubiquinol oxidation by the dimeric cytochrome bc1 complex.Biochem Biophys Acta1555: 166\u2013173, 2002.","DOI":"10.1016\/S0005-2728(02)00273-6"},{"key":"R66","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M303734200"},{"key":"R67","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M303139200"},{"key":"R68","doi-asserted-by":"publisher","DOI":"10.1126\/science.283.5407.1482"},{"key":"R69","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00752.x"},{"key":"R70","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0701924"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00415.2004","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,7,8]],"date-time":"2021-07-08T03:07:15Z","timestamp":1625713635000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00415.2004"}},"issued":{"date-parts":[[2005,8]]},"references-count":70,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2005,8]]}},"alternative-id":["10.1152\/ajprenal.00415.2004"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00415.2004","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2005,8]]}},{"indexed":{"date-parts":[[2026,3,19]],"date-time":"2026-03-19T12:58:02Z","timestamp":1773925082680,"version":"3.50.1"},"reference-count":60,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2012,2,1]]},"abstract":"<jats:p>Insulin receptors in podocytes are essential for normal kidney function. Here, we show that insulin evokes a rapid increase in the surface expression of canonical transient receptor potential-6 channel (TRPC6) channels in cultured podocytes, but caused a decrease in surface expression of TRPC5. These effects are accompanied by a marked increase in outwardly rectifying cationic currents that can be blocked by 10 \u03bcM SKF96365 or 100 \u03bcM La<jats:sup>3+<\/jats:sup>. Application of oleoyl-2-acetyl- sn-glycerol (OAG) also increased SKF96365- and La<jats:sup>3+<\/jats:sup>-sensitive cationic currents in podocytes. Importantly, current responses to a combination of OAG and insulin were the same amplitude as those evoked by either agent applied alone. This occlusion effect suggests that OAG and insulin are targeting the same population of channels. In addition, shRNA knockdown of TRPC6 markedly reduced cationic currents stimulated by insulin. The effects of insulin on TRPC6 were mimicked by treating podocytes with H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>. Insulin treatment rapidly increased the generation of H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>in podocytes, and it increased the surface expression of the NADPH oxidase NOX4 in cultured podocytes. Basal and insulin-stimulated surface expression of TRPC6 were reduced by pretreatment with diphenylene iodonium, an inhibitor of NADPH oxidases and other flavin-dependent enzymes, by siRNA knockdown of NOX4, and by manganese (III) tetrakis (4-benzoic acid) porphyrin chloride, a membrane-permeable mimetic of superoxide dismutase and catalase. These observations suggest that insulin increases generation of ROS in part through activation of NADPH oxidases, and that this step contributes to modulation of podocyte TRPC6 channels.<\/jats:p>","DOI":"10.1152\/ajprenal.00423.2011","type":"journal-article","created":{"date-parts":[[2011,10,27]],"date-time":"2011-10-27T00:28:37Z","timestamp":1319675317000},"page":"F298-F307","source":"Crossref","is-referenced-by-count":106,"title":["Insulin increases surface expression of TRPC6 channels in podocytes: role of NADPH oxidases and reactive oxygen species"],"prefix":"10.1152","volume":"302","author":[{"given":"Eun Young","family":"Kim","sequence":"first","affiliation":[{"name":"Department of Biology and Biochemistry, University of Houston, Houston, Texas"}]},{"given":"Marc","family":"Anderson","sequence":"additional","affiliation":[{"name":"Department of Biology and Biochemistry, University of Houston, Houston, Texas"}]},{"given":"Stuart E.","family":"Dryer","sequence":"additional","affiliation":[{"name":"Department of Biology and Biochemistry, University of Houston, Houston, Texas"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI114700"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/S0076-6879(02)49337-8"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00044.2005"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1172\/JCI106667"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009070721"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1007\/BF00252683"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1007\/BF00253406"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1988.255.2.F250"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.2337\/db06-0693"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.54.11.3095"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1006\/abbi.1997.0341"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00298.2010"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M804249200"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2005.103143"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.130135897"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M109.093500"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00014.2011"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0007771"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1161\/01.ATV.0000112024.13727.2c"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1038\/16711"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0607465103"},{"key":"B21a","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00388.2010"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M211484200"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00283.2001"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1995.tb09984.x"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1124\/mol.108.051912"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00354.2009"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00140.2008"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.22567"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00206.2010"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0012859"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115641"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.47"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.227"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M105061200"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1016\/j.cellsig.2005.03.023"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1042\/bj2710515"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006091010"},{"key":"B39","author":"Nijenhuis T","journal-title":"Am J Pathol"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00020.2002"},{"key":"B41","doi-asserted-by":"crossref","first-page":"3","DOI":"10.1111\/j.1748-1716.2010.02147.x","volume":"200","author":"Persson P","year":"2010","journal-title":"Acta Physiol (Oxf)"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1002\/jcb.23088"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.ph.48.030186.003301"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1038\/ng1592"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00559.2007"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00077.2008"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M007597200"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1126\/scisignal.2001200"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1159\/000186248"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00809.2010"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010030246"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009121253"},{"key":"B52a","doi-asserted-by":"publisher","DOI":"10.1159\/000257517"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2010.08.015"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.2010.00920.x"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1126\/science.1106215"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.2010.00636.x"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.3181\/0901-RM-11"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1016\/j.biochi.2010.11.001"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1006\/abio.1997.2391"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00423.2011","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,4,14]],"date-time":"2024-04-14T04:38:13Z","timestamp":1713069493000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00423.2011"}},"issued":{"date-parts":[[2012,2,1]]},"references-count":60,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2012,2,1]]}},"alternative-id":["10.1152\/ajprenal.00423.2011"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00423.2011","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2012,2,1]]}},{"indexed":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T09:15:07Z","timestamp":1773306907784,"version":"3.50.1"},"reference-count":26,"publisher":"American Physiological Society","issue":"12","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2014,12,15]]},"abstract":"<jats:p> Oxidative stress is a major determinant of acute kidney injury (AKI); however, the effects of an AKI on renal redox system are unclear, and few existing AKI markers are suitable for evaluating oxidative stress. We measured urinary levels of the redox-regulatory protein thioredoxin 1 (TRX1) in patients with various kinds of kidney disease and in mice with renal ischemia-reperfusion injury. Urinary TRX1 levels were markedly higher in patients with AKI than in those with chronic kidney disease or in healthy subjects. In a receiver operating characteristic curve analysis to differentiate between AKI and other renal diseases, the area under the curve for urinary TRX1 was 0.94 (95% confidence interval, 0.90\u20130.98), and the sensitivity and specificity were 0.88 and 0.88, respectively, at the optimal cutoff value of 43.0 \u03bcg\/g creatinine. Immunostaining revealed TRX1 to be diffusely distributed in the tubules of normal kidneys, but to be shifted to the brush borders or urinary lumen in injured tubules in both mice and humans with AKI. Urinary TRX1 in AKI was predominantly in the oxidized form. In cultured human proximal tubular epithelial cells, hydrogen peroxide specifically and dose dependently increased TRX1 levels in the culture supernatant, while reducing intracellular levels. These findings suggest that urinary TRX1 is an oxidative stress-specific biomarker useful for distinguishing AKI from chronic kidney disease and healthy kidneys. <\/jats:p>","DOI":"10.1152\/ajprenal.00381.2013","type":"journal-article","created":{"date-parts":[[2014,10,2]],"date-time":"2014-10-02T07:59:08Z","timestamp":1412236748000},"page":"F1342-F1351","source":"Crossref","is-referenced-by-count":33,"title":["Renal redox dysregulation in AKI: application for oxidative stress marker of AKI"],"prefix":"10.1152","volume":"307","author":[{"given":"Kenji","family":"Kasuno","sequence":"first","affiliation":[{"name":"Division of Nephrology, Department of General Medicine, School of Medicine, University of Fukui, Fukui, Japan;"}]},{"given":"Kiichi","family":"Shirakawa","sequence":"additional","affiliation":[{"name":"Department of Nephrology and Dialysis, Kitano Hospital, Tazuke Kofukai Medical Research Institute, Osaka, Japan;"}]},{"given":"Haruyoshi","family":"Yoshida","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of General Medicine, School of Medicine, University of Fukui, Fukui, Japan;"}]},{"given":"Kiyoshi","family":"Mori","sequence":"additional","affiliation":[{"name":"Medical Innovation Center, Kyoto University Graduate School of Medicine, Kyoto, Japan;"}]},{"given":"Hideki","family":"Kimura","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of General Medicine, School of Medicine, University of Fukui, Fukui, Japan;"}]},{"given":"Naoki","family":"Takahashi","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of General Medicine, School of Medicine, University of Fukui, Fukui, Japan;"}]},{"given":"Yasunari","family":"Nobukawa","sequence":"additional","affiliation":[{"name":"Intensive Care Unit, Fukui University Hospital, Fukui, Japan;"}]},{"given":"Kenji","family":"Shigemi","sequence":"additional","affiliation":[{"name":"Intensive Care Unit, Fukui University Hospital, Fukui, Japan;"}]},{"given":"Sawaka","family":"Tanabe","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular Surgery, Department of Surgery, School of Medicine, University of Fukui, Fukui, Japan;"}]},{"given":"Narihisa","family":"Yamada","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular Surgery, Department of Surgery, School of Medicine, University of Fukui, Fukui, Japan;"}]},{"given":"Takaaki","family":"Koshiji","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular Surgery, Department of Surgery, School of Medicine, University of Fukui, Fukui, Japan;"}]},{"given":"Fumiaki","family":"Nogaki","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Shimada Municipal Hospital, Shizuoka, Japan;"}]},{"given":"Hitoshi","family":"Kusano","sequence":"additional","affiliation":[{"name":"Department of Nephrology and Dialysis, Kitano Hospital, Tazuke Kofukai Medical Research Institute, Osaka, Japan;"}]},{"given":"Takahiko","family":"Ono","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Atami Hospital, International University of Health and Welfare, Shizuoka, Japan;"}]},{"given":"Kazuko","family":"Uno","sequence":"additional","affiliation":[{"name":"Louis Pasteur Center for Medical Research, Kyoto, Japan;"}]},{"given":"Hajime","family":"Nakamura","sequence":"additional","affiliation":[{"name":"Department of Preventive Medicine, Kitano Hospital, Tazuke Kofukai Medical Research Institute, Osaka, Japan;"}]},{"given":"Junji","family":"Yodoi","sequence":"additional","affiliation":[{"name":"Department of Biological Responses, Institute for Virus Research, Graduate School of Medicine, Kyoto University, Kyoto, Japan; and"},{"name":"Department of Bioinspired Science, Ewha Womans University, Seoul, Korea."}]},{"given":"Eri","family":"Muso","sequence":"additional","affiliation":[{"name":"Department of Nephrology and Dialysis, Kitano Hospital, Tazuke Kofukai Medical Research Institute, Osaka, Japan;"}]},{"given":"Masayuki","family":"Iwano","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of General Medicine, School of Medicine, University of Fukui, Fukui, Japan;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.03520807"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002729"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1097\/SHK.0000000000000052"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010010128"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/j.jacc.2009.12.046"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002224"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000138232.68452.3B"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.bi.54.070185.001321"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00224.x"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1253\/jcj.65.491"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1098-2825(1996)10:5<257::AID-JCLA5>3.0.CO;2-5"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.172.1.442"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(05)70238-5"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1097\/MCC.0b013e328332f69e"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00435.x"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.3899\/jrheum.120879"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa054209"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(05)74811-X"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.191498798"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1080\/10715760701487682"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/0165-2478(95)00213-O"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1089\/ars.2000.2.4-695"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1172\/JCI200422353"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1002\/j.1460-2075.1989.tb03436.x"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1089\/ars.2007.1949"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1001\/jama.294.7.813"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00381.2013","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T23:58:42Z","timestamp":1567987122000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00381.2013"}},"issued":{"date-parts":[[2014,12,15]]},"references-count":26,"journal-issue":{"issue":"12","published-print":{"date-parts":[[2014,12,15]]}},"alternative-id":["10.1152\/ajprenal.00381.2013"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00381.2013","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2014,12,15]]}},{"indexed":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T07:37:59Z","timestamp":1773301079034,"version":"3.50.1"},"reference-count":41,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2004,2]]},"abstract":"<jats:p>ANG II induces secretion and activation of transforming growth factor-\u03b2 (TGF-\u03b2) by glomerular mesangial cells. However, the mechanisms that operate this are unclear. Thrombospondin-1 (TSP-1), which is produced by mesangial cells in damaged glomeruli, is one of several molecules known to activate the latent TGF-\u03b2<jats:sub>1<\/jats:sub>complex. Therefore, we examined whether the ANG II-induced activation of latent TGF-\u03b2<jats:sub>1<\/jats:sub>in human mesangial cells (HMC) operates via TSP-1. The addition of ANG II (1-100 nM) to HMC significantly increased TSP-1 mRNA within 6 h, followed by an increase in TSP-1 protein production as shown by Western blot analysis of cells and immunoassay of the culture supernatant. Production of ANG II-induced TSP-1 mRNA and protein was completely inhibited by an ANG II type 1 (AT<jats:sub>1<\/jats:sub>)-receptor antagonist but was unaffected by an AT<jats:sub>2<\/jats:sub>-receptor antagonist. Use of a TSP-1-specific blocking peptide demonstrated that the ANG II-induced activation of latent TGF-\u03b2<jats:sub>1<\/jats:sub>operates via TSP-1. Next, we investigated the role of ERK1\/2, p38 MAPK, and JNK in ANG II-induced TSP-1 production in HMC. The addition of the upstream ERK1\/2 inhibitor PD-98059 did not affect ANG II-induced TSP-1 production, whereas addition of either the p38 MAPK inhibitor SB-203580 or the JNK inhibitor SP-600125 significantly reduced TSP-1 production. In conclusion, this study has demonstrated that ANG II-induced activation of latent TGF-\u03b2<jats:sub>1<\/jats:sub>in HMC operates via TSP-1. Furthermore, ANG II-induced TSP-1 production is dependent on p38 MAPK and JNK signaling.<\/jats:p>","DOI":"10.1152\/ajprenal.00139.2003","type":"journal-article","created":{"date-parts":[[2004,1,31]],"date-time":"2004-01-31T01:13:21Z","timestamp":1075511601000},"page":"F278-F287","source":"Crossref","is-referenced-by-count":126,"title":["Angiotensin II induces thrombospondin-1 production in human mesangial cells via p38 MAPK and JNK: a mechanism for activation of latent TGF-\u03b2<sub>1<\/sub>"],"prefix":"10.1152","volume":"286","author":[{"given":"Takayuki","family":"Naito","sequence":"first","affiliation":[]},{"given":"Takao","family":"Masaki","sequence":"additional","affiliation":[]},{"given":"David J.","family":"Nikolic-Paterson","sequence":"additional","affiliation":[]},{"given":"Chie","family":"Tanji","sequence":"additional","affiliation":[]},{"given":"Noriaki","family":"Yorioka","sequence":"additional","affiliation":[]},{"given":"Nobuoki","family":"Kohno","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"REF1","doi-asserted-by":"publisher","DOI":"10.1016\/S1357-2725(96)00171-9"},{"key":"REF2","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.21.1.29"},{"key":"REF3","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.372"},{"key":"REF4","doi-asserted-by":"crossref","unstructured":"Angel Pand Karin M.The role of Jun, Fos and the AP-1 complex in cell-proliferation and transformation.Biochim Biophys Acta1072: 129-157, 1991.","DOI":"10.1016\/0304-419X(91)90011-9"},{"key":"REF5","doi-asserted-by":"publisher","DOI":"10.1177\/002215549904700412"},{"key":"REF6","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa011161"},{"key":"REF7","doi-asserted-by":"publisher","DOI":"10.1016\/S0167-4889(97)00029-3"},{"key":"REF8","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.25.14843"},{"key":"REF9","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)81460-9"},{"key":"REF10","doi-asserted-by":"crossref","unstructured":"Donoviel DB, Framson P, Eldrige CF, Cooke M, Kobayashi S, and Bornstein P.Structual analysis and expression of the human thrombospondin gene promoter.J Biol Chem263: 18590-18593, 1988.","DOI":"10.1016\/S0021-9258(18)37324-1"},{"key":"REF11","doi-asserted-by":"publisher","DOI":"10.1016\/S0008-6363(01)00345-5"},{"key":"REF12","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.483"},{"key":"atypb1","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.36.4.511"},{"key":"REF14","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117251"},{"key":"REF15","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.96"},{"key":"REF16","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1992.259"},{"key":"REF17","doi-asserted-by":"crossref","unstructured":"Kang DH, Joly AH, Oh SW, Hugo C, Kerjaschki D, Gordon KL, Mazzali M, Jefferson JA, Hughes J, Madsen KM, Schreiner GF, and Johnson RJ.Impaired angiogenesis in the remnant kidney model. I. Potential role of vascular endothelial growth factor and thrombospondin-1.J Am Soc Nephrol12: 1434-1447, 2001.","DOI":"10.1681\/ASN.V1271434"},{"key":"REF18","unstructured":"Kropf J, Schurek JO, Wollner A, and Gressner AM.Immunological measurement of transforming growth factor-\u03b21(TGF-\u03b21) in blood: assay development and comparison.Clin Chem43: 1965-1974, 1997."},{"key":"REF19","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.83.8.824"},{"key":"REF20","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.40.24313"},{"key":"REF21","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa011303"},{"key":"REF22","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.188"},{"key":"REF23","doi-asserted-by":"publisher","DOI":"10.1016\/S0167-4781(01)00345-1"},{"key":"REF24","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)64649-4"},{"key":"REF25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00181.2002"},{"key":"REF26","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.52"},{"key":"REF27","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.13.7304"},{"key":"REF28","doi-asserted-by":"crossref","unstructured":"Schultz-Cherry S, Lawler J, and Murphy-Ullrich JE.The type 1 repeats of thrombospondin 1 activate latent transforming growth factor-\u03b2.J Biol Chem269: 26783-26788, 1994.","DOI":"10.1016\/S0021-9258(18)47087-1"},{"key":"REF29","doi-asserted-by":"publisher","DOI":"10.1172\/JCI114846"},{"key":"REF30","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.27.16047"},{"key":"REF31","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/cdf643"},{"key":"REF32","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(96)11445-8"},{"key":"REF33","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.84.5.505"},{"key":"REF34","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00067.x"},{"key":"REF35","doi-asserted-by":"publisher","DOI":"10.1152\/ajplung.2000.279.5.L895"},{"key":"REF36","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.24.15022"},{"key":"REF37","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.50.32447"},{"key":"REF38","unstructured":"Wolf G, Haberstroh U, and Neilson EG.Angiotensin II stimulates the proliferation and biosynthesis of type I collagen in cultured murine mesangial cells.Am J Pathol140: 95-107, 1992."},{"key":"REF39","doi-asserted-by":"crossref","unstructured":"Wolf Gand Neilson EG.Angiotensin II as a renal growth factor.J Am Soc Nephrol3: 1531-1540, 1993.","DOI":"10.1681\/ASN.V391531"},{"key":"REF40","doi-asserted-by":"crossref","unstructured":"Yevdokimova N, Wahab NA, and Mason RM.Thrombospondin-1 is the key activator of TGF-\u03b21in human mesangial cells exposed to high glucose.J Am Soc Nephrol12: 703-712, 2001.","DOI":"10.1681\/ASN.V124703"},{"key":"REF41","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-291X(02)00407-2"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00139.2003","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,6,14]],"date-time":"2021-06-14T05:34:40Z","timestamp":1623648880000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00139.2003"}},"issued":{"date-parts":[[2004,2]]},"references-count":41,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2004,2]]}},"alternative-id":["10.1152\/ajprenal.00139.2003"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00139.2003","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2004,2]]}},{"indexed":{"date-parts":[[2026,3,19]],"date-time":"2026-03-19T22:18:04Z","timestamp":1773958684984,"version":"3.50.1"},"reference-count":42,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2006,2]]},"abstract":"<jats:p> We have previously demonstrated that mouse proximal tubules in vitro respond to changes in luminal flow with proportional changes in Na<jats:sup>+<\/jats:sup> absorption (Du Z, Duan Y, Yan Q, Weinstein AM, Weinbaum S, and Wang T. Proc Natl Acad Sci USA 101: 13068\u201313073, 2004). It was hypothesized that brush-border microvilli function as a sensor to detect and amplify luminal hydrodynamic forces and transmit them to the actin cytoskeleton. In the present study we examine whether 1) flow-dependent HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup> transport is proportional to flow-dependent variations in microvillous torque (bending moment); 2) both luminal membrane Na<jats:sup>+<\/jats:sup>\/H<jats:sup>+<\/jats:sup> exchange (NHE3) and H<jats:sup>+<\/jats:sup>-ATPase activity are modulated by axial flow; and 3) paracellular permeabilities contribute to the flux perturbations. HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup> absorption is examined by microperfusion of mouse S2 proximal tubules in vitro, with varying perfusion rates, and in the presence of the Na\/H-exchange inhibitor EIPA, the H<jats:sup>+<\/jats:sup>-ATPase inhibitor bafilomycin, and the actin cytoskeleton inhibitor cytochalasin D. Paracellular permeability changes are assessed with measurements of epithelial HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup> permeability and transepithelial potential difference (PD). It is found that 1) an increase in perfusion rate enhances HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup> absorption and microvillous torque, and the fractional changes of each are nearly identical; 2) inhibition of NHE3 by EIPA, or H<jats:sup>+<\/jats:sup>-ATPase by bafilomycin, produced only partial inhibition of flow-stimulated bicarbonate transport; 3) disruption of the actin cytoskeleton by cytochalasin D blocked the increment of HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup> absorption by high flow; and 4) HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup> permeability and transepithelial PD are not modulated by flow. We conclude that flow-dependent modulation of proximal tubule HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup> reabsorption is due to changes in both NHE3 and H<jats:sup>+<\/jats:sup>-ATPase activity within the luminal cell membrane and this requires an intact actin cytoskeleton. Paracellular permeability changes do not contribute to this flow dependence. Perfusion-absorption balance in the proximal tubule is a direct effect of flow-induced torque on brush-border microvilli to regulate luminal cell membrane transporter activity. <\/jats:p>","DOI":"10.1152\/ajprenal.00255.2005","type":"journal-article","created":{"date-parts":[[2005,9,6]],"date-time":"2005-09-06T20:34:57Z","timestamp":1126038897000},"page":"F289-F296","source":"Crossref","is-referenced-by-count":69,"title":["Axial flow modulates proximal tubule NHE3 and H-ATPase activities by changing microvillus bending moments"],"prefix":"10.1152","volume":"290","author":[{"given":"Zhaopeng","family":"Du","sequence":"first","affiliation":[]},{"given":"Qingshang","family":"Yan","sequence":"additional","affiliation":[]},{"given":"Yi","family":"Duan","sequence":"additional","affiliation":[]},{"given":"Sheldon","family":"Weinbaum","sequence":"additional","affiliation":[]},{"given":"Alan M.","family":"Weinstein","sequence":"additional","affiliation":[]},{"given":"Tong","family":"Wang","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1982.243.1.F53"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1983.245.4.F478"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1172\/JCI107248"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1172\/JCI110767"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1172\/JCI110282"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1978.235.6.F592"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1172\/JCI105888"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1982.242.5.F532"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1983.245.5.F622"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1172\/JCI114255"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0405179101"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00261.2002"},{"key":"R13","unstructured":"Earley LE and Schrier RW. Intrarenal control of sodium excretion by hemodynamic and physical factors. In: Handbook of Physiology. Renal Physiology. Bethesda, MD: Am Physiol Soc, 1973, sect. 8, chapt. 22, p. 721\u2013762."},{"key":"R14","unstructured":"Gertz KH and Boylan JW. Glomerular-tubular balance. In: Handbook of Physiology. Renal Physiology. Bethesda, MD: Am Physiol Soc, 1973, sect. 8, chapt. 23, p. 763\u2013790."},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1981.180"},{"key":"R16","doi-asserted-by":"crossref","unstructured":"Green R, Windhager EE, and Giebisch G. Protein oncotic pressure effects on proximal tubular fluid movement in the rat. Am J Physiol 226: 265\u2013276, 1974.","DOI":"10.1152\/ajplegacy.1974.226.2.265"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.4.F698"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1981.99"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1981.241.4.F386"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1172\/JCI106816"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1980.238.6.F499"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.270.2.F344"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1984.247.4.F637"},{"key":"R24","doi-asserted-by":"crossref","unstructured":"Lewy JE and Windhager EE. Peritubular control of proximal tubular fluid reabsorption in the rat kidney. Am J Physiol 214: 943\u2013954, 1968.","DOI":"10.1152\/ajplegacy.1968.214.5.943"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1988.254.6.F851"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115715"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.342"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1007\/BF00580680"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.262.1.F47"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1007\/BF00592457"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1113\/expphysiol.1996.sp003921"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.ph.52.030190.003425"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1007\/BF00586722"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1038\/969"},{"key":"R35","unstructured":"Ullrich KJ. Permeability characteristics of the mammalian nephron. In: Handbook of Physiology. Renal Physiology. Bethesda, MD: Am Physiol Soc, 1973, sect. 8, chapt. 12, p. 377\u2013398."},{"key":"R36","unstructured":"Wang T and Chan YL. Mechanism of angiotensin II action on proximal tubular transport. J Pharmacol Exp Ther 252: 689\u2013695, 1990."},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.281.6.F1117"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.2.F298"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.258.3.F612"},{"key":"R40","unstructured":"Wilcox CS and Baylis C. Glomerular-tubular balance and proximal regulation. In: The Kidney: Physiology and Pathophysiology, edited by Seldin DW and Giebisch G. New York: Raven, 1985, p. 985\u20131012."},{"key":"R41","unstructured":"Windhager EE. Sodium chloride transport. In: Membrane Transport in Biology, edited by Giebisch G. Berlin: Springer-Verlag, 1979, vol. IV, p. 145\u2013214."},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.6.F870"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00255.2005","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:04:11Z","timestamp":1567969451000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00255.2005"}},"issued":{"date-parts":[[2006,2]]},"references-count":42,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2006,2]]}},"alternative-id":["10.1152\/ajprenal.00255.2005"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00255.2005","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2006,2]]}},{"indexed":{"date-parts":[[2026,3,18]],"date-time":"2026-03-18T22:39:34Z","timestamp":1773873574554,"version":"3.50.1"},"reference-count":50,"publisher":"American Physiological Society","issue":"5","funder":[{"DOI":"10.13039\/100000066","name":"HHS | NIH | National Institute of Environmental Health Sciences (NIEHS)","doi-asserted-by":"publisher","award":["T32 ES007015"],"award-info":[{"award-number":["T32 ES007015"]}],"id":[{"id":"10.13039\/100000066","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000057","name":"HHS | NIH | National Institute of General Medical Sciences (NIGMS)","doi-asserted-by":"publisher","award":["NIH T32 GM07356"],"award-info":[{"award-number":["NIH T32 GM07356"]}],"id":[{"id":"10.13039\/100000057","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)","doi-asserted-by":"publisher","award":["F30DK093173"],"award-info":[{"award-number":["F30DK093173"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)","doi-asserted-by":"publisher","award":["U54 DK104310"],"award-info":[{"award-number":["U54 DK104310"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"name":"NIH","award":["UO1ES020952"],"award-info":[{"award-number":["UO1ES020952"]}]},{"name":"NIH","award":["UO1ES020952"],"award-info":[{"award-number":["UO1ES020952"]}]},{"name":"NIH","award":["RC2ESO18764"],"award-info":[{"award-number":["RC2ESO18764"]}]},{"name":"NIH","award":["R01 ES001332"],"award-info":[{"award-number":["R01 ES001332"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2018,11,1]]},"abstract":"<jats:p> Estrogens, acting synergistically with androgens, are known from animal experiments to be important in lower urinary tract symptoms (LUTS) and benign prostate enlargement. Human exposure to environmental estrogens occurs throughout the life span, but the urologic health risks in men are largely unknown. Bisphenol A (BPA) is an endocrine disruptor implicated in male urogenital malformations. Given the role of estrogens in male LUTS, we studied the effects of BPA administered in combination with testosterone (T) on the urinary voiding behavior of adult male mice. Adult male mice underwent subcutaneous implantation with slow-release pellets of 25 mg BPA or 2.5 mg estradiol-17\u03b2 (E<jats:sub>2<\/jats:sub>), plus 25 mg T, and were compared with untreated (UNT) mice that underwent sham surgery. We studied urinary voiding behavior noninvasively for 1 mo before treatment and for 4 mo after treatment. After euthanasia, we evaluated bladder volume and mass. Mice treated with T+BPA had increased bladder volume ( P &lt; 0.05) and mass ( P &lt; 0.01) compared with UNT mice. After 4 mo of treatment with T+BPA, three of five mice developed voiding dysfunction in the form of droplet voiding or an intermediate pattern of voiding different from both UNT and T+E<jats:sub>2<\/jats:sub>-treated mice. Treatment of male mice with BPA or estradiol induces voiding dysfunction that manifests at later time points, implicating the endocrine disruptor, BPA, as a contributor to male LUTS. <\/jats:p>","DOI":"10.1152\/ajprenal.00582.2017","type":"journal-article","created":{"date-parts":[[2018,7,18]],"date-time":"2018-07-18T09:46:21Z","timestamp":1531907181000},"page":"F1208-F1216","source":"Crossref","is-referenced-by-count":25,"title":["Endocrine disruptor bisphenol A is implicated in urinary voiding dysfunction in male mice"],"prefix":"10.1152","volume":"315","author":[{"given":"Tristan M.","family":"Nicholson","sequence":"first","affiliation":[{"name":"Department of Urology, University of Washington, Seattle, Washington"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5189-3601","authenticated-orcid":false,"given":"Jalissa L.","family":"Nguyen","sequence":"additional","affiliation":[{"name":"Molecular and Environmental Toxicology Center, University of Wisconsin-Madison, Madison, Wisconsin"}]},{"given":"Glen E.","family":"Leverson","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Wisconsin-Madison, Madison, Wisconsin"}]},{"given":"Julia A.","family":"Taylor","sequence":"additional","affiliation":[{"name":"Division of Biological Sciences, University of Missouri, Columbia, Missouri"}]},{"given":"Frederick S.","family":"vom Saal","sequence":"additional","affiliation":[{"name":"Division of Biological Sciences, University of Missouri, Columbia, Missouri"}]},{"given":"Ronald W.","family":"Wood","sequence":"additional","affiliation":[{"name":"Department of Urology, University of Rochester School of Medicine and Dentistry, Rochester, New York"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9807-2090","authenticated-orcid":false,"given":"William A.","family":"Ricke","sequence":"additional","affiliation":[{"name":"Molecular and Environmental Toxicology Center, University of Wisconsin-Madison, Madison, Wisconsin"},{"name":"U54 George M. O\u2019Brien Center, University of Wisconsin-Madison, Madison, Wisconsin"},{"name":"Department of Urology, University of Wisconsin-Madison, Madison, Wisconsin"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbr.2007.05.007"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1095\/biolreprod.110.087502"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1210\/jcem.79.4.7962278"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1002\/pros.20791"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1289\/ehp.10753"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/j.envres.2011.05.014"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0055905"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1016\/j.eururo.2006.02.018"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1002\/14651858.CD011179.pub2"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1126\/science.182.4115.939"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1038\/137996a0"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1093\/annweh\/wxw021"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0110509"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/j.eururo.2009.02.026"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1001\/jama.300.11.1303"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.3909\/riu0519"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/j.urology.2004.04.036"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1093\/humrep\/dep381"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/j.etap.2015.03.007"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0055387"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/j.juro.2011.01.074"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0008673"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1093\/toxsci\/kfx101"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1210\/en.2012-1522"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1016\/j.diff.2011.04.006"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.2001.81.4.1535"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.3389\/neuro.08.010.2009"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1002\/ijc.21614"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1007\/3-540-27671-8_8"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1289\/ehp.1408989"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1016\/j.urology.2007.01.011"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1080\/10473289.2001.10464292"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1289\/ehp.1003170"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1289\/EHP150"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1289\/ehp.1104114"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.5402\/2012\/965243"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1289\/ehp.0800376"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.3109\/00365599509180541"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0048311"},{"key":"B40","volume-title":"Bisphenol A Alternatives in Thermal Paper","author":"U.S. Environmental Protection Agency","year":"2014"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1590\/S1413-81232012000200015"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1289\/ehp.0901716"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1177\/074823379801400115"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1289\/ehp.7713"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1016\/j.mce.2014.09.028"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pgen.1004949"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1016\/j.jsbmb.2011.01.015"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1289\/ehp.5494"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1007\/s40572-016-0102-3"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1016\/j.urology.2005.12.019"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00582.2017","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,20]],"date-time":"2019-09-20T17:40:37Z","timestamp":1569001237000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00582.2017"}},"issued":{"date-parts":[[2018,11,1]]},"references-count":50,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2018,11,1]]}},"alternative-id":["10.1152\/ajprenal.00582.2017"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00582.2017","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2018,11,1]]}},{"indexed":{"date-parts":[[2026,3,21]],"date-time":"2026-03-21T18:53:58Z","timestamp":1774119238877,"version":"3.50.1"},"reference-count":50,"publisher":"American Physiological Society","issue":"8","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2012,10,15]]},"abstract":"<jats:p>The number of the chronic renal failure (CRF) patients is increasing explosively. Hypertension, proteinuria, inflammation, fibrosis, and oxidative stress are intertwined in a complicated manner that leads to the progression of CRF. However, the therapeutic strategies to delay its progression are limited. Since serine proteases are involved in many processes that contribute to these risk factors, we investigated the effects of a synthetic serine protease inhibitor, camostat mesilate (CM), on the progression of CRF in 5\/6 nephrectomized (Nx) rats. Eighteen male Sprague-Dawley rats were divided into three groups: a sham-operated group ( n = 6), a vehicle-treated Nx group ( n = 6), and a CM-treated Nx group ( n = 6). Following the 9-wk study period, both proteinuria and serum creatinine levels were substantially increased in the vehicle-treated Nx group, and treatment with CM significantly reduced proteinuria and serum creatinine levels. The levels of podocyte-associated proteins in glomeruli, such as nephrin and synaptopodin, were markedly decreased by 5\/6 nephrectomy, and this was significantly ameliorated by CM. CM also suppressed the levels of inflammatory and fibrotic marker mRNAs including transforming growth factor-\u03b21, TNF-\u03b1, collagen types I, III, and IV, and reduced glomerulosclerosis, glomerular hypertrophy, and interstitial fibrosis in histological studies. Furthermore, CM decreased the expression of NADPH oxidase component mRNAs, as well as reactive oxygen species generation and advanced oxidative protein product levels. Our present results strongly suggest the possibility that CM could be a useful therapeutic agent against the progression of CRF.<\/jats:p>","DOI":"10.1152\/ajprenal.00706.2011","type":"journal-article","created":{"date-parts":[[2012,7,26]],"date-time":"2012-07-26T02:39:05Z","timestamp":1343270345000},"page":"F1126-F1135","source":"Crossref","is-referenced-by-count":24,"title":["Effect of a serine protease inhibitor on the progression of chronic renal failure"],"prefix":"10.1152","volume":"303","author":[{"given":"Manabu","family":"Hayata","sequence":"first","affiliation":[{"name":"Department of Nephrology, Kumamoto University Graduate School of Medical Sciences, Kumamoto, Japan; and"}]},{"given":"Yutaka","family":"Kakizoe","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Kumamoto University Graduate School of Medical Sciences, Kumamoto, Japan; and"}]},{"given":"Kohei","family":"Uchimura","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Kumamoto University Graduate School of Medical Sciences, Kumamoto, Japan; and"}]},{"given":"Jun","family":"Morinaga","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Kumamoto University Graduate School of Medical Sciences, Kumamoto, Japan; and"}]},{"given":"Rika","family":"Yamazoe","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Kumamoto University Graduate School of Medical Sciences, Kumamoto, Japan; and"}]},{"given":"Teruhiko","family":"Mizumoto","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Kumamoto University Graduate School of Medical Sciences, Kumamoto, Japan; and"}]},{"given":"Tomoaki","family":"Onoue","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Kumamoto University Graduate School of Medical Sciences, Kumamoto, Japan; and"}]},{"given":"Miki","family":"Ueda","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Kumamoto University Graduate School of Medical Sciences, Kumamoto, Japan; and"}]},{"given":"Naoki","family":"Shiraishi","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Kumamoto University Graduate School of Medical Sciences, Kumamoto, Japan; and"}]},{"given":"Masataka","family":"Adachi","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Kumamoto University Graduate School of Medical Sciences, Kumamoto, Japan; and"}]},{"given":"Taku","family":"Miyoshi","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Kumamoto University Graduate School of Medical Sciences, Kumamoto, Japan; and"}]},{"given":"Yoshiki","family":"Sakai","sequence":"additional","affiliation":[{"name":"Research Headquarters, Ono Pharmaceutical Company, Limited, Osaka, Japan"}]},{"given":"Kimio","family":"Tomita","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Kumamoto University Graduate School of Medical Sciences, Kumamoto, Japan; and"}]},{"given":"Kenichiro","family":"Kitamura","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Kumamoto University Graduate School of Medical Sciences, Kumamoto, Japan; and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/S0024-3205(98)00031-9"},{"key":"B2","doi-asserted-by":"crossref","first-page":"1213","DOI":"10.1681\/ASN.V971213","volume":"9","author":"Abbate M","year":"1998","journal-title":"J Am Soc Nephrol"},{"key":"B3","doi-asserted-by":"crossref","first-page":"14170","DOI":"10.1016\/S0021-9258(18)77283-9","volume":"265","author":"Amaya Y","year":"1990","journal-title":"J Biol Chem"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00217.2009"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajplung.2001.281.3.L556"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-003-1377-9"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.168.7.3577"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfl444"},{"key":"B9","doi-asserted-by":"crossref","first-page":"2080","DOI":"10.1681\/ASN.V12102080","volume":"12","author":"Bobadilla NA","year":"2001","journal-title":"J Am Soc Nephrol"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1983.72"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1016\/j.jaci.2006.02.047"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1084\/jem.191.3.455"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1992.103"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00138.x"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1038\/labinvest.3700203"},{"key":"B16","doi-asserted-by":"crossref","first-page":"1016","DOI":"10.1681\/ASN.V1161016","volume":"11","author":"Grandaliano G","year":"2000","journal-title":"J Am Soc Nephrol"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00396.2002"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1097\/00003246-199909000-00040"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00729.x"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1981.241.1.F85"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/S1056-8727(98)00016-6"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/0165-2478(91)90243-4"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1159\/000187824"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1084\/jem.168.3.1169"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1097\/HJH.0b013e32832c7d23"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000034910.58454.FD"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00044.x"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1172\/JCI109662"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1992.165"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1097\/HJH.0b013e328317a762"},{"key":"B31","doi-asserted-by":"crossref","first-page":"5435","DOI":"10.1016\/S0021-9258(19)70805-9","volume":"255","author":"Mainardi CL","year":"1980","journal-title":"J Biol Chem"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1172\/JCI7840"},{"key":"B33","first-page":"119","volume":"32","author":"Matsubara M","year":"1989","journal-title":"Clin Nephrol"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1016\/0891-6632(91)90060-3"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M805766200"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00500.2007"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1984.147"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1172\/JCI27699"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.0590051626.x"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.055003945.x"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.0902129"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1989.96"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000255636.11931.a2"},{"key":"B44","first-page":"95","volume":"79","author":"Shimamura T","year":"1975","journal-title":"Am J Pathol"},{"key":"B45","doi-asserted-by":"crossref","first-page":"2151","DOI":"10.4049\/jimmunol.133.4.2151","volume":"133","author":"Speer CP","year":"1984","journal-title":"J Immunol"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2744(77)90097-3"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1097\/TP.0b013e3181d72117"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1097\/01.CCM.0000060005.48885.2B"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00702.x"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.186"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00706.2011","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,6,24]],"date-time":"2023-06-24T17:39:27Z","timestamp":1687628367000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00706.2011"}},"issued":{"date-parts":[[2012,10,15]]},"references-count":50,"journal-issue":{"issue":"8","published-print":{"date-parts":[[2012,10,15]]}},"alternative-id":["10.1152\/ajprenal.00706.2011"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00706.2011","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2012,10,15]]}},{"indexed":{"date-parts":[[2026,3,21]],"date-time":"2026-03-21T19:00:15Z","timestamp":1774119615770,"version":"3.50.1"},"reference-count":10,"publisher":"American Physiological Society","issue":"5","funder":[{"name":"l\u2019Association pour l\u2019Utilisation du Rein Artificiel"},{"name":"Foundation Philancia"},{"DOI":"10.13039\/501100001665","name":"Agence Nationale de la Recherche","doi-asserted-by":"publisher","award":["ANR-16-CE14-0031-01[PROSTARGET]"],"award-info":[{"award-number":["ANR-16-CE14-0031-01[PROSTARGET]"]}],"id":[{"id":"10.13039\/501100001665","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001665","name":"Agence Nationale de la Recherche","doi-asserted-by":"publisher","award":["ANR-18-IBHU-0001"],"award-info":[{"award-number":["ANR-18-IBHU-0001"]}],"id":[{"id":"10.13039\/501100001665","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2023,5,1]]},"DOI":"10.1152\/ajprenal.00029.2023","type":"journal-article","created":{"date-parts":[[2023,3,9]],"date-time":"2023-03-09T16:42:33Z","timestamp":1678380153000},"page":"F431-F432","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["Novel insight on physiological regulation of the Cl<sup>\u2212<\/sup>\/HCO3\u2212 exchanger pendrin"],"prefix":"10.1152","volume":"324","author":[{"given":"R\u00e9gine","family":"Chambrey","sequence":"first","affiliation":[{"name":"Unit\u00e9 Mixte de Recherche INSERM 1283\/CNRS 8199, European Genomic Institute for Diabetes, Lille, France"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1067-0844","authenticated-orcid":false,"given":"Dominique","family":"Eladari","sequence":"additional","affiliation":[{"name":"Service de M\u00e9decine de Pr\u00e9cision des Maladies         M\u00e9taboliques et R\u00e9nales, CHU Amiens-Picardie, Universit\u00e9 de Picardie Jules Verne, Amiens, France"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.071516798"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI40145"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000088321.67254.B7"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfw393"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2012080787"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00254.2002"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00128.2022"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00211.2004"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2011.03.022"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2018.05.001"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00029.2023","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,4,10]],"date-time":"2023-04-10T13:56:03Z","timestamp":1681134963000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00029.2023"}},"issued":{"date-parts":[[2023,5,1]]},"references-count":10,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2023,5,1]]}},"alternative-id":["10.1152\/ajprenal.00029.2023"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00029.2023","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2023,5,1]]},"assertion":[{"value":"2023-02-09","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2023-03-03","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2023-03-03","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2023-04-10","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,3,19]],"date-time":"2026-03-19T20:37:35Z","timestamp":1773952655485,"version":"3.50.1"},"reference-count":62,"publisher":"American Physiological Society","issue":"11","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2015,6,1]]},"abstract":"<jats:p> Early life malnutrition results in structural alterations in the kidney, predisposing offspring to later life renal dysfunction. Kidneys of adults who were growth restricted at birth have substantial variations in nephron endowment. Animal models have indicated renal structural and functional consequences in offspring exposed to suboptimal intrauterine nutrition. Mitochondrial bioenergetics play a key role in renal energy metabolism, growth, and function. We hypothesized that moderate maternal nutrient reduction (MNR) would adversely impact fetal renal mitochondrial expression in a well-established nonhuman primate model that produces intrauterine growth reduction at term. Female baboons were fed normal chow diet or 70% of control diet (MNR). Fetal kidneys were harvested at cesarean section at 0.9 gestation (165 days gestation). Human Mitochondrial Energy Metabolism and Human Mitochondria Pathway PCR Arrays were used to analyze mitochondrially relevant mRNA expression. In situ protein content was detected by immunohistochemistry. Despite the smaller overall size, the fetal kidney weight-to-body weight ratio was not affected. We demonstrated fetal sex-specific differential mRNA expression encoding mitochondrial metabolite transport and dynamics proteins. MNR-related differential gene expression was more evident in female fetuses, with 16 transcripts significantly altered, including 14 downregulated and 2 upregulated transcripts. MNR impacted 10 transcripts in male fetuses, with 7 downregulated and 3 upregulated transcripts. The alteration in mRNA levels was accompanied by a decrease in mitochondrial protein cytochrome c oxidase subunit VIc. In conclusion, transcripts encoding fetal renal mitochondrial energy metabolism proteins are nutrition sensitive in a sex-dependent manner. We speculate that these differences lead to decreased mitochondrial fitness that contributes to renal dysfunction in later life. <\/jats:p>","DOI":"10.1152\/ajprenal.00419.2014","type":"journal-article","created":{"date-parts":[[2015,3,11]],"date-time":"2015-03-11T21:43:11Z","timestamp":1426110191000},"page":"F1217-F1228","source":"Crossref","is-referenced-by-count":33,"title":["Effects of moderate global maternal nutrient reduction on fetal baboon renal mitochondrial gene expression at 0.9 gestation"],"prefix":"10.1152","volume":"308","author":[{"given":"Susana P.","family":"Pereira","sequence":"first","affiliation":[{"name":"Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal;"},{"name":"Department of Life Sciences, School of Sciences and Technology, University of Coimbra, Coimbra, Portugal;"},{"name":"Center for Pregnancy and Newborn Research, University of Texas Health Science Center, San Antonio, Texas; and"}]},{"given":"Paulo J.","family":"Oliveira","sequence":"additional","affiliation":[{"name":"Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal;"}]},{"given":"Ludgero C.","family":"Tavares","sequence":"additional","affiliation":[{"name":"Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal;"},{"name":"Department of Life Sciences, School of Sciences and Technology, University of Coimbra, Coimbra, Portugal;"}]},{"given":"Ant\u00f3nio J.","family":"Moreno","sequence":"additional","affiliation":[{"name":"Department of Life Sciences, School of Sciences and Technology, University of Coimbra, Coimbra, Portugal;"}]},{"given":"Laura A.","family":"Cox","sequence":"additional","affiliation":[{"name":"Department of Genetics, Texas Biomedical Research Institute, San Antonio, Texas"}]},{"given":"Peter W.","family":"Nathanielsz","sequence":"additional","affiliation":[{"name":"Center for Pregnancy and Newborn Research, University of Texas Health Science Center, San Antonio, Texas; and"}]},{"given":"Mark J.","family":"Nijland","sequence":"additional","affiliation":[{"name":"Center for Pregnancy and Newborn Research, University of Texas Health Science Center, San Antonio, Texas; and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1009838108"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2005.084947"},{"key":"B3","first-page":"1","volume":"28","author":"Assis T","year":"2011","journal-title":"J Morphol Sci"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2005.02.001"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/j.placenta.2012.06.009"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbadis.2010.03.002"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1111\/j.1399-0004.2006.00684.x"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00051.2011"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1155\/2012\/760580"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2006.106872"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejogrb.2004.01.011"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.2174\/156720507780362236"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra022567"},{"key":"B15","first-page":"122A","volume":"15","author":"Drever N","year":"2008","journal-title":"Reprod Sci"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/S0070-2153(06)77002-8"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1155\/2012\/989037"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1186\/1471-2369-14-209"},{"key":"B19","doi-asserted-by":"crossref","first-page":"195","DOI":"10.1016\/j.cbi.2008.03.001","volume":"173","author":"Fernandes MA","year":"2008","journal-title":"Chem Biol Interact"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1042\/bj2330249"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/j.earlhumdev.2005.06.007"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.90724.2008"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(89)80068-X"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1159\/000313957"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1016\/j.earlhumdev.2006.07.008"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00018.x"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00582.x"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.3945\/ajcn.112.040352"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa020549"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000093196.59829.DF"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1530\/JOE-13-0012"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1210\/en.2008-1648"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002747"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1038\/nature05292"},{"key":"B35","first-page":"967","volume":"24","author":"Lucas SR","year":"1991","journal-title":"Braz J Med Biol Res"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.09712.x"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.5041\/RMMJ.10061"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1016\/j.cbi.2010.09.027"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1210\/endo-107-1-155"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.00332.2012"},{"key":"B41","first-page":"19","volume":"26","author":"Merlet-B\u00e9nichou C","year":"1997","journal-title":"Adv Nephrol Necker Hosp"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1016\/j.placenta.2010.01.006"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1007\/s004670050587"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2009.184168"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2006.122101"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1289\/ehp.00108s3545"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0038867"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1016\/j.tiv.2009.06.032"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1016\/j.envpol.2013.05.049"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1016\/j.mcna.2004.11.010"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1177\/0192623312444025"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1086\/515527"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1159\/000188022"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-0684.2004.00067.x"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-0684.2004.00066.x"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1016\/0272-6386(95)90119-1"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1038\/nrendo.2011.138"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1038\/nature08368"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00280.2009"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1007\/BF02691063"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2008.12.042"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.107.091603"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1155\/2012\/136942"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00419.2014","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T21:09:36Z","timestamp":1567976976000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00419.2014"}},"issued":{"date-parts":[[2015,6,1]]},"references-count":62,"journal-issue":{"issue":"11","published-print":{"date-parts":[[2015,6,1]]}},"alternative-id":["10.1152\/ajprenal.00419.2014"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00419.2014","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2015,6,1]]}},{"indexed":{"date-parts":[[2026,3,23]],"date-time":"2026-03-23T12:02:02Z","timestamp":1774267322587,"version":"3.50.1"},"reference-count":64,"publisher":"American Physiological Society","issue":"5","funder":[{"name":"Texas A&M College of Pharmacy","award":["Startup Grant"],"award-info":[{"award-number":["Startup Grant"]}]},{"name":"UA Merit Award","award":["BX002006"],"award-info":[{"award-number":["BX002006"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2019,11,1]]},"abstract":"<jats:p> The popular anticancer drug cisplatin causes many adverse side effects, the most serious of which is acute kidney injury (AKI). Emerging evidence from laboratory and clinical studies suggests that the AKI pathogenesis involves oxidative stress pathways; therefore, regulating such pathways may offer protection. Urolithin A (UA), a gut metabolite of the dietary tannin ellagic acid, possesses antioxidant properties and has shown promise in mouse models of AKI. However, therapeutic potential of UA is constrained by poor bioavailability. We aimed to improve oral bioavailability of UA by formulating it into biodegradable nanoparticles that use a surface-conjugated ligand targeting the gut-expressed transferrin receptor. Nanoparticle encapsulation of UA led to a sevenfold enhancement in oral bioavailability compared with native UA. Treatment with nanoparticle UA also significantly attenuated the histopathological hallmarks of cisplatin-induced AKI and reduced mortality by 63% in the mouse model. Expression analyses indicated that nanoparticle UA therapy coincided with oxidative stress mitigation and downregulation of nuclear factor erythroid 2-related factor 2- and P53-inducible genes. Additionally, normalization of miRNA (miR-192-5p and miR-140-5p) implicated in AKI, poly(ADP-ribose) polymerase 1 levels, antiapoptotic signaling, intracellular NAD<jats:sup>+<\/jats:sup>, and mitochondrial oxidative phosphorylation were observed in the treatment group. Our findings suggest that nanoparticles greatly increase the oral bioavailability of UA, leading to improved survival rates in AKI mice, in part by reducing renal oxidative and apoptotic stress. <\/jats:p>","DOI":"10.1152\/ajprenal.00346.2019","type":"journal-article","created":{"date-parts":[[2019,9,18]],"date-time":"2019-09-18T09:16:21Z","timestamp":1568798181000},"page":"F1255-F1264","source":"Crossref","is-referenced-by-count":53,"title":["Oral delivery of nanoparticle urolithin A normalizes cellular stress and improves survival in mouse model of cisplatin-induced AKI"],"prefix":"10.1152","volume":"317","author":[{"given":"Dianxiong","family":"Zou","sequence":"first","affiliation":[{"name":"Department of Pharmaceutical Sciences, Irma Lerma Rangel College of Pharmacy, Texas A&M University, College Station, Texas"}]},{"given":"Raghu","family":"Ganugula","sequence":"additional","affiliation":[{"name":"Department of Pharmaceutical Sciences, Irma Lerma Rangel College of Pharmacy, Texas A&M University, College Station, Texas"}]},{"given":"Meenakshi","family":"Arora","sequence":"additional","affiliation":[{"name":"Department of Pharmaceutical Sciences, Irma Lerma Rangel College of Pharmacy, Texas A&M University, College Station, Texas"}]},{"given":"Mary B.","family":"Nabity","sequence":"additional","affiliation":[{"name":"Department of Veterinary Pathobiology, Texas A&M University College of Veterinary Medicine and Biomedical Sciences, College Station, Texas"}]},{"given":"David","family":"Sheikh-Hamad","sequence":"additional","affiliation":[{"name":"Department of Medicine, Baylor College of Medicine, Houston, Texas"}]},{"given":"M. N. V. Ravi","family":"Kumar","sequence":"additional","affiliation":[{"name":"Department of Pharmaceutical Sciences, Irma Lerma Rangel College of Pharmacy, Texas A&M University, College Station, Texas"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.5552-09.2010"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2015.01.002"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/j.molcel.2015.01.034"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/0016-5085(86)90687-6"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/0016-5085(86)90687-6"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1021\/jf9025794"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1021\/jf050384i"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1186\/1478-811X-8-31"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1038\/srep38868"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/j.jconrel.2016.06.016"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1038\/nrrheum.2015.159"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.3390\/cancers10040126"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1208\/s12248-012-9377-y"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1093\/jat\/32.2.140"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1016\/j.biotechadv.2015.02.010"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/j.addr.2003.10.015"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1021\/acsmacrolett.7b00035"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1111\/bph.13816"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1021\/jacs.6b13231"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1017\/S0007114510000826"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.117.242420"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/physiolgenomics.00239.2007"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2011.120"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.3390\/ijms17111826"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1517\/17425247.5.6.703"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/j.bmcl.2011.07.086"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2443.2003.00640.x"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00262.2004"},{"key":"B29","first-page":"1135","volume":"18","author":"Ju SM","year":"2014","journal-title":"Eur Rev Med Pharmacol Sci"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0406731102"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.08070715"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1016\/j.yexcr.2017.09.019"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1089\/ars.2010.3644"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1146\/annurev-pharmtox-011112-140320"},{"key":"B35","first-page":"85","volume":"37","author":"Makris K","year":"2016","journal-title":"Clin Biochem Rev"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.3390\/toxins2112490"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2015.328"},{"key":"B38","first-page":"243","volume":"34","author":"Nowsheen S","year":"2012","journal-title":"Exp Oncol"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1155\/2014\/967826"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2007-03-079616"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1016\/j.ijbiomac.2016.04.065"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1126\/scitranslmed.3007049"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-4939-1215-5_24"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1080\/10717544.2018.1501119"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1038\/nm.4132"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1038\/srep29501"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1208\/s12249-018-1262-2"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2012050469"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1016\/j.ajpath.2011.11.001"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00081.2005"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000060577.94532.06"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1089\/ars.2017.7342"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000042803.28024.92"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1038\/nrm2147"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005121371"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009030253"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00353.2010"},{"key":"B58","first-page":"594","volume":"295","author":"Xia CQ","year":"2000","journal-title":"J Pharmacol Exp Ther"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013121270"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1007\/s00018-016-2202-5"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013080902"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1007\/s11255-016-1485-7"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1016\/j.yexcr.2016.12.015"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2012.173"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00346.2019","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,11,7]],"date-time":"2019-11-07T09:05:08Z","timestamp":1573117508000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00346.2019"}},"issued":{"date-parts":[[2019,11,1]]},"references-count":64,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2019,11,1]]}},"alternative-id":["10.1152\/ajprenal.00346.2019"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00346.2019","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2019,11,1]]}},{"indexed":{"date-parts":[[2026,3,21]],"date-time":"2026-03-21T20:22:33Z","timestamp":1774124553349,"version":"3.50.1"},"reference-count":39,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2007,7]]},"abstract":"<jats:p> Acute kidney injury (AKI) is associated with significant mortality, which increases further when combined with acute lung injury. Experiments in rodents have shown that kidney ischemia-reperfusion injury (IRI) facilitates lung injury and inflammation. To identify potential ischemia-specific lung molecular pathways involved, we conducted global gene expression profiling of lung 6 or 36 h following 1) bilateral kidney IRI, 2) bilateral nephrectomy (BNx), and 3) sham laparotomy in C57BL\/6J mice. Bronchoalveolar lavage fluid analysis revealed increased total protein, and lung histology revealed increased cellular inflammation following IRI, but not BNx, compared with sham controls. Total RNA from whole lung was isolated and hybridized to 430MOEA (22,626 genes) GeneChips ( n = 3\/group), which were analyzed by robust multichip average and significance analysis of microarrays and linked to gene ontology (GO) terms using MAPPFinder. The microarray power analysis predicted that the false discovery rate ( q &lt; 1%) and \u226550%-fold change compared with sham would represent significant changes in gene expression. Analysis identified 266 and 455 ischemia-specific, AKI-associated lung genes with increased expression and 615 and 204 with decreased expression at 6 and 36 h, respectively, compared with sham controls. Real-time PCR analysis validated select array changes in lung serum amyloid A3 and endothelin-1. GO analysis revealed significant activation ( Z &gt; 1.95) of several proinflammatory and proapoptotic biological processes. Ischemic AKI induces functional and transcriptional changes in the lung distinct from those induced by uremia alone. Further investigation using this lung molecular signature induced by kidney IRI will provide mechanistic insights and new therapies for critically ill patients with AKI. <\/jats:p>","DOI":"10.1152\/ajprenal.00023.2007","type":"journal-article","created":{"date-parts":[[2007,2,28]],"date-time":"2007-02-28T03:11:13Z","timestamp":1172632273000},"page":"F30-F40","source":"Crossref","is-referenced-by-count":165,"title":["Ischemic acute kidney injury induces a distant organ functional and genomic response distinguishable from bilateral nephrectomy"],"prefix":"10.1152","volume":"293","author":[{"given":"Heitham T.","family":"Hassoun","sequence":"first","affiliation":[]},{"given":"Dmitry N.","family":"Grigoryev","sequence":"additional","affiliation":[]},{"given":"Mihaela L.","family":"Lie","sequence":"additional","affiliation":[]},{"given":"Manchang","family":"Liu","sequence":"additional","affiliation":[]},{"given":"Chris","family":"Cheadle","sequence":"additional","affiliation":[]},{"given":"Rubin M.","family":"Tuder","sequence":"additional","affiliation":[]},{"given":"Hamid","family":"Rabb","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.177.5.3380"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1186\/cc3879"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.176.11.7015"},{"key":"R4","doi-asserted-by":"crossref","unstructured":"Chen YC, Fang JT, Tien YC, Chang MY, Huang CC. Organ system failures predict prognosis in critically ill patients with acute renal failure requiring dialysis. Chang Gung Med J 23: 8\u201313, 2000.","DOI":"10.1081\/JDI-100103492"},{"key":"R5","doi-asserted-by":"crossref","unstructured":"Colletti LM, Cortis A, Lukacs N, Kunkel SL, Green M, Strieter RM. Tumor necrosis factor up-regulates intercellular adhesion molecule 1, which is important in the neutrophil-dependent lung and liver injury associated with hepatic ischemia and reperfusion in the rat. Shock 3: 182\u2013191, 1998.","DOI":"10.1097\/00024382-199809000-00006"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1038\/ng0502-19"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1016\/j.surg.2003.12.012"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1001\/jama.281.4.354"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1097\/00024382-199408000-00010"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1164\/rccm.200303-372OC"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1093\/biostatistics\/kxh015"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1186\/gb-2003-4-1-r7"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1186\/gb-2004-5-5-r34"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1186\/1471-2164-6-62"},{"key":"R15","doi-asserted-by":"crossref","unstructured":"Habre W, Petak F, Ruchonnet-Metrailler I, Donati Y, Tolsa JF, Lele E, Albu G, Beghetti M, Barazzone-Argiroffo C. The role of endothelin-1 in hyperoxia-induced lung injury in mice. Respir Res 27: 7:45, 2006.","DOI":"10.1186\/1465-9921-7-45"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1097\/00024382-200115010-00001"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006050494"},{"key":"R18","doi-asserted-by":"crossref","unstructured":"Irizarry R, Gautier L, Cope L. An R Package for Analyses of Affymetrix Oligonucleotide Arrays. New York: Springer, 2003.","DOI":"10.1007\/0-387-21679-0_4"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000064946.94590.46"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00460.x"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1097\/01.CCM.0000114575.08269.F6"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1001\/jama.1996.03530430033035"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.00522.2005"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1152\/ajplung.00109.2005"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1097\/00000658-199810000-00008"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000014692.19351.52"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1097\/00005373-199412000-00002"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)62318-8"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1164\/rccm.200411-1547OC"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00753.x"},{"key":"R31","unstructured":"Savransky V, Molls R, Bevans S, King L, Tuder R, Rabb H. Rapid upregulation of lung keratinocyte chemokine (KC) in ischemic acute renal failure (Abstract). J Am Soc Nephro 16: 624A, 2005."},{"key":"R32","unstructured":"Sun HC, Qian XM, Nie SN, Wu XH. Serial analysis of gene expression in mice with lipopolysaccharide-induced acute lung injury. Chin J Traumatol 8: 67\u201373, 2005."},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199605303342207"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.091062498"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1152\/physiolgenomics.2000.2.1.29"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1186\/1471-2164-5-87"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1203\/01.pdr.0000185269.93228.29"},{"key":"R38","doi-asserted-by":"crossref","unstructured":"Zallen G, Moore EE, Tamura DY, Johnson JL, Biffl WL, Silliman CC. Posthemorrhagic shock mesenteric lymph primes circulating neutrophils and provokes lung injury. J Surg Res 1583: 83\u201388, 1999.","DOI":"10.1006\/jsre.1999.5569"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006040358"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00023.2007","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T22:35:23Z","timestamp":1567982123000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00023.2007"}},"issued":{"date-parts":[[2007,7]]},"references-count":39,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2007,7]]}},"alternative-id":["10.1152\/ajprenal.00023.2007"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00023.2007","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2007,7]]}},{"indexed":{"date-parts":[[2026,3,25]],"date-time":"2026-03-25T16:29:12Z","timestamp":1774456152339,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1987,9,1]]},"abstract":"<jats:p> In this study we investigated the ultrastructure of the proximal tubule during alterations in fluid flow to determine whether previously observed changes in solute and water reabsorption may be related to alterations in cell ultrastructure. In each kidney, two proximal tubules (S2 segments) were perfused simultaneously at 5 and 45 nl\/min. Subsequently, cell ultrastructure of control and experimental tubules was examined by electron microscopy in combination with morphometry. Changes in flow rate greatly modified the geometry of the tubule epithelium. Enhanced flow increased luminal diameter and decreased cell height. The number of microvilli per square micrometer of luminal epithelial surface area decreased with increased flow rate from a control value of 42.5 to 35.5 at high flow. However, the total number of microvilli per millimeter tubule length did not change. Thus the distance between microvilli was dependent on flow rate and was estimated to be 621, 741, and 904 A in low flow, control, and high flow tubules, respectively. We suggest that increased flow rate, perhaps by altering transepithelial hydrostatic pressure gradients, leads to an increase in the distance between the microvilli and to other alterations in cellular ultrastructure that may contribute to the augmentation of solute and water reabsorption. <\/jats:p>","DOI":"10.1152\/ajprenal.1987.253.3.f582","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T22:55:52Z","timestamp":1513983352000},"page":"F582-F587","source":"Crossref","is-referenced-by-count":8,"title":["Effects of flow rate on proximal tubule ultrastructure"],"prefix":"10.1152","volume":"253","author":[{"given":"A. B.","family":"Maunsbach","sequence":"first","affiliation":[]},{"given":"G. H.","family":"Giebisch","sequence":"additional","affiliation":[]},{"given":"B. A.","family":"Stanton","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1987.253.3.F582","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:52:29Z","timestamp":1567957949000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1987.253.3.F582"}},"issued":{"date-parts":[[1987,9,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1987,9,1]]}},"alternative-id":["10.1152\/ajprenal.1987.253.3.F582"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1987.253.3.f582","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1987,9,1]]}},{"indexed":{"date-parts":[[2026,3,25]],"date-time":"2026-03-25T22:17:09Z","timestamp":1774477029972,"version":"3.50.1"},"reference-count":77,"publisher":"American Physiological Society","issue":"2","funder":[{"DOI":"10.13039\/100016229","name":"HHS | NIH | NCI | Basic Research Laboratory","doi-asserted-by":"publisher","award":["CA68485"],"award-info":[{"award-number":["CA68485"]}],"id":[{"id":"10.13039\/100016229","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000052","name":"HHS | NIH | NIH Office of the Director","doi-asserted-by":"publisher","award":["OD021577"],"award-info":[{"award-number":["OD021577"]}],"id":[{"id":"10.13039\/100000052","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000052","name":"HHS | NIH | NIH Office of the Director","doi-asserted-by":"publisher","award":["S10OD021630"],"award-info":[{"award-number":["S10OD021630"]}],"id":[{"id":"10.13039\/100000052","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000053","name":"HHS | NIH | National Eye Institute","doi-asserted-by":"publisher","award":["EY08126"],"award-info":[{"award-number":["EY08126"]}],"id":[{"id":"10.13039\/100000053","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK119793"],"award-info":[{"award-number":["DK119793"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK107798"],"award-info":[{"award-number":["DK107798"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK121848"],"award-info":[{"award-number":["DK121848"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK057521"],"award-info":[{"award-number":["DK057521"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK007540"],"award-info":[{"award-number":["DK007540"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK043351"],"award-info":[{"award-number":["DK043351"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK069921"],"award-info":[{"award-number":["DK069921"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK127589"],"award-info":[{"award-number":["DK127589"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK088327"],"award-info":[{"award-number":["DK088327"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK134879"],"award-info":[{"award-number":["DK134879"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK110375"],"award-info":[{"award-number":["DK110375"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK20593"],"award-info":[{"award-number":["DK20593"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK58404"],"award-info":[{"award-number":["DK58404"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK59637"],"award-info":[{"award-number":["DK59637"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100019592","name":"Veterans Administration Medical Center","doi-asserted-by":"publisher","award":["I01 BX002196"],"award-info":[{"award-number":["I01 BX002196"]}],"id":[{"id":"10.13039\/100019592","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2024,2,1]]},"abstract":"<jats:p> This study defines a new signaling mechanism by which angiotensin II modulates oxidative stress and blood pressure. <\/jats:p>","DOI":"10.1152\/ajprenal.00139.2023","type":"journal-article","created":{"date-parts":[[2023,12,7]],"date-time":"2023-12-07T09:00:53Z","timestamp":1701939653000},"page":"F202-F218","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":10,"title":["Angiotensin II acts through Rac1 to upregulate pendrin: role of NADPH oxidase"],"prefix":"10.1152","volume":"326","author":[{"given":"Truyen D.","family":"Pham","sequence":"first","affiliation":[{"name":"Renal Division, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia, United States"}]},{"given":"Jill W.","family":"Verlander","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Hypertension and Renal Transplantation, The University of Florida College of Medicine, Gainesville, Florida, United States"}]},{"given":"Chao","family":"Chen","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Hypertension and Renal Transplantation, The University of Florida College of Medicine, Gainesville, Florida, United States"}]},{"given":"Vladimir","family":"Pech","sequence":"additional","affiliation":[{"name":"Renal Division, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia, United States"}]},{"given":"Hailey I.","family":"Kim","sequence":"additional","affiliation":[{"name":"Renal Division, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia, United States"}]},{"given":"Young Hee","family":"Kim","sequence":"additional","affiliation":[{"name":"Renal Division, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0046-0600","authenticated-orcid":false,"given":"I. David","family":"Weiner","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Hypertension and Renal Transplantation, The University of Florida College of Medicine, Gainesville, Florida, United States"},{"name":"Nephrology and Hypertension Section, Gainesville Veterans Affairs Medical Center, Gainesville, Florida, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3890-151X","authenticated-orcid":false,"given":"Ginger L.","family":"Milne","sequence":"additional","affiliation":[{"name":"Division of Clinical Pharmacology, Vanderbilt University Medical Center, Nashville, Tennessee, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2983-8133","authenticated-orcid":false,"given":"Roy","family":"Zent","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, United States"},{"name":"Department of Veterans Affairs Hospital, Nashville, Tennessee, United States"}]},{"given":"Fabian","family":"Bock","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, United States"},{"name":"Department of Veterans Affairs Hospital, Nashville, Tennessee, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5011-7798","authenticated-orcid":false,"given":"Dennis","family":"Brown","sequence":"additional","affiliation":[{"name":"Program in Membrane Biology, Division of Nephrology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0791-3411","authenticated-orcid":false,"given":"Amity","family":"Eaton","sequence":"additional","affiliation":[{"name":"Program in Membrane Biology, Division of Nephrology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2786-8849","authenticated-orcid":false,"given":"Susan M.","family":"Wall","sequence":"additional","affiliation":[{"name":"Renal Division, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia, United States"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00037.2002"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.071516798"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00147.2002"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000145863.96091.89"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000088321.67254.B7"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00114.2011"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1111\/cge.12789"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1136\/jmg.2008.063610"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.5.F730"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00361.2006"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007030277"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2012.282"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1710964114"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00154.2013"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1007\/s00109-008-0399-y"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2011070734"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.3390\/cancers12030665"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1172\/JCI43124"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1093\/ajh\/hpu224"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1038\/labinvest.2017.2"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.18632\/oncotarget.18540"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.109.214601"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.170.11.5652"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.569"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.202103080"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1210\/en.2004-1102"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.141241098"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2017080826"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00277.2010"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00050.2002"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90581.2008"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00151.2007"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00664.2011"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1021\/pr1011476"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00239.x"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.5.F913"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1161\/01.cir.101.14.1722"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00011.2019"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1002\/dvg.20335"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.86.14.5429"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2017030243"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1210\/en.2007-0864"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M703571200"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-4939-9424-3_8"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1089\/ars.2019.7915"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1016\/j.jbc.2021.100347"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200401000-00013"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1161\/01.hyp.0000032100.23772.98"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.3945\/ajcn.112.034918"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006121333"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M414610200"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-4939-9424-3_2"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1002\/path.4255"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1016\/j.biochi.2007.05.003"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1089\/ars.2006.8.1597"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00060.2004"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000101968.09376.79"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00626.2004"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00250.2005"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00044.2005"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1016\/s0378-1119(01)00449-8"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1016\/j.freeradbiomed.2008.08.013"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.105.538934"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.105.573709"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1007\/s40292-016-0175-y"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1016\/j.redox.2022.102527"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1096\/fj.04-2882fje"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00543.2009"},{"key":"B69","doi-asserted-by":"publisher","DOI":"10.1016\/0891-5849(95)02021-7"},{"key":"B70","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00368.2011"},{"key":"B71","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00576.2017"},{"key":"B72","doi-asserted-by":"publisher","DOI":"10.1096\/fj.202200160R"},{"key":"B73","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2019080804"},{"key":"B74","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2019050551"},{"key":"B75","doi-asserted-by":"publisher","DOI":"10.1016\/j.celrep.2018.06.072"},{"key":"B76","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2013.10.005"},{"key":"B77","doi-asserted-by":"publisher","DOI":"10.1007\/s11906-015-0552-2"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00139.2023","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,2,7]],"date-time":"2024-02-07T14:13:32Z","timestamp":1707315212000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00139.2023"}},"issued":{"date-parts":[[2024,2,1]]},"references-count":77,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2024,2,1]]}},"alternative-id":["10.1152\/ajprenal.00139.2023"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00139.2023","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2024,2,1]]},"assertion":[{"value":"2023-05-22","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2023-11-14","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2023-11-14","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2024-01-16","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,3,14]],"date-time":"2026-03-14T03:28:57Z","timestamp":1773458937696,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1982,12,1]]},"abstract":"<jats:p> To assess the effect of renal nerve stimulation on sodium, chloride, and water transport in the loop of Henle, experiments were performed in anesthetized hydropenic and isotonic saline volume-expanded rats using renal clearance and Henle's loop microperfusion techniques (end-proximal convoluted tubule perfusion site, early distal convoluted tubule collection site). As compared with the control period values, low-frequency (less than 1.0 Hz) renal nerve stimulation decreased absolute and fractional urinary flow rate and sodium and chloride excretion without affecting mean arterial pressure, glomerular filtration rate, renal blood flow, or renal vascular resistance. In the loop of Henle, the absorptive transport of water was not affected, whereas the absorptive transport of sodium and chloride was increased in both hydropenic (Na 111 +\/- 49 peq\/min) and isotonic saline volume-expanded rats (Na 154 +\/- 69 peq\/min, Cl 180 +\/- 52 peq\/min) during low-frequency renal nerve stimulation. Low-frequency renal nerve stimulation decreases urinary sodium and chloride excretion via a direct effect of increasing renal tubular sodium and chloride reabsorption. In addition to the established effect of increasing proximal tubular sodium reabsorption, Henle's loop sodium and chloride absorption are also increased, supporting a physiological role for the adrenergic innervation of these structures. <\/jats:p>","DOI":"10.1152\/ajprenal.1982.243.6.f576","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T15:43:20Z","timestamp":1513957400000},"page":"F576-F580","source":"Crossref","is-referenced-by-count":10,"title":["Effect of renal nerve stimulation on NaCl and H2O transport in Henle's loop of the rat"],"prefix":"10.1152","volume":"243","author":[{"given":"G. F.","family":"DiBona","sequence":"first","affiliation":[]},{"given":"L. L.","family":"Sawin","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1982.243.6.F576","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:27:11Z","timestamp":1567967231000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1982.243.6.F576"}},"issued":{"date-parts":[[1982,12,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1982,12,1]]}},"alternative-id":["10.1152\/ajprenal.1982.243.6.F576"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1982.243.6.f576","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1982,12,1]]}},{"indexed":{"date-parts":[[2026,3,14]],"date-time":"2026-03-14T02:47:09Z","timestamp":1773456429260,"version":"3.50.1"},"reference-count":31,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,8,1]]},"abstract":"<jats:p> In addition to its role as a physical barrier, the urothelium is considered to play an active role in mechanosensation. A key mechanism is the release of transient mediators that activate purinergic P2 receptors and transient receptor potential (TRP) channels to effect changes in intracellular Ca<jats:sup>2+<\/jats:sup>. Despite the implied importance of these receptors and channels in urothelial tissue homeostasis and dysfunctional bladder disease, little is known about their functional expression by the human urothelium. To evaluate the expression and function of P2X and P2Y receptors and TRP channels, the human ureter and bladder were used to separate urothelial and stromal tissues for RNA isolation and cell culture. RT-PCR using stringently designed primer sets was used to establish which P2 and TRP species were expressed at the transcript level, and selective agonists\/antagonists were used to confirm functional expression by monitoring changes in intracellular Ca<jats:sup>2+<\/jats:sup> and in a scratch repair assay. The results confirmed the functional expression of P2Y<jats:sub>4<\/jats:sub> receptors and excluded nonexpressed receptors\/channels (P2X<jats:sub>1<\/jats:sub>, P2X<jats:sub>3<\/jats:sub>, P2X<jats:sub>6<\/jats:sub>, P2Y<jats:sub>6<\/jats:sub>, P2Y<jats:sub>11<\/jats:sub>, TRPV5, and TRPM8), while a dearth of specific agonists confounded the functional validation of expressed P2X<jats:sub>2<\/jats:sub>, P2X<jats:sub>4<\/jats:sub>, P2Y<jats:sub>1<\/jats:sub>, P2Y<jats:sub>2<\/jats:sub>, TRPV2, TRPV3, TRPV6 and TRPM7 receptors\/channels. Although a conventional response was elicited in control stromal-derived cells, the urothelial cell response to well-characterized TRPV1 and TRPV4 agonists\/antagonists revealed unexpected anomalies. In addition, agonists that invoked an increase in intracellular Ca<jats:sup>2+<\/jats:sup> promoted urothelial scratch repair, presumably through the release of ATP. The study raises important questions about the ligand selectivity of receptor\/channel targets expressed by the urothelium. These pathways are important in urothelial tissue homeostasis, and this opens the possibility of selective drug targeting. <\/jats:p>","DOI":"10.1152\/ajprenal.00127.2013","type":"journal-article","created":{"date-parts":[[2013,5,30]],"date-time":"2013-05-30T00:52:54Z","timestamp":1369875174000},"page":"F396-F406","source":"Crossref","is-referenced-by-count":44,"title":["Functional expression of purinergic P2 receptors and transient receptor potential channels by the human urothelium"],"prefix":"10.1152","volume":"305","author":[{"given":"Saqib","family":"Shabir","sequence":"first","affiliation":[{"name":"Jack Birch Unit of Molecular Carcinogenesis, Department of Biology, University of York, York, United Kingdom;"}]},{"given":"William","family":"Cross","sequence":"additional","affiliation":[{"name":"Jack Birch Unit of Molecular Carcinogenesis, Department of Biology, University of York, York, United Kingdom;"},{"name":"Pyrah Department of Urology, St James's University Hospital, Leeds, United Kingdom; and"}]},{"given":"Lisa A.","family":"Kirkwood","sequence":"additional","affiliation":[{"name":"Jack Birch Unit of Molecular Carcinogenesis, Department of Biology, University of York, York, United Kingdom;"}]},{"given":"Joanna F.","family":"Pearson","sequence":"additional","affiliation":[{"name":"Jack Birch Unit of Molecular Carcinogenesis, Department of Biology, University of York, York, United Kingdom;"}]},{"given":"Peter A.","family":"Appleby","sequence":"additional","affiliation":[{"name":"Department of Computer Science, Kroto Research Institute, University of Sheffield, Sheffield, United Kingdom"}]},{"given":"Dawn","family":"Walker","sequence":"additional","affiliation":[{"name":"Department of Computer Science, Kroto Research Institute, University of Sheffield, Sheffield, United Kingdom"}]},{"given":"Ian","family":"Eardley","sequence":"additional","affiliation":[{"name":"Jack Birch Unit of Molecular Carcinogenesis, Department of Biology, University of York, York, United Kingdom;"},{"name":"Pyrah Department of Urology, St James's University Hospital, Leeds, United Kingdom; and"}]},{"given":"Jennifer","family":"Southgate","sequence":"additional","affiliation":[{"name":"Jack Birch Unit of Molecular Carcinogenesis, Department of Biology, University of York, York, United Kingdom;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1007\/978-3-642-16499-6_19"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/j.biomaterials.2008.04.033"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2011.226860"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1007\/978-3-642-16499-6_10"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1038\/ncpuro0672"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.231243698"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.22-18-08063.2002"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00118.2004"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1002\/nau.20372"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/j.juro.2009.08.022"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00321.2006"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00040.2005"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1007\/s00210-008-0391-7"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00599.2009"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1111\/j.1464-410X.2007.07251.x"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1111\/j.1464-410X.2004.05047.x"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1111\/j.1464-410X.2012.011145.x"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0045339"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/j.ceca.2008.02.008"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1038\/nature09851"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/j.juro.2011.04.112"},{"key":"B22","first-page":"583","volume":"71","author":"Southgate J","year":"1994","journal-title":"Lab Invest"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1002\/0471221201.ch12"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00234.2005"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1097\/01.ju.0000099660.46774.3c"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/j.urology.2009.02.066"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1111\/j.1464-410X.2004.04858.x"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1016\/j.yexcr.2005.02.004"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.4161\/chan.3.3.8555"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00334.2011"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00349.2010"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00127.2013","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:46:12Z","timestamp":1567971972000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00127.2013"}},"issued":{"date-parts":[[2013,8,1]]},"references-count":31,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2013,8,1]]}},"alternative-id":["10.1152\/ajprenal.00127.2013"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00127.2013","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2013,8,1]]}},{"indexed":{"date-parts":[[2026,3,14]],"date-time":"2026-03-14T03:24:20Z","timestamp":1773458660199,"version":"3.50.1"},"reference-count":30,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2006,7]]},"abstract":"<jats:p>In this study, we engineered a Madin-Darby canine kidney (MDCK) type I cell line to stably express the mouse urea transporter UT-A2. Monolayers of MDCK-mUT-A2 cells had a basal phloretin-inhibitable urea permeability of 8.4 \u00d7 10<jats:sup>\u22126<\/jats:sup>\u00b1 0.3 cm\/s. Treatment of MDCK-mUT-A2 monolayers with AVP led to a rapid dose-dependent increase in trans-monolayer phloretin-inhibitable urea flux. The temporal pattern of response was markedly different from that observed for MDCK cells expressing rat UT-A1. Exposure of MDCK-mUT-A2 cells to either 10 \u03bcM forskolin or 250 \u03bcM 8-bromo cAMP also increased urea flux rate. Inclusion of the PKA inhibitor H89 (10 \u03bcM) had no effect on the forskolin-stimulated increase in urea flux across MDCK-mUT-A2 monolayers. Treatment with either 10 \u03bcM CPA or 1 mM ATP also caused an increase in UT-A2-mediated urea flux, although these responses where transient compared with those induced by AVP or elevated cAMP. Taken together, these results show for the first time that UT-A2 is acutely sensitive to AVP, cAMP, or increased intracellular calcium.<\/jats:p>","DOI":"10.1152\/ajprenal.00423.2005","type":"journal-article","created":{"date-parts":[[2006,2,1]],"date-time":"2006-02-01T03:43:31Z","timestamp":1138765411000},"page":"F122-F128","source":"Crossref","is-referenced-by-count":18,"title":["Urea flux across MDCK-mUT-A2 monolayers is acutely sensitive to AVP, cAMP, and [Ca<sup>2+<\/sup>]<sub>i<\/sub>"],"prefix":"10.1152","volume":"291","author":[{"given":"Elizabeth A.","family":"Potter","sequence":"first","affiliation":[]},{"given":"Gavin","family":"Stewart","sequence":"additional","affiliation":[]},{"given":"Craig P.","family":"Smith","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1159\/000045476"},{"key":"R2","doi-asserted-by":"crossref","unstructured":"Bagnasco SM, Peng T, Nakayama Y, and Sands JM.Differential expression of individual UT-A urea transporter isoforms in rat kidney.J Am Soc Nephrol11: 1980\u20131986, 2000.","DOI":"10.1681\/ASN.V11111980"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1038\/361315a0"},{"key":"R4","doi-asserted-by":"crossref","unstructured":"Demaurex N, Lew D, and Krause K.Cyclopiazonic acid depletes intracellular Ca2+stores and activates an influx pathway for divalent cations in HL-60 cells.J Biol Chem267: 2318\u20132324, 1992.","DOI":"10.1016\/S0021-9258(18)45880-2"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.267.6.F998"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0401704101"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00264.2001"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00263.2001"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00499.2003"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1016\/S0024-3205(97)01149-1"},{"key":"R11","unstructured":"Karakashian A, Timmer RT, Klein JD, Gunn RB, Sands JM, and Bagnasco SM.Cloning and characterization of two new isoforms of the rat kidney urea transporter: UT-A3 and UT-A4.J Am Soc Nephrol10: 230\u2013237, 1999."},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.268.4.F671"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.21.12973"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.93.11.5495"},{"key":"R15","doi-asserted-by":"crossref","unstructured":"Olives B, Neau P, Bailly P, Hediger MA, Rousselet G, Cartron JP, and Ripoche P.Cloning and functional expression of a urea transporter from human bone marrow cells.J Biol Chem269: 31649\u201331652, 1994.","DOI":"10.1016\/S0021-9258(18)31744-7"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.65.092101.142638"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.272.5.F654"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.4.F620"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119077"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118194"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1007\/s00232-001-0048-7"},{"key":"R22","unstructured":"Smith C, Shayakul C, You G, Lee WS, Martial S, Mackenzie HS, Sands JM, Knepper MA, and Hediger MA.Molecular characterization and regulation of expression of the vasopressin-regulated urea transporter.J Am Soc Nephrol6: 329, 1995."},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1172\/JCI113534"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00334.2003"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.2.F325"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.25.16.7357-7363.2005"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.1.F52"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M200207200"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1038\/365844a0"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.0054.2001"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00423.2005","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,7,23]],"date-time":"2021-07-23T11:03:18Z","timestamp":1627038198000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00423.2005"}},"issued":{"date-parts":[[2006,7]]},"references-count":30,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2006,7]]}},"alternative-id":["10.1152\/ajprenal.00423.2005"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00423.2005","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2006,7]]}},{"indexed":{"date-parts":[[2026,3,14]],"date-time":"2026-03-14T03:41:46Z","timestamp":1773459706455,"version":"3.50.1"},"reference-count":31,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2002,3,1]]},"abstract":"<jats:p> We utilized immunofluorescent immunolabeling of renal tissue sections to identify and count tubules at specified depths of the rat renal inner medulla. We used primary antibodies to aquaporin-1 (AQP1; labeling thin descending limbs), aquaporin-2 (AQP2; labeling inner medullary collecting ducts), the rat kidney-specific chloride channel (ClC-K1; labeling thin ascending limbs), and von Willebrand factor (labeling descending vasa recta). Secondary antibodies conjugated to different fluorophores were used, giving up to a three-color display. Labeled structures were then identified and counted. At each level sampled in the inner medulla, many more thin limbs were labeled by ClC-K1 than AQP1. In addition, thin limbs were found to label with antibodies to ClC-K1 on both sides of their hairpin turns. We conclude that the descending thin limbs shift from expressing AQP1 to expressing ClC-K1 some distance before the point where they turn and begin to ascend. Mathematical models can use our quantitative data to explore implications for the urine-concentrating mechanism. <\/jats:p>","DOI":"10.1152\/ajprenal.00340.2000","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T15:34:32Z","timestamp":1425396872000},"page":"F553-F557","source":"Crossref","is-referenced-by-count":17,"title":["Immunomorphometric study of rat renal inner medulla"],"prefix":"10.1152","volume":"282","author":[{"given":"Raymond","family":"Mejia","sequence":"first","affiliation":[{"name":"Mathematical Research Branch, National Institutes of Health, Bethesda 20892-2690; and"}]},{"given":"James B.","family":"Wade","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland 21201"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.263.3.F417"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.264.2.F337"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1172\/JCI5704"},{"key":"B4","first-page":"168","volume":"13","author":"Chou C-L","year":"1993","journal-title":"Semin Nephrol"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1007\/BF00317960"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.264.3.F388"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1172\/JCI107572"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1988.254.3.F323"},{"key":"B9","doi-asserted-by":"crossref","first-page":"180","DOI":"10.1152\/ajplegacy.1973.224.1.180","volume":"224","author":"Jamison RL","year":"1973","journal-title":"Am J Physiol"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1172\/JCI108633"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.1.F96"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1977.118"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1172\/JCI106401"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1972.97"},{"key":"B15","first-page":"320","volume":"6","author":"Kriz W.","year":"1976","journal-title":"Curr Probl Clin Biochem"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1007\/BF00519771"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1007\/BF00520711"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117672"},{"key":"B19","doi-asserted-by":"crossref","first-page":"824","DOI":"10.1152\/ajplegacy.1970.218.3.824","volume":"218","author":"Marsh DJ.","year":"1970","journal-title":"Am J Physiol"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.257.6.F1146"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1983.245.6.F743"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.90.24.11663"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.268.6.F1023"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5320(66)80101-6"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.2.F202"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1972.75"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.256.2.F218"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.2.F414"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117626"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.272.5.F678"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.1.F52"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00340.2000","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T17:59:25Z","timestamp":1567965565000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00340.2000"}},"issued":{"date-parts":[[2002,3,1]]},"references-count":31,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2002,3,1]]}},"alternative-id":["10.1152\/ajprenal.00340.2000"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00340.2000","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2002,3,1]]}},{"indexed":{"date-parts":[[2026,3,14]],"date-time":"2026-03-14T03:45:24Z","timestamp":1773459924596,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1995,12,1]]},"abstract":"<jats:p> The P2u class of nucleotide receptors is linked to mobilization of intracellular Ca2+ in many cell types, including the renal collecting duct cells. In the present studies, we examined the effects of nucleotides (ATP, UTP, and ADP; 10 microM each) on the arginine vasopressin (AVP, 0.1 nM)-stimulated osmotic water permeability (Pf) in in vitro perfused terminal inner medullary collecting ducts (IMCD) of rat. ATP or UTP, when added to the bath, decreased the AVP-stimulated Pf by approximately 40%. These effects were reversible upon withdrawal of the nucleotides. However, addition of ADP to the bath or sham exchange of the bath had no significant effect on the Pf. Furthermore, ATP did not have any significant effect on the Pf stimulated either by a membrane-permeant, nonhydrolyzable adenosine 3',5'-cyclic monophosphate (cAMP) analogue [8-(4-chlorophenylthio)-cAMP, 0.1 mM] o by forskolin (1 microM). In line with these findings, ATP decreased the AVP-stimulated cAMP levels in IMCD suspensions to approximately 68%. In addition, ATP did not exert an inhibitory effect on the AVP-stimulated Pf in the presence of calphostin C (150 nM), an inhibitor of protein kinase C. These results lead us to conclude the following: 1) agonist occupancy of the putative nucleotide receptor in the terminal IMCD causes an inhibition of AVP-stimulated Pf; and 2) this effect is due to a decrease in cellular cAMP levels, most likely resulting from activation of the phosphoinositide signaling pathway. <\/jats:p>","DOI":"10.1152\/ajprenal.1995.269.6.f863","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T05:21:03Z","timestamp":1514006463000},"page":"F863-F869","source":"Crossref","is-referenced-by-count":49,"title":["Extracellular nucleotide receptor inhibits AVP-stimulated water permeability in inner medullary collecting duct"],"prefix":"10.1152","volume":"269","author":[{"given":"B. K.","family":"Kishore","sequence":"first","affiliation":[{"name":"Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lungand Blood Institute, National Institutes of Health, Bethesda, Maryland20892, USA."}]},{"given":"C. L.","family":"Chou","sequence":"additional","affiliation":[{"name":"Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lungand Blood Institute, National Institutes of Health, Bethesda, Maryland20892, USA."}]},{"given":"M. A.","family":"Knepper","sequence":"additional","affiliation":[{"name":"Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lungand Blood Institute, National Institutes of Health, Bethesda, Maryland20892, USA."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1995.269.6.F863","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:58:09Z","timestamp":1567972689000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1995.269.6.F863"}},"issued":{"date-parts":[[1995,12,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1995,12,1]]}},"alternative-id":["10.1152\/ajprenal.1995.269.6.F863"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1995.269.6.f863","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1995,12,1]]}},{"indexed":{"date-parts":[[2026,3,16]],"date-time":"2026-03-16T11:34:13Z","timestamp":1773660853763,"version":"3.50.1"},"reference-count":53,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2002,9,1]]},"abstract":"<jats:p>C-type natriuretic peptide (CNP) possesses well-established cardiovascular properties. Although present in the mammalian kidney, CNP production in human kidney and its modulation in human renal disease remain less defined. We investigated the presence of CNP in normal human kidney and in patients with nephrotic syndrome (NS). We also addressed whether or not a low-protein diet (LPD) alters plasma CNP and urinary CNP excretion in NS. In situ hybridization studies demonstrated CNP mRNA expression in tubular cells and glomeruli of normal human kidneys. CNP immunoreactivity was positive in proximal, distal, and medullary collecting duct tubular cells in both controls and patients with NS. The ratios of plasma CNP and urinary CNP to creatinine were significantly higher in patients with NS compared with controls. Urinary CNP, but not plasma CNP, was significantly lowered in patients with NS after an LPD. Similarly, the ratios of urinary protein to creatinine and urinary albumin to creatinine, but not urinary guanosine 3\u2032,5\u2032-cyclic monophosphate to creatinine, decreased significantly with an LPD. These data confirm and extend previous reports and demonstrate for the first time the presence of CNP in human kidney with NS. We also report increased plasma CNP concentration and urinary CNP excretion in NS patients and a significant reduction of CNP excretion with an LPD. Our findings demonstrate that CNP metabolism is altered in patients with NS and support the hypothesis that activation of renal CNP can be partially offset by an LPD. These results underscore that the beneficial effect of an LPD on protein excretion is paralleled by a substantial reduction in intrarenal CNP release.<\/jats:p>","DOI":"10.1152\/ajprenal.00372.2001","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:35:50Z","timestamp":1425414950000},"page":"F464-F472","source":"Crossref","is-referenced-by-count":30,"title":["CNP production in the kidney and effects of protein intake restriction in nephrotic syndrome"],"prefix":"10.1152","volume":"283","author":[{"given":"Alessandro","family":"Cataliotti","sequence":"first","affiliation":[{"name":"Cardiorenal Research Laboratory, Division of Cardiovascular Diseases and Nephrology, Department of Internal Medicine, Mayo Clinic and Foundation, Rochester, Minnesota 55905;"}]},{"given":"Mauro","family":"Giordano","sequence":"additional","affiliation":[{"name":"Department of Geriatric Medicine and Metabolic Diseases, Second University of Naples, Naples 803131; and"}]},{"given":"Emanuela","family":"De Pascale","sequence":"additional","affiliation":[{"name":"Department of Geriatric Medicine and Metabolic Diseases, Second University of Naples, Naples 803131; and"}]},{"given":"Gelsomina","family":"Giordano","sequence":"additional","affiliation":[{"name":"Department of Geriatric Medicine and Metabolic Diseases, Second University of Naples, Naples 803131; and"}]},{"given":"Pietro","family":"Castellino","sequence":"additional","affiliation":[{"name":"Istituto di Clinica Medica L. Condorelli, University of Catania, Catania 95124, Italy"}]},{"given":"Michihisa","family":"Jougasaki","sequence":"additional","affiliation":[{"name":"Cardiorenal Research Laboratory, Division of Cardiovascular Diseases and Nephrology, Department of Internal Medicine, Mayo Clinic and Foundation, Rochester, Minnesota 55905;"}]},{"given":"Lisa C.","family":"Costello","sequence":"additional","affiliation":[{"name":"Cardiorenal Research Laboratory, Division of Cardiovascular Diseases and Nephrology, Department of Internal Medicine, Mayo Clinic and Foundation, Rochester, Minnesota 55905;"}]},{"given":"Guido","family":"Boerrigter","sequence":"additional","affiliation":[{"name":"Cardiorenal Research Laboratory, Division of Cardiovascular Diseases and Nephrology, Department of Internal Medicine, Mayo Clinic and Foundation, Rochester, Minnesota 55905;"}]},{"given":"Toshihiro","family":"Tsuruda","sequence":"additional","affiliation":[{"name":"Cardiorenal Research Laboratory, Division of Cardiovascular Diseases and Nephrology, Department of Internal Medicine, Mayo Clinic and Foundation, Rochester, Minnesota 55905;"}]},{"given":"Paola","family":"Belluardo","sequence":"additional","affiliation":[{"name":"Istituto di Clinica Medica L. Condorelli, University of Catania, Catania 95124, Italy"}]},{"given":"Shang-Chiun","family":"Lee","sequence":"additional","affiliation":[{"name":"Cardiorenal Research Laboratory, Division of Cardiovascular Diseases and Nephrology, Department of Internal Medicine, Mayo Clinic and Foundation, Rochester, Minnesota 55905;"}]},{"given":"Brenda","family":"Huntley","sequence":"additional","affiliation":[{"name":"Cardiorenal Research Laboratory, Division of Cardiovascular Diseases and Nephrology, Department of Internal Medicine, Mayo Clinic and Foundation, Rochester, Minnesota 55905;"}]},{"given":"Sharon","family":"Sandberg","sequence":"additional","affiliation":[{"name":"Cardiorenal Research Laboratory, Division of Cardiovascular Diseases and Nephrology, Department of Internal Medicine, Mayo Clinic and Foundation, Rochester, Minnesota 55905;"}]},{"given":"Lorenzo S.","family":"Malatino","sequence":"additional","affiliation":[{"name":"Istituto di Clinica Medica L. Condorelli, University of Catania, Catania 95124, Italy"}]},{"suffix":"Jr.","given":"John C.","family":"Burnett","sequence":"additional","affiliation":[{"name":"Cardiorenal Research Laboratory, Division of Cardiovascular Diseases and Nephrology, Department of Internal Medicine, Mayo Clinic and Foundation, Rochester, Minnesota 55905;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.31.3.802"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2125.1998.00803.x"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1042\/cs0950195"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1210\/endo.130.1.1309350"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00895.x"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.4065\/76.11.1111"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1995.268.1.R201"},{"key":"B8","first-page":"S22","volume":"3","author":"Chen HH","year":"1998","journal-title":"J Cardiovasc Pharmacol"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.29.6.1296"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1993.264.2.R290"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.266.3.F491"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1042\/cs0780565"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1096\/fasebj.3.2.2521610"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/0006-291X(91)90627-J"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1016\/0006-291X(90)91260-Y"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00791.x"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1994.1166"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1093\/ajcp\/92.2.166"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1986.250.4.F613"},{"key":"B20","first-page":"S144","volume":"55","author":"Igaki T","year":"1996","journal-title":"Kidney Int Suppl"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1986.36"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1210\/endo-129-2-1104"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-199917040-00017"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199807303390507"},{"key":"B25","doi-asserted-by":"crossref","first-page":"1946","DOI":"10.1093\/clinchem\/29.11.1946","volume":"29","author":"Lott JA","year":"1983","journal-title":"Clin Chem"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1126\/science.2823385"},{"key":"B27","first-page":"S100","volume":"9","author":"Maroni BJ.","year":"1998","journal-title":"J Am Soc Nephrol"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1985.10"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.329"},{"key":"B30","first-page":"211","volume":"10","author":"Moulin B","year":"1990","journal-title":"Int J Clin Pharmacol Res"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1016\/0891-6632(91)90048-T"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1994.267.6.R1653"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199804233381707"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1997.273.4.R1457"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1992.263.5.C1001"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.229"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1007\/PL00005140"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1677\/joe.0.1580035"},{"key":"B39","doi-asserted-by":"crossref","first-page":"S126","DOI":"10.1681\/ASN.V210s126","volume":"2","author":"Sterzel RB","year":"1992","journal-title":"J Am Soc Nephrol"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1992.262.1.H308"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1992.263.4.H1318"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1016\/0006-291X(90)92401-K"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1210\/endo.130.1.1309330"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.19.6.762"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115933"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1210\/endo.133.6.8243333"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1993.1448"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1042\/cs0780481"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1016\/0006-291X(91)91614-I"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.24.6.758"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1987.154"},{"key":"B52","first-page":"152","volume":"117","author":"Vaziri ND","year":"1991","journal-title":"J Lab Clin Med"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1172\/JCI116947"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00372.2001","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,5,1]],"date-time":"2022-05-01T09:35:11Z","timestamp":1651397711000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00372.2001"}},"issued":{"date-parts":[[2002,9,1]]},"references-count":53,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2002,9,1]]}},"alternative-id":["10.1152\/ajprenal.00372.2001"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00372.2001","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2002,9,1]]}},{"indexed":{"date-parts":[[2026,3,16]],"date-time":"2026-03-16T11:55:14Z","timestamp":1773662114177,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1997,1,1]]},"abstract":"<jats:p> The development of urolithiasis is a multifaceted process, starting at urine supersaturation and ending with the formation of mature renal calculi. The retention of microcrystals by the urothelial cell membrane is a critical event in the process. The current study examines calcium oxalate monohydrate (COM) crystal attachment to inner medullary collecting duct (IMCD) cells following selective changes in cell membrane phospholipid composition. Both primary culture of IMCD cells and a continuous IMCD cell line were used for these studies. Cell membrane composition was selectively altered by either exogenous addition of membrane phospholipids or using membrane lipid scrambling agents. Enrichment with anionic phospholipids was found to greatly increase attachment of crystals to the cells. This increased attachment correlated with the exposure of phosphatidylserine (PS) on the exofacial leaflet of the cell membrane as demonstrated by the use of the membrane scrambling agent A-23187. Furthermore, the increased COM attachment following PS exposure could be blocked by incubating the cells with the PS-specific binding protein, annexin V. These results support the hypothesis that exposure of PS head groups on the papillary epithelial cell surface may mediate stone crystal attachment to the kidney tubule cell epithelium in the renal papilla, possibly as an initiating event in urolithiasis. <\/jats:p>","DOI":"10.1152\/ajprenal.1997.272.1.f55","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T08:32:04Z","timestamp":1514017924000},"page":"F55-F62","source":"Crossref","is-referenced-by-count":18,"title":["Surface exposure of phosphatidylserine increases calcium oxalate crystal attachment to IMCD cells"],"prefix":"10.1152","volume":"272","author":[{"given":"M. W.","family":"Bigelow","sequence":"first","affiliation":[{"name":"Department of Medicine, Medical College of Wisconsin, Milwaukee 53295,USA."}]},{"given":"J. H.","family":"Wiessner","sequence":"additional","affiliation":[{"name":"Department of Medicine, Medical College of Wisconsin, Milwaukee 53295,USA."}]},{"given":"J. G.","family":"Kleinman","sequence":"additional","affiliation":[{"name":"Department of Medicine, Medical College of Wisconsin, Milwaukee 53295,USA."}]},{"given":"N. S.","family":"Mandel","sequence":"additional","affiliation":[{"name":"Department of Medicine, Medical College of Wisconsin, Milwaukee 53295,USA."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1997.272.1.F55","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:15:38Z","timestamp":1567973738000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1997.272.1.F55"}},"issued":{"date-parts":[[1997,1,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1997,1,1]]}},"alternative-id":["10.1152\/ajprenal.1997.272.1.F55"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1997.272.1.f55","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1997,1,1]]}},{"indexed":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T16:47:27Z","timestamp":1773420447264,"version":"3.50.1"},"reference-count":191,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2002,12,1]]},"abstract":"<jats:p>Cl<jats:sup>\u2212<\/jats:sup>channels are involved in a range of functions, including regulation of cell volume and\/or intracellular pH, acidification of intracellular vesicles, and vectorial transport of NaCl across many epithelia. Numerous Cl<jats:sup>\u2212<\/jats:sup>channels have been identified in the kidney, based on single-channel properties such as conductance, anion selectivity, gating, and response to inhibitors. The molecular counterpart of many of these Cl<jats:sup>\u2212<\/jats:sup>channels is still not known. This review will focus on gene-targeted mouse models disrupting two structural classes of Cl<jats:sup>\u2212<\/jats:sup>channels that are relevant for the kidney: the CLC family of voltage-gated Cl<jats:sup>\u2212<\/jats:sup>channels and the CFTR. Disruption of several members of the CLC family in the mouse provided useful models for various inherited diseases of the kidney, including Dent's disease and diabetes insipidus. Mice with disrupted CFTR are valuable models for cystic fibrosis (CF), the most common autosomal recessive, lethal disease in Caucasians. Although CFTR is expressed in various nephron segments, there is no overt renal phenotype in CF. Analysis of CF mice has been useful to identify the role and potential interactions of CFTR in the kidney. Furthermore, observations made in CF mice are potentially relevant to all other models of Cl<jats:sup>\u2212<\/jats:sup>channel knockouts because they emphasize the importance of alternative Cl<jats:sup>\u2212<\/jats:sup>pathways in such models.<\/jats:p>","DOI":"10.1152\/ajprenal.00184.2002","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:36:32Z","timestamp":1425414992000},"page":"F1176-F1191","source":"Crossref","is-referenced-by-count":49,"title":["Chloride channels in the kidney: lessons learned from knockout animals"],"prefix":"10.1152","volume":"283","author":[{"given":"Olivier","family":"Devuyst","sequence":"first","affiliation":[{"name":"Division of Nephrology, Universit\u00e9Catholique de Louvain Medical School, B-1200 Brussels, Belgium; and"}]},{"given":"William B.","family":"Guggino","sequence":"additional","affiliation":[{"name":"Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1007\/s002329900444"},{"key":"B2","doi-asserted-by":"crossref","first-page":"17677","DOI":"10.1016\/S0021-9258(17)32494-8","volume":"269","author":"Adachi S","year":"1994","journal-title":"J Biol Chem"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.1.F79"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1159\/000182987"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.ph.53.030191.003001"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajplung.1992.263.1.L1"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.133.1.29"},{"key":"B8","first-page":"213","volume":"7","author":"Assael BM","year":"1986","journal-title":"Int J Pediatr Nephrol"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1038\/348637a0"},{"key":"B10","doi-asserted-by":"crossref","first-page":"464","DOI":"10.1016\/S0022-3565(24)37481-6","volume":"285","author":"Bailey MA","year":"1998","journal-title":"J Pharmacol Exp Ther"},{"key":"B11","first-page":"S29","volume":"65","author":"Bailly C.","year":"1998","journal-title":"Kidney Int"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1038\/352070a0"},{"key":"B13","doi-asserted-by":"crossref","first-page":"2145","DOI":"10.1242\/jcs.114.11.2145","volume":"114","author":"Barg S","year":"2001","journal-title":"J Cell Sci"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.9.5372"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1111\/j.1432-1033.1997.00367.x"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-3476(05)81602-6"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1111\/j.1651-2227.1982.tb09528.x"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1038\/ng752"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/20.6.1289"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1999.79.1.S175"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1126\/science.1373908"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1992.262.3.C752"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.93.19.10206"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00875.x"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1053\/snep.2001.20929"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1038\/35065099"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.4.F562"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/S0074-7696(08)61772-6"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.91.2.479"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1998.274.3.R718"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/10.25.2861"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1038\/ng0895-445"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1016\/S0076-6879(98)92050-X"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.88.20.9262"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.304"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1002\/j.1460-2075.1996.tb00432.x"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(05)61224-X"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.3.F723"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/8.2.247"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.91.19.8984"},{"key":"B44","first-page":"186","volume":"12","author":"Donckerwolcke RA","year":"1992","journal-title":"Child Nephrol Urol"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1038\/359211a0"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1038\/415287a"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1152\/ajplung.00207.2001"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1038\/35107099"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1038\/29319"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1038\/37391"},{"key":"B51","first-page":"2053","volume":"3","author":"Fisher SE","year":"1994","journal-title":"Hum Mol Genet"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.2.896"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1007\/s004240100655"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1038\/363263a0"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.2000.279.4.C1088"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1985.65.3.760"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.1995.268.3.G505"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.1997.272.2.G393"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1999.79.1.S193"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1994.266.5.C1478"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1995.sp020715"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.14.8075"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9343(01)00740-9"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1996.270.1.C389"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200205000-00007"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1007\/BF02254769"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1007\/BF00580776"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.9.5620"},{"key":"B69","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.3.F352"},{"key":"B70","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00061.x"},{"key":"B71","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.6.F982"},{"key":"B72","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-5793(98)00112-4"},{"key":"B73","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.5.F951"},{"key":"B74","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117709"},{"key":"B75","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00203.x"},{"key":"B76","doi-asserted-by":"publisher","DOI":"10.1152\/ajplung.1997.272.4.L752"},{"key":"B77","doi-asserted-by":"publisher","DOI":"10.1172\/JCI107572"},{"key":"B78","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1987.37"},{"key":"B79","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00029.2001"},{"key":"B80","doi-asserted-by":"publisher","DOI":"10.1038\/348510a0"},{"key":"B81","doi-asserted-by":"publisher","DOI":"10.1172\/JCI5731"},{"key":"B82","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM198808043190502"},{"key":"B83","doi-asserted-by":"publisher","DOI":"10.1016\/0896-6273(94)90215-1"},{"key":"B84","doi-asserted-by":"publisher","DOI":"10.1177\/106002808902301214"},{"key":"B85","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.2001.0449f.x"},{"key":"B86","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.2000.00027.x"},{"key":"B87","doi-asserted-by":"crossref","first-page":"2507","DOI":"10.1681\/ASN.V12112507","volume":"12","author":"Kibble J","year":"2001","journal-title":"J Am Soc Nephrol"},{"key":"B88","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.91.15.6943"},{"key":"B89","first-page":"1025","volume":"74","author":"Kishore BK","year":"1996","journal-title":"Lab Invest"},{"key":"B90","doi-asserted-by":"publisher","DOI":"10.1016\/S0955-0674(97)80034-8"},{"key":"B91","doi-asserted-by":"crossref","first-page":"1327","DOI":"10.1681\/ASN.V1271327","volume":"12","author":"Kobayashi K","year":"2001","journal-title":"J Am Soc Nephrol"},{"key":"B92","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1972.97"},{"key":"B93","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.253.6.F1206"},{"key":"B94","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(01)00206-9"},{"key":"B95","doi-asserted-by":"publisher","DOI":"10.1016\/0003-9861(88)90473-0"},{"key":"B96","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1998.78.1.247"},{"key":"B97","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.21.14670"},{"key":"B98","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1997.272.2.C657"},{"key":"B99","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-3476(84)80375-3"},{"key":"B100","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.0192.2001"},{"key":"B101","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/6.8.1233"},{"key":"B102","doi-asserted-by":"publisher","DOI":"10.1038\/379445a0"},{"key":"B103","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119262"},{"key":"B104","doi-asserted-by":"publisher","DOI":"10.1038\/ng1097-179"},{"key":"B105","doi-asserted-by":"publisher","DOI":"10.1038\/383340a0"},{"key":"B106","doi-asserted-by":"crossref","first-page":"14568","DOI":"10.1016\/S0021-9258(18)42078-9","volume":"267","author":"Lukacs GL","year":"1992","journal-title":"J Biol Chem"},{"key":"B107","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.275.5.F761"},{"key":"B108","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.21.12174"},{"key":"B109","doi-asserted-by":"publisher","DOI":"10.1172\/JCI4074"},{"key":"B111","doi-asserted-by":"publisher","DOI":"10.1038\/5036"},{"key":"B112","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.93.15.8083"},{"key":"B113","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.bi.55.070186.003311"},{"key":"B114","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118176"},{"key":"B115","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M106968200"},{"key":"B116","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.270.6.F1038"},{"key":"B117","doi-asserted-by":"publisher","DOI":"10.1007\/s004240100671"},{"key":"B118","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.63.1.607"},{"key":"B119","doi-asserted-by":"publisher","DOI":"10.1152\/ajplung.1996.271.5.L829"},{"key":"B120","doi-asserted-by":"publisher","DOI":"10.1165\/ajrcmb.12.6.7766424"},{"key":"B121","doi-asserted-by":"publisher","DOI":"10.1038\/35056009"},{"key":"B122","doi-asserted-by":"publisher","DOI":"10.1172\/JCI1496"},{"key":"B123","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/2.10.1561"},{"key":"B124","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-002-0788-y"},{"key":"B125","doi-asserted-by":"publisher","DOI":"10.1038\/415008a"},{"key":"B126","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(01)69068-2"},{"key":"B127","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/15.6.747"},{"key":"B128","doi-asserted-by":"crossref","first-page":"2285","DOI":"10.1681\/ASN.V11122285","volume":"11","author":"Persu A","year":"2000","journal-title":"J Am Soc Nephrol"},{"key":"B129","doi-asserted-by":"publisher","DOI":"10.1038\/35042597"},{"key":"B130","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M105441200"},{"key":"B131","doi-asserted-by":"publisher","DOI":"10.1038\/85429"},{"key":"B132","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.2000.279.1.C1"},{"key":"B133","doi-asserted-by":"publisher","DOI":"10.1038\/ng0593-35"},{"key":"B134","doi-asserted-by":"publisher","DOI":"10.1021\/bi00116a026"},{"key":"B135","doi-asserted-by":"crossref","first-page":"1451","DOI":"10.1681\/ASN.V571451","volume":"5","author":"Reinhart SC","year":"1995","journal-title":"J Am Soc Nephrol"},{"key":"B136","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(97)09174-5"},{"key":"B137","doi-asserted-by":"publisher","DOI":"10.1038\/ng0396-280"},{"key":"B138","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.6.F957"},{"key":"B139","doi-asserted-by":"publisher","DOI":"10.1097\/00045391-199603000-00011"},{"key":"B140","doi-asserted-by":"publisher","DOI":"10.1172\/JCI113410"},{"key":"B141","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00718.x"},{"key":"B142","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199904153401507"},{"key":"B143","doi-asserted-by":"publisher","DOI":"10.1007\/BF01871011"},{"key":"B144","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.94.14.7633"},{"key":"B145","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M010642200"},{"key":"B146","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1999.79.1.S145"},{"key":"B147","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.7.3879"},{"key":"B148","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(05)80011-X"},{"key":"B149","doi-asserted-by":"publisher","DOI":"10.1007\/BF00373843"},{"key":"B150","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.26.15542"},{"key":"B151","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1999.79.1.S23"},{"key":"B152","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-3495(91)82336-0"},{"key":"B153","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.41.25537"},{"key":"B154","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.2.F238"},{"key":"B155","doi-asserted-by":"publisher","DOI":"10.1038\/ng1097-171"},{"key":"B156","doi-asserted-by":"publisher","DOI":"10.1038\/ng0696-183"},{"key":"B157","doi-asserted-by":"publisher","DOI":"10.1038\/ng1096-152"},{"key":"B158","doi-asserted-by":"publisher","DOI":"10.1126\/science.257.5073.1083"},{"key":"B159","first-page":"457","volume":"109","author":"Stanton BA.","year":"1997","journal-title":"Wien Klin Wochenschr"},{"key":"B160","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.52.31172"},{"key":"B161","doi-asserted-by":"publisher","DOI":"10.1111\/j.1651-2227.1991.tb11833.x"},{"key":"B162","doi-asserted-by":"publisher","DOI":"10.1016\/S0896-6273(01)00189-1"},{"key":"B163","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1996.270.3.C711"},{"key":"B164","doi-asserted-by":"publisher","DOI":"10.1126\/science.7543698"},{"key":"B165","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1998.78.4.1165"},{"key":"B166","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.090091297"},{"key":"B167","doi-asserted-by":"publisher","DOI":"10.1007\/s002329900049"},{"key":"B168","doi-asserted-by":"publisher","DOI":"10.1038\/356057a0"},{"key":"B169","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.1.F148"},{"key":"B170","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.5.F792"},{"key":"B171","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/2.3.213"},{"key":"B172","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.5.F802"},{"key":"B173","doi-asserted-by":"crossref","first-page":"3821","DOI":"10.1016\/S0021-9258(18)53545-6","volume":"268","author":"Uchida S","year":"1993","journal-title":"J Biol Chem"},{"key":"B174","doi-asserted-by":"crossref","first-page":"23451","DOI":"10.1016\/S0021-9258(17)31537-5","volume":"269","author":"Uchida S","year":"1994","journal-title":"J Biol Chem"},{"key":"B175","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117626"},{"key":"B176","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.272.5.F678"},{"key":"B177","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.2001.280.2.C373"},{"key":"B178","doi-asserted-by":"publisher","DOI":"10.1002\/j.1460-2075.1995.tb00119.x"},{"key":"B179","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1995.269.3.C683"},{"key":"B180","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.93.11.5401"},{"key":"B181","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/3.4.547"},{"key":"B182","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.130.4.821"},{"key":"B183","doi-asserted-by":"crossref","first-page":"1331","DOI":"10.1681\/ASN.V1171331","volume":"11","author":"Waldegger S","year":"2000","journal-title":"J Am Soc Nephrol"},{"key":"B184","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/9.20.2937"},{"key":"B185","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.268.2.F204"},{"key":"B187","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(93)90353-R"},{"key":"B188","first-page":"473","volume":"87","author":"Wrong OM","year":"1994","journal-title":"Q J Med"},{"key":"B189","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)81570-6"},{"key":"B190","doi-asserted-by":"publisher","DOI":"10.1038\/46045"},{"key":"B191","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.10.5808"},{"key":"B192","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.4.F552"},{"key":"B193","doi-asserted-by":"publisher","DOI":"10.1172\/JCI113691"},{"key":"B194","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200105000-00019"},{"key":"B195","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118253"},{"key":"B196","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.481"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00184.2002","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,5,20]],"date-time":"2025-05-20T17:51:31Z","timestamp":1747763491000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00184.2002"}},"issued":{"date-parts":[[2002,12,1]]},"references-count":191,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2002,12,1]]}},"alternative-id":["10.1152\/ajprenal.00184.2002"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00184.2002","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2002,12,1]]}},{"indexed":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T16:47:51Z","timestamp":1773420471918,"version":"3.50.1"},"reference-count":73,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2000,7,1]]},"abstract":"<jats:p>A mathematical model of the outer medullary collecting duct (OMCD) has been developed, consisting of \u03b1-intercalated cells and a paracellular pathway, and which includes Na<jats:sup>+<\/jats:sup>, K<jats:sup>+<\/jats:sup>, Cl<jats:sup>\u2212<\/jats:sup>, HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup>, CO<jats:sub>2<\/jats:sub>, H<jats:sub>2<\/jats:sub>CO<jats:sub>3<\/jats:sub>, phosphate, ammonia, and urea. Proton secretion across the luminal cell membrane is mediated by both H<jats:sup>+<\/jats:sup>-ATPase and H-K-ATPase, with fluxes through the H-K-ATPase given by a previously developed kinetic model (Weinstein AM. Am J Physiol Renal Physiol 274: F856\u2013F867, 1998). The flux across each ATPase is substantial, and variation in abundance of either pump can be used to control OMCD proton secretion. In comparison with the H<jats:sup>+<\/jats:sup>-ATPase, flux through the H-K-ATPase is relatively insensitive to changes in lumen pH, so as luminal acidification proceeds, proton secretion shifts toward this pathway. Peritubular HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup>exit is via a conductive pathway and via the Cl<jats:sup>\u2212<\/jats:sup>\/HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup>exchanger, AE1. To represent AE1, a kinetic model has been developed based on transport studies obtained at 38\u00b0C in red blood cells. (Gasbjerg PK, Knauf PA, and Brahm J. J Gen Physiol 108: 565\u2013575, 1996; Knauf PA, Gasbjerg PK, and Brahm J. J Gen Physiol 108: 577\u2013589, 1996). Model calculations indicate that if all of the chloride entry via AE1 recycles across a peritubular chloride channel and if this channel is anything other than highly selective for chloride, then it should conduct a substantial fraction of the bicarbonate exit. Since both luminal membrane proton pumps are sensitive to small changes in cytosolic pH, variation in density of either AE1 or peritubular anion conductance can modulate OMCD proton secretory rate. With respect to the OMCD in situ, available buffer is predicted to be abundant, including delivered HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup>and HPO<jats:sub>4<\/jats:sub><jats:sup>2\u2212<\/jats:sup>, as well as peritubular NH<jats:sub>3<\/jats:sub>. Thus, buffer availability is unlikely to exert a regulatory role in total proton secretion by this tubule segment.<\/jats:p>","DOI":"10.1152\/ajprenal.2000.279.1.f24","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T12:43:17Z","timestamp":1514032997000},"page":"F24-F45","source":"Crossref","is-referenced-by-count":38,"title":["A mathematical model of the outer medullary collecting duct of the rat"],"prefix":"10.1152","volume":"279","author":[{"given":"Alan M.","family":"Weinstein","sequence":"first","affiliation":[{"name":"Department of Physiology and Biophysics, Weill Medical College of Cornell University, New York, New York 10021"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.86.14.5429"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.86.2.215"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.267.3.F450"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.1.F116"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1985.249.4.F485"},{"key":"B6","doi-asserted-by":"crossref","first-page":"1476","DOI":"10.1681\/ASN.V571476","volume":"5","author":"Bastani B.","year":"1995","journal-title":"J Am Soc Nephrol"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1007\/BF00585112"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1172\/JCI114264"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.87.19.7457"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2736(88)90022-3"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1983.244.4.F442"},{"key":"B12","doi-asserted-by":"crossref","first-page":"9537","DOI":"10.1016\/S0021-9258(17)39268-2","volume":"260","author":"Falke JJ","year":"1985","journal-title":"J Biol Chem"},{"key":"B13","doi-asserted-by":"crossref","first-page":"9545","DOI":"10.1016\/S0021-9258(17)39269-4","volume":"260","author":"Falke JJ","year":"1985","journal-title":"J Biol Chem"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.260.2.F264"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.262.1.F1"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/0304-4157(86)90010-9"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.267.4.F573"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.266"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1973.sp010234"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.108.6.565"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.259.5.F778"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.262.4.F692"},{"key":"B23","first-page":"146","volume":"13","author":"Gillin AG","year":"1993","journal-title":"Semin Nephrol"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.252.3.F491"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.74.3.351"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1980.38"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1988.255.2.F220"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.95.2.347"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1982.182"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1172\/JCI111635"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.108.6.577"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1977.118"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1985.248.4.F500"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1986.250.1.F70"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.256.1.F79"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1007\/BF00581796"},{"key":"B37","first-page":"S131","volume":"40","author":"Koeppen B","year":"1991","journal-title":"Kidney Int"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1987.41"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1007\/BF00372960"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.270.1.F116"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.259.6.F902"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1021\/bi961443b"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1983.244.3.F289"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1980.20"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1983.245.6.F670"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1172\/JCI114913"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.4.F687"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.90.24.11663"},{"key":"B49","first-page":"62","volume":"103","author":"Passow H.","year":"1986","journal-title":"Rev Physiol Biochem Pharmacol"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.91.12.5340"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1980.139"},{"key":"B52","doi-asserted-by":"crossref","first-page":"913","DOI":"10.1681\/ASN.V105913","volume":"10","author":"Sabolic I","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1981.146"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.260.4.F506"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.252.6.F1148"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1985.60"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1980.6"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1982.242.5.F514"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1981.144"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1172\/JCI110905"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.263.6.F1063"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1172\/JCI4836"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.89.14.6418"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119301"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.1.F139"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1988.255.1.F115"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.270.3.F432"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.4.F606"},{"key":"B69","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.265.3.F406"},{"key":"B70","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.5.F841"},{"key":"B71","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.5.F856"},{"key":"B72","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1981.123"},{"key":"B73","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1990.302"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.2000.279.1.F24","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:39:38Z","timestamp":1660189178000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.2000.279.1.F24"}},"issued":{"date-parts":[[2000,7,1]]},"references-count":73,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2000,7,1]]}},"alternative-id":["10.1152\/ajprenal.2000.279.1.F24"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.2000.279.1.f24","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2000,7,1]]}},{"indexed":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T17:21:53Z","timestamp":1773422513096,"version":"3.50.1"},"reference-count":33,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2002,7,1]]},"abstract":"<jats:p>The luminal uptake ofl-cystine and cationic amino acids by (re)absorptive epithelia, as found in the small intestine and the proximal kidney tubule, is mediated by the transport system b<jats:sup>0,+<\/jats:sup>, which is defective in cystinuria. Expression studies in Xenopus laevis oocytes and other nonepithelial cells as well as genetic studies on cystinuria patients have demonstrated that two gene products, the glycoprotein rBAT and the multitransmembrane-domain protein b<jats:sup>0,+<\/jats:sup>AT, are required for system b<jats:sup>0,+<\/jats:sup>function. To study the biosynthesis, surface expression, polarity, and function of this heterodimer in an epithelial context, we established stable Madin-Darby canine kidney (MDCK) cell lines expressing rBAT and\/or b<jats:sup>0,+<\/jats:sup>AT. Confocal immunofluorescence microscopy shows that both subunits depend on each other for apical surface expression. Immunoprecipitation of biosynthetically labeled proteins indicates that b<jats:sup>0,+<\/jats:sup>AT is stable in the absence of rBAT, whereas rBAT is rapidly degraded in the absence of b<jats:sup>0,+<\/jats:sup>AT. When both are coexpressed, they associate covalently and rBAT becomes fully glycosylated and more stable. Functional experiments show that the expressed transport is of the high-affinity b<jats:sup>0,+<\/jats:sup>-type and is restricted to the apical side of the epithelia. In conclusion, coexpression experiments in MDCK cell epithelia strongly suggest that the intracellular association of rBAT and b<jats:sup>0,+<\/jats:sup>AT is required for the surface expression of either subunit, which together form a functional heterocomplex at the apical cell membrane.<\/jats:p>","DOI":"10.1152\/ajprenal.00212.2001","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:32:35Z","timestamp":1425414755000},"page":"F181-F189","source":"Crossref","is-referenced-by-count":44,"title":["Apical heterodimeric cystine and cationic amino acid transporter expressed in MDCK cells"],"prefix":"10.1152","volume":"283","author":[{"given":"Christian","family":"Bauch","sequence":"first","affiliation":[{"name":"Institute of Physiology, University of Z\u00fcrich, CH-8057 Z\u00fcrich, Switzerland"}]},{"given":"Fran\u00e7ois","family":"Verrey","sequence":"additional","affiliation":[{"name":"Institute of Physiology, University of Z\u00fcrich, CH-8057 Z\u00fcrich, Switzerland"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.11.5.1657"},{"key":"B2","doi-asserted-by":"crossref","first-page":"14842","DOI":"10.1016\/S0021-9258(18)82410-3","volume":"268","author":"Bertran J","year":"1993","journal-title":"J Biol Chem"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.89.12.5601"},{"key":"B4","doi-asserted-by":"crossref","first-page":"13957","DOI":"10.1016\/S0021-9258(18)66965-0","volume":"261","author":"Boerner P","year":"1986","journal-title":"J Biol Chem"},{"key":"B5","doi-asserted-by":"crossref","first-page":"25581","DOI":"10.1016\/S0021-9258(18)47289-4","volume":"269","author":"Busch AE","year":"1994","journal-title":"J Biol Chem"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1038\/ng0494-420"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.41.28845"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.30.17761"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.14.9543"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(94)01262-8"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1038\/12652"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/10.4.305"},{"key":"B13","doi-asserted-by":"crossref","first-page":"27060","DOI":"10.1016\/S0021-9258(19)74218-5","volume":"268","author":"Furriols M","year":"1993","journal-title":"J Biol Chem"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(91)80801-9"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1021\/bi0009791"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/0378-1119(92)90687-K"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.263.6.F1087"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1038\/26246"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.0590051821.x"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200009000-00015"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1998.78.4.969"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.10.12.4135"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.275.19.14331"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.41.29005"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.49.34948"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1988.68.3.911"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1007\/s004240050403"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.89.1.1"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.89.17.8230"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1007\/s002329900595"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1007\/s004240000274"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.89.12.5596"},{"key":"B33","doi-asserted-by":"crossref","first-page":"649","DOI":"10.1016\/S0021-9258(18)48543-2","volume":"267","author":"Yamauchi A","year":"1992","journal-title":"J Biol Chem"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00212.2001","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,5,1]],"date-time":"2022-05-01T09:32:32Z","timestamp":1651397552000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00212.2001"}},"issued":{"date-parts":[[2002,7,1]]},"references-count":33,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2002,7,1]]}},"alternative-id":["10.1152\/ajprenal.00212.2001"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00212.2001","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2002,7,1]]}},{"indexed":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T17:52:54Z","timestamp":1773424374147,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1996,8,1]]},"abstract":"<jats:p> CHIF is a recently cloned, corticosteroid-induced gene which evokes K+ channel activity in oocytes (B. Attali, H. Latter, N. Rachamim, and H. Garty. Proc. Natl. Acad. Sci. USA 92: 6092-6096, 1995). To further characterize the possible role of this gene in epithelial ion transport, we have studied its epithelial distribution and hormonal induction. Northern hybridizations indicate that the zonal distribution of CHIF mRNA in kidney is: papilla &gt;&gt;medulla&gt;&gt; cortex. High levels of CHIF were also detected in a primary culture from inner medullary collecting duct (IMCD). Perfusing rats with &lt; 20 nM aldosterone through osmotic minipumps evoked a 22.4 +\/- 1.9-fold increase in colonic CHIF. A significant increase was observed 3 h after administrating the corticosteroid, but maximal response was detected only after a 72-h incubation. This response appears to be mineralocorticoid specific; perfusing or injecting rats with maximal doses of dexamethasone did not evoke a further increase in CHIF mRNA. In contrast, high levels of CHIF are expressed in kidney papilla and IMCD primary culture, irrespective of corticosteroid treatment. Thus, like the apical Na+ channel and the H(+)-K(+)-adenosinetriphosphatase, CHIF is mineralocorticoid induced in the colon but constitutively expressed in kidney. <\/jats:p>","DOI":"10.1152\/ajprenal.1996.271.2.f322","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T01:30:13Z","timestamp":1513992613000},"page":"F322-F329","source":"Crossref","is-referenced-by-count":23,"title":["Aldosterone induction and epithelial distribution of CHIF"],"prefix":"10.1152","volume":"271","author":[{"given":"H.","family":"Wald","sequence":"first","affiliation":[{"name":"Department of Membrane Research and Biophysics, Weizmann Institute ofScience, Rehovot, Israel."}]},{"given":"O.","family":"Goldstein","sequence":"additional","affiliation":[{"name":"Department of Membrane Research and Biophysics, Weizmann Institute ofScience, Rehovot, Israel."}]},{"given":"C.","family":"Asher","sequence":"additional","affiliation":[{"name":"Department of Membrane Research and Biophysics, Weizmann Institute ofScience, Rehovot, Israel."}]},{"given":"Y.","family":"Yagil","sequence":"additional","affiliation":[{"name":"Department of Membrane Research and Biophysics, Weizmann Institute ofScience, Rehovot, Israel."}]},{"given":"H.","family":"Garty","sequence":"additional","affiliation":[{"name":"Department of Membrane Research and Biophysics, Weizmann Institute ofScience, Rehovot, Israel."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1996.271.2.F322","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:05:35Z","timestamp":1567958735000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1996.271.2.F322"}},"issued":{"date-parts":[[1996,8,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1996,8,1]]}},"alternative-id":["10.1152\/ajprenal.1996.271.2.F322"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1996.271.2.f322","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1996,8,1]]}},{"indexed":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T17:52:55Z","timestamp":1773424375139,"version":"3.50.1"},"reference-count":29,"publisher":"American Physiological Society","issue":"3","funder":[{"DOI":"10.13039\/100000968","name":"American Heart Association (AHA)","doi-asserted-by":"publisher","award":["17POST33660468"],"award-info":[{"award-number":["17POST33660468"]}],"id":[{"id":"10.13039\/100000968","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000968","name":"American Heart Association (AHA)","doi-asserted-by":"publisher","award":["15GRNT22930030"],"award-info":[{"award-number":["15GRNT22930030"]}],"id":[{"id":"10.13039\/100000968","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000968","name":"American Heart Association (AHA)","doi-asserted-by":"publisher","award":["17GRNT3292002"],"award-info":[{"award-number":["17GRNT3292002"]}],"id":[{"id":"10.13039\/100000968","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100006955","name":"Office of Extramural Research, National Institutes of Health (OER)","doi-asserted-by":"publisher","award":["T32HL00744536A1"],"award-info":[{"award-number":["T32HL00744536A1"]}],"id":[{"id":"10.13039\/100006955","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100006955","name":"Office of Extramural Research, National Institutes of Health (OER)","doi-asserted-by":"publisher","award":["K12GM11726"],"award-info":[{"award-number":["K12GM11726"]}],"id":[{"id":"10.13039\/100006955","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100006955","name":"Office of Extramural Research, National Institutes of Health (OER)","doi-asserted-by":"publisher","award":["F32DK104572"],"award-info":[{"award-number":["F32DK104572"]}],"id":[{"id":"10.13039\/100006955","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2018,3,1]]},"abstract":"<jats:p> epithelial Na<jats:sup>+<\/jats:sup> channel, ENaC, is the final arbiter of sodium excretion in the kidneys. As such, discretionary control of ENaC by hormones is critical to the fine-tuning of electrolyte and water excretion and, consequently, blood pressure. Casein kinase 2 (CK2) phosphorylates ENaC. Phosphorylation by CK2 is necessary for normal ENaC activity. We tested the physiological importance of CK2 regulation of ENaC as the degree to which ENaC activity is dependent on CK2 phosphorylation in the living organism is unknown. This was addressed using patch-clamp analysis of ENaC in completely split-open collecting ducts and whole animal physiological studies of sodium excretion in mice. We also used ENaC-harboring CK2 phosphorylation site mutations to elaborate the mechanism. We found that ENaC activity in ex vivo preparations of murine collecting duct had a significant decrease in activity in response to selective antagonism of CK2. In whole animal experiments selective antagonism of CK2 caused a natriuresis similar to benzamil, but not additive to benzamil, suggesting an ENaC-dependent mechanism. Regulation of ENaC by CK2 was abolished by mutation of the canonical CK2 phosphorylation sites in beta and gamma ENaC. Together, these results demonstrate that the appropriate regulation of ENaC by CK2 is necessary for the normal physiological role played by this key renal ion channel in the fine-tuning of sodium excretion. <\/jats:p>","DOI":"10.1152\/ajprenal.00469.2017","type":"journal-article","created":{"date-parts":[[2017,10,11]],"date-time":"2017-10-11T20:25:35Z","timestamp":1507753535000},"page":"F367-F372","source":"Crossref","is-referenced-by-count":12,"title":["Physiological regulation of the epithelial Na<sup>+<\/sup> channel by casein kinase II"],"prefix":"10.1152","volume":"314","author":[{"given":"Jonathan M.","family":"Berman","sequence":"first","affiliation":[{"name":"Department of Cellular and Integrative Physiology, University of Texas Health Science Center at San Antonio, San Antonio, Texas"}]},{"given":"Elena","family":"Mironova","sequence":"additional","affiliation":[{"name":"Department of Cellular and Integrative Physiology, University of Texas Health Science Center at San Antonio, San Antonio, Texas"}]},{"given":"James D.","family":"Stockand","sequence":"additional","affiliation":[{"name":"Department of Cellular and Integrative Physiology, University of Texas Health Science Center at San Antonio, San Antonio, Texas"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1007\/s11010-005-2943-1"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M704532200"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00373.2002"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00608.2007"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.101.3.329"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0402178101"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1007\/s11010-011-0961-8"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2265.2005.02255.x"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013090931"},{"key":"B10","first-page":"1279","volume":"77","author":"Frank J","year":"2008","journal-title":"Am Fam Physician"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1016\/j.vascn.2004.08.008"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M601112200"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.45.30012"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1002\/path.1613"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1016\/j.febslet.2014.07.032"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.C400080200"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2002.022293"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M116.753616"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M303327200"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1007\/978-94-007-7654-8"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(07)61299-9"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-62703-351-0_27"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1016\/j.conb.2008.08.008"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1021\/jm049854a"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2265.2008.03314.x"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-5793(01)02404-8"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M111717200"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1046\/j.1432-1033.2002.03154.x"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1530\/EJE-12-1000"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00469.2017","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,22]],"date-time":"2019-09-22T04:46:42Z","timestamp":1569127602000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00469.2017"}},"issued":{"date-parts":[[2018,3,1]]},"references-count":29,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2018,3,1]]}},"alternative-id":["10.1152\/ajprenal.00469.2017"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00469.2017","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2018,3,1]]}},{"indexed":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T17:15:40Z","timestamp":1773422140797,"version":"3.50.1"},"reference-count":31,"publisher":"American Physiological Society","issue":"5","funder":[{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK095029"],"award-info":[{"award-number":["DK095029"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK117865"],"award-info":[{"award-number":["DK117865"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000968","name":"American Heart Association","doi-asserted-by":"publisher","award":["19CDA34660148"],"award-info":[{"award-number":["19CDA34660148"]}],"id":[{"id":"10.13039\/100000968","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2019,11,1]]},"abstract":"<jats:p> cAMP is a critical second messenger of numerous endocrine signals affecting water-electrolyte transport in the renal tubule. Exchange protein directly activated by cAMP (Epac) is a relatively recently discovered downstream effector of cAMP, having the same affinity to the second messenger as protein kinase A, the classical cAMP target. Two Epac isoforms, Epac1 and Epac2, are abundantly expressed in the renal epithelium, where they are thought to regulate water and electrolyte transport, particularly in the proximal tubule and collecting duct. Recent characterization of renal phenotype in mice lacking Epac1 and Epac2 revealed a critical role of the Epac signaling cascade in urinary concentration as well as in Na<jats:sup>+<\/jats:sup> and urea excretion. In this review, we aim to critically summarize current knowledge of Epac relevance for renal function and to discuss the applicability of Epac-based strategies in the regulation of systemic water-electrolyte homeostasis. <\/jats:p>","DOI":"10.1152\/ajprenal.00373.2019","type":"journal-article","created":{"date-parts":[[2019,9,11]],"date-time":"2019-09-11T11:56:02Z","timestamp":1568202962000},"page":"F1094-F1097","source":"Crossref","is-referenced-by-count":9,"title":["A peek into Epac physiology in the kidney"],"prefix":"10.1152","volume":"317","author":[{"given":"Viktor N.","family":"Tomilin","sequence":"first","affiliation":[{"name":"Department of Integrative Biology and Pharmacology, The University of Texas Health Science Center at Houston, Houston, Texas"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5397-6897","authenticated-orcid":false,"given":"Oleh","family":"Pochynyuk","sequence":"additional","affiliation":[{"name":"Department of Integrative Biology and Pharmacology, The University of Texas Health Science Center at Houston, Houston, Texas"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1038\/sj.mp.4001340"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-007-0371-7"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00371.2009"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1096\/fj.201800435R"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M005552200"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M000600200"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M405893200"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M001113200"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1038\/24884"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1089\/ars.2017.7041"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1242\/jeb.028605"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2017.02.001"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.pharmtox.010909.105714"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2006.119644"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0503562103"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1126\/science.282.5397.2275"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00376.2011"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00394.2002"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbamcr.2011.12.011"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00448.2007"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M110856200"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1002\/ajmg.b.30976"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.21709"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M203571200"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00025.2017"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013070679"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008121225"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00480.x"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2001.012606"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00411.2005"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00544.2009"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00373.2019","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,10,16]],"date-time":"2019-10-16T11:18:07Z","timestamp":1571224687000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00373.2019"}},"issued":{"date-parts":[[2019,11,1]]},"references-count":31,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2019,11,1]]}},"alternative-id":["10.1152\/ajprenal.00373.2019"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00373.2019","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2019,11,1]]}},{"indexed":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T19:31:04Z","timestamp":1773430264819,"version":"3.50.1"},"reference-count":33,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2010,2]]},"abstract":"<jats:p> To examine the functional interaction between superoxide dismutase (SOD) and NADPH oxidase activity, we assessed renal responses to acute intra-arterial infusion of ANG II (0.5 ng\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7min<jats:sup>\u22121<\/jats:sup>) before and during administration of a SOD inhibitor, diethyldithiocarbamate (DETC, 0.5 mg\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7min<jats:sup>\u22121<\/jats:sup>), in enalaprilat-pretreated (33 \u03bcg\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7min<jats:sup>\u22121<\/jats:sup>) rats ( n = 11). Total (RBF) and regional (cortical, CBF; medullary; MBF) renal blood flows were determined by Transonic and laser-Doppler flowmetry, respectively. Renal cortical and medullary tissue NADPH oxidase activity in vitro was determined using the lucigenin-chemiluminescence method. DETC treatment alone resulted in decreases in RBF, CBF, MBF, glomerular filtration rate (GFR), urine flow (V), and sodium excretion (U<jats:sub>Na<\/jats:sub>V) as reported previously. Before DETC, ANG II infusion decreased RBF (\u221218 \u00b1 3%), CBF (\u221216 \u00b1 3%), MBF [\u22125 \u00b1 6%; P = not significant (NS)], GFR (\u221231 \u00b1 4%), V (\u221234 \u00b1 2%), and U<jats:sub>Na<\/jats:sub>V (\u221253 \u00b1 3%). During DETC infusion, ANG II also caused similar reductions in RBF (\u221220 \u00b1 4%), CBF (\u221219 \u00b1 3%), MBF (\u22122 \u00b1 2; P = NS), and in GFR (\u221222 \u00b1 7%), whereas renal excretory responses (V; \u221212 \u00b1 2%; U<jats:sub>Na<\/jats:sub>V; \u221224 \u00b1 4%) were significantly attenuated compared with those before DETC. In in vitro experiments, ANG II (100 \u03bcM) enhanced NADPH oxidase activity both in cortical [13,194 \u00b1 1,651 vs. 20,914 \u00b1 2,769 relative light units (RLU)\/mg protein] and in medullary (21,296 \u00b1 2,244 vs. 30,597 \u00b1 4,250 RLU\/mg protein) tissue. Application of DETC (1 mM) reduced the basal levels and prevented ANG II-induced increases in NADPH oxidase activity in both tissues. These results demonstrate that renal excretory responses to acute ANG II administration are attenuated during SOD inhibition, which seems related to a downregulation of NADPH oxidase in the deficient condition of SOD activity. <\/jats:p>","DOI":"10.1152\/ajprenal.00511.2009","type":"journal-article","created":{"date-parts":[[2009,11,19]],"date-time":"2009-11-19T03:17:47Z","timestamp":1258600667000},"page":"F401-F407","source":"Crossref","is-referenced-by-count":4,"title":["Attenuation of renal excretory responses to ANG II during inhibition of superoxide dismutase in anesthetized rats"],"prefix":"10.1152","volume":"298","author":[{"given":"Md. Abdul Hye","family":"Khan","sequence":"first","affiliation":[{"name":"Department of Physiology, Tulane University Health Sciences Center, New Orleans, Louisiana"}]},{"given":"Mohammed Toriqul","family":"Islam","sequence":"additional","affiliation":[{"name":"Department of Physiology, Tulane University Health Sciences Center, New Orleans, Louisiana"}]},{"given":"Alexander","family":"Castillo","sequence":"additional","affiliation":[{"name":"Department of Physiology, Tulane University Health Sciences Center, New Orleans, Louisiana"}]},{"given":"Dewan Syed Abdul","family":"Majid","sequence":"additional","affiliation":[{"name":"Department of Physiology, Tulane University Health Sciences Center, New Orleans, Louisiana"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00476.2002"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90628.2008"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/S0008-6363(02)00328-0"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000235682.47673.ab"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.86.5.494"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00715.2006"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1093\/cvr\/cvp073"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-5793(03)00876-7"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000200027.34925.93"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00090.2005"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1097\/HJH.0b013e3282efb195"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1038\/ajh.2008.242"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.100.12.1330"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/j.transproceed.2007.01.004"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1161\/hy0202.104137"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00294.2004"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00073.2004"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000074903.96928.91"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1161\/hy0202.103469"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90487.2008"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00987.2008"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1161\/hy0202.103821"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1007\/s11906-003-0070-5"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.2.F271"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1016\/j.trsl.2007.10.003"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00491.2002"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1084\/jem.175.5.1181"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1096\/fasebj.10.7.8635688"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.00456.2007"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00626.2004"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000242928.57344.92"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1007\/s10549-007-9798-y"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.37.2.547"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00511.2009","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T00:07:10Z","timestamp":1567987630000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00511.2009"}},"issued":{"date-parts":[[2010,2]]},"references-count":33,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2010,2]]}},"alternative-id":["10.1152\/ajprenal.00511.2009"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00511.2009","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2010,2]]}},{"indexed":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T12:08:23Z","timestamp":1773403703939,"version":"3.50.1"},"reference-count":64,"publisher":"American Physiological Society","issue":"11","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2015,12,1]]},"abstract":"<jats:p> Long noncoding RNAs (lncRNAs) are emerging as key species-specific regulators of cellular and disease processes. To identify potential lncRNAs relevant to acute and chronic renal epithelial injury, we performed unbiased whole transcriptome profiling of human proximal tubular epithelial cells (PTECs) in hypoxic and inflammatory conditions. RNA sequencing revealed that the protein-coding and noncoding transcriptomic landscape differed between hypoxia-stimulated and cytokine-stimulated human PTECs. Hypoxia- and inflammation-modulated lncRNAs were prioritized for focused followup according to their degree of induction by these stress stimuli, their expression in human kidney tissue, and whether exposure of human PTECs to plasma of critically ill sepsis patients with acute kidney injury modulated their expression. For three lncRNAs (MIR210HG, linc-ATP13A4-8, and linc-KIAA1737-2) that fulfilled our criteria, we validated their expression patterns, examined their loci for conservation and synteny, and defined their associated epigenetic marks. The lncRNA landscape characterized here provides insights into novel transcriptomic variations in the renal epithelial cell response to hypoxic and inflammatory stress. <\/jats:p>","DOI":"10.1152\/ajprenal.00290.2015","type":"journal-article","created":{"date-parts":[[2015,9,24]],"date-time":"2015-09-24T01:39:49Z","timestamp":1443058789000},"page":"F901-F913","source":"Crossref","is-referenced-by-count":69,"title":["The long noncoding RNA landscape in hypoxic and inflammatory renal epithelial injury"],"prefix":"10.1152","volume":"309","author":[{"given":"Jennie","family":"Lin","sequence":"first","affiliation":[{"name":"Renal Electrolyte and Hypertension Division, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania;"}]},{"given":"Xuan","family":"Zhang","sequence":"additional","affiliation":[{"name":"Cardiovascular Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania;"}]},{"given":"Chenyi","family":"Xue","sequence":"additional","affiliation":[{"name":"Cardiovascular Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania;"}]},{"given":"Hanrui","family":"Zhang","sequence":"additional","affiliation":[{"name":"Cardiovascular Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania;"}]},{"given":"Michael G. S.","family":"Shashaty","sequence":"additional","affiliation":[{"name":"Pulmonary, Allergy, and Critical Care Division, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania; and"}]},{"given":"Sager J.","family":"Gosai","sequence":"additional","affiliation":[{"name":"Department of Biology, University of Pennsylvania, Philadelphia, Pennsylvania;"}]},{"given":"Nuala","family":"Meyer","sequence":"additional","affiliation":[{"name":"Pulmonary, Allergy, and Critical Care Division, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania; and"}]},{"given":"Alison","family":"Grazioli","sequence":"additional","affiliation":[{"name":"Renal Electrolyte and Hypertension Division, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania;"}]},{"given":"Christine","family":"Hinkle","sequence":"additional","affiliation":[{"name":"Cardiovascular Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania;"}]},{"given":"Jennifer","family":"Caughey","sequence":"additional","affiliation":[{"name":"Cardiovascular Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania;"}]},{"given":"Wenjun","family":"Li","sequence":"additional","affiliation":[{"name":"Cardiovascular Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania;"}]},{"given":"Katalin","family":"Susztak","sequence":"additional","affiliation":[{"name":"Renal Electrolyte and Hypertension Division, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania;"}]},{"given":"Brian D.","family":"Gregory","sequence":"additional","affiliation":[{"name":"Department of Biology, University of Pennsylvania, Philadelphia, Pennsylvania;"}]},{"given":"Mingyao","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Biostatistics and Epidemiology, University of Pennsylvania, Philadelphia, Pennsylvania"}]},{"given":"Muredach P.","family":"Reilly","sequence":"additional","affiliation":[{"name":"Cardiovascular Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0127175"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00025.2012"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1369\/0022155411428468"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0079037"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1186\/s13148-015-0047-7"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000067652.51441.21"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1101\/gad.17446611"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1186\/1471-2105-10-421"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1126\/science.1240925"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1126\/science.1187197"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.02510706"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pgen.1000899"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1101\/gr.132159.111"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1038\/nature11233"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1093\/bioinformatics\/bts635"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbamem.2010.07.032"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1038\/nrd4422"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1186\/1479-5876-11-63"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/gkt1223"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2012101024"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1038\/nature08975"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/nature13596"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1038\/nature11993"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gft449"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfs100"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/j.celrep.2015.04.023"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.7.4135"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1038\/ncomms4979"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1038\/ng.3192"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.113.02569"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5001866"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1097\/01.tp.0000287190.86654.74"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1159\/000142934"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013050502"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1158\/1078-0432.CCR-07-0411"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1038\/nature11661"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1038\/nature14248"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1016\/j.tibs.2014.02.007"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014010028"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1186\/cc7940"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1161\/ATVBAHA.113.303123"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.00430111"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1373\/clinchem.2014.230359"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1186\/cc6848"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1097\/SHK.0b013e3182a64682"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005070757"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1038\/nature12943"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1369\/jhc.2009.953976"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1007\/s00125-003-1155-z"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/gkt1114"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-2143(97)90180-3"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1378\/chest.13-1962"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1146\/annurev-biochem-051410-092902"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1222878110"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1186\/1471-2164-14-S2-S7"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1159\/000351684"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1172\/JCI58662"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1038\/nbt.2450"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pgen.1003368"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2013.06.020"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2011.11.055"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1038\/ni.2846"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1186\/1471-2164-15-287"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1038\/mt.2015.31"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00290.2015","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T01:12:26Z","timestamp":1567991546000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00290.2015"}},"issued":{"date-parts":[[2015,12,1]]},"references-count":64,"journal-issue":{"issue":"11","published-print":{"date-parts":[[2015,12,1]]}},"alternative-id":["10.1152\/ajprenal.00290.2015"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00290.2015","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2015,12,1]]}},{"indexed":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T16:26:41Z","timestamp":1773419201329,"version":"3.50.1"},"reference-count":41,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2003,10]]},"abstract":"<jats:p> Elevations in plasma osmolality elicit reflex humoral and neural responses. The hypothalamic paraventricular nucleus (PVN) is important in humoral responses. We have investigated whether the PVN contributed to the renal nerve reduction that is normally elicited by increased plasma osmolality in the conscious rabbit. Renal sympathetic nerve activity (RSNA) was monitored after an intravenous infusion of hypertonic saline (1.7 M NaCl, 2 ml\/min for 7 min). The responses were examined in animals microinjected with muscimol (10 nmol) into, and outside, the PVN to acutely inhibit neuronal function or with kynurenate (25 nmol) to block glutamate receptors. Compared with vehicle, the maximum reduction in RSNA elicited by hypertonic saline was significantly less with muscimol or kynurenate pretreatment into the PVN. A similar study with kynurenate was also performed in sinoaortically denervated rabbits, and similar effects were observed. The effect was specific to the PVN because microinjections of the drugs outside the PVN had no effect on the response. The findings suggest that excitatory inputs into the PVN may be important in the neural responses elicited by elevations in plasma osmolality. <\/jats:p>","DOI":"10.1152\/ajprenal.00372.2002","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:39:30Z","timestamp":1425415170000},"page":"F640-F650","source":"Crossref","is-referenced-by-count":30,"title":["Glutamatergic input in the PVN is important in renal nerve response to  elevations in osmolality"],"prefix":"10.1152","volume":"285","author":[{"given":"Emilio","family":"Badoer","sequence":"first","affiliation":[{"name":"School of Medical Sciences, Royal Melbourne Institute of Technology  University, Bundoora 3083, Melbourne, Victoria, Australia"}]},{"given":"Chi-Wai","family":"Ng","sequence":"additional","affiliation":[{"name":"School of Medical Sciences, Royal Melbourne Institute of Technology  University, Bundoora 3083, Melbourne, Victoria, Australia"}]},{"given":"Robert","family":"De Matteo","sequence":"additional","affiliation":[{"name":"School of Medical Sciences, Royal Melbourne Institute of Technology  University, Bundoora 3083, Melbourne, Victoria, Australia"}]}],"member":"24","reference":[{"key":"REF1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00279.2002"},{"key":"REF2","doi-asserted-by":"crossref","unstructured":"Badoer E.  Cardiovascular role of parvocellular neurones in the paraventricular nucleus  of the hypothalamus. News Physiol Sci 11: 43\u201347,  1996.","DOI":"10.1152\/physiologyonline.1996.11.1.43"},{"key":"REF3","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(93)91403-F"},{"key":"REF4","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-8993(98)00140-1"},{"key":"REF5","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1998.274.2.R383"},{"key":"REF6","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-8993(02)02901-3"},{"key":"REF7","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.2000.278.5.R1157"},{"key":"REF8","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1975.sp010809"},{"key":"REF9","doi-asserted-by":"publisher","DOI":"10.1016\/0165-1838(79)90014-6"},{"key":"REF10","doi-asserted-by":"publisher","DOI":"10.1152\/jn.1997.77.6.3396"},{"key":"REF11","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1967.sp008148"},{"key":"REF12","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.2001.281.6.R1844"},{"key":"REF13","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.1998.tb02235.x"},{"key":"REF14","doi-asserted-by":"publisher","DOI":"10.1016\/S0306-4522(00)00411-5"},{"key":"REF15","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1994.74.2.323"},{"key":"REF16","doi-asserted-by":"publisher","DOI":"10.1016\/S0306-4522(98)00643-5"},{"key":"REF17","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.57.4.618"},{"key":"REF18","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(95)01326-1"},{"key":"REF19","doi-asserted-by":"publisher","DOI":"10.1016\/0165-1838(94)90117-1"},{"key":"REF20","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1998.275.4.R1334"},{"key":"REF21","doi-asserted-by":"publisher","DOI":"10.1002\/1096-9861(20000703)422:3<352::AID-CNE3>3.0.CO;2-F"},{"key":"REF22","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1994.267.1.R309"},{"key":"REF23","doi-asserted-by":"publisher","DOI":"10.1016\/0165-1838(91)90110-O"},{"key":"REF24","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1989.256.6.R1325"},{"key":"REF25","doi-asserted-by":"publisher","DOI":"10.1016\/0165-1838(87)90094-4"},{"key":"REF26","doi-asserted-by":"publisher","DOI":"10.1016\/0304-3940(75)90004-X"},{"key":"REF27","doi-asserted-by":"publisher","DOI":"10.1016\/0165-1838(88)90018-5"},{"key":"REF28","doi-asserted-by":"crossref","unstructured":"McKinley MJ,  Denton DA, Coghan JP, Harvey RB, McDougall JG, Rundgren M, and Scoggins  BA. Cerebral osmoregulation of renal sodium excretion\u2014a response  analogous to thirst and vasopressin release. Can J Physiol  Pharmacol 65:  1724\u20131729, 1986.","DOI":"10.1139\/y87-271"},{"key":"REF29","unstructured":"McKinley MJ and  Oldfield BJ. Circumventricular organs. In: The Human Nervous  System. New York: Academic, 1990, p.  415\u2013438."},{"key":"REF30","doi-asserted-by":"publisher","DOI":"10.1016\/0165-1838(91)90082-E"},{"key":"REF31","doi-asserted-by":"crossref","unstructured":"Nishida Y,  Sugimoto I, Morita H, Murakami H, Hosomi H, and Bishop V. Suppression of  renal sympathetic nerve activity during portal vein infusion of hypertonic  saline. Am J Physiol Regul Integr Comp Physiol 278: R97\u2013R103,  2000.","DOI":"10.1152\/ajpregu.1998.274.1.R97"},{"key":"REF32","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(91)90760-S"},{"key":"REF33","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-445X.2001.tb00034.x"},{"key":"REF34","doi-asserted-by":"publisher","DOI":"10.1007\/s002210050390"},{"key":"REF35","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-8993(98)00587-3"},{"key":"REF36","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.11-08-02321.1991"},{"key":"REF37","doi-asserted-by":"publisher","DOI":"10.1016\/S0165-1838(99)00031-4"},{"key":"REF38","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(88)90132-1"},{"key":"REF39","doi-asserted-by":"publisher","DOI":"10.1002\/cne.901940306"},{"key":"REF40","doi-asserted-by":"publisher","DOI":"10.1016\/0165-1838(95)00108-5"},{"key":"REF41","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.2000.279.6.E1207"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00372.2002","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T21:38:46Z","timestamp":1567978726000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00372.2002"}},"issued":{"date-parts":[[2003,10]]},"references-count":41,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2003,10]]}},"alternative-id":["10.1152\/ajprenal.00372.2002"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00372.2002","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2003,10]]}},{"indexed":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T16:22:19Z","timestamp":1773418939677,"version":"3.50.1"},"reference-count":36,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2000,5,1]]},"abstract":"<jats:p>Locally formed arachidonic acid (AA) metabolites are important as modulators of many aspects of renal tubular function, including regulation of the activity of tubular Na<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-ATPase. Here we examined the ontogeny of the AA metabolic pathways regulating proximal convoluted tubular (PCT) Na<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-ATPase activity in infant and adult rats. Eicosatetraynoic acid, an inhibitor of all AA-metabolizing pathways, abolished this effect. AA inhibition of PCT Na<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-ATPase was blocked by the 12-lipoxygenase inhibitor baicalein in infant but not in adult rats and by the specific cytochrome P-450 fatty acid \u03c9-hydroxylase inhibitor 17-octadecynoic acid in adult but not in infant rats. The lipoxygenase metabolite 12(S)-hydroxyeicosatetraenoic acid (HETE) and the cytochrome P-450 metabolite 20-HETE both inhibited PCT Na<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-ATPase in a protein kinase C-dependent manner, but the effect was significantly more pronounced in infant PCT. Lipoxygenase mRNA was only detected in infant cortex. Expression of renal isoforms of cytochrome P-450 mRNA was more prominent in adult cortex. In summary, the AA metabolic pathways that modulated the activity of rat renal proximal tubular Na<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-ATPase are age dependent.<\/jats:p>","DOI":"10.1152\/ajprenal.2000.278.5.f823","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T12:47:32Z","timestamp":1514033252000},"page":"F823-F829","source":"Crossref","is-referenced-by-count":20,"title":["Arachidonic acid metabolic pathways regulating activity of renal Na<sup>+<\/sup>-K<sup>+<\/sup>-ATPase are age dependent"],"prefix":"10.1152","volume":"278","author":[{"given":"Dailin","family":"Li","sequence":"first","affiliation":[{"name":"Department of Woman and Child Health, Pediatric Unit, Karolinska Institute, S-171 76 Stockholm, Sweden; and"}]},{"given":"Roger","family":"Belusa","sequence":"additional","affiliation":[{"name":"Department of Woman and Child Health, Pediatric Unit, Karolinska Institute, S-171 76 Stockholm, Sweden; and"}]},{"given":"Susana","family":"Nowicki","sequence":"additional","affiliation":[{"name":"Department of Woman and Child Health, Pediatric Unit, Karolinska Institute, S-171 76 Stockholm, Sweden; and"},{"name":"Centro de Investigaciones Endocrinologicas, Consejo Nacional de Investigaciones C\u0131\u0301entificas y T\u00e9cnicas, 1425 Buenos Aires, Argentina"}]},{"given":"Anita","family":"Aperia","sequence":"additional","affiliation":[{"name":"Department of Woman and Child Health, Pediatric Unit, Karolinska Institute, S-171 76 Stockholm, Sweden; and"}]}],"member":"24","reference":[{"key":"B1","unstructured":"Aperia A, Celsi G.Ontogenic processes in nephron epithelia: structure, enzymes, and function.The Kidney: Physiology and Pathophysiology2nd ed., Seldin DW, Giebisch G.11992803822RavenNew York"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1981.241.4.F356"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/0166-2236(88)90157-9"},{"key":"B4","doi-asserted-by":"crossref","first-page":"13937","DOI":"10.1016\/S0021-9258(18)68334-6","volume":"263","author":"Balcarek JM","year":"1988","journal-title":"J Biol Chem"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.6.F846"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(88)80055-3"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1126\/science.1846705"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1203\/00006450-199309000-00014"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/0003-9861(92)90260-4"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1016\/0076-6879(74)32029-0"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1089\/dna.1.1989.8.503"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.1994.tb52719.x"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1994.267.2.R579"},{"key":"B15","first-page":"675","volume":"21","author":"McGiff JC","year":"1990","journal-title":"Adv Prostaglandin Thromboxane Leukot Res"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.21.6.767"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-2999(97)01259-4"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119279"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/11.6.1759"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1203\/00006450-199603000-00024"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.262.1.F8"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.262.4.F591"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1007\/s002329900101"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1016\/S0300-9084(97)83495-5"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.266.3.F497"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1172\/JCI116215"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1007\/BF00874022"},{"key":"B28","first-page":"656","volume":"73","author":"Schwartzman ML","year":"1996","journal-title":"Nephron"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1038\/314620a0"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/0006-291X(82)91081-6"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.31.3.866"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1007\/BF02533870"},{"key":"B33","doi-asserted-by":"crossref","first-page":"15771","DOI":"10.1016\/S0021-9258(18)98476-0","volume":"266","author":"Toullec D","year":"1991","journal-title":"J Biol Chem"},{"key":"B34","doi-asserted-by":"crossref","first-page":"7982","DOI":"10.1016\/S0021-9258(19)57499-3","volume":"261","author":"Ueda N","year":"1986","journal-title":"J Biol Chem"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1111\/j.1432-1033.1993.tb17699.x"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.2.F461"},{"key":"B37","doi-asserted-by":"crossref","first-page":"474","DOI":"10.1016\/S0022-3565(25)38498-3","volume":"268","author":"Zou A-P","year":"1994","journal-title":"J Pharmacol Exp Ther"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.2000.278.5.F823","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,6,29]],"date-time":"2025-06-29T04:36:44Z","timestamp":1751171804000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.2000.278.5.F823"}},"issued":{"date-parts":[[2000,5,1]]},"references-count":36,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2000,5,1]]}},"alternative-id":["10.1152\/ajprenal.2000.278.5.F823"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.2000.278.5.f823","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2000,5,1]]}},{"indexed":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T16:21:29Z","timestamp":1773418889977,"version":"3.50.1"},"reference-count":38,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2002,10,1]]},"abstract":"<jats:p>We have used peptide-directed antibodies to each major renal Na transporter and channel proteins to screen renal homogenates for changes in Na transporter protein expression after initiation of dietary NaCl restriction. After equilibration on a NaCl-replete diet (2.0 meq \u00b7 200 g body wt<jats:sup>\u22121<\/jats:sup>\u00b7 day<jats:sup>\u22121<\/jats:sup>), rats were switched to a NaCl-deficient diet (0.02 meq \u00b7 200 g body wt<jats:sup>\u22121<\/jats:sup>\u00b7 day<jats:sup>\u22121<\/jats:sup>). Na excretion fell to 25% of baseline levels on day 1, followed by a further decrease &lt;4% of baseline levels on day 3, of NaCl restriction. The decreased Na excretion at day 1 occurred despite the absence of a significant increase in plasma aldosterone level or in the abundance of any of the major renal Na transporters. However, after a 1-day lag, plasma aldosterone levels increased in association with increases in abundances of three aldosterone-regulated Na transporter proteins: the thiazide-sensitive Na-Cl cotransporter (NCC), the \u03b1-subunit of the amiloride-sensitive epithelial Na channel (\u03b1-ENaC), and the 70-kDa form of \u03b3-ENaC. RNase protection assays of transporter mRNA levels revealed an increase in renal \u03b1-ENaC mRNA coincident with the increase in \u03b1-ENaC protein abundance. However, there was no change in NCC mRNA abundance, suggesting that the increase in NCC protein in response to dietary NaCl restriction was not a result of altered gene transcription. These results point to early regulatory processes that decrease renal Na excretion without an increase in the abundance of any Na transporter, followed by a late aldosterone-dependent response associated with upregulation of NCC and ENaC.<\/jats:p>","DOI":"10.1152\/ajprenal.00016.2002","type":"journal-article","created":{"date-parts":[[2013,8,19]],"date-time":"2013-08-19T19:58:09Z","timestamp":1376942289000},"page":"F648-F657","source":"Crossref","is-referenced-by-count":99,"title":["Time course of renal Na-K-ATPase, NHE3, NKCC2, NCC, and ENaC abundance changes with dietary NaCl restriction"],"prefix":"10.1152","volume":"283","author":[{"given":"Shyama","family":"Masilamani","sequence":"first","affiliation":[{"name":"Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892-1603;"}]},{"given":"Xiaoyan","family":"Wang","sequence":"additional","affiliation":[{"name":"Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892-1603;"}]},{"given":"Gheun-Ho","family":"Kim","sequence":"additional","affiliation":[{"name":"Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892-1603;"}]},{"given":"Heddwen","family":"Brooks","sequence":"additional","affiliation":[{"name":"Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892-1603;"}]},{"given":"Jakob","family":"Nielsen","sequence":"additional","affiliation":[{"name":"Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892-1603;"},{"name":"The Water and Salt Institute, University of Aarhus, DK-8000 Aarhus C, Denmark; and"}]},{"given":"Soren","family":"Nielsen","sequence":"additional","affiliation":[{"name":"The Water and Salt Institute, University of Aarhus, DK-8000 Aarhus C, Denmark; and"}]},{"given":"Kenzo","family":"Nakamura","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Iowa, and Veterans Affairs Medical Center, Iowa City, Iowa 52242"}]},{"given":"John B.","family":"Stokes","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Iowa, and Veterans Affairs Medical Center, Iowa City, Iowa 52242"}]},{"given":"Mark A.","family":"Knepper","sequence":"additional","affiliation":[{"name":"Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892-1603;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"crossref","first-page":"1335","DOI":"10.1681\/ASN.V1271335","volume":"12","author":"Abdallah JG","year":"2001","journal-title":"J Am Soc Nephrol"},{"key":"B2","first-page":"24A","volume":"11","author":"Abdallah JG","year":"2000","journal-title":"J Am Soc Nephrol"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1161\/hy02t2.102959"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.2001.0359k.x"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/0003-2697(87)90021-2"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1001\/jama.1996.03530440061038"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.1.F46"},{"key":"B8","doi-asserted-by":"crossref","first-page":"207","DOI":"10.1681\/ASN.V122207","volume":"12","author":"Ecelbarger CA","year":"2001","journal-title":"J Am Soc Nephrol"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.3.F619"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00984.x"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.2.F219"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.1.F112"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1981.240.6.F536"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1997.77.2.359"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.6.F1093"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.3.F425"},{"key":"B17","doi-asserted-by":"crossref","first-page":"935","DOI":"10.1681\/ASN.V105935","volume":"10","author":"Kim GH","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.1.F96"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.3.F459"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.24.14552"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.2.F257"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1172\/JCI7840"},{"key":"B24","doi-asserted-by":"crossref","first-page":"1813","DOI":"10.1681\/ASN.V8121813","volume":"8","author":"May A","year":"1997","journal-title":"J Am Soc Nephrol"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-199309000-00006"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1172\/JCI111183"},{"key":"B27","doi-asserted-by":"crossref","first-page":"38A","DOI":"10.1681\/ASN.V1261099","volume":"12","author":"Nielsen J","year":"2001","journal-title":"J Am Soc Nephrol"},{"key":"B28","doi-asserted-by":"crossref","first-page":"38A","DOI":"10.1681\/ASN.V1261099","volume":"12","author":"Nielsen J","year":"2001","journal-title":"J Am Soc Nephrol"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1007\/s004240050462"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1007\/BF00373903"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.18.12431"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00320.2001"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1998.274.6.C1699"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.2.F414"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.2000.279.3.C541"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.266.2.F240"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.2001.280.6.R1632"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1172\/JCI10366"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1007\/s004240100544"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00016.2002","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,3,4]],"date-time":"2022-03-04T03:45:05Z","timestamp":1646365505000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00016.2002"}},"issued":{"date-parts":[[2002,10,1]]},"references-count":38,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2002,10,1]]}},"alternative-id":["10.1152\/ajprenal.00016.2002"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00016.2002","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2002,10,1]]}},{"indexed":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T10:35:42Z","timestamp":1773398142580,"version":"3.50.1"},"reference-count":95,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2009,3]]},"abstract":"<jats:p>Polarized distribution of plasma membrane transporters and receptors in epithelia is essential for vectorial functions of epithelia. This polarity is maintained by sorting of membrane proteins into apical or basolateral transport containers in the trans-Golgi network and\/or endosomes followed by their delivery to the appropriate plasma membrane domains. Sorting depends on the recognition of sorting signals in proteins by specific sorting machinery. In the present review, we summarize experimental evidence for and against the hypothesis that N-glycans attached to the membrane proteins can act as apical sorting signals. Furthermore, we discuss the roles of N-glycans in the apical sorting event per se and their contribution to folding and quality control of glycoproteins in the endoplasmic reticulum or retention of glycoproteins in the plasma membrane. Finally, we review existing hypotheses on the mechanism of apical sorting and discuss the potential roles of the lectins, VIP36 and galectin-3, as putative apical sorting receptors.<\/jats:p>","DOI":"10.1152\/ajprenal.90340.2008","type":"journal-article","created":{"date-parts":[[2008,10,30]],"date-time":"2008-10-30T00:34:53Z","timestamp":1225326893000},"page":"F459-F469","source":"Crossref","is-referenced-by-count":176,"title":["Role of N-glycosylation in trafficking of apical membrane proteins in epithelia"],"prefix":"10.1152","volume":"296","author":[{"given":"Olga","family":"Vagin","sequence":"first","affiliation":[]},{"given":"Jeffrey A.","family":"Kraut","sequence":"additional","affiliation":[]},{"given":"George","family":"Sachs","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","unstructured":"Varki A, Cummings R, Esco J, Freeze H, Hart G, Marth J.Essentials of Glycobiology.Cold Spring Harbor, NY: Cold Spring Harbor Laboratory Press, 1999."},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1038\/14020"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.97.7.3254"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.74.14.6538-6545.2000"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.15.10318"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.146.2.313"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1021\/ja0496266"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1016\/S0959-440X(02)00364-0"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1152\/physiol.00032.2006"},{"key":"R10","unstructured":"Bulbarelli A, Sprocati T, Barberi M, Pedrazzini E, Borgese N.Trafficking of tail-anchored proteins: transport from the endoplasmic reticulum to the plasma membrane and sorting between surface domains in polarised epithelial cells.J Cell Sci115: 1689\u20131702, 2002."},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0803223105"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M605954200"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1002\/elps.200406014"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.8.11.2241"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1016\/j.cub.2005.12.046"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200407073"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-0854.2007.00539.x"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1007\/s00018-006-6210-8"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.002717"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00161.2006"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1093\/glycob\/cwj081"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.17.2.375"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1002\/j.1460-2075.1994.tb06437.x"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(95)90380-1"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1016\/j.ceb.2008.01.003"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)81650-5"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1186\/1471-2091-7-8"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1038\/ncb827"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1023\/A:1010623724749"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1038\/nrm1050"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/17.7.1919"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1016\/0960-9822(93)90226-E"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1126\/science.7939687"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M112188200"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1093\/glycob\/cwh082"},{"key":"R36","doi-asserted-by":"crossref","unstructured":"Hauri HP, Nufer O, Breuza L, Tekaya HB, Liang L.Lectins and protein traffic early in the secretory pathway.Biochem Soc Symp: 73\u201382, 2002.","DOI":"10.1042\/bss0690073"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00050.2006"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.139.3.613"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1126\/science.291.5512.2364"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.biochem.73.011303.073752"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-0854.2004.0181.x"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1016\/S1367-5931(99)00021-6"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M709384200"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M505757200"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1096\/fasebj.1.6.3315809"},{"key":"R46","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.43.31039"},{"key":"R47","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200611106"},{"key":"R48","doi-asserted-by":"crossref","unstructured":"Le Bivic A, Garcia M, Rodriguez-Boulan E.Ricin-resistant Madin-Darby canine kidney cells missort a major endogenous apical sialoglycoprotein.J Biol Chem268: 6909\u20136916, 1993.","DOI":"10.1016\/S0021-9258(18)53126-4"},{"key":"R49","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.142.1.51"},{"key":"R50","doi-asserted-by":"publisher","DOI":"10.1023\/A:1022247826750"},{"key":"R51","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M006774200"},{"key":"R52","doi-asserted-by":"publisher","DOI":"10.1253\/circj.70.885"},{"key":"R53","unstructured":"Meerson NR, Bello V, Delaunay JL, Slimane TA, Delautier D, Lenoir C, Trugnan G, Maurice M.Intracellular traffic of the ecto-nucleotide pyrophosphatase\/phosphodiesterase NPP3 to the apical plasma membrane of MDCK and Caco-2 cells: apical targeting occurs in the absence of N-glycosylation.J Cell Sci113: 4193\u20134202, 2000."},{"key":"R54","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M101907200"},{"key":"R55","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.03489"},{"key":"R56","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.00415.2006"},{"key":"R57","doi-asserted-by":"publisher","DOI":"10.1126\/science.1079474"},{"key":"R58","doi-asserted-by":"publisher","DOI":"10.1038\/ncb0403-287"},{"key":"R59","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.cellbio.19.110701.161425"},{"key":"R60","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.25.17961"},{"key":"R61","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M504228200"},{"key":"R62","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M211199200"},{"key":"R63","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.137.6.1255"},{"key":"R64","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2006.08.019"},{"key":"R65","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2005.09.041"},{"key":"R66","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-0854.2006.00522.x"},{"key":"R67","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.01386"},{"key":"R68","doi-asserted-by":"publisher","DOI":"10.1126\/science.1102109"},{"key":"R69","doi-asserted-by":"publisher","DOI":"10.1093\/glycob\/cwj063"},{"key":"R70","doi-asserted-by":"publisher","DOI":"10.1093\/glycob\/cwh008"},{"key":"R71","doi-asserted-by":"crossref","unstructured":"Potter BA, Hughey RP, Weisz OA.Role of N- and O-glycans in polarized biosynthetic sorting.Am J Physiol Cell Physiol290: C1\u2013C10, 2006.","DOI":"10.1152\/ajpcell.00333.2005"},{"key":"R72","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.E03-08-0550"},{"key":"R73","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-0854.2005.00371.x"},{"key":"R74","doi-asserted-by":"publisher","DOI":"10.1016\/j.biocel.2007.06.015"},{"key":"R75","doi-asserted-by":"publisher","DOI":"10.1038\/nrm1593"},{"key":"R76","doi-asserted-by":"publisher","DOI":"10.1016\/j.ceb.2004.06.013"},{"key":"R77","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.03225"},{"key":"R78","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.E03-05-0271"},{"key":"R79","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M703064200"},{"key":"R80","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/16.18.5501"},{"key":"R81","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.01596"},{"key":"R82","doi-asserted-by":"publisher","DOI":"10.1177\/002215540305100809"},{"key":"R83","doi-asserted-by":"publisher","DOI":"10.1247\/csf.28.155"},{"key":"R84","doi-asserted-by":"publisher","DOI":"10.1038\/42408"},{"key":"R85","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.biophys.32.110601.141803"},{"key":"R86","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.108.3.821"},{"key":"R87","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M008797200"},{"key":"R88","doi-asserted-by":"crossref","unstructured":"Urquhart P, Pang S, Hooper NM.N-glycans as apical targeting signals in polarized epithelial cells.Biochem Soc Symp: 39\u201345, 2005.","DOI":"10.1042\/bss0720039"},{"key":"R89","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M704713200"},{"key":"R90","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M405453200"},{"key":"R91","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M508262200"},{"key":"R92","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.148.4.727"},{"key":"R93","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.139.4.929"},{"key":"R94","doi-asserted-by":"publisher","DOI":"10.1042\/bst0290746"},{"key":"R95","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.3.1596"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.90340.2008","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,9,19]],"date-time":"2021-09-19T18:53:28Z","timestamp":1632077608000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.90340.2008"}},"issued":{"date-parts":[[2009,3]]},"references-count":95,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2009,3]]}},"alternative-id":["10.1152\/ajprenal.90340.2008"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.90340.2008","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2009,3]]}},{"indexed":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T02:17:47Z","timestamp":1773368267987,"version":"3.50.1"},"reference-count":63,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1998,11,1]]},"abstract":"<jats:p>For more than 15 years, there has been an ongoing debate regarding the nephron segment(s) most severely injured in acute renal failure (ARF) induced by an ischemic or toxic insult. Although some investigators have argued that the proximal tubule (and particularly the S3 segment) is the major target of injury in ARF, others have held the view that damage to the distal nephron [particularly the medullary thick ascending limb (MTAL) segment] plays a more important role in this disease. In this discussion, the first of three on different aspects of ARF that have been hotly debated, we have invited several experts to discuss their opinions on this issue. The goals of this first discussion (and the subsequent two articles in this forum) are to establish areas of consensus in each area of controversy and also to identify unanswered questions that represent important areas for future research.<\/jats:p>","DOI":"10.1152\/ajprenal.1998.275.5.f623","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T17:12:38Z","timestamp":1514049158000},"page":"F623-F632","source":"Crossref","is-referenced-by-count":78,"title":["Acute renal failure. I. Relative importance of proximal vs. distal tubular injury"],"prefix":"10.1152","volume":"275","member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1981.63"},{"issue":"17","key":"B2","first-page":"F522","volume":"248","author":"Bagnasco S.","year":"1985","journal-title":"Am. J. Physiol."},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.249"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-199605000-00011"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.2.3.251"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1210\/endo.137.1.8536636"},{"issue":"36","key":"B7","first-page":"F1059","volume":"267","author":"Brezis M.","year":"1994","journal-title":"Am. J. Physiol."},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.me.44.020193.000331"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1002\/jemt.1060090306"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199503093321006"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1172\/JCI111189"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1126\/science.6322305"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1984.9"},{"key":"B15","first-page":"327","volume":"116","author":"Brezis M.","year":"1984","journal-title":"Am. J. Pathol."},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1172\/JCI112171"},{"key":"B17","first-page":"545","volume":"96","author":"Cantin M.","year":"1979","journal-title":"Am. J. Pathol."},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119272"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1053\/ajkd.1998.v31.pm9531191"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1978.31"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1042\/cs0760019"},{"key":"B24","first-page":"770","volume":"63","author":"Gob\u00e9 G. C.","year":"1990","journal-title":"Lab. Invest."},{"issue":"33","key":"B25","first-page":"F1","volume":"264","author":"Goligorsky M.","year":"1993","journal-title":"Am. J. Physiol."},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/0925-4439(93)90071-8"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/0003-9861(92)90492-F"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-199505000-00011"},{"issue":"8","key":"B29","first-page":"F17","volume":"239","author":"Hanley M. J.","year":"1980","journal-title":"Am. J. Physiol."},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(12)80838-9"},{"key":"B31","first-page":"153","volume":"2","author":"Heyman S. N.","year":"1994","journal-title":"Exp. Nephrol."},{"key":"B32","doi-asserted-by":"crossref","first-page":"69","DOI":"10.1681\/ASN.V4169","volume":"4","author":"Heyman S.","year":"1993","journal-title":"J. Am. Soc. Nephrol."},{"key":"B33","first-page":"399","volume":"5","author":"Jaffe R.","year":"1997","journal-title":"Exp. Nephrol."},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118498"},{"issue":"10","key":"B36","first-page":"R3","volume":"241","author":"Kriz W.","year":"1981","journal-title":"Am. J. Physiol."},{"key":"B37","first-page":"60","volume":"11","author":"Lieberthal W.","year":"1988","journal-title":"Renal Physiol. Biochem."},{"issue":"41","key":"B38","first-page":"F430","volume":"272","author":"Molitoris B.","year":"1997","journal-title":"Am. J. Physiol."},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.231"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1007\/BF00212525"},{"key":"B41","first-page":"456","volume":"28","author":"Nagle R. B.","year":"1973","journal-title":"Lab. Invest."},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1016\/0002-9343(53)90143-0"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1172\/JCI102550"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1097\/00005792-198905000-00005"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1111\/j.1699-0463.1990.tb05046.x"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(12)80973-5"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.349"},{"issue":"37","key":"B48","first-page":"F664","volume":"268","author":"Price P.","year":"1995","journal-title":"Am. J. Physiol."},{"key":"B49","first-page":"174","volume":"20","author":"Rosen S.","year":"1994","journal-title":"Miner. Electrolyte Metab."},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.3109\/08860229209106636"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1097\/00007890-199002000-00041"},{"issue":"28","key":"B52","first-page":"F176","volume":"259","author":"Ruegg C. E.","year":"1990","journal-title":"Am. J. Physiol."},{"key":"B53","doi-asserted-by":"crossref","first-page":"1387","DOI":"10.1681\/ASN.V471387","volume":"4","author":"Safirstein R.","year":"1994","journal-title":"J. Am. Soc. Nephrol."},{"issue":"30","key":"B54","first-page":"F1095","volume":"261","author":"Safirstein R.","year":"1991","journal-title":"Am. J. Physiol."},{"key":"B55","first-page":"462","volume":"122","author":"Shanley P. F.","year":"1986","journal-title":"Am. J. Pathol."},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1203\/00006450-199408000-00001"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1097\/00005792-197909000-00003"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1993.148"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1016\/S0024-3205(96)00604-2"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199605303342207"},{"issue":"9","key":"B61","first-page":"F492","volume":"240","author":"Vandewalle A.","year":"1981","journal-title":"Am. J. Physiol."},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1978.87"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117214"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(12)80694-9"},{"key":"B65","first-page":"396","volume":"110","author":"Zager R. A.","year":"1987","journal-title":"J. Lab. Clin. Med."},{"issue":"20","key":"B66","first-page":"F87","volume":"251","author":"Zager R. A.","year":"1986","journal-title":"Am. J. Physiol."},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.65.5.1263"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1998.275.5.F623","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:51:52Z","timestamp":1660189912000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1998.275.5.F623"}},"editor":[{"given":"Wilfred","family":"Lieberthal","sequence":"first","affiliation":[{"name":"Renal Section, Boston Medical Center, Boston University School of Medicine, Boston 02118; and"}]},{"given":"Sanjay K.","family":"Nigam","sequence":"additional","affiliation":[{"name":"Renal Division, Brigham and Women\u2019s Hospital, Harvard Institutes of Medicine, Boston, Massachusetts 02115"}]}],"issued":{"date-parts":[[1998,11,1]]},"references-count":63,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1998,11,1]]}},"alternative-id":["10.1152\/ajprenal.1998.275.5.F623"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1998.275.5.f623","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1998,11,1]]}},{"indexed":{"date-parts":[[2026,3,14]],"date-time":"2026-03-14T10:36:11Z","timestamp":1773484571650,"version":"3.50.1"},"reference-count":28,"publisher":"American Physiological Society","issue":"2","funder":[{"DOI":"10.13039\/100000071","name":"HHS | NIH | National Institute of Child Health and Human Development (NICHD)","doi-asserted-by":"publisher","award":["HDO67541"],"award-info":[{"award-number":["HDO67541"]}],"id":[{"id":"10.13039\/100000071","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"HHS | NIH | National Heart, Lung, and Blood Institute (NHBLI)","doi-asserted-by":"publisher","award":["HL66072"],"award-info":[{"award-number":["HL66072"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"HHS | NIH | National Heart, Lung, and Blood Institute (NHBLI)","doi-asserted-by":"publisher","award":["HL51971"],"award-info":[{"award-number":["HL51971"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2016,8,1]]},"abstract":"<jats:p> Renal ischemia-reperfusion (I\/R) in male rats causes reductions in plasma testosterone, and infusion of testosterone 3 h postreperfusion is protective. We tested the hypotheses that acute high doses of testosterone promote renal injury after I\/R, and that acute low-dose testosterone is protective by the following: 1) increasing renal IL-10 and reducing TNF-\u03b1; 2) its effects on nitric oxide; and 3) reducing intrarenal T-cell infiltration. Rats were subjected to renal I\/R, followed by intravenous infusion of vehicle or testosterone (20, 50, or 100 \u03bcg\/kg) 3 h postreperfusion. Low-dose testosterone (20 \u03bcg\/kg) reduced plasma creatinine, increased nitrate\/nitrite excretion, increased intrarenal IL-10, and reduced intrarenal TNF-\u03b1, whereas 50 \u03bcg\/kg testosterone failed to reduce plasma creatinine, increased IL-10, but failed to reduce TNF-\u03b1. A higher dose of testosterone (100 mg\/kg) not only failed to reduce plasma creatinine, but significantly increased both IL-10 and TNF-\u03b1 compared with other groups. Low-dose nitro-l-arginine methyl ester (1 mg\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7day<jats:sup>\u22121<\/jats:sup>), given 2 days before I\/R, prevented low-dose testosterone (20 \u03bcg\/kg) from protecting against I\/R injury, and was associated with lack of increase in intrarenal IL-10. Intrarenal CD4<jats:sup>+<\/jats:sup> and CD8<jats:sup>+<\/jats:sup> T cells were significantly increased with I\/R, but were attenuated with low-dose testosterone, as were effector T helper 17 cells. The present studies suggest that acute, low-dose testosterone is protective against I\/R AKI in males due to its effects on inflammation by reducing renal T-cell infiltration and by shifting the balance to favor anti-inflammatory cytokine production rather than proinflammatory cytokines. <\/jats:p>","DOI":"10.1152\/ajprenal.00454.2015","type":"journal-article","created":{"date-parts":[[2016,6,1]],"date-time":"2016-06-01T23:47:56Z","timestamp":1464824876000},"page":"F395-F403","source":"Crossref","is-referenced-by-count":38,"title":["Low-dose testosterone protects against renal ischemia-reperfusion injury by increasing renal IL-10-to-TNF-\u03b1 ratio and attenuating T-cell infiltration"],"prefix":"10.1152","volume":"311","author":[{"given":"Chetan N.","family":"Patil","sequence":"first","affiliation":[{"name":"Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi;"},{"name":"The Women's Health Research Center, University of Mississippi Medical Center, Jackson, Mississippi; and"}]},{"given":"Kedra","family":"Wallace","sequence":"additional","affiliation":[{"name":"Department of Obstetrics and Gynecology, University of Mississippi Medical Center, Jackson, Mississippi;"},{"name":"The Women's Health Research Center, University of Mississippi Medical Center, Jackson, Mississippi; and"}]},{"given":"Babbette D.","family":"LaMarca","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, University of Mississippi Medical Center, Jackson, Mississippi;"},{"name":"The Women's Health Research Center, University of Mississippi Medical Center, Jackson, Mississippi; and"}]},{"given":"Mohadetheh","family":"Moulana","sequence":"additional","affiliation":[{"name":"Department of Psychiatry, University of Mississippi Medical Center, Jackson, Mississippi;"},{"name":"The Women's Health Research Center, University of Mississippi Medical Center, Jackson, Mississippi; and"}]},{"given":"Arnaldo","family":"Lopez-Ruiz","sequence":"additional","affiliation":[{"name":"Department of Medicine (Nephrology), University of Mississippi Medical Center, Jackson, Mississippi;"}]},{"given":"Andrea","family":"Soljancic","sequence":"additional","affiliation":[{"name":"Department of Medicine (Nephrology), University of Mississippi Medical Center, Jackson, Mississippi;"}]},{"given":"Luis A.","family":"Juncos","sequence":"additional","affiliation":[{"name":"Department of Medicine (Nephrology), University of Mississippi Medical Center, Jackson, Mississippi;"}]},{"given":"Joseph P.","family":"Grande","sequence":"additional","affiliation":[{"name":"Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota"}]},{"given":"Jane F.","family":"Reckelhoff","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi;"},{"name":"The Women's Health Research Center, University of Mississippi Medical Center, Jackson, Mississippi; and"}]}],"member":"24","reference":[{"key":"B1","first-page":"309","volume":"57","author":"Centers for Disease Control and Prevention","year":"2008","journal-title":"MMWR Morb Mortal Wkly Rep"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1136\/hrt.2010.217414"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.1993.tb13552.x"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/S1166-7087(14)70058-2"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1097\/FJC.0000000000000060"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1186\/cc4915"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013050502"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1172\/JCI38702"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2010.03.005"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00471.2009"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/j.genm.2012.02.003"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1136\/hrt.2010.195412"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/j.mayocp.2014.10.011"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2002.kid590.x"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014090868"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/j.lfs.2008.08.009"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M407629200"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/j.vph.2012.01.008"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/j.steroids.2010.12.012"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.600"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1186\/1476-9255-8-14"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.1400076"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00360.2012"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1248\/bpb.b14-00860"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejphar.2013.07.008"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfs360"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1159\/000443414"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1097\/01.TP.0000438622.89310.95"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00454.2015","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:43:39Z","timestamp":1567975419000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00454.2015"}},"issued":{"date-parts":[[2016,8,1]]},"references-count":28,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2016,8,1]]}},"alternative-id":["10.1152\/ajprenal.00454.2015"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00454.2015","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2016,8,1]]}},{"indexed":{"date-parts":[[2026,3,15]],"date-time":"2026-03-15T16:11:00Z","timestamp":1773591060390,"version":"3.50.1"},"reference-count":31,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2004,2]]},"abstract":"<jats:p> In macrophages, changes in intracellular calcium have been associated with activation of cellular processes that regulate cell adhesion and motility and are important for the response of macrophages to antigenic stimuli. The mammalian counterpart of the fish calcium-regulating hormone stanniocalcin-1 (STC1) is expressed in multiple organs including the thymus and spleen, and hence, we hypothesized that it may have a role in modulating the immune\/inflammatory response. Using murine macrophage-like (RAW264.7) and human monoblast-like (U937) cells to study chemotaxis in vitro, we found that STC1 attenuated chemokinesis and diminished the chemotactic response to monocyte chemotactic protein-1 (MCP-1) and stromal cell-derived factor-1\u03b1. Consistent with these findings, STC1 blunted the rise in intracellular calcium following MCP-1 stimulation in RAW264.7 cells. In vivo studies suggested differential expression of STC1 in obstructed kidney and localization to macrophages. MCP-1 and STC1 transcripts were both upregulated following ureteric obstruction, suggesting a functional association between the two genes. Our data suggest a role for mammalian STC1 in modulating the immune\/inflammatory response. <\/jats:p>","DOI":"10.1152\/ajprenal.00138.2003","type":"journal-article","created":{"date-parts":[[2004,1,31]],"date-time":"2004-01-31T01:13:21Z","timestamp":1075511601000},"page":"F356-F362","source":"Crossref","is-referenced-by-count":69,"title":["Stanniocalcin-1, an inhibitor of macrophage chemotaxis and chemokinesis"],"prefix":"10.1152","volume":"286","author":[{"given":"John","family":"Kanellis","sequence":"first","affiliation":[]},{"given":"Roger","family":"Bick","sequence":"additional","affiliation":[]},{"given":"Gabriela","family":"Garcia","sequence":"additional","affiliation":[]},{"given":"Luan","family":"Truong","sequence":"additional","affiliation":[]},{"given":"Chun Chui","family":"Tsao","sequence":"additional","affiliation":[]},{"given":"Dariush","family":"Etemadmoghadam","sequence":"additional","affiliation":[]},{"given":"Brian","family":"Poindexter","sequence":"additional","affiliation":[]},{"given":"Lili","family":"Feng","sequence":"additional","affiliation":[]},{"given":"Richard J.","family":"Johnson","sequence":"additional","affiliation":[]},{"given":"David","family":"Sheikh-Hamad","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"REF1","doi-asserted-by":"publisher","DOI":"10.1016\/S0303-7207(96)03929-9"},{"key":"REF2","doi-asserted-by":"publisher","DOI":"10.1016\/0303-7207(95)03601-3"},{"key":"REF3","doi-asserted-by":"publisher","DOI":"10.1084\/jem.188.1.193"},{"key":"REF4","doi-asserted-by":"crossref","unstructured":"Chomczynski P and Sacchi N. Single-step method of RNA isolation by acid guanidinium thiocyanate-phenol-chloroform extraction. Anal Biochem 162: 156-159, 1987.","DOI":"10.1016\/0003-2697(87)90021-2"},{"key":"REF5","doi-asserted-by":"publisher","DOI":"10.1159\/000052618"},{"key":"REF6","doi-asserted-by":"publisher","DOI":"10.1016\/S0303-7207(97)00243-8"},{"key":"REF7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.266.6.F926"},{"key":"REF8","unstructured":"Fontaine M. Corpuscles de Stannius et regulation ionique (Ca, K, Na) du milieu interieur de l'anguille (Anguilla anguilla L.). C R Acad Sc Paris Serie D 259: 875-878, 1964."},{"key":"REF9","doi-asserted-by":"publisher","DOI":"10.1016\/0303-7207(94)90130-9"},{"key":"REF10","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00153.x"},{"key":"REF11","doi-asserted-by":"crossref","unstructured":"Kaneto H, Fukuzaki A, Ishidoya S, Takeda A, Ogata Y, Sasaki T, Yamada S, and Orikasa S. mRNA expression of chemokines in rat kidneys with ureteral obstruction. Nippon Hinyokika Gakkai Zasshi 91: 69-74, 2000.","DOI":"10.5980\/jpnjurol1989.91.69"},{"key":"REF12","doi-asserted-by":"crossref","unstructured":"Lafeber FP, Flik G, Wendelaar Bonga SE, and Perry SF. Hypocalcin from Stannius corpuscles inhibits gill calcium uptake in trout. Am J Physiol Renal Fluid Electrolyte Physiol 254: F891-F896, 1988.","DOI":"10.1152\/ajpregu.1988.254.6.R891"},{"key":"REF13","doi-asserted-by":"publisher","DOI":"10.1016\/0898-6568(94)90042-6"},{"key":"REF14","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.immunol.19.1.497"},{"key":"REF15","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.1998.274.1.G96"},{"key":"REF16","doi-asserted-by":"publisher","DOI":"10.1097\/00062752-199603010-00010"},{"key":"REF17","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M205954200"},{"key":"REF18","doi-asserted-by":"publisher","DOI":"10.1126\/science.8235587"},{"key":"REF19","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.01071.2002"},{"key":"REF20","doi-asserted-by":"crossref","unstructured":"Sheikh-Hamad D, Rouse D, and Yang Y. Regulation of stanniocalcin in MDCK cells by hypertonicity and extracellular calcium. Am J Physiol Renal Physiol 278: F417-F424, 2000.","DOI":"10.1152\/ajprenal.2000.278.3.F417"},{"key":"REF21","unstructured":"Stannius H. Uber nebenniere bei knochenfischen. Arch Anat Physiol 6: 97-101, 1939."},{"key":"REF22","unstructured":"Tagaki Y, Hirano T, and Yamada J. Effects of the removal of the corpuscles of Stannius on the transport of calcium across the intestine of rainbow trout. Zool Sci 2: 523-530, 1985."},{"key":"REF23","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.303"},{"key":"REF24","unstructured":"Truong LD, Sheikh-Hamad D, Chakraborty S, and Suki WN. Cell apoptosis and proliferation in obstructive uropathy. Semin Nephrol 18: 641-651, 1998."},{"key":"REF25","unstructured":"Vielhauer V, Anders HJ, Mack M, Cihak J, Strutz F, Stangassinger M, Luckow B, Grone HJ, and Schlondorff D. Obstructive nephropathy in the mouse: progressive fibrosis correlates with tubulointerstitial chemokine expression and accumulation of CC chemokine receptor 2- and 5-positive leukocytes. J Am Soc Nephrol 12: 1173-1187, 2001."},{"key":"REF26","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.6.1871"},{"key":"REF27","doi-asserted-by":"publisher","DOI":"10.1016\/S0074-7696(08)60499-4"},{"key":"REF28","doi-asserted-by":"publisher","DOI":"10.1038\/35073616"},{"key":"REF29","doi-asserted-by":"publisher","DOI":"10.1006\/prep.1997.0857"},{"key":"REF30","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.97.7.3637"},{"key":"REF31","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/17.10.2830"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00138.2003","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T21:34:37Z","timestamp":1567978477000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00138.2003"}},"issued":{"date-parts":[[2004,2]]},"references-count":31,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2004,2]]}},"alternative-id":["10.1152\/ajprenal.00138.2003"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00138.2003","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2004,2]]}},{"indexed":{"date-parts":[[2026,3,15]],"date-time":"2026-03-15T06:57:35Z","timestamp":1773557855368,"version":"3.50.1"},"reference-count":38,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2014,8,1]]},"abstract":"<jats:p> Diabetic nephropathy is the leading cause of end-stage renal disease in humans in the Western world. The recent development of Na<jats:sup>+<\/jats:sup>-glucose cotransporter 2 (SGLT2) inhibitors offers a new antidiabetic therapy via enhanced glucose excretion. Whether this strategy exerts beneficial effects on the development of type 2 diabetic nephropathy is still largely unclear. We investigated the effects of the specific SGLT2 inhibitor empagliflozin in BTBR.Cg-Lep&lt;ob&gt;\/WiscJ (BTBR ob\/ ob) mice, which spontaneously develop type 2 diabetic nephropathy. In the first experiment, BTBR ob\/ ob mice received either a diet containing 300 ppm empagliflozin or equicaloric placebo chow for 12 wk. In the second experiment, BTBR ob\/ ob mice received 1 \u03bcg\u00b7kg body wt<jats:sup>\u22121<\/jats:sup>\u00b7day<jats:sup>\u22121<\/jats:sup> ANG II to induce arterial hypertension and were separated into the same two diet groups for 6 wk. In both experiments, empagliflozin treatment enhanced glucosuria, thereby lowering blood glucose. Independently of hypertension, empagliflozin reduced albuminuria in diabetic mice. However, empagliflozin treatment affected diabetes-related glomerular hypertrophy, markers of renal inflammation, and mesangial matrix expansion only in BTBR ob\/ ob mice without hypertension. In summary, empagliflozin demonstrated significant antihyperglycemic effects, differentially ameliorating early features of diabetic nephropathy in BTBR ob\/ ob mice with and without hypertension. <\/jats:p>","DOI":"10.1152\/ajprenal.00145.2014","type":"journal-article","created":{"date-parts":[[2014,6,19]],"date-time":"2014-06-19T04:23:24Z","timestamp":1403151804000},"page":"F317-F325","source":"Crossref","is-referenced-by-count":169,"title":["The SGLT2 inhibitor empagliflozin ameliorates early features of diabetic nephropathy in BTBR <i>ob<\/i>\/<i>ob<\/i> type 2 diabetic mice with and without hypertension"],"prefix":"10.1152","volume":"307","author":[{"given":"Florian","family":"Gembardt","sequence":"first","affiliation":[{"name":"Division of Nephrology, Department of Internal Medicine III, University Hospital Carl Gustav Carus at the Technische Universit\u00e4t Dresden, Dresden, Germany; and"}]},{"given":"Christoph","family":"Bartaun","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Internal Medicine III, University Hospital Carl Gustav Carus at the Technische Universit\u00e4t Dresden, Dresden, Germany; and"}]},{"given":"Natalia","family":"Jarzebska","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Internal Medicine III, University Hospital Carl Gustav Carus at the Technische Universit\u00e4t Dresden, Dresden, Germany; and"}]},{"given":"Eric","family":"Mayoux","sequence":"additional","affiliation":[{"name":"Divison of Research, Boehringer Ingelheim Pharma, Biberach\/Riss, Germany"}]},{"given":"Vladimir T.","family":"Todorov","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Internal Medicine III, University Hospital Carl Gustav Carus at the Technische Universit\u00e4t Dresden, Dresden, Germany; and"}]},{"given":"Bernd","family":"Hohenstein","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Internal Medicine III, University Hospital Carl Gustav Carus at the Technische Universit\u00e4t Dresden, Dresden, Germany; and"}]},{"given":"Christian","family":"Hugo","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Internal Medicine III, University Hospital Carl Gustav Carus at the Technische Universit\u00e4t Dresden, Dresden, Germany; and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1136\/bmj.321.7258.412"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.2337\/dc13-S011"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(10)60407-2"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/j.surg.2008.03.018"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00180.2008"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000141"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1210\/jc.2011-2260"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M113.469486"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1097\/01.mjt.0000178781.89789.25"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1007\/BF01221856"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2009.10.009"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00254.2009"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1038\/oby.2008.443"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.2337\/dc13-0663"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.2337\/db11-1029"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa1007994"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1994.74.4.993"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009121290"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119592"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejphar.2009.07.001"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.176.9.5577"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.112.201889"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1210\/jc.2009-0473"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2012050445"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00518.2013"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00270.2005"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00450.2011"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.04010609"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1111\/acel.12008"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00357.2011"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000051700.07403.27"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00520.2013"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010030246"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00409.2012"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1146\/annurev-physiol-020911-153333"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.2337\/dc09-0517"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1155\/2012\/645969"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00292.2011"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00145.2014","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T01:04:12Z","timestamp":1567991052000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00145.2014"}},"issued":{"date-parts":[[2014,8,1]]},"references-count":38,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2014,8,1]]}},"alternative-id":["10.1152\/ajprenal.00145.2014"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00145.2014","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2014,8,1]]}},{"indexed":{"date-parts":[[2026,3,18]],"date-time":"2026-03-18T04:25:17Z","timestamp":1773807917520,"version":"3.50.1"},"reference-count":64,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2009,5]]},"abstract":"<jats:p>TNF-\u03b1 and NF-\u03baB play important roles in the development of inflammation in chronic renal failure (CRF). In hepatic cells, curcumin is shown to antagonize TNF-\u03b1-elicited NF-\u03baB activation. In this study, we hypothesized that if inflammation plays a key role in renal failure then curcumin should be effective in improving CRF. The effectiveness of curcumin was compared with enalapril, a compound known to ameliorate human and experimental CRF. Investigation was conducted in Sprague-Dawley rats where CRF was induced by 5\/6 nephrectomy (Nx). The Nx animals were divided into untreated (Nx), curcumin-treated (curcumin), and enalapril-treated (enalapril) groups. Sham-operated animals served as a control. Renal dysfunction in the Nx group, as evidenced by elevated blood urea nitrogen, plasma creatinine, proteinuria, segmental sclerosis, and tubular dilatation, was significantly reduced by curcumin and enalapril treatment. However, only enalapril significantly improved blood pressure. Compared with the control, the Nx animals had significantly higher plasma and kidney TNF-\u03b1, which was associated with NF-\u03baB activation and macrophage infiltration in the kidney. These changes were effectively antagonized by curcumin and enalapril treatment. The decline in the anti-inflammatory peroxisome proliferator-activated receptor \u03b3 (PPAR\u03b3) seen in Nx animals was also counteracted by curcumin and enalapril. Studies in mesangial cells were carried out to further establish that the anti-inflammatory effect of curcumin in vivo was mediated essentially by antagonizing TNF-\u03b1. Curcumin dose dependently antagonized the TNF-\u03b1-mediated decrease in PPAR\u03b3 and blocked transactivation of NF-\u03baB and repression of PPAR\u03b3, indicating that the anti-inflamatory property of curcumin may be responsible for alleviating CRF in Nx animals.<\/jats:p>","DOI":"10.1152\/ajprenal.90732.2008","type":"journal-article","created":{"date-parts":[[2009,2,18]],"date-time":"2009-02-18T21:09:41Z","timestamp":1234991381000},"page":"F1146-F1157","source":"Crossref","is-referenced-by-count":115,"title":["Curcumin ameliorates renal failure in 5\/6 nephrectomized rats: role of inflammation"],"prefix":"10.1152","volume":"296","author":[{"given":"S. S.","family":"Ghosh","sequence":"first","affiliation":[]},{"given":"H. D.","family":"Massey","sequence":"additional","affiliation":[]},{"given":"R.","family":"Krieg","sequence":"additional","affiliation":[]},{"given":"Z. A.","family":"Fazelbhoy","sequence":"additional","affiliation":[]},{"given":"S.","family":"Ghosh","sequence":"additional","affiliation":[]},{"given":"D. A.","family":"Sica","sequence":"additional","affiliation":[]},{"given":"I.","family":"Fakhry","sequence":"additional","affiliation":[]},{"given":"T. W. B.","family":"Gehr","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006040377"},{"key":"R2","doi-asserted-by":"crossref","unstructured":"Aggarwal S\n                      , Ichikawa H, Takada Y, Sandur SK, Shishodia S, Aggarwal BB.\n                      Curcumin (diferuloylmethane) down-regulates expression of cell proliferation and antiapoptotic and metastatic gene products through suppression of IkappaBalpha kinase and Akt activation.\n                      Mol Pharmacol\n                      69\n                      : 195\u2013206, 2006.","DOI":"10.1124\/mol.105.017400"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1016\/j.mce.2005.02.003"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1016\/j.canlet.2008.03.025"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.103.055616"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1007\/s00345-008-0253-4"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1016\/j.atherosclerosis.2004.08.023"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.107.164384"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1007\/s10495-005-1055-4"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1016\/j.coph.2006.11.008"},{"key":"R11","doi-asserted-by":"crossref","unstructured":"Fu Y\n                      , Zheng S, Lin J, Ryerse J, Chen A.\n                      Curcumin protects the rat liver from CCl4-caused injury and fibrogenesis by attenuating oxidative stress and suppressing inflammation.\n                      Mol Pharmacol\n                      73\n                      : 399\u2013409, 2008.","DOI":"10.1124\/mol.107.039818"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00184.2006"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00658.x"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1097\/00000441-200212000-00002"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00054.x"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-008-0978-8"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1209954"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006020185"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00766.x"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.059002415.x"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1161\/ATVBAHA.107.147835"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1007\/s00018-008-7452-4"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1093\/carcin\/bgh165"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1016\/j.bone.2007.11.016"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1007\/978-0-387-46401-5_21"},{"key":"R26","unstructured":"Ireson C\n                      , Orr S, Jones DJ, Verschoyle R, Lim CK, Luo JL, Howells L, Plummer S, Jukes R, Williams M, Steward WP, Gescher A.\n                      Characterization of metabolites of the chemopreventive agent curcumin in human and rat hepatocytes and in the rat in vivo, and evaluation of their ability to inhibit phorbol ester-induced prostaglandin E\n                      2\n                      production.\n                      Cancer Res\n                      61\n                      : 1058\u20131064, 2001."},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.40.25252"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000015603.84788.47"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1016\/j.metabol.2006.10.007"},{"key":"R30","doi-asserted-by":"crossref","unstructured":"Kincaid-Smith P\n                      , Fairley KF, Farish S, Best JD, Proietto J.\n                      Reduction of proteinuria by rosiglitazone in non-diabetic renal disease.\n                      Nephrology (Carlton)\n                      13\n                      : 58\u201362, 2008.","DOI":"10.1111\/j.1440-1797.2007.00903.x"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1016\/j.urology.2005.09.028"},{"key":"R32","doi-asserted-by":"crossref","unstructured":"Li HL\n                      , Liu C, de Couto G, Ouzounian M, Sun M, Wang AB, Huang Y, He CW, Shi Y, Chen X, Nghiem MP, Liu Y, Chen M, Dawood F, Fukuoka M, Maekawa Y, Zhang L, Leask A, Ghosh AK, Kirshenbaum LA, Liu PP.\n                      Curcumin prevents and reverses murine cardiac hypertrophy.\n                      J Clin Invest\n                      118\n                      : 879\u2013893, 2008.","DOI":"10.1172\/JCI32865"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0b013e3282f2903c"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1016\/j.amjcard.2006.11.004"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.2000.2748"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.0590051899.x"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006091028"},{"key":"R38","doi-asserted-by":"crossref","unstructured":"Morimoto T\n                      , Sunagawa Y, Kawamura T, Takaya T, Wada H, Nagasawa A, Komeda M, Fujita M, Shimatsu A, Kita T, Hasegawa K.\n                      The dietary compound curcumin inhibits p300 histone acetyltransferase activity and prevents heart failure in rats.\n                      J Clin Invest\n                      118\n                      : 868\u2013878, 2008.","DOI":"10.1172\/JCI33160"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1111\/j.1742-7843.2007.00109.x"},{"key":"R40","doi-asserted-by":"crossref","unstructured":"Pan MH\n                      , Huang TM, Lin JK.\n                      Biotransformation of curcumin through reduction and glucuronidation in mice.\n                      Drug Metab Dispos\n                      27\n                      : 486\u2013494, 1999.","DOI":"10.1016\/S0090-9556(24)15211-7"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00500.2007"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1016\/0300-483X(81)90027-5"},{"key":"R43","doi-asserted-by":"crossref","unstructured":"Remuzzi G\n                      , Perico N, Macia M, Ruggenenti P.\n                      The role of renin-angiotensin-aldosterone system in the progression of chronic kidney disease.\n                      Kidney Int Suppl\n                      99\n                      : S57\u2013S65, 2005.","DOI":"10.1111\/j.1523-1755.2005.09911.x"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1172\/JCI36150"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.62.s82.4.x"},{"key":"R46","doi-asserted-by":"publisher","DOI":"10.1093\/carcin\/bgm123"},{"key":"R47","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5001620"},{"key":"R48","doi-asserted-by":"publisher","DOI":"10.1007\/978-0-387-46401-5_20"},{"key":"R49","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.2006.04468.x"},{"key":"R50","doi-asserted-by":"publisher","DOI":"10.1016\/S0076-6879(05)00015-7"},{"key":"R51","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-5793(98)01304-0"},{"key":"R52","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00200.x"},{"key":"R53","doi-asserted-by":"publisher","DOI":"10.1089\/ars.2007.1769"},{"key":"R54","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.00411.2003"},{"key":"R55","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2000.00327.x"},{"key":"R56","doi-asserted-by":"publisher","DOI":"10.3317\/jraas.2007.017"},{"key":"R57","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.107.123638"},{"key":"R58","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.00456.2007"},{"key":"R59","doi-asserted-by":"publisher","DOI":"10.1210\/en.2008-0262"},{"key":"R60","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.00474.2002"},{"key":"R61","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.2001.281.6.G1397"},{"key":"R62","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2008.07.068"},{"key":"R63","doi-asserted-by":"crossref","unstructured":"Zhang B\n                      , Berger J, Hu E, Szalkowski D, White-Carrington S, Spiegelman BM, Moller DE.\n                      Negative regulation of peroxisome proliferator-activated receptor-gamma gene expression contributes to the antiadipogenic effects of tumor necrosis factor-alpha.\n                      Mol Endocrinol\n                      10\n                      : 1457\u20131466, 1996.","DOI":"10.1210\/mend.10.11.8923470"},{"key":"R64","doi-asserted-by":"publisher","DOI":"10.1172\/JCI30485"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.90732.2008","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,2,7]],"date-time":"2025-02-07T15:13:07Z","timestamp":1738941187000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.90732.2008"}},"issued":{"date-parts":[[2009,5]]},"references-count":64,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2009,5]]}},"alternative-id":["10.1152\/ajprenal.90732.2008"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.90732.2008","relation":{"has-review":[{"id-type":"doi","id":"10.3410\/f.1157160.617274","asserted-by":"object"}]},"ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2009,5]]}},{"indexed":{"date-parts":[[2026,3,6]],"date-time":"2026-03-06T15:23:54Z","timestamp":1772810634304,"version":"3.50.1"},"reference-count":38,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2010,5]]},"abstract":"<jats:p>Akt\/PKB is known to regulate the facilitative glucose carrier GLUT4. Nothing is known, however, of the role of Akt\/PKB in the regulation of renal epithelial transport. To explore whether Akt2\/PKB\u03b2 influences the Na<jats:sup>+<\/jats:sup>-coupled glucose cotransporter SGLT1, human SGLT1 was expressed in Xenopus laevis oocytes with or without Akt\/PKB, and electrogenic glucose transport was determined by dual-electrode voltage clamp. The coexpression of Akt\/PKB in SGLT1-expressing oocytes was followed by an increase in glucose-induced currents. To study the functional significance of Akt\/PKB-sensitive renal glucose transport, further experiments were performed in gene-targeted mice lacking functional Akt2\/PKB\u03b2 ( akt2<jats:sup>\u2212\/\u2212<\/jats:sup>) and in their wild-type littermates ( akt2<jats:sup>+\/+<\/jats:sup>). Plasma glucose concentration was significantly higher in akt2<jats:sup>\u2212\/\u2212<\/jats:sup>mice than in akt2<jats:sup>+\/+<\/jats:sup>mice but was virtually identical to the plasma glucose concentration in fructose-treated akt2<jats:sup>+\/+<\/jats:sup>mice. Urinary glucose excretion was significantly higher in akt2<jats:sup>\u2212\/\u2212<\/jats:sup>mice compared with akt2<jats:sup>+\/+<\/jats:sup>mice with or without fructose treatment. Moreover, the glucose-induced depolarization of proximal tubular cells was significantly smaller in isolated, perfused renal tubules from akt2<jats:sup>\u2212\/\u2212<\/jats:sup>mice than in those from akt2<jats:sup>+\/+<\/jats:sup>mice. In conclusion, Akt2\/PKB\u03b2 plays a role in the regulation of renal glucose transport.<\/jats:p>","DOI":"10.1152\/ajprenal.00592.2009","type":"journal-article","created":{"date-parts":[[2010,2,17]],"date-time":"2010-02-17T20:45:03Z","timestamp":1266439503000},"page":"F1113-F1117","source":"Crossref","is-referenced-by-count":13,"title":["Regulation of renal tubular glucose reabsorption by Akt2\/PKB\u03b2"],"prefix":"10.1152","volume":"298","author":[{"given":"Daniela S.","family":"Kempe","sequence":"first","affiliation":[{"name":"Department of Physiology, University of T\u00fcbingen, T\u00fcbingen, Germany;"}]},{"given":"Gulab","family":"Siraskar","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of T\u00fcbingen, T\u00fcbingen, Germany;"}]},{"given":"Henning","family":"Fr\u00f6hlich","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of T\u00fcbingen, T\u00fcbingen, Germany;"}]},{"given":"Anja T.","family":"Umbach","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of T\u00fcbingen, T\u00fcbingen, Germany;"}]},{"given":"Michael","family":"St\u00fcbs","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of T\u00fcbingen, T\u00fcbingen, Germany;"}]},{"given":"Florian","family":"Weiss","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of T\u00fcbingen, T\u00fcbingen, Germany;"}]},{"given":"Teresa F.","family":"Ackermann","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of T\u00fcbingen, T\u00fcbingen, Germany;"}]},{"given":"Harald","family":"V\u00f6lkl","sequence":"additional","affiliation":[{"name":"Department of Physiology and Medical Physics, Medical University of Innsbruck, Innsbruck, Austria;"}]},{"given":"Morris J.","family":"Birnbaum","sequence":"additional","affiliation":[{"name":"Division of Endocrinology, Diabetes and Metabolism, University of Pennsylvania, Philadelphia, Pennsylvania; and"}]},{"given":"David","family":"Pearce","sequence":"additional","affiliation":[{"name":"Department of Medicine (Nephrology), University of California, San Francisco, California"}]},{"given":"Michael","family":"F\u00f6ller","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of T\u00fcbingen, T\u00fcbingen, Germany;"}]},{"given":"Florian","family":"Lang","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of T\u00fcbingen, T\u00fcbingen, Germany;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90238.2008"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1002\/j.1460-2075.1996.tb01045.x"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/S0960-9822(06)00336-8"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00024.2006"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007030263"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004080638"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1159\/000185543"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1159\/000185554"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00090.2008"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1126\/science.292.5522.1728"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.C100462200"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1038\/oby.2004.104"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M802623200"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00382.2005"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1210\/en.2005-0850"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1042\/bj3390319"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1159\/000113758"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00050.2005"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.97.14.8157"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/cdf387"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M701923200"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007080940"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1016\/j.lfs.2008.09.014"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1159\/000113756"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006070699"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007050626"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1159\/000110439"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1159\/000071068"},{"key":"B29","doi-asserted-by":"crossref","first-page":"2003","DOI":"10.1681\/ASN.V12102003","volume":"12","author":"Vallon V","year":"2001","journal-title":"J Am Soc Nephrol"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0505860102"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.108.186445"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006111229"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1159\/000016341"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1016\/S1043-2760(02)00662-8"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000050223.34749.F4"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2796.2006.01746.x"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008040445"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006111194"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00592.2009","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,10,23]],"date-time":"2021-10-23T02:13:24Z","timestamp":1634955204000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00592.2009"}},"issued":{"date-parts":[[2010,5]]},"references-count":38,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2010,5]]}},"alternative-id":["10.1152\/ajprenal.00592.2009"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00592.2009","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2010,5]]}},{"indexed":{"date-parts":[[2026,3,9]],"date-time":"2026-03-09T22:31:51Z","timestamp":1773095511296,"version":"3.50.1"},"reference-count":40,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,1,15]]},"abstract":"<jats:p>Epoxyeicosatrienoic acids, hydrolyzed by soluble epoxide hydrolase (sEH), have multiple biological functions, including the regulation of vascular tone, renal tubular transport, and being anti-inflammatory. Inhibitors of sEH have been demonstrated to be antihypertensive and renal protective. To elucidate the role of sEH in glomerulonephritis, we first determined the expression of sEH in human kidney by examining biopsies from 153 patients with a variety of glomerulonephritis, including minimal-change, membranous, and IgA nephropathy. Immunohistochemical staining of frozen kidney biopsy samples revealed sEH preferentially expressed in the renal proximal tubular cells, and its expression increased in all patients with glomerulonephritis. The level of sEH in the cortex was positively correlated with proteinuria and negatively with serum albumin level. To investigate the role of sEH in proteinuria-induced renal damage, we incubated purified urine protein from patients with rat renal proximal tubular epithelial cells in vitro. The level of sEH was elevated, as were monocyte chemoattractant protein 1 and the process of tubular epithelial-to-mesenchymal transition, characterized with increased \u03b1-smooth muscle actin (\u03b1-SMA) and decreased E-cadherin. These effects were attenuated by administration of a potent sEH inhibitor and mimicked with adenovirus-mediated sEH overexpression. In adriamycin-induced nephropathic mice, sEH inhibitor did not ameliorate proteinuria or level of serum albumin but reduced the long-term elevated serum creatinine level, interstitial inflammation, fibrosis, and \u03b1-SMA expression. Thus upregulation of sEH in proximal tubular cells in chronic proteinuric kidney diseases may mediate proteinuria-induced renal damage; sEH inhibition by increasing renal eicosanoid levels could prevent the progression of chronic proteinuric kidney diseases.<\/jats:p>","DOI":"10.1152\/ajprenal.00129.2012","type":"journal-article","created":{"date-parts":[[2012,11,15]],"date-time":"2012-11-15T01:46:22Z","timestamp":1352943982000},"page":"F168-F176","source":"Crossref","is-referenced-by-count":22,"title":["Upregulation of soluble epoxide hydrolase in proximal tubular cells mediated proteinuria-induced renal damage"],"prefix":"10.1152","volume":"304","author":[{"given":"Qian","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Nephrology, Peking University Third Hospital, Beijing, China;"},{"name":"Department of Geriatric Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, China; and"}]},{"given":"Wei","family":"Pang","sequence":"additional","affiliation":[{"name":"Department of Physiology and Pathophysiology, Peking University Health Science Center, Key Laboratory of Molecular Cardiovascular Science of the Ministry of Education, Beijing, China;"}]},{"given":"Zhuan","family":"Cui","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Peking University Third Hospital, Beijing, China;"}]},{"given":"Junbao","family":"Shi","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Peking University Third Hospital, Beijing, China;"}]},{"given":"Yan","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Physiology and Pathophysiology, Peking University Health Science Center, Key Laboratory of Molecular Cardiovascular Science of the Ministry of Education, Beijing, China;"}]},{"given":"Bo","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Physiology and Pathophysiology, Peking University Health Science Center, Key Laboratory of Molecular Cardiovascular Science of the Ministry of Education, Beijing, China;"}]},{"given":"Yunfeng","family":"Zhou","sequence":"additional","affiliation":[{"name":"Department of Physiology and Pathophysiology, Peking University Health Science Center, Key Laboratory of Molecular Cardiovascular Science of the Ministry of Education, Beijing, China;"}]},{"given":"Youfei","family":"Guan","sequence":"additional","affiliation":[{"name":"Department of Physiology and Pathophysiology, Peking University Health Science Center, Key Laboratory of Molecular Cardiovascular Science of the Ministry of Education, Beijing, China;"}]},{"given":"Bruce D.","family":"Hammock","sequence":"additional","affiliation":[{"name":"Department of Entomology and Cancer Center, University of California, Davis, California"}]},{"given":"Yue","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Peking University Third Hospital, Beijing, China;"}]},{"given":"Yi","family":"Zhu","sequence":"additional","affiliation":[{"name":"Department of Physiology and Pathophysiology, Peking University Health Science Center, Key Laboratory of Molecular Cardiovascular Science of the Ministry of Education, Beijing, China;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0703229104"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0811022106"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.78.3.415"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.44.29254"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1097\/FJC.0b013e3181506445"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/j.yjmcc.2009.10.022"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1369\/jhc.5A6808.2005"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1177\/002215540405200403"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/j.tcm.2007.11.002"},{"key":"B10","first-page":"147","volume":"23","author":"Hallan SI","year":"2010","journal-title":"J Nephrol"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00004.2007"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00350.2004"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1097\/FJC.0b013e3181e96e0c"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1038\/nrd2875"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1161\/hy0202.103788"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000176237.74820.75"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000153792.29478.1d"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0011979"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1517\/17425250902932923"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.00710.2010"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/j.tips.2006.11.002"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.110.161695"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1161\/STROKEAHA.109.567768"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0039165"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00098.2009"},{"key":"B26","doi-asserted-by":"crossref","first-page":"2314","DOI":"10.1093\/clinchem\/39.11.2314","volume":"39","author":"Marshall T","year":"1993","journal-title":"Clin Chem"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1007\/BF00332483"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1007\/s10565-008-9071-0"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/j.prostaglandins.2009.04.004"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0409591102"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1194\/jlr.R800038-JLR200"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00402.2006"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.36"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejps.2010.03.018"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1155\/2012\/601786"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00342.x"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00165.2003"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.111.259325"},{"key":"B39","first-page":"1244","volume":"15","author":"Zhao X","year":"2004","journal-title":"J Am Soc Nephrol"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1016\/j.pharmthera.2009.12.002"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00129.2012","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2020,7,16]],"date-time":"2020-07-16T03:41:06Z","timestamp":1594870866000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00129.2012"}},"issued":{"date-parts":[[2013,1,15]]},"references-count":40,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2013,1,15]]}},"alternative-id":["10.1152\/ajprenal.00129.2012"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00129.2012","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2013,1,15]]}},{"indexed":{"date-parts":[[2026,3,10]],"date-time":"2026-03-10T13:48:19Z","timestamp":1773150499091,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1993,2,1]]},"abstract":"<jats:p> Antidiuretic hormone and parathyroid hormone (PTH) inhibit HCO3- absorption by the rat medullary thick ascending limb (MTAL). Studies were performed on rat MTAL tubule suspension to specify the H(+)-HCO3- membrane transporters affected by these hormones and the implicated intracellular second messengers. Arginine vasopressin (AVP) and PTH stimulated cell adenosine 3',5'-cyclic monophosphate (cAMP) production with a relative rank order potency of AVP &gt; rat PTH-(1-34) &gt; bovine PTH-(1-84). Significant cell acidification in HCO3- -CO2-free medium, monitored in 2'7'-bis(carboxyethyl)-5(6')-carboxyfluorescein-loaded cells, was caused by 0.1 nM AVP, 1 nM rat PTH-(1-34), but not by &lt; 100 nM bovine PTH-(1-84), as well as by 10(-4) M 8-bromo-cAMP and 2 x 10(-5) M forskolin; 10 nM AVP or rat PTH-(1-34) did not alter the intracellular pH when Na+\/H+ antiport was inhibited by 2 mM amiloride. Prostaglandin E2 (PGE2, 10(-6) M), which inhibited AVP-stimulated cell cAMP production, reduced by 35% the cell acidification response to 10 nM AVP. AVP and 8-bromo-cAMP inhibited Na+\/H+ antiport-dependent cell pH recovery from intracellular acidification, which was explained by a decrease in the Vmax of the antiporter. AVP did not directly affect K(+)-HCO3- cotransport and plasma membrane H(+)-ATPase of rat MTAL cells. Cytosolic calcium ([Ca2+]i), monitored in fura-2-loaded cells, was unaffected by up to 1 nM AVP, 100 nM PTH, glucagon, calcitonin, and oxytocin, and 1 microM PGE2; however, 100 nM AVP, but not 1-desamino-8-D-AVP (dDAVP), caused a peak increase in [Ca2+]i, even in the absence of extracellular Ca2+, and stimulated cell accumulation of [3H]inositol phosphates.(ABSTRACT TRUNCATED AT 250 WORDS) <\/jats:p>","DOI":"10.1152\/ajprenal.1993.264.2.f354","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T05:21:35Z","timestamp":1514006495000},"page":"F354-F364","source":"Crossref","is-referenced-by-count":15,"title":["cAMP-dependent control of Na+\/H+ antiport by AVP, PTH, and PGE2 in rat medullary thick ascending limb cells"],"prefix":"10.1152","volume":"264","author":[{"given":"P.","family":"Borensztein","sequence":"first","affiliation":[{"name":"Physiologie et Endocrinologie Cellulaire Renale, Institut National dela Sante et de la Recherche Medicale, Unite 356, Universite Pierre et MarieCurie, Paris, France."}]},{"given":"P.","family":"Juvin","sequence":"additional","affiliation":[{"name":"Physiologie et Endocrinologie Cellulaire Renale, Institut National dela Sante et de la Recherche Medicale, Unite 356, Universite Pierre et MarieCurie, Paris, France."}]},{"given":"C.","family":"Vernimmen","sequence":"additional","affiliation":[{"name":"Physiologie et Endocrinologie Cellulaire Renale, Institut National dela Sante et de la Recherche Medicale, Unite 356, Universite Pierre et MarieCurie, Paris, France."}]},{"given":"J.","family":"Poggioli","sequence":"additional","affiliation":[{"name":"Physiologie et Endocrinologie Cellulaire Renale, Institut National dela Sante et de la Recherche Medicale, Unite 356, Universite Pierre et MarieCurie, Paris, France."}]},{"given":"M.","family":"Paillard","sequence":"additional","affiliation":[{"name":"Physiologie et Endocrinologie Cellulaire Renale, Institut National dela Sante et de la Recherche Medicale, Unite 356, Universite Pierre et MarieCurie, Paris, France."}]},{"given":"M.","family":"Bichara","sequence":"additional","affiliation":[{"name":"Physiologie et Endocrinologie Cellulaire Renale, Institut National dela Sante et de la Recherche Medicale, Unite 356, Universite Pierre et MarieCurie, Paris, France."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1993.264.2.F354","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:29:12Z","timestamp":1567960152000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1993.264.2.F354"}},"issued":{"date-parts":[[1993,2,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1993,2,1]]}},"alternative-id":["10.1152\/ajprenal.1993.264.2.F354"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1993.264.2.f354","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1993,2,1]]}},{"indexed":{"date-parts":[[2026,3,10]],"date-time":"2026-03-10T13:48:05Z","timestamp":1773150485516,"version":"3.50.1"},"reference-count":35,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2004,2]]},"abstract":"<jats:p>The effect of arginine vasopressin (AVP) and\/or atrial natriuretic peptide (ANP) on the regulation of intracellular pH (pH<jats:sub>i<\/jats:sub>) via H<jats:sup>+<\/jats:sup>-ATPase and of cytosolic calcium ([Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>) was investigated in Madin-Darby canine kidney (MDCK) cells by the fluorescent probes BCECF-AM and fluo-4-AM, respectively. The pH<jats:sub>i<\/jats:sub>recovery rate was examined after intracellular acidification following an NH<jats:sub>4<\/jats:sub>Cl pulse, in the presence of zero Na<jats:sup>+<\/jats:sup>plus Schering 28080 (a specific inhibitor of H<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-ATPase). AVP (10<jats:sup>-12<\/jats:sup>-10<jats:sup>-6<\/jats:sup>M) increased the rate of pH<jats:sub>i<\/jats:sub>recovery and [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>in a dose-dependent manner. V<jats:sub>1<\/jats:sub>- or V<jats:sub>2<\/jats:sub>-receptor antagonists impaired the effect of AVP on both processes, and DDAVP (10<jats:sup>-12<\/jats:sup>-10<jats:sup>-6<\/jats:sup>M; a V<jats:sub>2<\/jats:sub>-selective agonist) caused a dose-dependent stimulation of them. [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>or cAMP (as increased by 10<jats:sup>-5<\/jats:sup>M thapsigargin or 8-BrcAMP, respectively) alone had no effect on H<jats:sup>+<\/jats:sup>-ATPase, but their synergic action was necessary to stimulate H<jats:sup>+<\/jats:sup>-ATPase. In agreement with these findings, ANP (10<jats:sup>-6<\/jats:sup>M) or dimethyl-BAPTA-AM (5 \u00d7 10<jats:sup>-5<\/jats:sup>M), impairing the increase of [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>in response to AVP, blocks the stimulatory effect of AVP on H<jats:sup>+<\/jats:sup>-ATPase.<\/jats:p>","DOI":"10.1152\/ajprenal.00121.2003","type":"journal-article","created":{"date-parts":[[2004,1,31]],"date-time":"2004-01-31T01:13:21Z","timestamp":1075511601000},"page":"F402-F408","source":"Crossref","is-referenced-by-count":16,"title":["Arginine vasopressin stimulates H<sup>+<\/sup>-ATPase in MDCK cells via V<sub>1<\/sub>(cell Ca<sup>2+<\/sup>) and V<sub>2<\/sub>(cAMP) receptors"],"prefix":"10.1152","volume":"286","author":[{"given":"Maria","family":"Oliveira-Souza","sequence":"first","affiliation":[{"name":"Department of Physiology and Biophysics, Instituto de Ci\u00eancias Biom\u00e9dicas, University of S\u00e3o Paulo, S\u00e3o Paulo 05508-900, Brazil"}]},{"given":"Raif","family":"Musa-Aziz","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, Instituto de Ci\u00eancias Biom\u00e9dicas, University of S\u00e3o Paulo, S\u00e3o Paulo 05508-900, Brazil"}]},{"given":"Gerhard","family":"Malnic","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, Instituto de Ci\u00eancias Biom\u00e9dicas, University of S\u00e3o Paulo, S\u00e3o Paulo 05508-900, Brazil"}]},{"given":"Margarida","family":"de Mello Aires","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, Instituto de Ci\u00eancias Biom\u00e9dicas, University of S\u00e3o Paulo, S\u00e3o Paulo 05508-900, Brazil"}]}],"member":"24","reference":[{"key":"REF1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115398"},{"key":"REF2","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.425"},{"key":"REF3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.264.2.F354"},{"key":"REF4","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.67.1.91"},{"key":"REF5","doi-asserted-by":"crossref","unstructured":"Brewer CBand Roth MG.Polarized exocytosis in MDCK cells is regulated by phosphorylation.J Cell Sci108: 789-796, 1995.","DOI":"10.1242\/jcs.108.2.789"},{"key":"REF6","doi-asserted-by":"publisher","DOI":"10.1172\/JCI113888"},{"key":"REF7","doi-asserted-by":"crossref","unstructured":"Burgess WJ, Balment RJ, and Beck JS.Effects of luminal vasopressin on intracellular calcium in microperfused rat medullary thick ascending limb.Renal Physiol Biochem17: 1-9, 1994.","DOI":"10.1159\/000173782"},{"key":"REF8","doi-asserted-by":"publisher","DOI":"10.1038\/314443a0"},{"key":"REF9","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.ph.56.030194.003245"},{"key":"REF10","doi-asserted-by":"publisher","DOI":"10.1007\/s002329900378"},{"key":"REF11","doi-asserted-by":"publisher","DOI":"10.1007\/s004240000411"},{"key":"REF12","doi-asserted-by":"publisher","DOI":"10.1007\/BF00374853"},{"key":"REF13","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.79.14.4327"},{"key":"REF14","doi-asserted-by":"publisher","DOI":"10.1016\/0014-2999(96)00620-6"},{"key":"REF15","doi-asserted-by":"crossref","unstructured":"Grynkiewicz G, Poenie M, and Tsien RY.A new generation of Ca2+indicators with greatly improved fluorescence properties.J Biol Chem260: 3440-3450, 1985.","DOI":"10.1016\/S0021-9258(19)83641-4"},{"key":"REF16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.257.5.F777"},{"key":"REF17","doi-asserted-by":"publisher","DOI":"10.1007\/s00232-001-0028-y"},{"key":"REF18","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00366.x"},{"key":"REF19","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.107"},{"key":"REF20","doi-asserted-by":"publisher","DOI":"10.1016\/0006-291X(85)91735-8"},{"key":"REF21","doi-asserted-by":"publisher","DOI":"10.1016\/S0955-0674(00)00120-4"},{"key":"REF22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00056.2001"},{"key":"REF23","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9629(15)41815-4"},{"key":"REF24","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00604.x"},{"key":"REF25","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00993.x"},{"key":"REF26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.5.F944"},{"key":"REF27","doi-asserted-by":"publisher","DOI":"10.1016\/0304-4165(81)90307-X"},{"key":"REF28","doi-asserted-by":"publisher","DOI":"10.1172\/JCI111871"},{"key":"REF29","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1993.265.2.C432"},{"key":"REF30","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.1041590306"},{"key":"REF31","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.01066.2000"},{"key":"REF32","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.102.5.1638"},{"key":"REF33","doi-asserted-by":"publisher","DOI":"10.1007\/s004240050255"},{"key":"REF34","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.1989.257.3.G317"},{"key":"REF35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.5.F1068"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00121.2003","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,6,14]],"date-time":"2021-06-14T05:34:48Z","timestamp":1623648888000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00121.2003"}},"issued":{"date-parts":[[2004,2]]},"references-count":35,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2004,2]]}},"alternative-id":["10.1152\/ajprenal.00121.2003"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00121.2003","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2004,2]]}},{"indexed":{"date-parts":[[2026,3,9]],"date-time":"2026-03-09T14:38:54Z","timestamp":1773067134680,"version":"3.50.1"},"reference-count":55,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2009,4]]},"abstract":"<jats:p>The principal mediators of renal phosphate (P<jats:sub>i<\/jats:sub>) reabsorption are the SLC34 family proteins NaPi-IIa and NaPi-IIc, localized to the proximal tubule (PT) apical membrane. Their abundance is regulated by circulatory factors and dietary P<jats:sub>i<\/jats:sub>. Although their physiological importance has been confirmed in knockout animal studies, significant P<jats:sub>i<\/jats:sub>reabsorptive capacity remains, which suggests the involvement of other secondary-active P<jats:sub>i<\/jats:sub>transporters along the nephron. Here we show that a member of the SLC20 gene family (PiT-2) is localized to the brush-border membrane (BBM) of the PT epithelia and that its abundance, confirmed by Western blot and immunohistochemistry of rat kidney slices, is regulated by dietary P<jats:sub>i<\/jats:sub>. In rats treated chronically on a high-P<jats:sub>i<\/jats:sub>(1.2%) diet, there was a marked decrease in the apparent abundance of PiT-2 protein in kidney slices compared with those from rats kept on a chronic low-P<jats:sub>i<\/jats:sub>(0.1%) diet. In Western blots of BBM from rats that were switched from a chronic low- to high-P<jats:sub>i<\/jats:sub>diet, NaPi-IIa showed rapid downregulation after 2 h; PiT-2 was also significantly downregulated at 24 h and NaPi-IIc after 48 h. For the converse dietary regime, NaPi-IIa showed adaptation within 8 h, whereas PiT-2 and NaPi-IIc showed a slower adaptive trend. Our findings suggest that PiT-2, until now considered as a ubiquitously expressed P<jats:sub>i<\/jats:sub>housekeeping transporter, is a novel mediator of P<jats:sub>i<\/jats:sub>reabsorption in the PT under conditions of acute P<jats:sub>i<\/jats:sub>deprivation, but with a different adaptive time course from NaPi-IIa and NaPi-IIc.<\/jats:p>","DOI":"10.1152\/ajprenal.90623.2008","type":"journal-article","created":{"date-parts":[[2008,12,11]],"date-time":"2008-12-11T01:17:08Z","timestamp":1228958228000},"page":"F691-F699","source":"Crossref","is-referenced-by-count":150,"title":["The Na<sup>+<\/sup>-P<sub>i<\/sub>cotransporter PiT-2 (SLC20A2) is expressed in the apical membrane of rat renal proximal tubules and regulated by dietary P<sub>i<\/sub>"],"prefix":"10.1152","volume":"296","author":[{"given":"Ricardo","family":"Villa-Bellosta","sequence":"first","affiliation":[]},{"given":"Silvia","family":"Ravera","sequence":"additional","affiliation":[]},{"given":"Victor","family":"Sorribas","sequence":"additional","affiliation":[]},{"given":"Gerti","family":"Stange","sequence":"additional","affiliation":[]},{"given":"Moshe","family":"Levi","sequence":"additional","affiliation":[]},{"given":"Heini","family":"Murer","sequence":"additional","affiliation":[]},{"given":"J\u00fcrg","family":"Biber","sequence":"additional","affiliation":[]},{"given":"Ian C.","family":"Forster","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0505882102"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.2000.279.4.C1135"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.9.5372"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.69.040705.141729"},{"key":"R5","unstructured":"Berndt TJ, Kumar R.Clinical disturbances of phosphate homeostasis. In:Seldin and Giebisch's The Kidney, edited by Alpern RJ and Hebert SC. New York, NY: Academic, 2008, p. 1989\u20132006."},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1038\/nprot.2007.156"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1007\/s002329900394"},{"key":"R8","doi-asserted-by":"crossref","unstructured":"Chien ML, Foster JL, Douglas JL, Garcia JV.The amphotropic murine leukemia virus receptor gene encodes a 71-kilodalton protein that is induced by phosphate depletion.J Virol71: 4564\u20134570, 1997.","DOI":"10.1128\/JVI.71.6.4564-4570.1997"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.266.5.F767"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1074\/mcp.M500078-MCP200"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1999.277.2.H543"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5001813"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.4.F644"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.00272.2004"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000161997.24797.c0"},{"key":"R16","doi-asserted-by":"crossref","unstructured":"Gottschalk CW, Lassiter WE, Mylle M.Localization of urine acidification in the mammalian kidney.Am J Physiol198: 581\u2013585, 1960.","DOI":"10.1152\/ajplegacy.1960.198.3.581"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.135"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.91.15.7071"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00075.2006"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1055\/s-2005-870096"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.267.5.F900"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0b013e3281c55ef1"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000216409.20863.e7"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119289"},{"key":"R25","doi-asserted-by":"crossref","unstructured":"Madjdpour C, Bacic D, Kaissling B, Murer H, Biber J.Segment-specific expression of sodium-phosphate cotransporters NaPi-IIa and -IIc and interacting proteins in mouse renal proximal tubules.Pflugers Arch448: 402\u2013410, 2004.","DOI":"10.1007\/s00424-004-1253-x"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1159\/000107069"},{"key":"R27","unstructured":"Murer H, Forster I, Hilfiker H, Pfister M, Kaissling B, Lotscher M, Biber J.Cellular\/molecular control of renal Na\/Pi-cotransport.Kidney Int Suppl65: S2\u2013S10, 1998."},{"key":"R28","unstructured":"Murer H, Forster IC, Hernando N, Biber J.Proximal Tubular Handling of Phosphate: Na\/Pi-Cotransporters and their Regulation. In:Seldin and Giebisch's The Kidney, edited by Alpern RJ and Hebert SC. New York, NY: Acdemic, 2008, p. 1979\u20131988."},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.2000.80.4.1373"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1991.260.5.C885"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.2133\/dmpk.23.22"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-008-0530-5"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-003-1010-6"},{"key":"R34","doi-asserted-by":"crossref","unstructured":"Olah Z, Lehel C, Anderson WB, Eiden MV, Wilson CA.The cellular receptor for gibbon ape leukemia virus is a novel high affinity sodium-dependent phosphate transporter.J Biol Chem269: 25426\u201325431, 1994.","DOI":"10.1016\/S0021-9258(18)47267-5"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1007\/s004240050573"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00064.2007"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.055003976.x"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.75.12.5584-5592.2001"},{"key":"R39","doi-asserted-by":"crossref","unstructured":"Saliba KJ, Martin RE, Broer A, Henry RI, McCarthy CS, Downie MJ, Allen RJ, Mullin KA, McFadden GI, Broer S, Kirk K.Sodium-dependent uptake of inorganic phosphate by the intracellular malaria parasite.Nature443: 582\u2013585, 2006.","DOI":"10.1038\/nature05149"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M200943200"},{"key":"R41","unstructured":"Segawa H, Onitsuka A, Aranami F, Tomeo Y, Kaneko I, Furutani J, Ito M, Matsumoto M, Li M, Amizuka N, Kuwahata M, Miyamoto KI.Npt2a and Npt2c in mice play distinct and synergistic roles in inorganic phosphate metabolism and skeletal development.J Amer Soc NephrolSA-FC101, 2007."},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00097.2004"},{"key":"R43","unstructured":"Segel IH.Enzyme Kinetics: Behavior and Analysis of Rapid Equilibrium and Steady-state Enzyme Systems.New York, NY: Wiley, 1975."},{"key":"R44","doi-asserted-by":"crossref","unstructured":"Szczepanska-Konkel M, Yusufi AN, VanScoy M, Webster SK, Dousa TP.Phosphonocarboxylic acids as specific inhibitors of Na+-dependent transport of phosphate across renal brush border membrane.J Biol Chem261: 6375\u20136383, 1986.","DOI":"10.1016\/S0021-9258(19)84572-6"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1210\/endo.139.4.5925"},{"key":"R46","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00252.2003"},{"key":"R47","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1998.275.2.H527"},{"key":"R48","doi-asserted-by":"crossref","unstructured":"Traebert M, Lotscher M, Aschwanden R, Ritthaler T, Biber J, Murer H, Kaissling B.Distribution of the sodium\/phosphate transporter during postnatal ontogeny of the rat kidney.J Am Soc Nephrol10: 1407\u20131415, 1999.","DOI":"10.1681\/ASN.V1071407"},{"key":"R49","doi-asserted-by":"crossref","unstructured":"Vieira FL, Malnic G.Hydrogen ion secretion by rat renal cortical tubules as studied by an antimony microelectrode.Am J Physiol214: 710\u2013718, 1968.","DOI":"10.1152\/ajplegacy.1968.214.4.710"},{"key":"R50","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002703"},{"key":"R51","doi-asserted-by":"publisher","DOI":"10.1161\/ATVBAHA.106.132266"},{"key":"R52","doi-asserted-by":"publisher","DOI":"10.1016\/j.taap.2008.05.026"},{"key":"R53","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00228.2007"},{"key":"R54","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00293.2004"},{"key":"R55","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.00104-07"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.90623.2008","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,9,27]],"date-time":"2021-09-27T12:36:58Z","timestamp":1632746218000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.90623.2008"}},"issued":{"date-parts":[[2009,4]]},"references-count":55,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2009,4]]}},"alternative-id":["10.1152\/ajprenal.90623.2008"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.90623.2008","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2009,4]]}},{"indexed":{"date-parts":[[2026,3,10]],"date-time":"2026-03-10T18:18:31Z","timestamp":1773166711689,"version":"3.50.1"},"reference-count":30,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2010,7]]},"abstract":"<jats:p>Prolactin is a natriuretic hormone and acts by inhibiting the activity of renal tubular Na<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-ATPase activity. These effects require an intact renal dopamine system. Here, we have studied by which mechanism prolactin and dopamine interact in Sprague-Dawley rat renal tissue. Na<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-ATPase activity was measured as ouabain-sensitive ATP hydrolysis in microdissected renal proximal tubular segments. Intracellular signaling pathways were studied by a variety of different techniques, including Western blotting using phosphospecific antibodies, immunoprecipitation, and biotinylation assays. We found that dopamine and prolactin regulated Na<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-ATPase activity via similar signaling pathways, including protein kinase A, protein kinase C, and phosphoinositide 3-kinase activation. The cross talk between prolactin and dopamine 1-like receptors was explained by a heterologous recruitment of dopamine 1-like receptors to the plasma membrane in renal proximal tubular cells. Prolactin had no effect on Na<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-ATPase activity in spontaneously hypertensive rats, a rat strain with a blunted response to dopamine. These results further emphasize the central role of the renal dopamine system in the interactive regulation of renal tubular salt balance.<\/jats:p>","DOI":"10.1152\/ajprenal.00582.2009","type":"journal-article","created":{"date-parts":[[2010,5,13]],"date-time":"2010-05-13T00:55:27Z","timestamp":1273712127000},"page":"F49-F54","source":"Crossref","is-referenced-by-count":23,"title":["Prolactin and dopamine 1-like receptor interaction in renal proximal tubular cells"],"prefix":"10.1152","volume":"299","author":[{"given":"Susanne","family":"Crambert","sequence":"first","affiliation":[{"name":"Pediatric Unit, Department of Women's and Children's Health, Karolinska Institutet, Stockholm, Sweden"}]},{"given":"Agneta","family":"Sj\u00f6berg","sequence":"additional","affiliation":[{"name":"Pediatric Unit, Department of Women's and Children's Health, Karolinska Institutet, Stockholm, Sweden"}]},{"given":"Ann-Christine","family":"Ekl\u00f6f","sequence":"additional","affiliation":[{"name":"Pediatric Unit, Department of Women's and Children's Health, Karolinska Institutet, Stockholm, Sweden"}]},{"given":"Fernando","family":"Ibarra","sequence":"additional","affiliation":[{"name":"Pediatric Unit, Department of Women's and Children's Health, Karolinska Institutet, Stockholm, Sweden"}]},{"given":"Ulla","family":"Holtb\u00e4ck","sequence":"additional","affiliation":[{"name":"Pediatric Unit, Department of Women's and Children's Health, Karolinska Institutet, Stockholm, Sweden"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.252.1.F39"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1979.tb06310.x"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.62.1.621"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.256.2.F370"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1210\/edrv.19.3.0334"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.10.5573"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-201X.2002.00996.x"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1997.273.6.C1981"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.9.5.1209"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.28.17726"},{"key":"B11","doi-asserted-by":"crossref","first-page":"9368","DOI":"10.1016\/S0021-9258(17)37117-X","volume":"269","author":"Fisone G","year":"1994","journal-title":"J Biol Chem"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.2000.80.4.1523"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00318.2001"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.13.7271"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-201x.2000.00661.x"},{"key":"B16","first-page":"739","volume":"8","author":"H\u00fcgl SR","year":"2007","journal-title":"J Pancreas"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00586.x"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-201X.2002.00984.x"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.270.5.F862"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1172\/JCI114371"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-002-0899-5"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(12)80337-4"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005080894"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1210\/en.2006-1577"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1530\/eje.0.1450065"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.268.6.F1185"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1007\/s003600050117"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5001708"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.100128297"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1042\/CS20070018"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00582.2009","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,10,27]],"date-time":"2021-10-27T17:24:55Z","timestamp":1635355495000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00582.2009"}},"issued":{"date-parts":[[2010,7]]},"references-count":30,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2010,7]]}},"alternative-id":["10.1152\/ajprenal.00582.2009"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00582.2009","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2010,7]]}},{"indexed":{"date-parts":[[2026,3,11]],"date-time":"2026-03-11T12:09:07Z","timestamp":1773230947097,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1991,11,1]]},"abstract":"<jats:p> Recent micropuncture studies in rats have demonstrated the existence of oscillatory states in nephron filtration mediated by tubuloglomerular feedback (TGF). We develop a minimal mathematical model of the TGF system, consisting of a first-order hyperbolic partial differential equation describing thick ascending limb (TAL) NaCl reabsorption and an empirical feedback relation. An analytic bifurcation analysis of this model provides fundamental insight into how oscillatory states depend on the physiological parameters of the model. In the special case of no solute backleak in the TAL, the emergence of oscillations explicitly depends on two nondimensional parameters. The first corresponds to the delay time of the TGF response across the juxtaglomerular apparatus, and the second corresponds to the product of the slope of the TGF response curve at the steady-state operating point and the space derivative of the steady-state NaCl concentration profile in the TAL at the macula densa. Numerical calculations for the case without TAL backleak are consistent with this result. Numerical simulation of the more general case with TAL backleak shows that the bifurcation analysis still provides useful predictions concerning nephron dynamics. With typical parameter values, the analysis predicts that the TGF system will be in oscillatory state. However, the system is near enough to the boundary of the nonoscillatory region so that small changes in parameter values could result in nonoscillatory behavior. <\/jats:p>","DOI":"10.1152\/ajprenal.1991.261.5.f904","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T09:17:21Z","timestamp":1514020641000},"page":"F904-F919","source":"Crossref","is-referenced-by-count":48,"title":["Bifurcation analysis of TGF-mediated oscillations in SNGFR"],"prefix":"10.1152","volume":"261","author":[{"given":"H. E.","family":"Layton","sequence":"first","affiliation":[{"name":"Department of Mathematics, Duke University, Durham, North Carolina27706."}]},{"given":"E. B.","family":"Pitman","sequence":"additional","affiliation":[{"name":"Department of Mathematics, Duke University, Durham, North Carolina27706."}]},{"given":"L. C.","family":"Moore","sequence":"additional","affiliation":[{"name":"Department of Mathematics, Duke University, Durham, North Carolina27706."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1991.261.5.F904","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:20:17Z","timestamp":1567974017000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1991.261.5.F904"}},"issued":{"date-parts":[[1991,11,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1991,11,1]]}},"alternative-id":["10.1152\/ajprenal.1991.261.5.F904"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1991.261.5.f904","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1991,11,1]]}},{"indexed":{"date-parts":[[2026,3,11]],"date-time":"2026-03-11T13:52:43Z","timestamp":1773237163478,"version":"3.50.1"},"reference-count":20,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1998,8,1]]},"abstract":"<jats:p> Cerebrospinal fluid (CSF) plays an important role in the brain\u2019s adaptive response to acute osmotic disturbances. In the present experiments, the effect of 48-h dehydration on CSF formation and absorption rates was studied in conscious adult sheep. Animals had cannulas chronically implanted into the lateral cerebral ventricles and cisterna magna to enable the ventriculocisternal perfusion. A 48-h water deprivation altered neither CSF production nor resistance to CSF absorption. However, in the water-depleted sheep, intraventricular pressure tended to be lower than that found under control conditions. This likely resulted from decreased extracellular fluid volume and a subsequent drop in central venous pressure occurring in dehydrated animals. In conclusion, our findings provide evidence for the maintenance of CSF production during mild dehydration, which may play a role in the regulation of fluid balance in the brain during chronic hyperosmotic stress. <\/jats:p>","DOI":"10.1152\/ajprenal.1998.275.2.f235","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T12:17:09Z","timestamp":1514031429000},"page":"F235-F238","source":"Crossref","is-referenced-by-count":5,"title":["Cerebrospinal fluid formation and absorption  in dehydrated sheep"],"prefix":"10.1152","volume":"275","author":[{"given":"Adam","family":"Chodobski","sequence":"first","affiliation":[{"name":"Howard Florey Institute of Experimental Physiology and Medicine, University of Melbourne, Parkville, Victoria 3052, Australia"}]},{"given":"Joanna","family":"Szmydynger-Chodobska","sequence":"additional","affiliation":[{"name":"Howard Florey Institute of Experimental Physiology and Medicine, University of Melbourne, Parkville, Victoria 3052, Australia"}]},{"given":"Michael J.","family":"McKinley","sequence":"additional","affiliation":[{"name":"Howard Florey Institute of Experimental Physiology and Medicine, University of Melbourne, Parkville, Victoria 3052, Australia"}]}],"member":"24","reference":[{"issue":"31","key":"B1","first-page":"R860","volume":"262","author":"Chodobski A.","year":"1992","journal-title":"Am. J. Physiol."},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2736(94)90326-3"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1991.sp018793"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1007\/978-3-642-76226-0_3"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1093\/brain\/91.4.707"},{"issue":"25","key":"B7","first-page":"F1059","volume":"256","author":"DePasquale M.","year":"1989","journal-title":"Am. J. Physiol."},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.63.2.373"},{"issue":"27","key":"B9","first-page":"R94","volume":"258","author":"Faraci F. M.","year":"1990","journal-title":"Am. J. Physiol."},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.me.44.020193.001445"},{"key":"B11","doi-asserted-by":"crossref","first-page":"775","DOI":"10.1152\/ajplegacy.1962.203.5.775","volume":"203","author":"Heisey S. R.","year":"1962","journal-title":"Am. J. Physiol."},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1097\/00001756-199604260-00020"},{"key":"B14","doi-asserted-by":"crossref","first-page":"56","DOI":"10.1152\/ajplegacy.1974.226.1.56","volume":"226","author":"Mouw D. R.","year":"1974","journal-title":"Am. J. Physiol."},{"issue":"20","key":"B15","first-page":"R621","volume":"251","author":"Park R. G.","year":"1986","journal-title":"Am. J. Physiol."},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(90)90874-B"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(92)90731-N"},{"issue":"22","key":"B18","first-page":"F538","volume":"253","author":"Pullen R. G. L.","year":"1987","journal-title":"Am. J. Physiol."},{"issue":"7","key":"B19","first-page":"F42","volume":"238","author":"Rosenberg G. A.","year":"1980","journal-title":"Am. J. Physiol."},{"issue":"20","key":"B20","first-page":"R197","volume":"251","author":"Somero G. N.","year":"1986","journal-title":"Am. J. Physiol."},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-4159.1993.tb13428.x"},{"issue":"13","key":"B22","first-page":"H239","volume":"244","author":"Wiig H","year":"1983","journal-title":"Am. J. Physiol."}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1998.275.2.F235","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T17:21:51Z","timestamp":1567963311000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1998.275.2.F235"}},"issued":{"date-parts":[[1998,8,1]]},"references-count":20,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1998,8,1]]}},"alternative-id":["10.1152\/ajprenal.1998.275.2.F235"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1998.275.2.f235","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1998,8,1]]}},{"indexed":{"date-parts":[[2026,3,9]],"date-time":"2026-03-09T09:19:07Z","timestamp":1773047947417,"version":"3.50.1"},"reference-count":32,"publisher":"American Physiological Society","issue":"5","funder":[{"DOI":"10.13039\/501100012166","name":"National Key Research and Development Program of China","doi-asserted-by":"publisher","award":["2020YFC2005000"],"award-info":[{"award-number":["2020YFC2005000"]}],"id":[{"id":"10.13039\/501100012166","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100007620","name":"Department of Education of Liaoning Province","doi-asserted-by":"publisher","award":["507123"],"award-info":[{"award-number":["507123"]}],"id":[{"id":"10.13039\/501100007620","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Dalian Young Star of Science and Technology","award":["2019RQ116"],"award-info":[{"award-number":["2019RQ116"]}]},{"name":"Liaoning BaiQianWan Talents Program"},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81970606"],"award-info":[{"award-number":["81970606"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81970595"],"award-info":[{"award-number":["81970595"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2021,11,1]]},"abstract":"<jats:p> In the present study, we found that alisol B 23-acetate (ABA), an identified natural farnesoid X receptor (FXR) agonist from the well-known traditional Chinese medicine Alismatis rhizoma, protects against ischemic acute kidney injury (AKI) in an FXR-dependent manner, as reflected by improved renal function, reduced renal tubular apoptosis, ameliorated oxidative stress, and suppressed inflammatory factor expression. Therefore, ABA may have great potential as a novel therapeutic agent in the treatment of AKI in the future. <\/jats:p>","DOI":"10.1152\/ajprenal.00193.2021","type":"journal-article","created":{"date-parts":[[2021,9,27]],"date-time":"2021-09-27T07:13:01Z","timestamp":1632726781000},"page":"F617-F628","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":24,"title":["A naturally occurring FXR agonist, alisol B 23-acetate, protects against renal ischemia-reperfusion injury"],"prefix":"10.1152","volume":"321","author":[{"given":"Zhi-Lin","family":"Luan","sequence":"first","affiliation":[{"name":"Advanced Institute for Medical Sciences, Dalian Medical University, Dalian, People\u2019s Republic of China"},{"name":"Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Dalian Medical University, Dalian, People\u2019s Republic of China"},{"name":"Dalian Key Laboratory for Nuclear Receptors in Major Metabolic Diseases, Dalian, People\u2019s Republic of China"}]},{"given":"Wen-Hua","family":"Ming","sequence":"additional","affiliation":[{"name":"Advanced Institute for Medical Sciences, Dalian Medical University, Dalian, People\u2019s Republic of China"}]},{"given":"Xiao-Wan","family":"Sun","sequence":"additional","affiliation":[{"name":"Advanced Institute for Medical Sciences, Dalian Medical University, Dalian, People\u2019s Republic of China"}]},{"given":"Cong","family":"Zhang","sequence":"additional","affiliation":[{"name":"Advanced Institute for Medical Sciences, Dalian Medical University, Dalian, People\u2019s Republic of China"}]},{"given":"Yang","family":"Zhou","sequence":"additional","affiliation":[{"name":"Advanced Institute for Medical Sciences, Dalian Medical University, Dalian, People\u2019s Republic of China"}]},{"given":"Feng","family":"Zheng","sequence":"additional","affiliation":[{"name":"Advanced Institute for Medical Sciences, Dalian Medical University, Dalian, People\u2019s Republic of China"},{"name":"Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Dalian Medical University, Dalian, People\u2019s Republic of China"},{"name":"Dalian Key Laboratory for Nuclear Receptors in Major Metabolic Diseases, Dalian, People\u2019s Republic of China"}]},{"given":"Yong-Liang","family":"Yang","sequence":"additional","affiliation":[{"name":"Center for Molecular Medicine, School of Life Science and Biotechnology, Dalian University of Technology, Dalian, People\u2019s Republic of China"}]},{"given":"You-Fei","family":"Guan","sequence":"additional","affiliation":[{"name":"Advanced Institute for Medical Sciences, Dalian Medical University, Dalian, People\u2019s Republic of China"},{"name":"Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Dalian Medical University, Dalian, People\u2019s Republic of China"},{"name":"Dalian Key Laboratory for Nuclear Receptors in Major Metabolic Diseases, Dalian, People\u2019s Republic of China"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4060-2423","authenticated-orcid":true,"given":"Xiao-Yan","family":"Zhang","sequence":"additional","affiliation":[{"name":"Health Science Center, East China Normal University, Shanghai, People\u2019s Republic of China"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2017.2"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2016010105"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2015.85"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(19)32563-2"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1038\/s41581-018-0052-0"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009060636"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1159\/000437352"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1007\/s40620-020-00793-2"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.12861\/jrip.2015.06"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/j.mam.2020.100935"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1126\/science.284.5418.1362"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.3390\/ijms17071105"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1038\/cr.2008.289"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/s0092-8674(00)00062-3"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1172\/JCI25604"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1053\/j.gastro.2017.01.014"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1136\/gut.2010.212159"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1323977111"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1803945115"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.2337\/db10-0019"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.2337\/db06-1642"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M115.694323"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1038\/srep37234"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-017-10168-6"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.3389\/fphar.2018.00053"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.19540\/j.cnki.cjcmm.20190616.201"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.3109\/0886022X.2012.723582"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.23876\/j.krcp.19.062"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra032401"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2008.11.034"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.02140215"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.2174\/0929867323666160112122858"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00193.2021","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,10,25]],"date-time":"2021-10-25T12:45:24Z","timestamp":1635165924000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00193.2021"}},"issued":{"date-parts":[[2021,11,1]]},"references-count":32,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2021,11,1]]}},"alternative-id":["10.1152\/ajprenal.00193.2021"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00193.2021","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2021,11,1]]},"assertion":[{"value":"2021-05-19","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2021-09-21","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2021-10-20","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,3,7]],"date-time":"2026-03-07T15:25:50Z","timestamp":1772897150162,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1991,7,1]]},"abstract":"<jats:p> We report the localization of insulin-like growth factor I (IGF-I) and a 25-kDa form of insulin-like growth factor-binding protein (IGF-BP-1) in adult rat kidney. The antigens were localized using a rabbit anti-human IGF-I antibody, and a rabbit anti-human IGF-BP-1 antibody raised against human 25-kDa IGF-BP-1 purified from amniotic fluid. Immunohistochemistry by the avidin-biotin peroxidase conjugate technique showed that both peptides are located in the same nephron segments, in the same cell types. The most intense staining was in papillary collecting ducts. There was moderate staining also in cortical collecting ducts and medullary thick ascending limbs of Henle's loop. In collecting ducts the antigens were shown to be present in principal cells but not in intercalated cells. In distal convoluted tubules, cortical thick ascending limbs, and in structures presumptively identified as thin limbs of Henle's loops there was only modest staining. The macula densa, however, lacked immunoreactivity. Colocalization of IGF-I and IGF-BP-1 in the same cells supports the notion, derived from studies on cultured cells, that the actions of IGF-I may be modified by IGF-BPs that are present in the same location. <\/jats:p>","DOI":"10.1152\/ajprenal.1991.261.1.f22","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T18:39:32Z","timestamp":1513967972000},"page":"F22-F28","source":"Crossref","is-referenced-by-count":2,"title":["Colocalization of insulin-like growth factor-binding protein with insulin-like growth factor I"],"prefix":"10.1152","volume":"261","author":[{"given":"S.","family":"Kobayashi","sequence":"first","affiliation":[{"name":"Department of Pathology, University of Texas Health Science Center, San Antonio 78284-\u20137750."}]},{"given":"D. R.","family":"Clemmons","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Texas Health Science Center, San Antonio 78284-\u20137750."}]},{"given":"M. A.","family":"Venkatachalam","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Texas Health Science Center, San Antonio 78284-\u20137750."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1991.261.1.F22","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:25:25Z","timestamp":1567956325000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1991.261.1.F22"}},"issued":{"date-parts":[[1991,7,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1991,7,1]]}},"alternative-id":["10.1152\/ajprenal.1991.261.1.F22"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1991.261.1.f22","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1991,7,1]]}},{"indexed":{"date-parts":[[2026,3,8]],"date-time":"2026-03-08T22:24:23Z","timestamp":1773008663925,"version":"3.50.1"},"reference-count":91,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2008,9]]},"abstract":"<jats:p> Hyponatremia is the most common electrolyte abnormality in hospitalized patients. When symptomatic (hyponatremic encephalopathy), the overall morbidity is 34%. Individuals most susceptible to death or permanent brain damage are prepubescent children and menstruant women. Failure of the brain to adapt to the hyponatremia leads to brain damage. Major factors that can impair brain adaptation include hypoxia and peptide hormones. In children, physical factors\u2014discrepancy between skull size and brain size\u2014are important in the genesis of brain damage. In adults, certain hormones\u2014estrogen and vasopressin (usually elevated in cases of hyponatremia)\u2014have been shown to impair brain adaptation, decreasing both cerebral blood flow and oxygen utilization. Initially, hyponatremia leads to an influx of water into the brain, primarily through glial cells and largely via the water channel aquaporin (AQP)4. Water is thus shunted into astrocytes, which swell, largely preserving neuronal cell volume. The initial brain response to swelling is adaptation, utilizing the Na<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-ATPase system to extrude cellular Na<jats:sup>+<\/jats:sup>. In menstruant women, estrogen + vasopressin inhibits the Na<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-ATPase system and decreases cerebral oxygen utilization, impairing brain adaptation. Cerebral edema compresses the respiratory centers and also forces blood out of the brain, both lowering arterial Po<jats:sub>2<\/jats:sub> and decreasing oxygen utilization. The hypoxemia further impairs brain adaptation. Hyponatremic encephalopathy leads to brain damage when brain adaptation is impaired and is a consequence of both cerebral hypoxia and peptide hormones. <\/jats:p>","DOI":"10.1152\/ajprenal.00502.2007","type":"journal-article","created":{"date-parts":[[2008,5,1]],"date-time":"2008-05-01T01:07:09Z","timestamp":1209604029000},"page":"F619-F624","source":"Crossref","is-referenced-by-count":195,"title":["Brain cell volume regulation in hyponatremia: role of sex, age, vasopressin, and hypoxia"],"prefix":"10.1152","volume":"295","author":[{"given":"Juan Carlos","family":"Ayus","sequence":"first","affiliation":[]},{"given":"Steven G.","family":"Achinger","sequence":"additional","affiliation":[]},{"given":"Allen","family":"Arieff","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1038\/nrn1824"},{"key":"R2","unstructured":"Achinger SG, Ayus JC. Fluid and electrolytes. In: Critical Care (4th ed.), edited by Civetta D, Taylor A, Kirby JM. Philadelphia, PA: Lippincott, 2006."},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.256.1.F113"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.265.4.F463"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1990.258.4.R924"},{"key":"R6","doi-asserted-by":"crossref","unstructured":"Amiry-Moghaddam M, Ottersen OP. The molecular basis of water transport in the brain. Nat Rev Neurosci 12: 991\u20131001, 2003.","DOI":"10.1038\/nrn1252"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1677\/joe.0.0930319"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM198606123142401"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1016\/j.amjmed.2006.05.009"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1001\/jama.1993.03510100080037"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1136\/bmj.304.6836.1218"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1995.268.5.R1143"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1542\/peds.103.6.1292"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1212\/WNL.46.2.323"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1001\/jama.281.24.2299"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1001\/archinte.1997.00440230101013"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1378\/chest.107.2.517"},{"key":"R18","doi-asserted-by":"crossref","unstructured":"Ayus JC, Armstrong DL, Arieff AI. Effects of hypernatraemia in the central nervous system and its therapy in rats and rabbits. J Physiol 492.1: 243\u2013255, 1996.","DOI":"10.1113\/jphysiol.1996.sp021305"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000187"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.257.1.F18"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM198711053171905"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1985.248.5.F711"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-132-9-200005020-00005"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-117-11-891"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.1986.250.4.E352"},{"key":"R27","unstructured":"Betz AL. Transport of ions across the blood-brain barrier. Fed Proc 45: 2050\u20132054, 1986."},{"key":"R28","unstructured":"Bradbury MWB. The structure and function of the blood-brain barrier. Fed Proc 43: 186\u2013190, 1984."},{"key":"R29","unstructured":"Bradley EL, Etheridge MS, Arieff AI. Causes of brain damage in patients with severe symptomatic hyponatremia: analysis of 344 patients over 30 years (Abstract). J Am Soc Nephrol 16: 44A, 2005."},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1007\/s10549-005-9053-3"},{"key":"R32","unstructured":"Cheong JL, Cady EB, Penrice J, Wyatt JS, Cox IJ, Robertson NJ. Proton MR spectroscopy in neonates with perinatal cerebral hypoxic-ischemic injury. Am J Neuroradiol 27: 1546\u20131554, 2006."},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.256.6.F1059"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1002\/ana.410040410"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(87)91502-2"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1097\/00004424-199105000-00022"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1990.258.1.R94"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.281.4.F674"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9343(96)00274-4"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1989.256.4.R880"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.1989.257.2.E284"},{"key":"R42","doi-asserted-by":"crossref","unstructured":"Fraser CL, Swanson RA. Female sex hormones inhibit volume regulation in rat brain astrocyte culture. Am J Physiol Cell Physiol 267: C909\u2013C914, 1994.","DOI":"10.1152\/ajpcell.1994.267.4.C909"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0605796103"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1016\/0024-3205(92)90459-3"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1016\/j.ijdevneu.2006.05.003"},{"key":"R46","unstructured":"Griggs RC, Arieff AI. Hypoxia and the central nervous system. In: Metabolic Brain Dysfunction in Systemic Disorders, edited by Griggs RC, Arieff AI. Boston, MA: Little, Brown, 1992, p. 39\u201354."},{"key":"R47","doi-asserted-by":"publisher","DOI":"10.1016\/0304-3940(87)90568-4"},{"key":"R48","doi-asserted-by":"publisher","DOI":"10.1136\/bmj.322.7289.780"},{"key":"R49","doi-asserted-by":"publisher","DOI":"10.1016\/S0074-7742(08)60035-5"},{"key":"R50","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.93.18.9493"},{"key":"R51","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfi082"},{"key":"R52","doi-asserted-by":"publisher","DOI":"10.1038\/325253a0"},{"key":"R53","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1994.266.4.R1169"},{"key":"R54","doi-asserted-by":"publisher","DOI":"10.1001\/archpedi.1991.02160090037018"},{"key":"R55","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M701411200"},{"key":"R56","unstructured":"Kimelberg HK. Swelling and volume control in brain astroglial cells. In: Advances in Comparative and Environmental Physiology Series, edited by Gilles R. Heidelberg, Germany: Springer, 1991, p. 81\u2013110."},{"key":"R57","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.76.4.551"},{"key":"R58","unstructured":"Kucharczyk J, Fraser CL, Arieff AI. Central nervous system manifestations of hyponatremia. In: Metabolic Brain Dysfunction in Systemic Disorders (1st ed.), edited by Griggs R, Arieff AI. Boston, MA: Little, Brown, 1992, p. 55\u201386."},{"key":"R59","unstructured":"Lang F, Busch GL, Volkl H, Haussinger D. Cell volume: a second message in regulation of cellular function. News Physiol Sci 10: 18\u201322, 1995."},{"key":"R60","doi-asserted-by":"publisher","DOI":"10.1172\/JCI114587"},{"key":"R61","doi-asserted-by":"publisher","DOI":"10.1038\/310061a0"},{"key":"R62","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.57.1.1"},{"key":"R63","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.252.4.F661"},{"key":"R63A","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfg394"},{"key":"R64","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.90.15.7275"},{"key":"R65","unstructured":"Nzerue CM, Baffoe-Bonnie H, You W, Falana B, Dai S. Predictors of outcome in hospitalized patients with severe hyponatremia. J Natl Med Assoc 95: 335\u2013343, 2003."},{"key":"R66","doi-asserted-by":"publisher","DOI":"10.1172\/JCI114830"},{"key":"R67","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.1041280211"},{"key":"R69","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-006-0411-0"},{"key":"R70","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1993.265.5.C1191"},{"key":"R71","doi-asserted-by":"publisher","DOI":"10.1016\/j.amjmed.2006.05.002"},{"key":"R72","doi-asserted-by":"publisher","DOI":"10.1126\/science.3616619"},{"key":"R73","unstructured":"Rollin C, Arieff A, Fraser C, Kucharczyk J, Norman D, Sarnacki P. Gonadal steroid effects on ATP-stimulated sodium transport in pig brain synaptosomes (Abstract). Soc Neurosci Abstr 13: 22.26, 1987."},{"key":"R74","unstructured":"Rosenberg GA, Estrada E, Kyner WT. Vasopressin-induced brain edema is mediated by the V1 receptor. Adv Neurol 52: 149\u2013154, 1990."},{"key":"R75","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.1999.276.3.E596"},{"key":"R76","unstructured":"Sarrel PM, Lufkin EG, Oursler MJ, Keefe D. Estrogen actions in arteries, bone, and brain. Sci Am Sci Med 1: 44\u201353, 1994."},{"key":"R77","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.1988.254.5.G687"},{"key":"R78","doi-asserted-by":"publisher","DOI":"10.1148\/radiology.185.3.1438745"},{"key":"R79","doi-asserted-by":"publisher","DOI":"10.1212\/WNL.18.2.127"},{"key":"R80","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuroscience.2004.09.053"},{"key":"R81","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2006.12.040"},{"key":"R82","doi-asserted-by":"publisher","DOI":"10.1007\/3-211-30714-1_82"},{"key":"R83","doi-asserted-by":"publisher","DOI":"10.1016\/0002-9343(92)90748-Z"},{"key":"R84","unstructured":"Van Bree JB, de Boer AG, Verhoef JC, Danhof M, Breimer DD. Transport of vasopressin fragments across the blood-brain barrier: in vitro studies using monolayer cultures of bovine brain endothelial cells. J Pharmacol Exp Ther 249: 901\u2013905, 1989."},{"key":"R85","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-199307000-00015"},{"key":"R86","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(91)90806-7"},{"key":"R87","doi-asserted-by":"publisher","DOI":"10.1172\/JCI116953"},{"key":"R88","unstructured":"Vexler ZS, Roberts TPL, Kucharczyk J, Arieff AI. Severe brain edema associated with cumulative effects of hyponatremic encephalopathy and ischemic hypoxia. In: Brain Edema IX, edited by Ito U, Baethmann A, Hossman KA, Kuroiwa T, Marmarou A, Reulen HJ, Takakura K. Vienna: Springer, 1994, p. 246\u2013249."},{"key":"R89","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117728"},{"key":"R90","unstructured":"Vieweg WVR. Special topics in water balance in schizophrenia. In: Water Balance in Schizophrenia, edited by Schnur DB and Kirch DG. Arlington, VA: American Psychiatric Press, 1996, p. 43\u201352."},{"key":"R91","doi-asserted-by":"publisher","DOI":"10.1042\/bj0770030"},{"key":"R92","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M603917200"},{"key":"R93","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2736(90)90097-8"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00502.2007","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T22:45:00Z","timestamp":1567982700000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00502.2007"}},"issued":{"date-parts":[[2008,9]]},"references-count":91,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2008,9]]}},"alternative-id":["10.1152\/ajprenal.00502.2007"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00502.2007","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2008,9]]}},{"indexed":{"date-parts":[[2026,3,24]],"date-time":"2026-03-24T04:04:43Z","timestamp":1774325083004,"version":"3.50.1"},"reference-count":38,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1997,11,1]]},"abstract":"<jats:p> Renal juxtaglomerular (JG) cells are specialized myoepithelioid cells located in the afferent arteriole at the entrance to the glomerulus. Their main function and distinctive feature is the synthesis and release of renin, the key hormone-enzyme of the renin-angiotensin system that regulates arterial blood pressure. Despite their relevance to health and disease, not much is known about factors that confer and\/or maintain JG cell identity. To identify genes uniquely expressed in JG cells, we used a cell culture model and RNA differential display. JG cells cultured for 2 days express renin and renin mRNA, but after 10 days in culture they no longer contain or release renin and renin mRNA is reduced 700-fold. We report one cDNA differentially expressed in the 2-day JG cell culture that detects a 2.6-kb mRNA expressed at higher levels in newborn than adult kidney. Screening a 2-day culture JG cell cDNA library yielded clones representing differentially spliced transcripts. These cDNAs encode one unique protein (Zis) containing zinc fingers and domains characteristic of splicing factors and RNA binding proteins. Northern blot analysis confirmed Zis mRNA expression in differentiated JG cells, and identified an additional unique 1.5-kb transcript. The Zis transcripts are developmentally regulated in kidney and a number of other organs. The features of the Zis protein and its organ distribution suggest a possible role in regulation of transcription and\/or splicing, both important steps for controlling developmentally expressed genes. <\/jats:p>","DOI":"10.1152\/ajprenal.1997.273.5.f731","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T09:37:38Z","timestamp":1514021858000},"page":"F731-F738","source":"Crossref","is-referenced-by-count":25,"title":["Zis: a developmentally regulated gene expressed in juxtaglomerular cells"],"prefix":"10.1152","volume":"273","author":[{"given":"Elena A.","family":"Karginova","sequence":"first","affiliation":[{"name":"Departments of Pediatrics and Internal Medicine, University of Virginia Health Sciences Center, Charlottesville, Virginia 22908"}]},{"given":"Ellen Steward","family":"Pentz","sequence":"additional","affiliation":[{"name":"Departments of Pediatrics and Internal Medicine, University of Virginia Health Sciences Center, Charlottesville, Virginia 22908"}]},{"given":"Irina G.","family":"Kazakova","sequence":"additional","affiliation":[{"name":"Departments of Pediatrics and Internal Medicine, University of Virginia Health Sciences Center, Charlottesville, Virginia 22908"}]},{"given":"Victoria F.","family":"Norwood","sequence":"additional","affiliation":[{"name":"Departments of Pediatrics and Internal Medicine, University of Virginia Health Sciences Center, Charlottesville, Virginia 22908"}]},{"given":"Robert M.","family":"Carey","sequence":"additional","affiliation":[{"name":"Departments of Pediatrics and Internal Medicine, University of Virginia Health Sciences Center, Charlottesville, Virginia 22908"}]},{"given":"R. Ariel","family":"Gomez","sequence":"additional","affiliation":[{"name":"Departments of Pediatrics and Internal Medicine, University of Virginia Health Sciences Center, Charlottesville, Virginia 22908"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.90.2.542"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/0378-1119(95)00571-4"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1101\/gad.3.4.431"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.84.16.5605"},{"issue":"27","key":"B6","first-page":"F649","volume":"258","author":"Carey R. M.","year":"1990","journal-title":"Am. J. Physiol."},{"key":"B7","first-page":"532","volume":"15","author":"Chomczynski P.","year":"1993","journal-title":"Biotechniques"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.81.7.1991"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.10.7.3376"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1038\/363640a0"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1038\/359162a0"},{"key":"B12","first-page":"13","volume":"186","author":"Delius H.","year":"1994","journal-title":"Curr. Top. Microbiol. Immunol."},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1016\/0003-2697(83)90418-9"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(93)80749-K"},{"issue":"28","key":"B15","first-page":"F660","volume":"259","author":"Gomez R. A.","year":"1990","journal-title":"Am. J. Physiol."},{"issue":"23","key":"B16","first-page":"F900","volume":"254","author":"Gomez R. A.","year":"1988","journal-title":"Am. J. Physiol."},{"issue":"26","key":"B17","first-page":"F850","volume":"257","author":"Gomez R. A.","year":"1989","journal-title":"Am. J. Physiol."},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.17.4.469"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.15.8.4562"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.10.5.488"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1038\/348257a0"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/12.2.857"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.115.4.887"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.83.13.4769"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1177\/33.4.3884706"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/21.14.3269"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1126\/science.1354393"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.89.4.1301"},{"key":"B29","first-page":"545","volume":"5","author":"McGrath E. M.","year":"1994","journal-title":"J. Am. Soc. Nephrol."},{"key":"B30","first-page":"2","volume":"154","author":"Okayama H.","year":"1987","journal-title":"Methods Enzymol."},{"key":"B31","first-page":"162","volume":"6","author":"Oste C.","year":"1988","journal-title":"Biotechniques"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.74.12.5463"},{"key":"B34","first-page":"1079","volume":"2","author":"Sealey J. E.","year":"1977","journal-title":"Cardiovasc. Med."},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.ge.23.120189.002523"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/12.1Part2.505"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.118.5.991"},{"issue":"35","key":"B39","first-page":"F911","volume":"266","author":"Tufro-McReddie A.","year":"1994","journal-title":"Am. J. Physiol."},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1016\/0022-2836(87)90688-7"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1101\/gad.6.5.837"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1997.273.5.F731","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T17:04:22Z","timestamp":1567962262000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1997.273.5.F731"}},"issued":{"date-parts":[[1997,11,1]]},"references-count":38,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1997,11,1]]}},"alternative-id":["10.1152\/ajprenal.1997.273.5.F731"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1997.273.5.f731","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1997,11,1]]}},{"indexed":{"date-parts":[[2026,3,24]],"date-time":"2026-03-24T04:04:46Z","timestamp":1774325086306,"version":"3.50.1"},"reference-count":32,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2002,10,1]]},"abstract":"<jats:p>To test the role of epithelial Na channels in the day-to-day regulation of renal Na excretion, rats were infused via osmotic minipumps with the Na channel blocker amiloride at rates that achieved drug concentrations of 2\u20135 \u03bcM in the lumen of the distal nephron. Daily Na excretion rates were unchanged, although amiloride-treated animals tended to excrete more Na in the afternoon and less in the late evening than controls. When the rats were given a low-Na diet, Na excretion rates were elevated in the amiloride-treated group within 4 h and remained higher than controls for at least 48 h. Adrenalectomized animals responded similarly to the low-Na diet. In contrast, rats infused with polythiazide at rates designed to inhibit NaCl transport in the distal tubule were able to conserve Na as well as did the controls. Injection of aldosterone (2 \u03bcg\/100 g body wt) decreased Na excretion in control animals after a 1-h delay. This effect was largely abolished in amiloride-treated rats. On the basis of quantitative analysis of the results, we conclude that activation of amiloride-sensitive channels by mineralocorticoids accounts for 50\u201380% of the immediate natriuretic response of the kidney to a reduction in Na intake. Furthermore, the channels are necessary to achieve minimal rates of Na excretion during more chronic Na deprivation.<\/jats:p>","DOI":"10.1152\/ajprenal.00379.2001","type":"journal-article","created":{"date-parts":[[2013,8,19]],"date-time":"2013-08-19T19:58:09Z","timestamp":1376942289000},"page":"F717-F726","source":"Crossref","is-referenced-by-count":33,"title":["Epithelial Na channels and short-term renal response to salt deprivation"],"prefix":"10.1152","volume":"283","author":[{"given":"Gustavo","family":"Frindt","sequence":"first","affiliation":[{"name":"Department of Physiology and Biophysics, Weill Medical College of Cornell University, New York, New York 10021"}]},{"given":"Tiffany","family":"McNair","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, Weill Medical College of Cornell University, New York, New York 10021"}]},{"given":"Anke","family":"Dahlmann","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, Weill Medical College of Cornell University, New York, New York 10021"}]},{"given":"Emily","family":"Jacobs-Palmer","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, Weill Medical College of Cornell University, New York, New York 10021"}]},{"given":"Lawrence G.","family":"Palmer","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, Weill Medical College of Cornell University, New York, New York 10021"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"crossref","first-page":"472","DOI":"10.1016\/S0022-3565(25)27727-8","volume":"157","author":"Baer JE","year":"1967","journal-title":"J Pharmacol Exp Ther"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1982.242.3.C131"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1038\/ng0396-248"},{"key":"B4","doi-asserted-by":"crossref","first-page":"91","DOI":"10.1681\/ASN.V1191","volume":"1","author":"Chen Z","year":"1990","journal-title":"J Am Soc Nephrol"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1007\/BF01953312"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.15.5.451"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1159\/000181544"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.60.1.179"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.1.F112"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.90.7.2749"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1966.sp007954"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1016\/0009-8981(73)90466-X"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1988.254.6.R1001"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1038\/ng0396-325"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.24.14552"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1007\/BF01871102"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1985.54"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.1.F161"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.84.5.1464"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.6.F900"},{"key":"B22","first-page":"38A","volume":"12","author":"Oh YK","year":"2001","journal-title":"J Am Soc Nephrol"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.35.2.550"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.102.1.25"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1007\/978-3-642-79565-7_10"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1172\/JCI112433"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.2000.80.1.277"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(94)90250-X"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1038\/ng0696-248"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1172\/JCI111935"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1046\/j.1440-1681.2000.03204.x"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.1.F143"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00728.x"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00379.2001","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,4,30]],"date-time":"2025-04-30T14:00:02Z","timestamp":1746021602000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00379.2001"}},"issued":{"date-parts":[[2002,10,1]]},"references-count":32,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2002,10,1]]}},"alternative-id":["10.1152\/ajprenal.00379.2001"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00379.2001","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2002,10,1]]}},{"indexed":{"date-parts":[[2026,3,28]],"date-time":"2026-03-28T04:49:01Z","timestamp":1774673341235,"version":"3.50.1"},"reference-count":60,"publisher":"American Physiological Society","issue":"4","funder":[{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)","doi-asserted-by":"publisher","award":["R01 DK059600"],"award-info":[{"award-number":["R01 DK059600"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)","doi-asserted-by":"publisher","award":["P30 DK079337"],"award-info":[{"award-number":["P30 DK079337"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)","doi-asserted-by":"publisher","award":["F31 DK115169-01"],"award-info":[{"award-number":["F31 DK115169-01"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2018,10,1]]},"abstract":"<jats:p>\n                    Chronic kidney disease (CKD) is a condition with significant morbidity and mortality that affects 15% of adults in the United States. One cause of CKD is acute kidney injury (AKI), which commonly occurs secondary to sepsis, ischemic events, and drug-induced nephrotoxicity. Unilateral ischemia-reperfusion injury (UIRI) without contralateral nephrectomy (CLN) and repeated low-dose cisplatin (RLDC) models of AKI to CKD demonstrate responses characteristic of the transition; however, previous studies have not effectively compared the pathogenesis. We demonstrate both models instigate renal dysfunction, inflammatory cytokine responses, and fibrosis. However, the models exhibit differences in urinary excretory function, inflammatory cell infiltration, and degree of fibrotic response. UIRI without CLN demonstrated worsening perfusion and function, measured with\n                    <jats:sup>99m<\/jats:sup>\n                    Tc-mercaptoacetyltriglycine-3 imaging, and physiologic compensation in the contralateral kidney. Furthermore, UIRI without CLN elicited a robust inflammatory response that was characterized by a prolonged polymorphonuclear cell and natural killer cell infiltrate and an early expansion of kidney resident macrophages, followed by T-cell infiltration. Symmetrical diminished function occurred in RLDC kidneys and progressively worsened until day 17 of the study. Surprisingly, RLDC mice demonstrated a decrease in inflammatory cell numbers relative to controls. However, RLDC kidneys expressed increased levels of kidney injury molecule-1 (KIM-1), high mobility group box-1 ( HMGB1), and colony stimulating factor-1 ( CSF-1), which likely recruits inflammatory cells in response to injury. These data emphasize how the divergent etiologies of AKI to CKD models affect the kidney microenvironment and outcomes. This study provides support for subtyping AKI by etiology in human studies, aiding in the elucidation of injury-specific pathophysiologic mechanisms of the AKI to CKD transition.\n                  <\/jats:p>","DOI":"10.1152\/ajprenal.00179.2018","type":"journal-article","created":{"date-parts":[[2018,6,13]],"date-time":"2018-06-13T11:35:39Z","timestamp":1528889739000},"page":"F1107-F1118","source":"Crossref","is-referenced-by-count":75,"title":["Divergent effects of AKI to CKD models on inflammation and fibrosis"],"prefix":"10.1152","volume":"315","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3273-9849","authenticated-orcid":false,"given":"L. M.","family":"Black","sequence":"first","affiliation":[{"name":"Nephrology Research and Training Center, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4182-1545","authenticated-orcid":false,"given":"J. M.","family":"Lever","sequence":"additional","affiliation":[{"name":"Nephrology Research and Training Center, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama"}]},{"given":"A. M.","family":"Traylor","sequence":"additional","affiliation":[{"name":"Nephrology Research and Training Center, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama"}]},{"given":"B.","family":"Chen","sequence":"additional","affiliation":[{"name":"Nephrology Research and Training Center, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama"}]},{"given":"Z.","family":"Yang","sequence":"additional","affiliation":[{"name":"Nephrology Research and Training Center, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama"}]},{"given":"S. K.","family":"Esman","sequence":"additional","affiliation":[{"name":"Nephrology Research and Training Center, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama"}]},{"given":"Y.","family":"Jiang","sequence":"additional","affiliation":[{"name":"Nephrology Research and Training Center, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama"}]},{"given":"G. R.","family":"Cutter","sequence":"additional","affiliation":[{"name":"Department of Biostatistics, University of Alabama at Birmingham, Birmingham, Alabama"}]},{"given":"R.","family":"Boddu","sequence":"additional","affiliation":[{"name":"Nephrology Research and Training Center, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama"}]},{"given":"J. F.","family":"George","sequence":"additional","affiliation":[{"name":"Nephrology Research and Training Center, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama"},{"name":"Department of Surgery, University of Alabama at Birmingham, Birmingham, Alabama"}]},{"given":"A.","family":"Agarwal","sequence":"additional","affiliation":[{"name":"Nephrology Research and Training Center, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama"},{"name":"Department of Veterans Affairs, Birmingham, Alabama"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.13111215"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1007\/s10753-014-9953-7"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1111\/apha.12914"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00546.2010"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1007\/s11096-013-9912-7"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00049.2017"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00335.2015"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1136\/bmj.1.4185.427"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra1214243"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00164.2016"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0070464"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1080\/01926230601187430"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejphar.2014.07.025"},{"key":"B15","doi-asserted-by":"crossref","first-page":"551","DOI":"10.1016\/S0022-3565(25)32105-1","volume":"213","author":"Dobyan DC","year":"1980","journal-title":"J Pharmacol Exp Ther"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1002\/14651858.CD003374.pub4"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2015020204"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1111\/nep.12363"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00369.2016"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/j.matbio.2018.02.006"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002447"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1002\/mpo.2950180105"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0158765"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-011-1992-9"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1146\/annurev-physiol-022516-034219"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014060612"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014080770"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1146\/annurev-physiol-022516-034227"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.3892\/or.2014.3202"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007111182"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.08070715"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0152153"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009060615"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1038\/labinvest.2017.130"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2013.153"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1038\/srep23975"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.500"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1172\/jci.insight.94716"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.3390\/toxins2112490"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2014.294"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1200\/JCO.1992.10.9.1460"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1989.118"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1155\/2016\/6232909"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1177\/019262338601400106"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00083.2007"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1159\/000314656"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1007\/BF00685091"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1016\/j.pharmthera.2012.07.003"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2011.31"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00279.2012"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00512.2015"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00636.2017"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1177\/0960327110377521"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1053\/j.semnuclmed.2010.09.003"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1634\/theoncologist.2017-0015"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002033"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2017.119"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00431.2011"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010050484"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007090982"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1172\/JCI60363"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00179.2018","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,7,4]],"date-time":"2025-07-04T23:20:46Z","timestamp":1751671246000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00179.2018"}},"issued":{"date-parts":[[2018,10,1]]},"references-count":60,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2018,10,1]]}},"alternative-id":["10.1152\/ajprenal.00179.2018"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00179.2018","relation":{"has-review":[{"id-type":"doi","id":"10.3410\/f.733445233.793547723","asserted-by":"object"}]},"ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2018,10,1]]}},{"indexed":{"date-parts":[[2026,3,29]],"date-time":"2026-03-29T12:52:59Z","timestamp":1774788779157,"version":"3.50.1"},"reference-count":42,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2007,7]]},"abstract":"<jats:p> Since epoxyeicosatrienoic acids (EETs) affect sodium reabsorption in renal tubules and dilate the renal vasculature, we have examined their effects on renal hemodynamics and sodium balance in male rats fed a high-fat (HF) diet by fenofibrate, a peroxisome proliferator-activated receptor-\u03b1 (PPAR-\u03b1) agonist and an inducer of cytochrome P-450 (CYP) epoxygenases; by N-methanesulfonyl-6-(2-proparyloxyphenyl)hexanamide (MSPPOH), a selective EET biosynthesis inhibitor; and by 12-(3-adamantane-1-yl-ureido)dodecanoic acid (AUDA), a selective inhibitor of soluble epoxide hydrolase. In rats treated with fenofibrate (30 mg\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7day<jats:sup>\u22121<\/jats:sup> ig) or AUDA (50 mg\/l in drinking water) for 2 wk, mean arterial pressure, renal vascular resistance, and glomerular filtration rate were lower but renal blood flow was higher than in vehicle-treated control rats. In addition, fenofibrate and AUDA decreased cumulative sodium balance in the HF rats. Treatment with MSPPOH (20 mg\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7day<jats:sup>\u22121<\/jats:sup> iv) + fenofibrate for 2 wk reversed renal hemodynamics and sodium balance to the levels in control HF rats. Moreover, fenofibrate caused a threefold increase in renal cortical CYP epoxygenase activity, whereas the fenofibrate-induced elevation of this activity was attenuated by MSPPOH. Western blot analysis showed that fenofibrate induced the expression of CYP epoxygenases in renal cortex and microvessels and that the induction effect of fenofibrate was blocked by MSPPOH. These results demonstrate that the fenofibrate-induced increase of CYP epoxygenase expression and the AUDA-induced stabilization of EET production in the kidneys cause renal vascular dilation and reduce sodium retention, contributing to the improvement of abnormal renal hemodynamics and hypertension in HF rats. <\/jats:p>","DOI":"10.1152\/ajprenal.00004.2007","type":"journal-article","created":{"date-parts":[[2007,4,19]],"date-time":"2007-04-19T00:38:47Z","timestamp":1176943127000},"page":"F342-F349","source":"Crossref","is-referenced-by-count":64,"title":["Increasing or stabilizing renal epoxyeicosatrienoic acid production attenuates abnormal renal function and hypertension in obese rats"],"prefix":"10.1152","volume":"293","author":[{"given":"Hui","family":"Huang","sequence":"first","affiliation":[]},{"given":"Christophe","family":"Morisseau","sequence":"additional","affiliation":[]},{"given":"JingFeng","family":"Wang","sequence":"additional","affiliation":[]},{"given":"Tianxin","family":"Yang","sequence":"additional","affiliation":[]},{"given":"John R.","family":"Falck","sequence":"additional","affiliation":[]},{"given":"Bruce D.","family":"Hammock","sequence":"additional","affiliation":[]},{"given":"Mong-Heng","family":"Wang","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.27.4.926"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000111139.94378.74"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.35.4.1009"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00388.2002"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1097\/01.fjc.0000189600.74157.6d"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00713.2003"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1016\/j.phrs.2003.11.016"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000052314.95497.78"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.22.3.292"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1016\/0041-008X(83)90342-3"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1172\/JCI7013"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1177\/153537020623101112"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.6.F965"},{"key":"R14","doi-asserted-by":"crossref","unstructured":"Imig JD. Epoxide hydrolase and epoxygenase metabolites as therapeutic targets for renal diseases. Am J Physiol Renal Physiol 289: F496\u2013F503, 2005.","DOI":"10.1152\/ajprenal.00350.2004"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1161\/hy0202.103788"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000176237.74820.75"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1096\/fj.05-4341fje"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000153792.29478.1d"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0508081102"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)63142-2"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1016\/j.plipres.2004.10.001"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00278.2003"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00324.2003"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00021.2001"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1081\/DMR-100101915"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1016\/0006-2952(87)90292-9"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0503279102"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1096\/fj.04-3128fje"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1016\/S0306-3623(96)00246-7"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1016\/S0163-7827(03)00049-3"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000153317.06072.2e"},{"key":"R32","unstructured":"Wang MH, Brand-Schieber E, Zand BA, Nguyen X, Falck JR, Balu N, Laniado Schwartzman M. Cytochrome P450-derived arachidonic acid metabolism in the rat kidney: characterization of selective inhibitors. J Pharmacol Exp Ther 284: 966\u2013973, 1998."},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000090123.55365.BA"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.200409140"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.31.1.225"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.19.12551"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0609158103"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1006\/abbi.1997.9922"},{"key":"R39","unstructured":"Zhao X, Yamamoto T, Newman JW, Kim IH, Watanabe T, Hammock BD, Stewart J, Pollock JS, Pollock DM, Imig JD. Soluble epoxide hydrolase inhibition protects the kidney from hypertension-induced damage. J Am Soc Nephrol 15: 1244\u20131253, 2004."},{"key":"R40","doi-asserted-by":"crossref","unstructured":"Zhou Y, Chang HH, Du J, Wang CY, Dong Z, Wang MH. Renal epoxyeicosatrienoic acid synthesis during pregnancy. Am J Physiol Renal Physiol 288: F221\u2013F226, 2005.","DOI":"10.1152\/ajprenal.00170.2004"},{"key":"R41","doi-asserted-by":"crossref","unstructured":"Zhou Y, Huang H, Chang HH, Du J, Wu JF, Wang CY, Wang MH. Induction of renal 20-hydroxyeicosatetraenoic acid by clofibrate attenuates high-fat diet-induced hypertension in rats. J Pharmacol Exp Ther 317: 11\u201318, 2006.","DOI":"10.1124\/jpet.105.095356"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1016\/j.amjhyper.2004.10.033"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00004.2007","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T22:37:31Z","timestamp":1567982251000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00004.2007"}},"issued":{"date-parts":[[2007,7]]},"references-count":42,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2007,7]]}},"alternative-id":["10.1152\/ajprenal.00004.2007"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00004.2007","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2007,7]]}},{"indexed":{"date-parts":[[2026,3,28]],"date-time":"2026-03-28T02:59:14Z","timestamp":1774666754321,"version":"3.50.1"},"reference-count":148,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2010,11]]},"abstract":"<jats:p>Renal proximal tubules are highly sensitive to ischemic and toxic insults and are affected in diverse genetic disorders, of which nephropathic cystinosis is the most common. The disease is caused by mutations in the CTNS gene, encoding the lysosomal cystine transporter cystinosin, and is characterized by accumulation of cystine in the lysosomes throughout the body. In the majority of the patients, this leads to generalized proximal tubular dysfunction (also called DeToni-Debr\u00e9-Fanconi syndrome) in the first year and progressive renal failure during the first decade. Extrarenal organs are affected by cystinosis as well, with clinical symptoms manifesting mostly after 10 yr of age. The cystine-depleting agent cysteamine significantly improves life expectancy of patients with cystinosis, but offers no cure, pointing to the complexity of the disease mechanism. In this review, current knowledge on the pathogenesis of cystinosis is described and placed in perspective of future research.<\/jats:p>","DOI":"10.1152\/ajprenal.00318.2010","type":"journal-article","created":{"date-parts":[[2010,9,9]],"date-time":"2010-09-09T01:41:51Z","timestamp":1283996511000},"page":"F905-F916","source":"Crossref","is-referenced-by-count":92,"title":["The pathogenesis of cystinosis: mechanisms beyond cystine accumulation"],"prefix":"10.1152","volume":"299","author":[{"given":"Martijn J.","family":"Wilmer","sequence":"first","affiliation":[{"name":"Laboratory of Genetic Endocrine and Metabolic Diseases, Department of Laboratory Medicine, Radboud University Nijmegen Medical Centre, The Netherlands;"},{"name":"Laboratory of Pediatrics, Catholic University, Leuven;"}]},{"given":"Francesco","family":"Emma","sequence":"additional","affiliation":[{"name":"Department of Nephrology and Urology, Division of Nephrology, Bambino Ges\u00fa, Rome, Italy; and"}]},{"given":"Elena N.","family":"Levtchenko","sequence":"additional","affiliation":[{"name":"Laboratory of Pediatrics, Catholic University, Leuven;"},{"name":"Department of Pediatrics, University Hospitals Leuven, Belgium"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1515\/bchm2.1903.38.5-6.557"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1089\/gte.2008.0014"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1006\/mgme.1998.2790"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1098-1004(199912)14:6<454::AID-HUMU2>3.0.CO;2-H"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/8.13.2507"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1111\/j.1399-0004.1995.tb03958.x"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/j.freeradbiomed.2010.01.011"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1992.263.2.C516"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-008-0507-4"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-003-1213-2"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-006-0009-6"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1126\/science.279.5349.349"},{"key":"B13","first-page":"137","volume":"10","author":"Broyer M","year":"1981","journal-title":"Adv Nephrol Necker Hosp"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002790"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1016\/j.clinbiochem.2007.02.005"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199105093241904"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M010562200"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.22.21.7622-7632.2002"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007080862"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2004.09.033"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.E05-02-0120"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/nrm778"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1432873100"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115103"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004110925"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00453.2009"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/0167-4889(86)90240-5"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1111\/j.1651-2227.1933.tb03611.x"},{"key":"B29","first-page":"597","volume":"37","author":"Debre R","year":"1934","journal-title":"Arch Med Enfants"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1172\/JCI110747"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006080833"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118535"},{"key":"B33","first-page":"257","volume":"133","author":"Fanconi G","year":"1931","journal-title":"Jahrbuch Kinderheilkunde"},{"key":"B34","first-page":"359","volume":"4","author":"Fanconi G","year":"1949","journal-title":"Helv Pediatr Acta"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1038\/12652"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000057852.35075.AC"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1111\/j.1399-0004.2005.00490.x"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1016\/0026-0495(87)90246-0"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1086\/302509"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M602500200"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M802681200"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/physiolgenomics.00193.2006"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-147-4-200708210-00006"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1126\/science.7112129"},{"key":"B45","first-page":"5085","volume-title":"The Metabolic and Molecular Bases of Inherited Disease","author":"Gahl WA","year":"2001"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra020552"},{"key":"B47","doi-asserted-by":"crossref","first-page":"9570","DOI":"10.1016\/S0021-9258(18)34109-7","volume":"257","author":"Gahl WA","year":"1982","journal-title":"J Biol Chem"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1042\/bj2280545"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.143.1.81"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(70)92411-6"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2736(73)90114-4"},{"key":"B52","doi-asserted-by":"crossref","first-page":"2224","DOI":"10.1093\/clinchem\/45.12.2224","volume":"45","author":"Graaf-Hess A","year":"1999","journal-title":"Clin Chem"},{"key":"B53","first-page":"42","volume-title":"Cystinosis","author":"Gubler M","year":"1999"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1159\/000096860"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.3109\/15513818409025883"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1038\/mt.2008.126"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117084"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1086\/427887"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1016\/0002-9343(62)90221-8"},{"key":"B60","doi-asserted-by":"crossref","first-page":"11727","DOI":"10.1016\/S0021-9258(17)44289-X","volume":"258","author":"Jonas AJ","year":"1983","journal-title":"J Biol Chem"},{"key":"B61","doi-asserted-by":"crossref","first-page":"3185","DOI":"10.1016\/S0021-9258(18)33425-2","volume":"257","author":"Jonas AJ","year":"1982","journal-title":"J Biol Chem"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/20.21.5940"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/ddh152"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1203\/PDR.0b013e31809fda89"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1016\/S0891-5849(99)00145-8"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1016\/j.jpeds.2004.03.056"},{"key":"B67","first-page":"2495","volume-title":"The Metabolic and Molecular Bases of Inherited Disease","author":"Kornfeld S","year":"1995"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2009.080939"},{"key":"B69","doi-asserted-by":"publisher","DOI":"10.1126\/science.186.4168.1040"},{"key":"B70","doi-asserted-by":"publisher","DOI":"10.1016\/j.taap.2004.10.004"},{"key":"B71","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-006-0005-x"},{"key":"B72","doi-asserted-by":"publisher","DOI":"10.1038\/ejhg.2009.13"},{"key":"B73","doi-asserted-by":"publisher","DOI":"10.5414\/CNP60386"},{"key":"B74","doi-asserted-by":"publisher","DOI":"10.5414\/CNP57349"},{"key":"B75","first-page":"283A","volume":"20","author":"Levtchenko EN","year":"2009","journal-title":"J Am Soc Nephrol"},{"key":"B76","doi-asserted-by":"publisher","DOI":"10.1203\/01.pdr.0000196334.46940.54"},{"key":"B77","first-page":"139","volume":"145","author":"Lignac GOE","year":"1924","journal-title":"Deut Arch Klin Med"},{"key":"B78","doi-asserted-by":"publisher","DOI":"10.1038\/nrm2217"},{"key":"B79","doi-asserted-by":"publisher","DOI":"10.1007\/PL00013448"},{"key":"B80","doi-asserted-by":"publisher","DOI":"10.1203\/01.pdr.0000196370.57200.da"},{"key":"B81","doi-asserted-by":"publisher","DOI":"10.1007\/BF00373881"},{"key":"B82","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfp648"},{"key":"B83","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbamem.2010.03.002"},{"key":"B84","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfn373"},{"key":"B85","doi-asserted-by":"publisher","DOI":"10.1515\/JBCPP.1990.1.1-4.357"},{"key":"B86","doi-asserted-by":"publisher","DOI":"10.1002\/ajmg.a.31194"},{"key":"B87","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.405"},{"key":"B88","first-page":"1993","volume-title":"GeneReviews","author":"Nesterova G","year":"2010"},{"key":"B89","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfp553"},{"key":"B90","doi-asserted-by":"publisher","DOI":"10.1136\/adc.78.4.387"},{"key":"B91","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0700330104"},{"key":"B92","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00021.2006"},{"key":"B93","doi-asserted-by":"publisher","DOI":"10.1007\/s00439-005-1255-6"},{"key":"B94","doi-asserted-by":"crossref","first-page":"125","DOI":"10.1097\/01.ASN.0000017940.40617.41","volume":"13","author":"Norden AG","year":"2002","journal-title":"J Am Soc Nephrol"},{"key":"B95","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-009-1199-5"},{"key":"B96","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000036867.49866.59"},{"key":"B97","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006050474"},{"key":"B98","doi-asserted-by":"publisher","DOI":"10.1136\/jcp.21.5.571"},{"key":"B99","doi-asserted-by":"publisher","DOI":"10.1007\/BF02633332"},{"key":"B100","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejphar.2009.10.053"},{"key":"B101","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00033.2009"},{"key":"B102","doi-asserted-by":"publisher","DOI":"10.1086\/323484"},{"key":"B103","doi-asserted-by":"crossref","first-page":"15011","DOI":"10.1016\/S0021-9258(18)48130-6","volume":"262","author":"Pisoni RL","year":"1987","journal-title":"J Biol Chem"},{"key":"B104","doi-asserted-by":"publisher","DOI":"10.1038\/35042597"},{"key":"B105","first-page":"1297","volume":"56","author":"Pras E","year":"1995","journal-title":"Am J Hum Genet"},{"key":"B106","doi-asserted-by":"crossref","first-page":"1028","DOI":"10.1681\/ASN.V181028","volume":"1","author":"Racusen LC","year":"1991","journal-title":"J Am Soc Nephrol"},{"key":"B107","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.324"},{"key":"B108","doi-asserted-by":"crossref","first-page":"8914","DOI":"10.1016\/S0021-9258(19)86787-X","volume":"254","author":"Reeves JP","year":"1979","journal-title":"J Biol Chem"},{"key":"B109","doi-asserted-by":"publisher","DOI":"10.1186\/1750-1172-2-16"},{"key":"B110","doi-asserted-by":"publisher","DOI":"10.1023\/A:1005545012776"},{"key":"B111","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.6"},{"key":"B112","doi-asserted-by":"publisher","DOI":"10.1038\/nrm2745"},{"key":"B113","doi-asserted-by":"publisher","DOI":"10.1172\/JCI114443"},{"key":"B114","author":"Sansanwal P","year":"2009","journal-title":"Pediatr Nephrol"},{"key":"B115","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009040383"},{"key":"B116","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfh266"},{"key":"B117","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-004-1445-9"},{"key":"B118","doi-asserted-by":"publisher","DOI":"10.1126\/science.157.3794.1321"},{"key":"B119","doi-asserted-by":"publisher","DOI":"10.1016\/0006-291X(67)90516-5"},{"key":"B120","doi-asserted-by":"publisher","DOI":"10.1126\/science.166.3909.1152"},{"key":"B121","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.01740407"},{"key":"B122","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006050500"},{"key":"B123","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.79.14.4446"},{"key":"B124","doi-asserted-by":"publisher","DOI":"10.1038\/239231a0"},{"key":"B125","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2009-03-213934"},{"key":"B126","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00413.2007"},{"key":"B127","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-010-1502-5"},{"key":"B128","doi-asserted-by":"publisher","DOI":"10.1038\/ng0695-246"},{"key":"B129","doi-asserted-by":"publisher","DOI":"10.1203\/00006450-198006000-00001"},{"key":"B130","doi-asserted-by":"publisher","DOI":"10.1042\/bj2080823"},{"key":"B131","doi-asserted-by":"publisher","DOI":"10.1172\/JCI108448"},{"key":"B132","doi-asserted-by":"publisher","DOI":"10.1203\/00006450-197912000-00010"},{"key":"B133","doi-asserted-by":"publisher","DOI":"10.1007\/s004670050278"},{"key":"B134","doi-asserted-by":"publisher","DOI":"10.1101\/gr.10.2.165"},{"key":"B135","doi-asserted-by":"publisher","DOI":"10.1038\/ng0498-319"},{"key":"B136","doi-asserted-by":"publisher","DOI":"10.1203\/00006450-197711100-00005"},{"key":"B137","doi-asserted-by":"publisher","DOI":"10.1016\/j.ymgme.2009.12.010"},{"key":"B138","doi-asserted-by":"publisher","DOI":"10.1002\/humu.20685"},{"key":"B139","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.108.110197"},{"key":"B140","doi-asserted-by":"crossref","first-page":"1204","DOI":"10.1681\/ASN.V1061204","volume":"10","author":"Wang Y","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B141","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2008.03.010"},{"key":"B142","doi-asserted-by":"publisher","DOI":"10.1007\/s00441-009-0882-y"},{"key":"B143","doi-asserted-by":"publisher","DOI":"10.1203\/PDR.0b013e318183fd67"},{"key":"B144","doi-asserted-by":"publisher","DOI":"10.1203\/PDR.0b013e31809fd9a7"},{"key":"B145","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2005.09.094"},{"key":"B146","doi-asserted-by":"publisher","DOI":"10.1007\/s10545-009-1118-8"},{"key":"B147","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/16.9.1769"},{"key":"B148","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00905.x"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00318.2010","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,11,9]],"date-time":"2021-11-09T07:04:39Z","timestamp":1636441479000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00318.2010"}},"issued":{"date-parts":[[2010,11]]},"references-count":148,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2010,11]]}},"alternative-id":["10.1152\/ajprenal.00318.2010"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00318.2010","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2010,11]]}},{"indexed":{"date-parts":[[2026,4,2]],"date-time":"2026-04-02T01:07:49Z","timestamp":1775092069440,"version":"3.50.1"},"reference-count":49,"publisher":"American Physiological Society","issue":"11","funder":[{"DOI":"10.13039\/100000901","name":"Juvenile Diabetes Research Foundation International (JDRF)","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000901","id-type":"DOI","asserted-by":"publisher"}]},{"name":"HHS | National Institutes of Health","award":["UL1 TR001120"],"award-info":[{"award-number":["UL1 TR001120"]}]},{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health (NIH)","doi-asserted-by":"publisher","award":["NIH RO1 DK 079996"],"award-info":[{"award-number":["NIH RO1 DK 079996"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health (NIH)","doi-asserted-by":"publisher","award":["NIH RO1 CA 131272"],"award-info":[{"award-number":["NIH RO1 CA 131272"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health (NIH)","doi-asserted-by":"publisher","award":["NIH RO1 DK 78971"],"award-info":[{"award-number":["NIH RO1 DK 78971"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000738","name":"U.S. Department of Veterans Affairs (VA)","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000738","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2015,6,1]]},"abstract":"<jats:p> Reactive oxygen species (ROS) generated by Nox NADPH oxidases may play a critical role in the pathogenesis of diabetic nephropathy (DN). The efficacy of the Nox1\/Nox4 inhibitor GKT137831 on the manifestations of DN was studied in OVE26 mice, a model of type 1 diabetes. Starting at 4\u20135 mo of age, OVE26 mice were treated with GKT137831 at 10 or 40 mg\/kg, once-a-day for 4 wk. At both doses, GKT137831 inhibited NADPH oxidase activity, superoxide generation, and hydrogen peroxide production in the renal cortex from diabetic mice without affecting Nox1 or Nox4 protein expression. The increased expression of fibronectin and type IV collagen was reduced in the renal cortex, including glomeruli, of diabetic mice treated with GKT137831. GKT137831 significantly reduced glomerular hypertrophy, mesangial matrix expansion, urinary albumin excretion, and podocyte loss in OVE26 mice. GKT137831 also attenuated macrophage infiltration in glomeruli and tubulointerstitium. Collectively, our data indicate that pharmacological inhibition of Nox1\/4 affords broad renoprotection in mice with preexisting diabetes and established kidney disease. This study validates the relevance of targeting Nox4 and identifies GKT137831 as a promising compound for the treatment of DN in type 1 diabetes. <\/jats:p>","DOI":"10.1152\/ajprenal.00396.2014","type":"journal-article","created":{"date-parts":[[2015,2,5]],"date-time":"2015-02-05T22:17:12Z","timestamp":1423174632000},"page":"F1276-F1287","source":"Crossref","is-referenced-by-count":168,"title":["Targeting NADPH oxidase with a novel dual Nox1\/Nox4 inhibitor attenuates renal pathology in type 1 diabetes"],"prefix":"10.1152","volume":"308","author":[{"given":"Yves","family":"Gorin","sequence":"first","affiliation":[{"name":"Department of Medicine, The University of Texas Health Science Center, San Antonio, Texas;"}]},{"given":"Rita C.","family":"Cavaglieri","sequence":"additional","affiliation":[{"name":"Department of Medicine, The University of Texas Health Science Center, San Antonio, Texas;"}]},{"given":"Khaled","family":"Khazim","sequence":"additional","affiliation":[{"name":"Department of Medicine, The University of Texas Health Science Center, San Antonio, Texas;"}]},{"given":"Doug-Yoon","family":"Lee","sequence":"additional","affiliation":[{"name":"Department of Medicine, The University of Texas Health Science Center, San Antonio, Texas;"}]},{"given":"Francesca","family":"Bruno","sequence":"additional","affiliation":[{"name":"Department of Medicine, The University of Texas Health Science Center, San Antonio, Texas;"}]},{"given":"Sachin","family":"Thakur","sequence":"additional","affiliation":[{"name":"Department of Medicine, The University of Texas Health Science Center, San Antonio, Texas;"}]},{"given":"Paolo","family":"Fanti","sequence":"additional","affiliation":[{"name":"Department of Medicine, The University of Texas Health Science Center, San Antonio, Texas;"},{"name":"Audie Leon Murphy Memorial Hospital Division, South Texas Veterans Health Care System, San Antonio, Texas; and"}]},{"given":"C\u00e9dric","family":"Szyndralewiez","sequence":"additional","affiliation":[{"name":"Genkyotex SA, Geneva, Switzerland"}]},{"given":"Jeffrey L.","family":"Barnes","sequence":"additional","affiliation":[{"name":"Department of Medicine, The University of Texas Health Science Center, San Antonio, Texas;"},{"name":"Audie Leon Murphy Memorial Hospital Division, South Texas Veterans Health Care System, San Antonio, Texas; and"}]},{"given":"Karen","family":"Block","sequence":"additional","affiliation":[{"name":"Department of Medicine, The University of Texas Health Science Center, San Antonio, Texas;"}]},{"given":"Hanna E.","family":"Abboud","sequence":"additional","affiliation":[{"name":"Department of Medicine, The University of Texas Health Science Center, San Antonio, Texas;"},{"name":"Audie Leon Murphy Memorial Hospital Division, South Texas Veterans Health Care System, San Antonio, Texas; and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/j.yexcr.2012.02.025"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1002\/hep.25938"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/j.freeradbiomed.2012.06.027"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2010.516"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00044.2005"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0906805106"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004080648"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1053\/j.ackd.2005.01.004"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009070721"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1089\/ars.2010.3829"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1042\/CS20110562"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00555.x"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1007\/s00125-013-3118-3"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1038\/nrd3403"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.2337\/db12-1504"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M110.136796"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.2337\/db08-1536"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.00217-13"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00522.2012"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.2174\/157016110793563816"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M502412200"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1042\/CS20130065"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1016\/j.freeradbiomed.2013.03.014"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.112.132159"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1126\/scitranslmed.3008182"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013040371"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013070810"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1016\/j.freeradbiomed.2012.05.007"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2010.263"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.pathol.4.110807.092150"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00028.2013"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1021\/jm100773e"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.111.243972"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00331.2011"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2008.070601"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1016\/j.jnutbio.2014.03.010"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2011.102"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1016\/j.vph.2012.02.012"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00028.2010"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1042\/CS20120330"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfs555"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1038\/nrendo.2010.212"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00316.2013"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.14814\/phy2.12192"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M110.143917"},{"key":"B46","first-page":"559A","volume":"23","author":"Wiesel P","year":"2012","journal-title":"J Am Soc Nephrol"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1089\/ars.2013.5357"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00511.2012"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.53.12.3248"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00396.2014","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T21:09:48Z","timestamp":1567976988000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00396.2014"}},"issued":{"date-parts":[[2015,6,1]]},"references-count":49,"journal-issue":{"issue":"11","published-print":{"date-parts":[[2015,6,1]]}},"alternative-id":["10.1152\/ajprenal.00396.2014"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00396.2014","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2015,6,1]]}},{"indexed":{"date-parts":[[2026,4,2]],"date-time":"2026-04-02T16:28:37Z","timestamp":1775147317303,"version":"3.50.1"},"reference-count":57,"publisher":"American Physiological Society","issue":"5","funder":[{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health","doi-asserted-by":"publisher","award":["R01DK117495"],"award-info":[{"award-number":["R01DK117495"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health","doi-asserted-by":"publisher","award":["R01DK61578"],"award-info":[{"award-number":["R01DK61578"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2021,5,1]]},"abstract":"<jats:p>The angiotensin II type 2 receptor agonist C21 has been known to have a renoprotective role in various kidney pathologies. C21 treatment (before renal ischemia) attenuated postischemic kidney injury, kidney dysfunction, and immune cell infiltration during the injury phase. Also, C21 treatment modulated the kidney microenvironment by enhancing anti-inflammatory responses mainly mediated by IL-10. During the repair phase, C21 treatment enhanced IL-10-secreting CD4 T cells and FoxP3-secreting regulatory T cells in Sprague\u2013Dawley rats.<\/jats:p>","DOI":"10.1152\/ajprenal.00507.2020","type":"journal-article","created":{"date-parts":[[2021,3,15]],"date-time":"2021-03-15T10:23:58Z","timestamp":1615803838000},"page":"F814-F825","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":21,"title":["Angiotensin type 2 receptor activation limits kidney injury during the early phase and induces Treg cells during the late phase of renal ischemia"],"prefix":"10.1152","volume":"320","author":[{"given":"Riyasat","family":"Ali","sequence":"first","affiliation":[{"name":"Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, Texas"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1674-711X","authenticated-orcid":false,"given":"Sanket","family":"Patel","sequence":"additional","affiliation":[{"name":"Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, Texas"}]},{"given":"Tahir","family":"Hussain","sequence":"additional","affiliation":[{"name":"Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, Texas"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/s0140-6736(95)92057-9"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.200"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1002\/wsbm.133"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2014.180"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1097\/00007890-199707270-00002"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.91.2.812"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.256.5.F794"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1007\/s00109-009-0491-y"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/j.clim.2008.08.016"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.177.5.3380"},{"key":"B11","doi-asserted-by":"crossref","first-page":"5506","DOI":"10.4049\/jimmunol.162.9.5506","volume":"162","author":"Daemen MA","year":"1999","journal-title":"J Immunol"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00486.2006"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002203"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119457"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1172\/JCI200112080"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1590\/s0100-879x2007000400015"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005080842"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2012070684"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2009.259"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/j.cellimm.2014.04.002"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1155\/2015\/360973"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1096\/fj.04-2960fje"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.109.147843"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1007\/s00109-016-1406-3"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1042\/bsr20190429"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.108.784868"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.111.00422"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1002\/stem.171"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.0903681"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1111\/jcmm.12574"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1097\/00007890-199502270-00022"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013050528"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.267.6.F1052"},{"key":"B34","first-page":"509","volume":"135","author":"Thornton MA","year":"1989","journal-title":"Am J Pathol"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118498"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119533"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.3.F525"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1097\/00007890-199810150-00028"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1038\/371336a0"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1097\/00007890-200209270-00005"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2011.140"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1097\/01.asn.0000089563.63641.a8"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1097\/00007890-200003150-00049"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.648"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1067\/mlc.2002.122832"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.314"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1159\/000329396"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2011.42"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1186\/s12929-020-0623-9"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1097\/HJH.0000000000000364"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejphar.2017.02.016"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008111160"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1038\/hr.2014.132"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfi265"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.4.F636"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1007\/s11906-003-0014-0"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.1.F79"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00507.2020","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,10,23]],"date-time":"2023-10-23T04:38:21Z","timestamp":1698035901000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00507.2020"}},"issued":{"date-parts":[[2021,5,1]]},"references-count":57,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2021,5,1]]}},"alternative-id":["10.1152\/ajprenal.00507.2020"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00507.2020","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2021,5,1]]},"assertion":[{"value":"2020-09-20","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2021-03-08","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2021-04-27","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,4,3]],"date-time":"2026-04-03T05:48:20Z","timestamp":1775195300851,"version":"3.50.1"},"reference-count":48,"publisher":"American Physiological Society","issue":"9","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2014,5,1]]},"abstract":"<jats:p>The renal glomerulus forms a selective filtration barrier that allows the passage of water, ions, and small solutes into the urinary space while restricting the passage of cells and macromolecules. The three layers of the glomerular filtration barrier include the vascular endothelium, glomerular basement membrane (GBM), and podocyte epithelium. Podocytes are capable of internalizing albumin and are hypothesized to clear proteins that traverse the GBM. The present study followed the fate of FITC-labeled albumin to establish the mechanisms of albumin endocytosis and processing by podocytes. Confocal imaging and total internal reflection fluorescence microscopy of immortalized human podocytes showed FITC-albumin endocytosis occurred preferentially across the basal membrane. Inhibition of clathrin-mediated endocytosis and caveolae-mediated endocytosis demonstrated that the majority of FITC-albumin entered podocytes through caveolae. Once internalized, FITC-albumin colocalized with EEA1 and LAMP1, endocytic markers, and with the neonatal Fc receptor, a marker for transcytosis. After preloading podocytes with FITC-albumin, the majority of loaded FITC-albumin was lost over the subsequent 60 min of incubation. A portion of the loss of albumin occurred via lysosomal degradation as pretreatment with leupeptin, a lysosomal protease inhibitor, partially inhibited the loss of FITC-albumin. Consistent with transcytosis of albumin, preloaded podocytes also progressively released FITC-albumin into the extracellular media. These studies confirm the ability of podocytes to endocytose albumin and provide mechanistic insight into cellular mechanisms and fates of albumin handling in podocytes.<\/jats:p>","DOI":"10.1152\/ajprenal.00532.2013","type":"journal-article","created":{"date-parts":[[2014,2,27]],"date-time":"2014-02-27T03:13:38Z","timestamp":1393470818000},"page":"F941-F951","source":"Crossref","is-referenced-by-count":61,"title":["Human podocytes perform polarized, caveolae-dependent albumin endocytosis"],"prefix":"10.1152","volume":"306","author":[{"given":"Evgenia","family":"Dobrinskikh","sequence":"first","affiliation":[{"name":"University of Colorado Anschutz Medical Campus, Aurora, Colorado; and"}]},{"given":"Kayo","family":"Okamura","sequence":"additional","affiliation":[{"name":"University of Colorado Anschutz Medical Campus, Aurora, Colorado; and"}]},{"given":"Jeffrey B.","family":"Kopp","sequence":"additional","affiliation":[{"name":"Kidney Disease Section, National Institute of Diabetes and Digestive and Kidney Disease. National Institutes of Health, Bethesda, Maryland"}]},{"given":"R. Brian","family":"Doctor","sequence":"additional","affiliation":[{"name":"University of Colorado Anschutz Medical Campus, Aurora, Colorado; and"}]},{"given":"Judith","family":"Blaine","sequence":"additional","affiliation":[{"name":"University of Colorado Anschutz Medical Campus, Aurora, Colorado; and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0711515105"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.2133\/dmpk.24.318"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/j.it.2006.05.004"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-4159.2009.06304.x"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1093\/intimm\/10.9.1289"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1111\/j.1582-4934.2007.00167.x"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2012.233403"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20021829"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1093\/cvr\/cvr279"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00183.2010"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00183.2010"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1993.264.4.C1003"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00208.x"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00272.2006"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010020199"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.67.031103.154845"},{"key":"B17","doi-asserted-by":"crossref","first-page":"632","DOI":"10.1681\/ASN.V114632","volume":"11","author":"Haymann JP","year":"2000","journal-title":"J Am Soc Nephrol"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.00286.2005"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2011.282"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1007\/s10875-010-9468-4"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1797.2005.00385.x"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.0346-04.2004"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1016\/j.yexcr.2012.02.031"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.139.1.193"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.2133\/dmpk.DMPK-11-RG-022"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0054817"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1986.250.6.F1055"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00144.2009"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200102084"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/j.cellsig.2011.09.022"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0057051"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002041"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00509.2009"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2011070666"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008090976"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0730776100"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000033277.32822.23"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M113.460832"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90638.2008"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.263.4.F601"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1155\/2012\/481520"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1007\/s004180100317"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1007\/s00795-008-0397-8"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2011.06.025"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1172\/JCI27100"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1152\/ajplung.00173.2005"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.2133\/dmpk.DMPK-11-RG-127"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00314.x"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00532.2013","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,3,27]],"date-time":"2022-03-27T21:57:59Z","timestamp":1648418279000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00532.2013"}},"issued":{"date-parts":[[2014,5,1]]},"references-count":48,"journal-issue":{"issue":"9","published-print":{"date-parts":[[2014,5,1]]}},"alternative-id":["10.1152\/ajprenal.00532.2013"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00532.2013","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2014,5,1]]}},{"indexed":{"date-parts":[[2026,4,6]],"date-time":"2026-04-06T22:36:21Z","timestamp":1775514981204,"version":"3.50.1"},"reference-count":79,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2004,4]]},"abstract":"<jats:p>In ischemic or hypoxic tissues, elevated Ca<jats:sup>2+<\/jats:sup>levels have emerged as one of the main damaging agents among other Ca<jats:sup>2+<\/jats:sup>-independent mechanisms of cellular injury. Because mitochondria, besides the endoplasmic reticulum, play a key role in the maintainance of cellular Ca<jats:sup>2+<\/jats:sup>homeostasis, alterations in the mitochondrial Ca<jats:sup>2+<\/jats:sup>content ([Ca<jats:sup>2+<\/jats:sup>]<jats:sub>m<\/jats:sub>) were monitored in addition to changes in cytosolic Ca<jats:sup>2+<\/jats:sup>concentration ([Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>) during metabolic inhibition (MI) in renal epithelial Madin-Darby canine kidney (MDCK) cells. [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>and [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>m<\/jats:sub>were monitored via, respectively, fura 2 and rhod 2 measurements. MI induced an increase in [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>reaching 631 \u00b1 78 nM in \u223c20 min, followed by a decrease to 118 \u00b1 9 nM in the next \u223c25 min. A pronounced drop in cellular ATP levels and a rapid increase in intracellular Na<jats:sup>+<\/jats:sup>concentrations in the first 20 min of MI excluded Ca<jats:sup>2+<\/jats:sup>efflux in the second phase via plasma membrane ATPases or Na<jats:sup>+<\/jats:sup>\/Ca<jats:sup>2+<\/jats:sup>exchangers (NCE). Mitochondrial rhod 2 intensities increased to 434 \u00b1 46% of the control value during MI, indicating that mitochondria sequester Ca<jats:sup>2+<\/jats:sup>during MI. The mitochondrial potential (\u0394\u03a8<jats:sub>m<\/jats:sub>) was lost in 20 min of MI, excluding mitochondrial Ca<jats:sup>2+<\/jats:sup>uptake via the \u0394\u03a8<jats:sub>m<\/jats:sub>-dependent mitochondrial Ca<jats:sup>2+<\/jats:sup>uniporter after 20 min of MI. Under Na<jats:sup>+<\/jats:sup>-free conditions, or when CGP-37157, a specific inhibitor of the mitochondrial NCE, was used, no drop in [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>was seen during MI, whereas the MI-induced increase in mitochondrial rhod 2 fluorescence was strongly reduced. To our knowledge, this study is the first to report that in metabolically inhibited renal epithelial cells mitochondria take up Ca<jats:sup>2+<\/jats:sup>via the NCE acting in the reverse mode.<\/jats:p>","DOI":"10.1152\/ajprenal.00284.2003","type":"journal-article","created":{"date-parts":[[2004,3,4]],"date-time":"2004-03-04T19:24:57Z","timestamp":1078428297000},"page":"F784-F794","source":"Crossref","is-referenced-by-count":44,"title":["Ca<sup>2+<\/sup>uptake in mitochondria occurs via the reverse action of the Na<sup>+<\/sup>\/Ca<sup>2+<\/sup>exchanger in metabolically inhibited MDCK cells"],"prefix":"10.1152","volume":"286","author":[{"given":"Ilse","family":"Smets","sequence":"first","affiliation":[{"name":"Department of Physiology, Limburgs Universitair Centrum\/Transnationale Universiteit Limburg, Biomedisch Onderzoeksinstituut, B-3590 Diepenbeek, Belgium"}]},{"given":"Adrian","family":"Caplanusi","sequence":"additional","affiliation":[{"name":"Department of Physiology, Limburgs Universitair Centrum\/Transnationale Universiteit Limburg, Biomedisch Onderzoeksinstituut, B-3590 Diepenbeek, Belgium"}]},{"given":"Sanda","family":"Despa","sequence":"additional","affiliation":[{"name":"Department of Physiology, Limburgs Universitair Centrum\/Transnationale Universiteit Limburg, Biomedisch Onderzoeksinstituut, B-3590 Diepenbeek, Belgium"}]},{"given":"Zsolt","family":"Molnar","sequence":"additional","affiliation":[{"name":"Department of Physiology, Limburgs Universitair Centrum\/Transnationale Universiteit Limburg, Biomedisch Onderzoeksinstituut, B-3590 Diepenbeek, Belgium"}]},{"given":"Mihai","family":"Radu","sequence":"additional","affiliation":[{"name":"Department of Physiology, Limburgs Universitair Centrum\/Transnationale Universiteit Limburg, Biomedisch Onderzoeksinstituut, B-3590 Diepenbeek, Belgium"}]},{"given":"Martin","family":"vandeVen","sequence":"additional","affiliation":[{"name":"Department of Physiology, Limburgs Universitair Centrum\/Transnationale Universiteit Limburg, Biomedisch Onderzoeksinstituut, B-3590 Diepenbeek, Belgium"}]},{"given":"Marcel","family":"Ameloot","sequence":"additional","affiliation":[{"name":"Department of Physiology, Limburgs Universitair Centrum\/Transnationale Universiteit Limburg, Biomedisch Onderzoeksinstituut, B-3590 Diepenbeek, Belgium"}]},{"given":"Paul","family":"Steels","sequence":"additional","affiliation":[{"name":"Department of Physiology, Limburgs Universitair Centrum\/Transnationale Universiteit Limburg, Biomedisch Onderzoeksinstituut, B-3590 Diepenbeek, Belgium"}]}],"member":"24","reference":[{"key":"REF1","doi-asserted-by":"publisher","DOI":"10.1016\/S0143-4160(02)00203-8"},{"key":"REF2","doi-asserted-by":"publisher","DOI":"10.1006\/jmcc.1993.1107"},{"key":"REF3","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.136.4.833"},{"key":"REF4","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1999.79.4.1127"},{"key":"REF5","doi-asserted-by":"publisher","DOI":"10.1046\/j.1432-1327.1999.00725.x"},{"key":"REF6","doi-asserted-by":"publisher","DOI":"10.1038\/35036035"},{"key":"REF7","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1991.261.3.C482"},{"key":"REF8","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M208393200"},{"key":"REF9","doi-asserted-by":"crossref","unstructured":"Carafoli E.Calcium pumps of the plasma membrane.Phys Rev71: 129-153, 1991.","DOI":"10.1152\/physrev.1991.71.1.129"},{"key":"REF10","doi-asserted-by":"publisher","DOI":"10.1016\/0304-4165(94)00190-9"},{"key":"REF11","doi-asserted-by":"publisher","DOI":"10.1016\/0006-2952(88)90623-5"},{"key":"REF12","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1993.2438"},{"key":"REF13","doi-asserted-by":"publisher","DOI":"10.1097\/00005344-199304000-00013"},{"key":"REF14","doi-asserted-by":"crossref","unstructured":"Cox DAand Matlib MA.A role for the mitochondrial Na+-Ca2+exchanger in the regulation of oxidative phosphorylation in isolated heart mitochondria.J Biol Chem268: 938-947, 1993.","DOI":"10.1016\/S0021-9258(18)54024-2"},{"key":"REF15","doi-asserted-by":"publisher","DOI":"10.1016\/S0955-0674(00)00110-1"},{"key":"REF16","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1994.266.6.C1803"},{"key":"REF17","doi-asserted-by":"publisher","DOI":"10.1054\/ceca.2000.0170"},{"key":"REF18","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.2000.00057.x"},{"key":"REF19","doi-asserted-by":"publisher","DOI":"10.3109\/08860229709026276"},{"key":"REF20","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1981.240.1.R3"},{"key":"REF21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.6.F837"},{"key":"REF22","doi-asserted-by":"crossref","unstructured":"Furukawa K, Tawada Y, and Shigekawa M.Regulation of the plasma membrane Ca2+pump by cyclic nucleotides in cultured vascular smooth muscle cells.J Biol Chem263: 8058-8065, 1988.","DOI":"10.1016\/S0021-9258(18)68441-8"},{"key":"REF23","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1098-2795(199906)53:2<222::AID-MRD11>3.0.CO;2-L"},{"key":"REF24","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-5793(99)00726-7"},{"key":"REF25","doi-asserted-by":"publisher","DOI":"10.1016\/S0008-6363(98)00104-7"},{"key":"REF26","doi-asserted-by":"crossref","unstructured":"Grynkiewicz G, Poenie M, and Tsien RY.A new generation of Ca2+indicators with greatly improved fluorescence properties.J Biol Chem260: 3440-3450, 1985.","DOI":"10.1016\/S0021-9258(19)83641-4"},{"key":"REF27","doi-asserted-by":"publisher","DOI":"10.1054\/ceca.2000.0168"},{"key":"REF28","doi-asserted-by":"publisher","DOI":"10.1080\/15216540152846000"},{"key":"REF29","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1994.267.2.C313"},{"key":"REF30","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1990.258.5.C755"},{"key":"REF31","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.71.3.547"},{"key":"REF32","doi-asserted-by":"publisher","DOI":"10.1016\/S0896-6273(00)80038-0"},{"key":"REF33","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.1997.tb52284.x"},{"key":"REF34","doi-asserted-by":"publisher","DOI":"10.1016\/S1570-9639(02)00438-7"},{"key":"REF35","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.180143997"},{"key":"REF36","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.137.3.633"},{"key":"REF37","doi-asserted-by":"crossref","unstructured":"Jung DW, Apel LM, and Brierly GP.Transmembrane gradients of free Na+in isolated heart mitochondria estimated using a fluorescent probe.Am J Physiol Cell Physiol262: C1047-C1055, 1992.","DOI":"10.1152\/ajpcell.1992.262.4.C1047"},{"key":"REF38","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.2.672"},{"key":"REF39","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(91)80444-8"},{"key":"REF40","doi-asserted-by":"crossref","unstructured":"Kawanishi T, Nieminen AL, Herman B, and Lemasters JJ.Suppression of Ca2+oscillations in cultured rat hepatocytes by chemical hypoxia.J Biol Chem266: 20062-20069, 1991.","DOI":"10.1016\/S0021-9258(18)54891-2"},{"key":"REF41","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-5793(99)01130-8"},{"key":"REF42","doi-asserted-by":"publisher","DOI":"10.1006\/taap.1994.1151"},{"key":"REF43","doi-asserted-by":"crossref","unstructured":"Kip SNand Strehler EE.Characterization of PMCA isoforms and their contribution to transcellular Ca2+flux in MDCK cells.Am J Physiol Renal Physiol284: F122-F132, 2003.","DOI":"10.1152\/ajprenal.00161.2002"},{"key":"REF44","unstructured":"Koenig K.Cellular response to laser radiation in fluorescence microscopes. In:Methods in Cellular Imaging, edited by Periasamy A. Oxford, UK: Oxford Univ. Press, 2001, p. 236-251."},{"key":"REF45","unstructured":"Kribben A, Edelstein CL, and Schrier RW.Pathophysiology of acute renal failure.J Nephrol12,Suppl2: S142-S151, 1999."},{"key":"REF46","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-2999(02)01842-3"},{"key":"REF47","doi-asserted-by":"crossref","unstructured":"Lang F, Friedrich F, Paulmichl M, Schobersberger W, Jungwirth A, Ritter M, Steidl M, Weiss H, Woll E, Tschernko E, Paulmichl M, and Hallbrucker C.Ion channels in Madin-Darby canine kidney cells.Ren Physiol Biochem13: 82-93, 1990.","DOI":"10.1159\/000173350"},{"key":"REF48","doi-asserted-by":"publisher","DOI":"10.1089\/152308602760598918"},{"key":"REF49","unstructured":"Levine JSand Lieberthal W.Terminal pathways to cell death. In:Acute Renal Failure: A Companion to Brenner & Rector's The Kidney, edited by Molitoris BA and Finn WF. Philadelphia, PA: Saunders, 2001, p. 30-59."},{"key":"REF50","doi-asserted-by":"crossref","unstructured":"Lynch RMand Balaban RS.Coupling of aerobic glycolysis and Na+-K+-ATPase in renal cell line MDCK.Am J Physiol Cell Physiol253: C269-C276, 1987.","DOI":"10.1152\/ajpcell.1987.253.2.C269"},{"key":"REF51","doi-asserted-by":"publisher","DOI":"10.1137\/0111030"},{"key":"REF52","doi-asserted-by":"publisher","DOI":"10.1172\/JCI113734"},{"key":"REF53","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.71.3.605"},{"key":"REF54","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.12.1.63"},{"key":"REF55","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2736(80)90235-7"},{"key":"REF56","doi-asserted-by":"crossref","unstructured":"Muallem Sand Karlish SJD.Catalytic and regulatory ATP-binding sites of the red cell Ca2+pump studied by irreversible modification with fluorescein isothiocyanate.J Biol Chem258: 169-175, 1983.","DOI":"10.1016\/S0021-9258(18)33236-8"},{"key":"REF57","doi-asserted-by":"publisher","DOI":"10.1002\/1096-9861(20001016)426:2<297::AID-CNE10>3.0.CO;2-O"},{"key":"REF58","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.2000.80.1.315"},{"key":"REF59","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.103.21.2617"},{"key":"REF60","doi-asserted-by":"publisher","DOI":"10.1016\/0076-6879(95)60154-6"},{"key":"REF61","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.2000.00037.x"},{"key":"REF62","doi-asserted-by":"publisher","DOI":"10.1054\/ceca.1999.0076"},{"key":"REF63","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.93.11.5489"},{"key":"REF64","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-5793(97)00669-8"},{"key":"REF65","doi-asserted-by":"publisher","DOI":"10.1054\/ceca.2000.0171"},{"key":"REF66","doi-asserted-by":"publisher","DOI":"10.1016\/S0028-3908(98)00198-1"},{"key":"REF67","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.88.9.3671"},{"key":"REF68","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.46.27510"},{"key":"REF69","doi-asserted-by":"publisher","DOI":"10.1016\/S0163-7258(00)00102-9"},{"key":"REF70","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1990.sp018094"},{"key":"REF71","doi-asserted-by":"publisher","DOI":"10.1096\/fasebj.9.2.7781924"},{"key":"REF72","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.26.16133"},{"key":"REF73","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2736(88)90490-7"},{"key":"REF74","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.1981.tb15490.x"},{"key":"REF75","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-3495(95)80285-7"},{"key":"REF76","doi-asserted-by":"crossref","unstructured":"Vieyra A, Nachbin L, de Dios-Abad E, Goldfeld M, Meyer-Fernandes JR, and de Moraes L.Comparison between calcium transport and adenosine triphosphatase activity in membrane vesicles derived from rabbit kidney proximal tubules.J Biol Chem261: 4247-4255, 1986.","DOI":"10.1016\/S0021-9258(17)35654-5"},{"key":"REF77","unstructured":"Wakata A, Belous AE, Knox CD, Pierce JM, Nicoud IB, Anderson CD, Pinson CW, and Chari RS.Mitochondrial calcium uptake during ischemia is regulated by cytosolic ATP:ADP ratio.J Surg Res114: 304, 2003."},{"key":"REF78","doi-asserted-by":"crossref","unstructured":"Wingrove DEand Gunter TE.Kinetics of mitochondrial calcium transport. I. Characteristics of the sodium-independent calcium efflux mechanism of liver mitochondria.J Biol Chem261: 15159-15165, 1986.","DOI":"10.1016\/S0021-9258(18)66846-2"},{"key":"REF79","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.110.2.201"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00284.2003","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,6,15]],"date-time":"2021-06-15T00:41:35Z","timestamp":1623717695000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00284.2003"}},"issued":{"date-parts":[[2004,4]]},"references-count":79,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2004,4]]}},"alternative-id":["10.1152\/ajprenal.00284.2003"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00284.2003","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2004,4]]}},{"indexed":{"date-parts":[[2026,4,3]],"date-time":"2026-04-03T14:19:08Z","timestamp":1775225948352,"version":"3.50.1"},"reference-count":68,"publisher":"American Physiological Society","issue":"2","funder":[{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["T32DK007726"],"award-info":[{"award-number":["T32DK007726"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["R01DK115438"],"award-info":[{"award-number":["R01DK115438"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100002347","name":"Bundesministerium f\u00fcr Bildung und Forschung","doi-asserted-by":"publisher","award":["STOP-FSGS 01GM1518B"],"award-info":[{"award-number":["STOP-FSGS 01GM1518B"]}],"id":[{"id":"10.13039\/501100002347","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2020,2,1]]},"abstract":"<jats:p>Mucin-type O-linked glycosylation, a posttranslational modification affecting the stability and biophysical characteristics of proteins, requires C1GalT1 (T synthase) and its obligate, X-linked chaperone Cosmc. Hypomorphic C1GalT1 mutations cause renal failure via not yet established mechanisms. We hypothesize that impaired Cosmc-dependent O-glycosylation in podocytes is sufficient to cause disease. Podocyte-specific Cosmc knockout mice were generated and phenotyped to test this hypothesis. Female heterozygous mice displaying mosaic inactivation of Cosmc in podocytes due to random X-linked inactivation were also examined. Mice with podocyte-specific Cosmc deletion develop profound albuminuria, foot process effacement, glomerular sclerosis, progressive renal failure, and impaired survival. Glomerular transcriptome analysis reveals early changes in cell adhesion, extracellular matrix organization, and chemokine-mediated signaling pathways, coupled with podocyte loss. Expression of the O-glycoprotein podoplanin was lost, while Tn antigen, representing immature O-glycans, was most abundantly found on podocalyxin. In contrast to hemizygous male and homozygous female animals, heterozygous female mosaic animals developed only mild albuminuria, focal foot process effacement, and nonprogressive kidney disease. Ultrastructurally, Cosmc-deficient podocytes formed Tn antigen-positive foot processes interdigitating with those of normal podocytes but not with other Cosmc-deficient cells. This suggests a cell nonautonomous mechanism for mucin-type O-glycoproteins in maintaining podocyte function. In summary, our findings demonstrated an essential and likely cell nonautonomous role for mucin-type O-glycosylation for podocyte function.<\/jats:p>","DOI":"10.1152\/ajprenal.00399.2019","type":"journal-article","created":{"date-parts":[[2020,1,6]],"date-time":"2020-01-06T16:54:30Z","timestamp":1578329670000},"page":"F518-F530","source":"Crossref","is-referenced-by-count":22,"title":["Cosmc-dependent mucin-type<i>O<\/i>-linked glycosylation is essential for podocyte function"],"prefix":"10.1152","volume":"318","author":[{"given":"Brian R.","family":"Stotter","sequence":"first","affiliation":[{"name":"Division of Nephrology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts"},{"name":"Division of Nephrology, Boston Children\u2019s Hospital, Harvard Medical School, Boston, Massachusetts"}]},{"given":"Brianna E.","family":"Talbot","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts"}]},{"given":"Diane E.","family":"Capen","sequence":"additional","affiliation":[{"name":"Center for Systems Biology\/Program in Membrane Biology, Massachusetts General Hospital, Boston, Massachusetts"}]},{"given":"Nadine","family":"Artelt","sequence":"additional","affiliation":[{"name":"Institute for Anatomy and Cell Biology, University Medicine Greifswald, Greifswald, Germany"}]},{"given":"Junwei","family":"Zeng","sequence":"additional","affiliation":[{"name":"National Center for Functional Glycomics, Department of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts"}]},{"given":"Yasuyuki","family":"Matsumoto","sequence":"additional","affiliation":[{"name":"National Center for Functional Glycomics, Department of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts"}]},{"given":"Nicole","family":"Endlich","sequence":"additional","affiliation":[{"name":"Institute for Anatomy and Cell Biology, University Medicine Greifswald, Greifswald, Germany"}]},{"given":"Richard D.","family":"Cummings","sequence":"additional","affiliation":[{"name":"National Center for Functional Glycomics, Department of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9973-9731","authenticated-orcid":false,"given":"Johannes S.","family":"Schlondorff","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0607872103"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.060003969.x"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1979.49"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.3389\/fmed.2018.00292"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1097-0215(19970703)72:1<119:AID-IJC17>3.0.CO;2-E"},{"key":"B6","first-page":"477","volume":"28","author":"Blau EB","year":"1973","journal-title":"Lab Invest"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2012.487"},{"key":"B8","first-page":"1141","volume":"151","author":"Breiteneder-Geleff S","year":"1997","journal-title":"Am J Pathol"},{"key":"B9","first-page":"113","volume-title":"Essentials of Glycobiology","author":"Brockhausen I","year":"2017","edition":"3"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1038\/nm.2261"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00245.2016"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.3390\/biom6030033"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2018050490"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1111\/tan.12900"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1172\/JCI36077"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2015040421"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1172\/JCI30954"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1159\/000481633"},{"key":"B19","first-page":"907","volume":"74","author":"Gelberg H","year":"1996","journal-title":"Lab Invest"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2013.169"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2014.204"},{"key":"B22","doi-asserted-by":"crossref","first-page":"760","DOI":"10.1681\/ASN.V104760","volume":"10","author":"Hiki Y","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2010.090539"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1016\/j.ekir.2019.06.012"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0029873"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1111\/j.1742-4658.2009.07429.x"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2012.08.037"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1038\/4371252a"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.262438199"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/j.ajpath.2011.12.023"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2018030238"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M602469200"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2008.080063"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1038\/nrm3231"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.3389\/fendo.2014.00160"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1038\/190372a0"},{"key":"B37","doi-asserted-by":"crossref","first-page":"2013","DOI":"10.1681\/ASN.V9112013","volume":"9","author":"Matsui K","year":"1998","journal-title":"J Am Soc Nephrol"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010090963"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1002\/gene.10164"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1177\/39.8.1856454"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2016.01.012"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-017-15993-3"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2018090951"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0000237"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008070782"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2014-04-572107"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1038\/nature13535"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1038\/labinvest.2015.78"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1016\/S0344-0338(87)80103-6"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1406619111"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1038\/s41581-019-0129-4"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.12688\/f1000research.7255.1"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2012040414"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/cdg342"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.201410017"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1021\/acsbiomaterials.7b00037"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2019.04.017"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-017-11553-x"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M117.798512"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1038\/emboj.2013.79"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)64239-3"},{"key":"B61a","doi-asserted-by":"publisher","DOI":"10.1093\/glycob\/cww086"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1038\/srep23642"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0914004107"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2011090947"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005010055"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005050488"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200311112"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00399.2019","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,10,10]],"date-time":"2022-10-10T02:52:42Z","timestamp":1665370362000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00399.2019"}},"issued":{"date-parts":[[2020,2,1]]},"references-count":68,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2020,2,1]]}},"alternative-id":["10.1152\/ajprenal.00399.2019"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00399.2019","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2020,2,1]]}},{"indexed":{"date-parts":[[2022,4,1]],"date-time":"2022-04-01T23:40:24Z","timestamp":1648856424813},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1988,8,1]]},"abstract":"<jats:p> Little is known of the regulatory steps in the cellular action of vasopressin (AVP) on the renal epithelium, subsequent to the cAMP generation. We studied cAMP-binding proteins in the medullary collecting tubule (MCT) and the thick ascending limb of Henle's loop (MTAL) microdissected from the rat kidney by use of photoaffinity labeling. Microdissected tubules were homogenized and photoaffinity labeled by incubation with 1 microM 32P-labeled 8-azido-adenosine 3',5'-cyclic monophosphate (N3-8-[32P]-cAMP); the incorporated 32P was analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and autoradiography. Both in MCT and MTAL preparations, the analyses showed incorporation of N3-8-[32P]cAMP into two bands (Mr = 49,000 and Mr = 55,000) that comigrated with standards of the cAMP-dependent protein kinase regulatory subunits RI and RII. In MCT, most of the 32P (80%) was incorporated into RI, whereas in MTAL the 32P incorporated into RI and RII was equivalent. When freshly dissected MCT segments were incubated with 10(-12)-10(-6) M AVP, the subsequent photoaffinity labeling of RI with N3-8-[32P]cAMP was markedly diminished in a dose-dependent manner compared with controls. Our results suggest that cAMP binds in MCT and MTAL to regulatory subunits RI and RII of cAMP-dependent protein kinase. However, in MCT the dominant type of cAMP-dependent protein kinase appears to be type I. The outlined procedure is suitable to indirectly measure the occupancy of RI by endogenous cAMP generated in MCT cells in response to physiological levels (10(-12) M) of AVP.(ABSTRACT TRUNCATED AT 250 WORDS) <\/jats:p>","DOI":"10.1152\/ajprenal.1988.255.2.f292","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T03:15:30Z","timestamp":1513998930000},"page":"F292-F300","source":"Crossref","is-referenced-by-count":3,"title":["cAMP-binding proteins in medullary tubules from rat kidney: effect of ADH"],"prefix":"10.1152","volume":"255","author":[{"given":"S. M.","family":"Gapstur","sequence":"first","affiliation":[{"name":"Department of Medicine, Mayo Clinic and Foundation, Rochester, Minnesota 55905."}]},{"given":"S.","family":"Homma","sequence":"additional","affiliation":[{"name":"Department of Medicine, Mayo Clinic and Foundation, Rochester, Minnesota 55905."}]},{"given":"T. P.","family":"Dousa","sequence":"additional","affiliation":[{"name":"Department of Medicine, Mayo Clinic and Foundation, Rochester, Minnesota 55905."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1988.255.2.F292","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:48:35Z","timestamp":1567972115000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1988.255.2.F292"}},"issued":{"date-parts":[[1988,8,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1988,8,1]]}},"alternative-id":["10.1152\/ajprenal.1988.255.2.F292"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1988.255.2.f292","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1988,8,1]]}},{"indexed":{"date-parts":[[2022,3,29]],"date-time":"2022-03-29T21:38:31Z","timestamp":1648589911132},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1987,1,1]]},"abstract":"<jats:p> The objective of this study was to examine the relationship between plasma angiotensin II (ANG II) and ANG II receptor binding to the glomerulus following acute renal failure (ARF) induced by an injection of glycerol (50%, 10 ml\/kg im). At 2 and 24 h after glycerol injection, ARF was documented by a rise in blood urea nitrogen (BUN) (normal, 18.6 +\/- 0.7; 2 h after glycerol 29.3 +\/- 2.3; 24 h after glycerol, 103.0 +\/- 12.0 mg\/dl; P less than 0.002 each experimental vs. normal) and creatinine (normal, 0.41 +\/- 0.02; 2 h after glycerol, 0.96 +\/- 0.10; 24 h after glycerol, 2.40 +\/- 0.30 mg\/dl; P less than 0.001, experimental vs. normal groups). Plasma ANG II rose from a control of 15.8 +\/- 3.1 to 26.9 +\/- 4.4 pg\/ml at 2 h and 49.5 +\/- 8.6 pg\/ml at 24 h after glycerol (P less than 0.05, experimental vs. normal). No changes in affinity or density of glomerular ANG II receptors were detected either at 2 or 24 h after glycerol injection despite the significant rise in plasma ANG II (glomerular ANG II receptors: normal, 1,000 +\/- 61; 2 h after glycerol, 896 +\/- 120; 24 h after glycerol, 936 +\/- 80 fmol\/mg). The 24-h infusion of ANG II in normal rats to achieve plasma levels identical to the 24 h ARF group caused ANG II receptor density to fall to 58.1 +\/- 8.6% of control values (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS) <\/jats:p>","DOI":"10.1152\/ajprenal.1987.252.1.f109","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T02:52:49Z","timestamp":1513997569000},"page":"F109-F114","source":"Crossref","is-referenced-by-count":0,"title":["Glomerular angiotensin II receptor modulation in glycerol-induced acute renal failure"],"prefix":"10.1152","volume":"252","author":[{"given":"B. M.","family":"Wilkes","sequence":"first","affiliation":[]},{"given":"P. F.","family":"Mento","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1987.252.1.F109","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:45:47Z","timestamp":1567971947000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1987.252.1.F109"}},"issued":{"date-parts":[[1987,1,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1987,1,1]]}},"alternative-id":["10.1152\/ajprenal.1987.252.1.F109"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1987.252.1.f109","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1987,1,1]]}},{"indexed":{"date-parts":[[2022,4,2]],"date-time":"2022-04-02T10:11:37Z","timestamp":1648894297774},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2018,2,1]]},"DOI":"10.1152\/ajprenal.zh2-8423-corr.2017","type":"journal-article","created":{"date-parts":[[2018,2,7]],"date-time":"2018-02-07T06:30:55Z","timestamp":1517985055000},"page":"F317-F317","source":"Crossref","is-referenced-by-count":0,"title":["CORRIGENDUM"],"prefix":"10.1152","volume":"314","member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.zh2-8423-corr.2017","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T10:57:24Z","timestamp":1567940244000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.zh2-8423-corr.2017"}},"issued":{"date-parts":[[2018,2,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2018,2,1]]}},"alternative-id":["10.1152\/ajprenal.zh2-8423-corr.2017"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.zh2-8423-corr.2017","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2018,2,1]]}},{"indexed":{"date-parts":[[2022,10,28]],"date-time":"2022-10-28T08:18:09Z","timestamp":1666945089744},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1992,5,1]]},"abstract":"<jats:p> The regulatory step for Ca(2+)- and calmodulin-dependent control of renin secretion was studied in rabbit renal cortical slices. Renin secretion was stimulated by adding the K(+)-H+ exchange ionophore nigericin or a weak base, benzylamine, to Ca(2+)-free incubation medium. Both nigericin and benzylamine can produce chemiosmotic swelling of acidic intracellular organelles in a pH gradient-dependent manner. Swelling of renin secretory granules may account for the stimulatory effects of these two agents on renin secretion. The stimulation of renin secretion by each of these agents was prevented by including Ca2+ in the incubation medium. The inhibitory effects of Ca2+ were reversed by the calmodulin antagonist calmidazolium, suggesting that the Ca2+ inhibition may be mediated by calmodulin. However, when renin secretion was first stimulated by nigericin or benzylamine in Ca(2+)-free medium, subsequent addition of Ca2+ to the incubation medium failed to reverse the stimulation. These results therefore suggest that Ca2+ acting through calmodulin may exert its inhibitory effects on renin secretion by blocking an early step in the cellular events that lead to renin secretion such as pH gradient-dependent swelling of renin secretory granule. <\/jats:p>","DOI":"10.1152\/ajprenal.1992.262.5.f793","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T03:53:48Z","timestamp":1514001228000},"page":"F793-F798","source":"Crossref","is-referenced-by-count":3,"title":["Calcium-dependent inhibitory step in control of renin secretion"],"prefix":"10.1152","volume":"262","author":[{"given":"C. S.","family":"Park","sequence":"first","affiliation":[{"name":"Department of Physiology, University of Ulsan College of Medicine,Seoul, Korea."}]},{"given":"C. D.","family":"Hong","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Ulsan College of Medicine,Seoul, Korea."}]},{"given":"T. W.","family":"Honeyman","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Ulsan College of Medicine,Seoul, Korea."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1992.262.5.F793","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:16:41Z","timestamp":1567959401000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1992.262.5.F793"}},"issued":{"date-parts":[[1992,5,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1992,5,1]]}},"alternative-id":["10.1152\/ajprenal.1992.262.5.F793"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1992.262.5.f793","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1992,5,1]]}},{"indexed":{"date-parts":[[2022,4,2]],"date-time":"2022-04-02T09:44:55Z","timestamp":1648892695925},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1977,4,1]]},"abstract":"<jats:p> The possibility that prostaglandins (PG) located in the renal medulla may influence renal excretion of sodium by a direct tubular action was examined by the addition of prostaglandins PGE2, PGF2alpha, and PGA2 to the peritubular and luminal surfaces of isolated perfused medullary thick ascending lumbs and collecting tubules from rabbit kidneys. The prostaglandins at both high (2.5 x 10(-4) M) and low (10 (-10) M, 10 (-7) M) concentrations had no effect on transepithelial potential difference and net sodium flux across these segments. Pretreatment of the animals with indomethacin did not influence the results. In vivo, both PGE2 and PGF2alpha, caused a natriuresis when infused directly into one renal artery, whereas PGA2 had no effect on sodium excretion. The prostaglandin inhibitors indomethacin, meclofenamate, and RO 20-5720 similarly had no direct effect on sodium transport in the nephron segments studied. It is concluded that the previously observed influence of prostaglandins and prostaglandin inhibitors on renal excretion of sodium in vivo are not mediated by a direct tubular action. <\/jats:p>","DOI":"10.1152\/ajprenal.1977.232.4.f383","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T20:12:25Z","timestamp":1513973545000},"page":"F383-F390","source":"Crossref","is-referenced-by-count":4,"title":["Influence of prostaglandins on sodium transport of isolated medullary nephron segments"],"prefix":"10.1152","volume":"232","author":[{"given":"L. G.","family":"Fine","sequence":"first","affiliation":[]},{"given":"W.","family":"Trizna","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1977.232.4.F383","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:58:15Z","timestamp":1567969095000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1977.232.4.F383"}},"issued":{"date-parts":[[1977,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1977,4,1]]}},"alternative-id":["10.1152\/ajprenal.1977.232.4.F383"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1977.232.4.f383","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1977,4,1]]}},{"indexed":{"date-parts":[[2022,4,2]],"date-time":"2022-04-02T09:16:59Z","timestamp":1648891019846},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1984,10,1]]},"abstract":"<jats:p> We previously demonstrated Na+-dependent 32Pi uptake in basolateral membrane vesicles from kidneys of normal dogs. We postulated that this reflects Na+-dependent Pi transport across the basolateral membrane into the proximal tubular cell in vivo that subserves cellular needs for Pi. To ascertain whether Pi transport across the basolateral membrane was enhanced in a condition in which delivery of Pi across the luminal membrane would be markedly decreased, we measured Na+-dependent 32Pi uptake in basolateral vesicles isolated from postobstructed and control kidneys of dogs following release of unilateral ureteral obstruction. Clearance of creatinine and filtered load of Pi were significantly decreased in postobstructed compared with control kidneys. Na+-dependent 32Pi uptake was increased in basolateral vesicles from postobstructed compared with control kidneys, as reflected by increased initial rate of uptake and an increased overshoot of 32Pi transport. Our findings are consistent with an adaptation resulting in increased transport of Pi across the basolateral membrane of the proximal tubular cell in unilateral ureteral obstruction. This process may provide required Pi to the cell under conditions in which decreased Pi is available for transport across the brush border membrane. <\/jats:p>","DOI":"10.1152\/ajprenal.1984.247.4.f543","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T16:18:34Z","timestamp":1513959514000},"page":"F543-F547","source":"Crossref","is-referenced-by-count":0,"title":["Uptake of Pi in basolateral vesicles after release of unilateral ureteral obstruction"],"prefix":"10.1152","volume":"247","author":[{"given":"S. J.","family":"Schwab","sequence":"first","affiliation":[]},{"given":"S.","family":"Klahr","sequence":"additional","affiliation":[]},{"given":"M. R.","family":"Hammerman","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1984.247.4.F543","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:32:34Z","timestamp":1567967554000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1984.247.4.F543"}},"issued":{"date-parts":[[1984,10,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1984,10,1]]}},"alternative-id":["10.1152\/ajprenal.1984.247.4.F543"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1984.247.4.f543","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1984,10,1]]}},{"indexed":{"date-parts":[[2022,4,2]],"date-time":"2022-04-02T07:14:20Z","timestamp":1648883660708},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1991,12,1]]},"abstract":"<jats:p> Immature rats display a blunted rise in urinary phosphate but not adenosine 3',5'-cyclic monophosphate (cAMP) excretion in response to parathyroid hormone (PTH), perhaps as a consequence of the increased demand for phosphate during growth. Because a major driving force for growth is growth hormone (GH), and in view of the fact that GH has been shown to promote renal phosphate retention in the immature animal, it is possible that GH may attenuate the phosphaturic effect of PTH. The objective of this study was to determine whether suppression of pulsatile GH release, during administration of a synthetic peptide antagonist to GH-releasing factor, i.e., [N-acetyl-Tyr1-D-Arg2]-GRF-(1-29)-NH2 (GRF-AN), alters the renal response to increasing doses of PTH (1.5-15.0 micrograms.100 g-1.h-1) in the acutely thyroparathyroidectomized immature rat. Baseline fractional excretion of phosphate (FEPi), before administration of PTH, was negligible in all groups (less than 0.05%). Infusion of PTH resulted in an attenuated rise in FEPi in immature control rats compared with adult control rats (from 3.8 +\/- 1.4% at lowest PTH dose to 16.7 +\/- 3.1% at highest dose in immature rats vs. 21.1 +\/- 3.5 to 31.9 +\/- 4.4% in adult rats, P less than 0.05). In contrast, immature rats treated for 2 days with GRF-AN (100 micrograms\/kg, twice daily) displayed an enhanced phosphaturic response (FEPi from 12.0 +\/- 4.2 to 42.9 +\/- 3.7%, P less than 0.05) compared with immature control rats, which was not different from that observed in control adult rats.(ABSTRACT TRUNCATED AT 250 WORDS) <\/jats:p>","DOI":"10.1152\/ajprenal.1991.261.6.f1110","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T09:30:08Z","timestamp":1514021408000},"page":"F1110-F1113","source":"Crossref","is-referenced-by-count":3,"title":["Suppression of growth hormone release restores phosphaturic response to PTH in immature rats"],"prefix":"10.1152","volume":"261","author":[{"given":"S. E.","family":"Mulroney","sequence":"first","affiliation":[{"name":"Department of Physiology and Biophysics, Georgetown University Schoolof Medicine, Washington, District of Columbia 20007."}]},{"given":"M. D.","family":"Lumpkin","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, Georgetown University Schoolof Medicine, Washington, District of Columbia 20007."}]},{"given":"A.","family":"Haramati","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, Georgetown University Schoolof Medicine, Washington, District of Columbia 20007."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1991.261.6.F1110","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:20:56Z","timestamp":1567974056000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1991.261.6.F1110"}},"issued":{"date-parts":[[1991,12,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1991,12,1]]}},"alternative-id":["10.1152\/ajprenal.1991.261.6.F1110"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1991.261.6.f1110","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1991,12,1]]}},{"indexed":{"date-parts":[[2022,4,3]],"date-time":"2022-04-03T16:24:11Z","timestamp":1649003051903},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1981,11,1]]},"abstract":"<jats:p> The process of combined convection and diffusion of solute across membranes of finite thickness is discussed. An exact solution is available for an open (nonsieving) homoporous membrane. This solution is nonlinear in the volume flux (Jv) for any nonzero volume flow and concentration difference. Extension to the more general case of a partially sieving membrane does not change the nonlinear form of this equation. A linearization of this transport equation about small Jv\/Ps yields an approximate equation (the arithmetic mean) that is useful over a reasonable range of conditions near equilibrium. The application of linear nonequilibrium thermodynamics to this process has led to the derivation of a third transport equation, linear in Jv but logarithmic in the concentrations. This finite difference equation is shown to give a less accurate approximation to the exact equation than does the arithmetic mean equation, even in regions near equilibrium. Use of approximate equations may lead to error when the solute reflection coefficient is determined from ultrafiltration experiments or when applied to the individual elements of a membrane array. The early origins of the concept of reflection and sieving coefficients and their relation to one another are discussed. The importance of structural detail in membranes, even at a fine-grained level, and the distinction between the terms \"homogeneous\" or \"black box\" and \"homoporous\" is emphasized. Although structural complexity creates problems in any attempt to write a transport equation without detailed knowledge of the membrane stucture, proper consideration of the local equation and its subsequent integration makes this fact explicit and allows for an assessment of the magnitude of these effects. <\/jats:p>","DOI":"10.1152\/ajprenal.1981.241.5.f469","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T14:01:28Z","timestamp":1513951288000},"page":"F469-F476","source":"Crossref","is-referenced-by-count":1,"title":["On equations for combined convective and diffusive transport of neutral solute across porous membranes"],"prefix":"10.1152","volume":"241","author":[{"given":"E. H.","family":"Bresler","sequence":"first","affiliation":[]},{"given":"L. J.","family":"Groome","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1981.241.5.F469","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:19:57Z","timestamp":1567966797000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1981.241.5.F469"}},"issued":{"date-parts":[[1981,11,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1981,11,1]]}},"alternative-id":["10.1152\/ajprenal.1981.241.5.F469"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1981.241.5.f469","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1981,11,1]]}},{"indexed":{"date-parts":[[2022,3,29]],"date-time":"2022-03-29T05:23:37Z","timestamp":1648531417577},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1983,6,1]]},"abstract":"<jats:p> Cortical collecting tubules were dissected from rabbit kidney and cultured in a hormonally defined serum-free medium. Morphologic studies of the cultured cells derived from the collecting tubule indicated that the cells maintained their epithelial nature. These studies also revealed the presence of two distinct cell types that closely resemble the principal and intercalated cell types of the cortical collecting tubule. Several biochemical characteristics of the cultured cells were found to be similar to previously reported values for the cortical collecting tubule. The cells retain hormonal responsiveness to antidiuretic hormone (ADH), as demonstrated by a 12-fold increase in cAMP in response to ADH. Cultured cortical collecting tubule cells produce prostaglandins, with prostaglandin E2 as the predominant cyclooxygenase product. This study presents the first morphologic and biochemical characterization of cortical collecting tubule epithelial cells grown in culture. <\/jats:p>","DOI":"10.1152\/ajprenal.1983.244.6.f724","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T15:47:42Z","timestamp":1513957662000},"page":"F724-F728","source":"Crossref","is-referenced-by-count":4,"title":["Cell culture of renal epithelium derived from rabbit microdissected cortical collecting tubules"],"prefix":"10.1152","volume":"244","author":[{"given":"M. G.","family":"Currie","sequence":"first","affiliation":[]},{"given":"B. R.","family":"Cole","sequence":"additional","affiliation":[]},{"given":"K.","family":"DeSchryver-Kecskemeti","sequence":"additional","affiliation":[]},{"given":"S.","family":"Holmberg","sequence":"additional","affiliation":[]},{"given":"P.","family":"Needleman","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1983.244.6.F724","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:27:25Z","timestamp":1567967245000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1983.244.6.F724"}},"issued":{"date-parts":[[1983,6,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1983,6,1]]}},"alternative-id":["10.1152\/ajprenal.1983.244.6.F724"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1983.244.6.f724","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1983,6,1]]}},{"indexed":{"date-parts":[[2022,4,4]],"date-time":"2022-04-04T05:42:18Z","timestamp":1649050938585},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2005,4]]},"DOI":"10.1152\/ajprenal.00010.2005","type":"journal-article","created":{"date-parts":[[2005,3,7]],"date-time":"2005-03-07T22:12:56Z","timestamp":1110233576000},"page":"F867-F869","source":"Crossref","is-referenced-by-count":0,"title":["CORRIGENDUM"],"prefix":"10.1152","volume":"288","member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00010.2005","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T21:49:10Z","timestamp":1567979350000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00010.2005"}},"issued":{"date-parts":[[2005,4]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2005,4]]}},"alternative-id":["10.1152\/ajprenal.00010.2005"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00010.2005","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2005,4]]}},{"indexed":{"date-parts":[[2022,3,29]],"date-time":"2022-03-29T01:08:11Z","timestamp":1648516091238},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2007,3]]},"DOI":"10.1152\/ajprenal.00014.2007","type":"journal-article","created":{"date-parts":[[2007,3,6]],"date-time":"2007-03-06T16:19:11Z","timestamp":1173197951000},"page":"F1102-F1102","source":"Crossref","is-referenced-by-count":0,"title":["2007 Carl W. Gottschalk Distinguished Lecturer of the American Physiological Society Renal Section"],"prefix":"10.1152","volume":"292","member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00014.2007","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:28:52Z","timestamp":1567970932000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00014.2007"}},"issued":{"date-parts":[[2007,3]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2007,3]]}},"alternative-id":["10.1152\/ajprenal.00014.2007"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00014.2007","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2007,3]]}},{"indexed":{"date-parts":[[2022,3,29]],"date-time":"2022-03-29T03:47:58Z","timestamp":1648525678134},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1990,8,1]]},"abstract":"<jats:p> To examine the specificity of the phosphonoformic acid (PFA) interaction with the Na(+)-dependent phosphate transporter of mouse renal brush-border membrane vesicles, we compared the effects of anions on Na(+)-dependent [14C]PFA binding and Na(+)-dependent phosphate transport. Inhibition of PFA binding was achieved by PFA (% control = 0 +\/- 1), sulfate (15 +\/- 2), arsenate (35 +\/- 1), phosphate (59 +\/- 2), and nitrate (68 +\/- 4), whereas inhibition of phosphate transport was only apparent with phosphate (0 +\/- 1), PFA (22 +\/- 4), and arsenate (37 +\/- 5). Succinate and gluconate had no effect on either Na(+)-dependent process. Under conditions where Na(+)-dependent PFA binding was maximally inhibited by phosphate (% control = 65 +\/- 4), further inhibition could be achieved by sulfate (26 +\/- 5%). Na(+)-dependent PFA binding was competitively inhibited by phosphate (apparent Ki = 8.9 +\/- 1.2 mM) and noncompetitively inhibited by sulfate (apparent Ki = 2.6 +\/- 0.5 mM). We found that PFA inhibited Na(+)-dependent sulfate transport (50% inhibition at 9 mM PFA) as well as Na(+)-dependent phosphate transport (50% inhibition at 0.5 mM PFA). We also examined the pH dependence of Na(+)-dependent PFA binding and Na(+)-dependent phosphate and sulfate transport. PFA binding was optimal at pH = 7.4, whereas phosphate transport increased with increasing pH, and sulfate transport increased with decreasing pH.(ABSTRACT TRUNCATED AT 250 WORDS) <\/jats:p>","DOI":"10.1152\/ajprenal.1990.259.2.f286","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T22:26:51Z","timestamp":1513981611000},"page":"F286-F292","source":"Crossref","is-referenced-by-count":1,"title":["Sulfate inhibits [14C]phosphonoformic acid binding to renal brush-border membranes"],"prefix":"10.1152","volume":"259","author":[{"given":"H. S.","family":"Tenenhouse","sequence":"first","affiliation":[{"name":"Department of Pediatrics, McGill University-Montreal Children'sHospital Research Institute, Quebec, Canada."}]},{"given":"J.","family":"Lee","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, McGill University-Montreal Children'sHospital Research Institute, Quebec, Canada."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1990.259.2.F286","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:18:59Z","timestamp":1567970339000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1990.259.2.F286"}},"issued":{"date-parts":[[1990,8,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1990,8,1]]}},"alternative-id":["10.1152\/ajprenal.1990.259.2.F286"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1990.259.2.f286","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1990,8,1]]}},{"indexed":{"date-parts":[[2022,3,30]],"date-time":"2022-03-30T22:12:17Z","timestamp":1648678337187},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1986,2,1]]},"abstract":"<jats:p> Reducing the daily Na intake of rabbits from approximately 4.4 to 0.1 meq\/kg body wt increases plasma aldosterone levels and the rate of amiloride-sensitive Na transport in the descending colon two- to threefold. The stimulation of Na transport is a result of an increase in the maximum transport capacity of the epithelium, whereas the affinity of Na to its transport system is not altered. Simultaneous with enhanced Na absorption, there is statistically significant K secretion of 0.25 mu eq . cm-2 . h-1 under short-circuit conditions. Transepithelial current-voltage relations in the absence and presence of amiloride were used to determine the Na permeability of the apical membrane and the intracellular Na activity of the Na-transporting cells. The Na content of the amiloride-sensitive cells was estimated from the kinetics of absorptive Na tracer fluxes. The stimulation of active Na transport under conditions of dietary Na restriction is associated with parallel increases in apical membrane Na permeability and the Na content of the amiloride-sensitive cells, but the intracellular Na activity and the activity of the epithelial Na-K-ATPase are not significantly altered. Taken together, these results suggest that endogenous aldosterone increases the number of conducting Na entry sites in the apical membrane of colonic epithelium and that there is activation of additional Na pump units in the basolateral membrane, brought about by cell swelling and possibly by an increase in the fraction of epithelial cells that participate in active Na transport. <\/jats:p>","DOI":"10.1152\/ajprenal.1986.250.2.f235","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T20:43:52Z","timestamp":1513975432000},"page":"F235-F245","source":"Crossref","is-referenced-by-count":1,"title":["Sodium absorption and potassium secretion in rabbit colon during sodium deficiency"],"prefix":"10.1152","volume":"250","author":[{"given":"K.","family":"Turnheim","sequence":"first","affiliation":[]},{"given":"H.","family":"Plass","sequence":"additional","affiliation":[]},{"given":"M.","family":"Grasl","sequence":"additional","affiliation":[]},{"given":"P.","family":"Krivanek","sequence":"additional","affiliation":[]},{"given":"H.","family":"Wiener","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1986.250.2.F235","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:38:10Z","timestamp":1567957090000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1986.250.2.F235"}},"issued":{"date-parts":[[1986,2,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1986,2,1]]}},"alternative-id":["10.1152\/ajprenal.1986.250.2.F235"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1986.250.2.f235","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1986,2,1]]}},{"indexed":{"date-parts":[[2022,3,29]],"date-time":"2022-03-29T10:51:18Z","timestamp":1648551078552},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1977,3,1]]},"abstract":"<jats:p> The renal cortex has an unusually high rate of palmitic acid utilization. The uptake, oxidation, and distribution of this fatty acid in the cortex, unlike other tissues, responds to variations in medium and tissue potassium content. This potassium dependency is mimicked and amplified by rubidium. These observations indicate that in the renal cortex, both potassium and rubidium promote the accumulation, oxidation, and esterification of palmitic acid. <\/jats:p>","DOI":"10.1152\/ajprenal.1977.232.3.f254","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T20:24:50Z","timestamp":1513974290000},"page":"F254-F259","source":"Crossref","is-referenced-by-count":0,"title":["Effect of potassium on utilization of (1-14C)palmitic acid in renal cortex of the rat"],"prefix":"10.1152","volume":"232","author":[{"given":"M. E.","family":"Wagner","sequence":"first","affiliation":[]},{"given":"H. O.","family":"Heinemann","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1977.232.3.F254","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:59:14Z","timestamp":1567969154000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1977.232.3.F254"}},"issued":{"date-parts":[[1977,3,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1977,3,1]]}},"alternative-id":["10.1152\/ajprenal.1977.232.3.F254"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1977.232.3.f254","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1977,3,1]]}},{"indexed":{"date-parts":[[2022,4,3]],"date-time":"2022-04-03T18:51:41Z","timestamp":1649011901141},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1977,4,1]]},"abstract":"<jats:p> Mechanisms for the concentrating defect produced by fluoride were examined in the rat. Free-water clearance at all levels of delivery was normal after 5 days of chronic fluoride administration in the hereditary hypothalamic diabetes insipidus rat. In the Sprague-Dawley rats, during moderate fluoride administration (120 micronmol\/kg per day), urine osmolality and cyclic AMP excretion decreased and urine volume increased, but after exogenous vasopressin, volume decreased and osmolality and cyclic AMP increased appropriately. During larger daily doses of fluoride (240 micronmol\/kg per day) urinary osmolality and cyclic AMP decreased and volume increased, which was similar to the changes seen during lower fluoride dosages, but these parameters did not change after exogenous vasopressin. These data suggest that ascending limb chloride reabsorption is unaltered by fluoride administration; in the presence of sufficient fluoride, collecting tubular cells apparently do not generate cyclic AMP or increase permeability appropriately in response to vasopressin. The postulated defect is felt to be due to either a decrease in ATP availability or to a direct inhibitory effect of fluoride on the vasopressin-dependent cyclic AMP generating system. <\/jats:p>","DOI":"10.1152\/ajprenal.1977.232.4.f335","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T15:12:25Z","timestamp":1513955545000},"page":"F335-F340","source":"Crossref","is-referenced-by-count":1,"title":["Effect of sodium fluoride on concentrating and diluting ability in the rat"],"prefix":"10.1152","volume":"232","author":[{"given":"J. D.","family":"Wallin","sequence":"first","affiliation":[]},{"given":"R. A.","family":"Kaplan","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1977.232.4.F335","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T14:58:10Z","timestamp":1567954690000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1977.232.4.F335"}},"issued":{"date-parts":[[1977,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1977,4,1]]}},"alternative-id":["10.1152\/ajprenal.1977.232.4.F335"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1977.232.4.f335","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1977,4,1]]}},{"indexed":{"date-parts":[[2022,4,3]],"date-time":"2022-04-03T20:43:07Z","timestamp":1649018587038},"reference-count":8,"publisher":"American Physiological Society","issue":"10","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2015,11,15]]},"DOI":"10.1152\/ajprenal.00398.2015","type":"journal-article","created":{"date-parts":[[2015,9,17]],"date-time":"2015-09-17T02:33:41Z","timestamp":1442457221000},"page":"F835-F835","source":"Crossref","is-referenced-by-count":0,"title":["Being dedicated"],"prefix":"10.1152","volume":"309","author":[{"given":"Helle A.","family":"Praetorius","sequence":"first","affiliation":[{"name":"Department of Biomedicine, Aarhus University, Aarhus, Denmark"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00294.2015"},{"key":"B1a","doi-asserted-by":"publisher","DOI":"10.1038\/sj.emboj.7600963"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2004.070839"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M411089200"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00336.2014"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1007\/s00232-001-0075-4"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1038\/nmeth.2647"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M506965200"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00398.2015","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T01:15:37Z","timestamp":1567991737000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00398.2015"}},"issued":{"date-parts":[[2015,11,15]]},"references-count":8,"journal-issue":{"issue":"10","published-print":{"date-parts":[[2015,11,15]]}},"alternative-id":["10.1152\/ajprenal.00398.2015"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00398.2015","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2015,11,15]]}},{"indexed":{"date-parts":[[2022,4,5]],"date-time":"2022-04-05T19:22:30Z","timestamp":1649186550828},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1996,7,1]]},"abstract":"<jats:p> The mechanism by which proteins that pass through the glomerular basal lamina are taken up by proximal tubule cells is incompletely characterized. Past work has identified the kinetics of albumin binding to renal brush-border membrane. We have now purified and characterized albumin binding protein (ABP) and shown its distribution in renal proximal tubular cells. ABP was purified from rat renal proximal tubular cell brush-border membrane by affinity chromatography with rat serum albumin-Sepharose. The resulting ABP had two apparent molecular masses (55 and 31 kDa) by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Antibodies to ABP were raised in rabbits and checked by immunoassay and immunoblotting. Light-microscopic immunohistochemistry showed ABP all along the proximal tubule in the pars convoluta and pars recta. Electron-microscopic immunohistochemistry showed labeling on microvilli and in apical endocytic vacuoles, dense apical tubules, and lysosomes. These results indicate that ABP is involved in proximal tubule endocytosis. <\/jats:p>","DOI":"10.1152\/ajprenal.1996.271.1.f101","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T06:50:32Z","timestamp":1514011832000},"page":"F101-F107","source":"Crossref","is-referenced-by-count":6,"title":["Characterization and distribution of albumin binding protein in normal rat kidney"],"prefix":"10.1152","volume":"271","author":[{"given":"A. L.","family":"Cessac-Guillemet","sequence":"first","affiliation":[{"name":"Laboratoire de Biologie Cellulaire, Universite Paris 7, France."}]},{"given":"F.","family":"Mounier","sequence":"additional","affiliation":[{"name":"Laboratoire de Biologie Cellulaire, Universite Paris 7, France."}]},{"given":"C.","family":"Borot","sequence":"additional","affiliation":[{"name":"Laboratoire de Biologie Cellulaire, Universite Paris 7, France."}]},{"given":"H.","family":"Bakala","sequence":"additional","affiliation":[{"name":"Laboratoire de Biologie Cellulaire, Universite Paris 7, France."}]},{"given":"M.","family":"Perichon","sequence":"additional","affiliation":[{"name":"Laboratoire de Biologie Cellulaire, Universite Paris 7, France."}]},{"given":"M.","family":"Schaeverbeke","sequence":"additional","affiliation":[{"name":"Laboratoire de Biologie Cellulaire, Universite Paris 7, France."}]},{"given":"J.","family":"Schaeverbeke","sequence":"additional","affiliation":[{"name":"Laboratoire de Biologie Cellulaire, Universite Paris 7, France."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1996.271.1.F101","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:06:54Z","timestamp":1567973214000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1996.271.1.F101"}},"issued":{"date-parts":[[1996,7,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1996,7,1]]}},"alternative-id":["10.1152\/ajprenal.1996.271.1.F101"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1996.271.1.f101","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1996,7,1]]}},{"indexed":{"date-parts":[[2022,4,5]],"date-time":"2022-04-05T21:43:01Z","timestamp":1649194981335},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1986,2,1]]},"abstract":"<jats:p> The renal renin-angiotensin system plays an important role in the control of renal hemodynamics and in the etiology of some types of hypertension. Angiotensinogen is the prohormone for angiotensins I and II. In the present communication, we report for the first time the presence of mRNA coding for angiotensinogen in the kidney. Indeed, the intrarenal location appears to be predominantly in the renal medulla. Additionally, an investigation of the effect of uninephrectomy on the intrarenal angiotensinogen mRNA suggests that regulation of mRNA levels in the kidney does occur. <\/jats:p>","DOI":"10.1152\/ajprenal.1986.250.2.f374","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T20:43:52Z","timestamp":1513975432000},"page":"F374-F377","source":"Crossref","is-referenced-by-count":1,"title":["Intrarenal localization of angiotensinogen mRNA by RNA-DNA dot-blot hybridization"],"prefix":"10.1152","volume":"250","author":[{"given":"T. A.","family":"Fried","sequence":"first","affiliation":[]},{"given":"E. A.","family":"Simpson","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1986.250.2.F374","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:38:20Z","timestamp":1567957100000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1986.250.2.F374"}},"issued":{"date-parts":[[1986,2,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1986,2,1]]}},"alternative-id":["10.1152\/ajprenal.1986.250.2.F374"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1986.250.2.f374","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1986,2,1]]}},{"indexed":{"date-parts":[[2022,3,29]],"date-time":"2022-03-29T16:40:01Z","timestamp":1648572001353},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1987,4,1]]},"abstract":"<jats:p> Micropuncture studies in anesthetized Munich-Wistar rats were undertaken to investigate the effects of calcium channel blockade on the glomerular hemodynamic responses to 3-Hz renal nerve stimulation. Stimulation alone increased afferent and efferent arteriolar resistances by 85 and 35%, respectively. Because of these increases both single nephron plasma flow and glomerular capillary hydrostatic pressure difference fell to levels significantly below control, leading to a 26% reduction in single nephron filtration rate (P less than 0.005). These changes, however, were largely attenuated during calcium channel blockade (verapamil, nifedipine). Single nephron filtration rate was only decreased by 14% (P less than 0.05) due to a reduction in single nephron plasma flow. The role of angiotensin II on the residual vasoconstrictive effect of stimulation was also investigated. Pretreatment with an angiotensin-converting enzyme inhibitor (MK 421) of rats infused with verapamil abolished the residual vasoconstriction. The data suggest that calcium influx is an important step for the vasoconstrictive effects of the renal nerves. Additionally, angiotensin II contributes to increased vascular resistance during renal nerve stimulation via a separate, calcium channel mechanism. <\/jats:p>","DOI":"10.1152\/ajprenal.1987.252.4.f613","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T21:13:31Z","timestamp":1513977211000},"page":"F613-F620","source":"Crossref","is-referenced-by-count":0,"title":["Modulation of renal adrenergic effector mechanisms by calcium entry blockers"],"prefix":"10.1152","volume":"252","author":[{"given":"J. C.","family":"Pelayo","sequence":"first","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1987.252.4.F613","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:44:40Z","timestamp":1567957480000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1987.252.4.F613"}},"issued":{"date-parts":[[1987,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1987,4,1]]}},"alternative-id":["10.1152\/ajprenal.1987.252.4.F613"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1987.252.4.f613","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1987,4,1]]}},{"indexed":{"date-parts":[[2022,3,31]],"date-time":"2022-03-31T14:48:23Z","timestamp":1648738103345},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1980,7,1]]},"abstract":"<jats:p> Treatment with disodium ethane-1-hydroxy-1,1-diphosphonate (EHDP) given in doses of 10 mg P\/kg s.c. for 7 days inhibits bone mineral retention and decreases the tubular capacity to reabsorb inorganic phosphate (Pi) in thyroparathyroidectomized (TPTX) rats. In the present work we show that pretreatment with EHDP depressed Na+-dependent Pi uptake by brush border membrane vesicles (BBMV) isolated from renal cortex of TPTX rats. The effect of EHDP was observed after feeding both high (1.2%) and low (0.2%) phosphorus diets. The EHDP-induced changes observed in vitro at the brush border level parallel the variations in the overall tubular Pi transport capacity as assessed by clearance techniques in conscious rats. Na+-dependent glucose uptake by BBMV, as well as alkaline phosphatase activity in cortical homogenates and in the BBMV were not affected by EHDP treatment. Accordingly, EHDP, given in doses that block bone mineral retention, appears to specifically affect the Na+-dependent transport of Pi across the luminal membrane of proximal tubules of renal cortex. <\/jats:p>","DOI":"10.1152\/ajprenal.1980.239.1.f13","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T07:55:11Z","timestamp":1513929311000},"page":"F13-F16","source":"Crossref","is-referenced-by-count":3,"title":["Effect of diphosphonate treatment on phosphate transport by renal brush border vesicles"],"prefix":"10.1152","volume":"239","author":[{"given":"R.","family":"Stoll","sequence":"first","affiliation":[]},{"given":"H.","family":"Fleisch","sequence":"additional","affiliation":[]},{"given":"J. P.","family":"Bonjour","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1980.239.1.F13","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T14:15:12Z","timestamp":1567952112000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1980.239.1.F13"}},"issued":{"date-parts":[[1980,7,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1980,7,1]]}},"alternative-id":["10.1152\/ajprenal.1980.239.1.F13"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1980.239.1.f13","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1980,7,1]]}},{"indexed":{"date-parts":[[2022,9,28]],"date-time":"2022-09-28T10:29:44Z","timestamp":1664360984326},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1982,12,1]]},"abstract":"<jats:p> To investigate whether dysfunction of the proximal tubule underlies maleic acid-(MA) induced type II (\u201cproximal\u201d) renal tubular acidosis (RTA II), we intravenously administered either MA or acetazolamide to eight conscious trained dogs undergoing water diuresis and examined the relationship between fractional solute-free water clearance (Ch2o\/GFR), a measure of NaCl reabsorption in the post-proximal nephron, and either fractional urine flow (V\/GFR), a measure of total solute rejected by the proximal tubule, or the sum of fractional excretion of Cl- and Ch2o\/GFR [(Ccl + Ch2o)\/GFR], a measure of proximally rejected solute that is potentially reabsorbable by the thick ascending limb. When MA or acetazolamide induced brisk bicarbonaturia at normal plasma bicarbonate concentrations: 1) V\/GFR, (Ccl + Ch20)GFR, and Ch2o\/GFR increased strikingly; 2) at any increment of Ch2o\/GFR ws not; 3) the increments of V\/GFR correlated positively with those of fractional excretion of bicarbonate (P less than 0.001); 4) during hyperchloremic acidosis, MA-induced bicarbonaturia was greatly attenuated; the increment in V\/GFR was halved and approximated that in Ch20\/GFR, which was unchanged; 5) when plasma bicarbonate was abruptly increased, bicarbonaturia increased strikingly and V\/GFR increased further but Ch20\/GFR and aminoaciduria did not. We conclude that MA induces a reduction in the net rate at which the proximal tubule reabsorbs HCO-3, Na+, and Cl-. This dysfunction underlies RTA II and evokes greatly increased reabsorption of Cl- and Na+ in the post-proximal tubule. <\/jats:p>","DOI":"10.1152\/ajprenal.1982.243.6.f604","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T15:43:20Z","timestamp":1513957400000},"page":"F604-F611","source":"Crossref","is-referenced-by-count":3,"title":["Dysfunction of the proximal tubule underlies maleic acid-induced type II renal tubular acidosis"],"prefix":"10.1152","volume":"243","author":[{"given":"H. A.","family":"Al-Bander","sequence":"first","affiliation":[]},{"given":"R. A.","family":"Weiss","sequence":"additional","affiliation":[]},{"given":"M. H.","family":"Humphreys","sequence":"additional","affiliation":[]},{"suffix":"Jr","given":"R. C.","family":"Morris","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1982.243.6.F604","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:27:14Z","timestamp":1567967234000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1982.243.6.F604"}},"issued":{"date-parts":[[1982,12,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1982,12,1]]}},"alternative-id":["10.1152\/ajprenal.1982.243.6.F604"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1982.243.6.f604","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1982,12,1]]}},{"indexed":{"date-parts":[[2023,12,26]],"date-time":"2023-12-26T09:01:44Z","timestamp":1703581304798},"reference-count":44,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2003,10]]},"abstract":"<jats:p>In a previous paper, we found that low ionic strength (I) reversibly reduced the glomerular charge density, suggesting increased volume of the charge-selective barrier. Because glutaraldehyde makes most structures rigid, we considered the isolated, perfusion-fixed rat kidney to be an ideal model for further analysis. The fixed kidneys were perfused with albumin solutions containing FITC-Ficoll at two different Is (I = 151 and 34 mM). At normal I, the fractional clearance (\u03b8) for albumin was 0.0049 (SE \u20130.0017, +0.0027, n = 6), whereas \u03b8 for neutral Ficoll<jats:sub>35.5\u00c5<\/jats:sub>of similar size was significantly higher 0.104 (SE 0.010, n = 5, P &lt; 0.001). At low I, \u03b8 for albumin was 0.0030 (SE \u20130.0011, +0.0018, n = 6, not significant from \u03b8<jats:sub>albumin<\/jats:sub>at normal I) and \u03b8 for Ficoll<jats:sub>35.5\u00c5<\/jats:sub>was identical to that at normal I, 0.104 (SE 0.015, n = 6, P &lt; 0.01 compared with \u03b8<jats:sub>albumin<\/jats:sub>at low I). According to a heterogeneous charged fiber model, low I reduced the fiber density from 0.056 to 0.0315, suggesting a 78% gel volume expansion. We conclude that 1) there is a significant glomerular charge barrier. 2) Solutions with low I increase the volume of the charge barrier even in kidneys fixed with glutaraldehyde. Our findings suggest that polysaccharide-rich structures, such as the endothelial cell coat, are key components in the glomerular barrier.<\/jats:p>","DOI":"10.1152\/ajprenal.00227.2001","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:39:30Z","timestamp":1425415170000},"page":"F722-F730","source":"Crossref","is-referenced-by-count":13,"title":["Dynamic alterations of glomerular charge density in fixed rat kidneys suggest involvement of endothelial cell coat"],"prefix":"10.1152","volume":"285","author":[{"given":"Giuliano","family":"Ciarimboli","sequence":"first","affiliation":[]},{"given":"Clara","family":"Hjalmarsson","sequence":"additional","affiliation":[]},{"given":"Arend","family":"B\u00f6kenkamp","sequence":"additional","affiliation":[]},{"given":"Hans-Joachim","family":"Schurek","sequence":"additional","affiliation":[]},{"given":"B\u00f6rje","family":"Haraldsson","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"REF1","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1097-0029(19970301)36:5<390::AID-JEMT9>3.0.CO;2-P"},{"key":"REF2","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-3495(74)85962-X"},{"key":"REF3","doi-asserted-by":"publisher","DOI":"10.1016\/0003-2697(76)90527-3"},{"key":"REF4","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1975.104"},{"key":"REF5","doi-asserted-by":"publisher","DOI":"10.1007\/s004249900120"},{"key":"REF6","doi-asserted-by":"publisher","DOI":"10.1042\/bj2970031"},{"key":"REF7","doi-asserted-by":"publisher","DOI":"10.1016\/0026-2862(80)90024-2"},{"key":"REF8","doi-asserted-by":"crossref","unstructured":"Deen WM, Lazzara MJ, and Myers BD.Structural determinants of glomerular permeability.Am J Physiol Renal Physiol281: F579\u2013F596, 2001.","DOI":"10.1152\/ajprenal.2001.281.4.F579"},{"key":"REF9","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.33.1.1"},{"key":"REF10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1980.238.2.F126"},{"key":"REF11","doi-asserted-by":"publisher","DOI":"10.1159\/000144810"},{"key":"REF12","doi-asserted-by":"publisher","DOI":"10.1097\/00004424-197707000-00008"},{"key":"REF13","doi-asserted-by":"publisher","DOI":"10.1172\/JCI116831"},{"key":"REF14","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1985.tb07637.x"},{"key":"REF15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.281.3.F503"},{"key":"REF16","doi-asserted-by":"publisher","DOI":"10.1006\/jcis.1996.0173"},{"key":"REF17","doi-asserted-by":"publisher","DOI":"10.1016\/S0376-7388(98)00260-9"},{"key":"REF18","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2818.1999.00430.x"},{"key":"REF19","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.47"},{"key":"REF20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.281.5.F860"},{"key":"REF21","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-201X.1998.0316f.x"},{"key":"REF22","doi-asserted-by":"publisher","DOI":"10.1042\/bj1030852"},{"key":"REF23","doi-asserted-by":"publisher","DOI":"10.1039\/tf9585401754"},{"key":"REF24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.3.F396"},{"key":"REF25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.1.F84"},{"key":"REF26","doi-asserted-by":"crossref","unstructured":"Oken Dand Flamenbaum W.Micropuncture studies of proximal tubule concentrations in normal and nephrotic rats.J Clin Invest50: 1498\u20131505, 1970.","DOI":"10.1172\/JCI106635"},{"key":"REF27","doi-asserted-by":"crossref","unstructured":"Oliver JP, Anderson S, Troy JL, Brenner BM, and Deen WM.Determination of glomerular size selectivity in the normal rat with Ficoll.J Am Soc Nephrol3: 214\u2013228, 1992.","DOI":"10.1681\/ASN.V32214"},{"key":"REF28","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1797.1996.tb00088.x"},{"key":"REF29","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-3495(00)76566-0"},{"key":"REF30","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1994.74.1.163"},{"key":"REF31","doi-asserted-by":"publisher","DOI":"10.1016\/S0021-9975(97)80033-3"},{"key":"REF32","doi-asserted-by":"publisher","DOI":"10.1007\/BF01506150"},{"key":"REF33","doi-asserted-by":"publisher","DOI":"10.1159\/000428777"},{"key":"REF34","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1981.240.6.F569"},{"key":"REF35","unstructured":"Sims Dand Horne M.Non-aqueous fixative preserves macromolecules on the endothelial cell surface: an in situ study.Eur J Morphol31: 251\u2013256, 1993."},{"key":"REF36","unstructured":"Sonnenburg-Hatzopoulos C, Assel E, Schurek H, and Stolte H.Glomerular albumin leakage and morphology after neutralization of polyanions. II. Discrepancy of protamine induced albuminuria and fine structure of the glomerular filtration barrier.J Submicrosc Cytol Pathol16: 741\u2013751, 1984."},{"key":"REF37","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1979.140"},{"key":"REF38","doi-asserted-by":"crossref","unstructured":"S\u00f6rensson J, Ohlson M, and Haraldsson B.A quantitative analysis of the glomerular charge barrier in the rat.Am J Physiol Renal Physiol280: F646\u2013F656, 2001.","DOI":"10.1152\/ajprenal.2001.280.4.F646"},{"key":"REF39","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-201x.1998.00315.x"},{"key":"REF40","doi-asserted-by":"crossref","unstructured":"Weiss C, Passow H, and Rothstein A.Autoregulation of flow in isolated rat kidney in the absence of red cells.Am J Physiol196: 1115\u20131118, 1959.","DOI":"10.1152\/ajplegacy.1959.196.5.1115"},{"key":"REF41","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-201X.1996.553306000.x"},{"key":"REF42","doi-asserted-by":"publisher","DOI":"10.1016\/0304-4165(94)90064-7"},{"key":"REF43","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.140"},{"key":"REF44","unstructured":"Zeh M.Zur glomerul\u00e4ren permeabilit\u00e4t geladener und ungeladener makromolekule (Doctoral Thesis). Hannover, Germany: Hannover Medical School, 1994."}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00227.2001","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,5,1]],"date-time":"2022-05-01T09:38:07Z","timestamp":1651397887000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00227.2001"}},"issued":{"date-parts":[[2003,10]]},"references-count":44,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2003,10]]}},"alternative-id":["10.1152\/ajprenal.00227.2001"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00227.2001","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2003,10]]}},{"indexed":{"date-parts":[[2024,5,14]],"date-time":"2024-05-14T03:15:36Z","timestamp":1715656536963},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1987,12,1]]},"abstract":"<jats:p> The hydronephrotic kidney of Inactin-anesthetized female Wistar rats was exteriorized in a controlled bath to directly observe preglomerular and postglomerular vessels via television microscopy. Nitrendipine, added to the bath in a concentration that did not alter blood pressure, induced a concentration-dependent dilation of preglomerular vessels. The arcuate artery maximally dilated by 29 +\/- 4%, the interlobular artery by 24 +\/- 5%, the afferent arteriole near the interlobular artery by 60 +\/- 9%, and near the glomerulus by 28 +\/- 13%. In contrast the efferent arteriole near the glomerulus dilated by only 11 +\/- 6% and near the welling point by 7 +\/- 9%. Similarly, diltiazem significantly dilated preglomerular vessels but not efferent arterioles. Acetylcholine significantly dilated all preglomerular vessels and dilated the afferent arterioles near the glomerulus (by 51 +\/- 8%) to a greater extent than the calcium blockers. Acetylcholine also significantly dilated the efferent arterioles (near the glomerulus by 26 +\/- 5% and near the welling point by 12 +\/- 3%). These data suggest that the tone of the preglomerular vessels of the hydronephrotic kidney is more dependent on the entry of extracellular calcium through calcium antagonist-sensitive channels (i.e., potential dependent) than is the tone of the afferent arterioles near the glomerulus and the efferent arterioles. <\/jats:p>","DOI":"10.1152\/ajprenal.1987.253.6.f1157","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T03:25:22Z","timestamp":1513999522000},"page":"F1157-F1163","source":"Crossref","is-referenced-by-count":12,"title":["Calcium antagonists preferentially dilate preglomerular vessels of hydronephrotic kidney"],"prefix":"10.1152","volume":"253","author":[{"given":"J. T.","family":"Fleming","sequence":"first","affiliation":[{"name":"Department of Physiology, University of Louisville, Kentucky40292."}]},{"given":"N.","family":"Parekh","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Louisville, Kentucky40292."}]},{"given":"M.","family":"Steinhausen","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Louisville, Kentucky40292."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1987.253.6.F1157","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:51:15Z","timestamp":1567972275000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1987.253.6.F1157"}},"issued":{"date-parts":[[1987,12,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1987,12,1]]}},"alternative-id":["10.1152\/ajprenal.1987.253.6.F1157"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1987.253.6.f1157","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1987,12,1]]}},{"indexed":{"date-parts":[[2024,6,27]],"date-time":"2024-06-27T06:31:50Z","timestamp":1719469910985},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1988,4,1]]},"abstract":"<jats:p> The transport of organic anions in the proximal tubule occurs primarily through the epithelial cells. This process involves movement across both the luminal and contraluminal membranes via specialized transport systems. Although some of the organic anions are taken up into the cell from the lumen, they can also be accumulated in tubule cells from the interstitial compartment by a variety of transporters. The relative affinities of anions for the different luminal and contraluminal transporters in concert with their conjugate driving forces determine the net directional movement, i.e., organic anion absorption or secretion. By use of the approach of stopped-flow microperfusion, it has been possible to characterize the contraluminal anion transporters in the rat. The following three different systems have been identified: 1) an exchange system for sulfate and oxalate; 2) a cotransport system for Na<jats:sup>+<\/jats:sup> and dicarboxylates; and 3) an exchange system (the so-called p-aminohippuric acid transport system) for hydrophobic anions and long-chain fatty acids. By use of a wide variety of different analogues, the substrate specificities for these different systems were determined. Substrates with two negative ionic charges or with one negative ionic charge and one or more negative partial charges interact with all three systems, depending on the distance between the two charged groups. Polyhalogenated substrates are preferred by the dicarboxylate system. Those substrates which interact only with the p-aminohippurate transport system possess a hydrophobic area and one negative ionic charge or two negative partial charges. <\/jats:p>","DOI":"10.1152\/ajprenal.1988.254.4.f453","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T22:22:12Z","timestamp":1513981332000},"page":"F453-F462","source":"Crossref","is-referenced-by-count":11,"title":["Contraluminal transport systems in the proximal renal tubule involved in secretion of organic anions"],"prefix":"10.1152","volume":"254","author":[{"given":"K. J.","family":"Ullrich","sequence":"first","affiliation":[{"name":"Max-Planck-Institut fur Biophysik, Frankfurt am Main, Federal Republic of Germany."}]},{"given":"G.","family":"Rumrich","sequence":"additional","affiliation":[{"name":"Max-Planck-Institut fur Biophysik, Frankfurt am Main, Federal Republic of Germany."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1988.254.4.F453","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:49:59Z","timestamp":1567957799000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1988.254.4.F453"}},"issued":{"date-parts":[[1988,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1988,4,1]]}},"alternative-id":["10.1152\/ajprenal.1988.254.4.F453"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1988.254.4.f453","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1988,4,1]]}},{"indexed":{"date-parts":[[2024,6,20]],"date-time":"2024-06-20T17:58:36Z","timestamp":1718906316494},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1984,4,1]]},"abstract":"<jats:p> The role of 1,25-dihydroxyvitamin D3 in regulating the maternal-to-fetal transfer of calcium and phosphorus across the placenta was examined by measuring maternal and fetal plasma levels of these elements in vitamin D-replete and -deficient rats. Pregnant rats in their 20th day of gestation and their fetuses were studied. Two diets with different calcium and phosphorus contents were used to produce either hypocalcemia or hypophosphatemia in the vitamin D-deficient rats. Calcium and phosphorus levels in fetal plasma were always higher than maternal values, and in vitamin D deficiency a twofold gradient of calcium and a fivefold gradient of phosphorus concentrations across the placenta were observed. Since protein levels in fetal plasma were approximately fivefold lower than maternal values, protein binding does not account for the higher fetal than maternal concentrations of plasma calcium. These results, together with previous data showing normal calcium content of vitamin D-deficient fetuses, indicate that 1,25-dihydroxyvitamin D3 and other vitamin D3 metabolites are not involved in the active transport of calcium and phosphorus across the placenta in the rat. <\/jats:p>","DOI":"10.1152\/ajprenal.1984.246.4.f526","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T16:28:42Z","timestamp":1513960122000},"page":"F526-F529","source":"Crossref","is-referenced-by-count":7,"title":["Placental transport of calcium and phosphorus is not regulated by vitamin D"],"prefix":"10.1152","volume":"246","author":[{"given":"R.","family":"Brommage","sequence":"first","affiliation":[]},{"given":"H. F.","family":"DeLuca","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1984.246.4.F526","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:32:59Z","timestamp":1567967579000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1984.246.4.F526"}},"issued":{"date-parts":[[1984,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1984,4,1]]}},"alternative-id":["10.1152\/ajprenal.1984.246.4.F526"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1984.246.4.f526","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1984,4,1]]}},{"indexed":{"date-parts":[[2022,4,2]],"date-time":"2022-04-02T19:38:20Z","timestamp":1648928300167},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1978,6,1]]},"abstract":"<jats:p> In rats, a diet depleted of potassium caused a significant hypokalemia and hypermagnesemia, a diuresis and natriuresis, a decrease in urinary and fecal excretion of potassium, a magnesiuria, and a decrease in fecal excretion of magnesium. Balance studies revealed that potassium metabolism was negative in potassium-depleted rats and that magnesium metabolism was positive and higher than in control rats. In potassium-depleted rats, potassium and magnesium contents in muscle were reduced, whereas the sodium level was increased and plasma aldosterone was significantly lower. Therefore, the elevation in plasma concentration of magnesium induced by a diet poor in potassium is the result of a more positive metabolic balance of magnesium and of shifting of magnesium from the tissue into the plasma compartment. Results of additional preliminary studies support the possibility that the hypermagnesemia may be mediated through the depression in mineralocorticoid activity induced by the depletion of potassium. <\/jats:p>","DOI":"10.1152\/ajprenal.1978.234.6.f466","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T20:45:29Z","timestamp":1513975529000},"page":"F466-F471","source":"Crossref","is-referenced-by-count":1,"title":["Magnesium metabolism in potassium-depleted rats"],"prefix":"10.1152","volume":"234","author":[{"given":"C. G.","family":"Duarte","sequence":"first","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1978.234.6.F466","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:01:40Z","timestamp":1567969300000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1978.234.6.F466"}},"issued":{"date-parts":[[1978,6,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1978,6,1]]}},"alternative-id":["10.1152\/ajprenal.1978.234.6.F466"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1978.234.6.f466","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1978,6,1]]}},{"indexed":{"date-parts":[[2022,3,31]],"date-time":"2022-03-31T13:06:21Z","timestamp":1648731981163},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1993,2,1]]},"abstract":"<jats:p> The existence of dopamine receptor subtypes outside the central nervous system has been suggested by pharmacological and biochemical techniques. Whether the renal dopamine receptors are distinct from those cloned from the brain remains to be determined. Indeed, the expression of any of these receptor genes in the kidney has not been demonstrated definitively. In this study, we amplified D1A receptor cDNA from microdissected proximal convoluted tubules of the rat kidney by reverse transcription-polymerase chain reaction; primers were based on the sequence of rat D1A cDNA cloned from the brain and corresponded to the third cytoplasmic loop of the receptor. Specificity of the amplified products was verified by restriction analysis, Southern blots, and sequencing. Furthermore, solution hybridization indicated the presence of a single ribonuclease-protected RNA species corresponding to the D1A receptor mRNA in proximal tubules. These studies report for the first time the presence of D1A receptor message in the kidney. <\/jats:p>","DOI":"10.1152\/ajprenal.1993.264.2.f280","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T10:21:35Z","timestamp":1514024495000},"page":"F280-F285","source":"Crossref","is-referenced-by-count":8,"title":["Expression of dopamine D1A receptor gene in proximal tubule of rat kidneys"],"prefix":"10.1152","volume":"264","author":[{"given":"I.","family":"Yamaguchi","sequence":"first","affiliation":[{"name":"Department of Pathology, University of Virginia Medical Center,Charlottesville 22908."}]},{"given":"P. A.","family":"Jose","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Virginia Medical Center,Charlottesville 22908."}]},{"given":"M. M.","family":"Mouradian","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Virginia Medical Center,Charlottesville 22908."}]},{"given":"L. M.","family":"Canessa","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Virginia Medical Center,Charlottesville 22908."}]},{"suffix":"Jr","given":"F. J.","family":"Monsma","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Virginia Medical Center,Charlottesville 22908."}]},{"given":"D. R.","family":"Sibley","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Virginia Medical Center,Charlottesville 22908."}]},{"given":"K.","family":"Takeyasu","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Virginia Medical Center,Charlottesville 22908."}]},{"given":"R. A.","family":"Felder","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Virginia Medical Center,Charlottesville 22908."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1993.264.2.F280","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:28:57Z","timestamp":1567974537000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1993.264.2.F280"}},"issued":{"date-parts":[[1993,2,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1993,2,1]]}},"alternative-id":["10.1152\/ajprenal.1993.264.2.F280"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1993.264.2.f280","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1993,2,1]]}},{"indexed":{"date-parts":[[2022,3,31]],"date-time":"2022-03-31T13:24:55Z","timestamp":1648733095945},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1987,4,1]]},"abstract":"<jats:p> This study examines the cellular mechanisms of acid secretion by the in vitro perfused late distal tubule of Amphiuma kidney. Acidification of tubule fluid occurred against an electrochemical gradient of 16 mV; thus H+ secretion was active. Amiloride (1 mM) or a reduction of sodium in the perfusion fluid (from 83.7 to 7.7 mM) partially reduced acidification. Amiloride, in the presence of low sodium, completely inhibited acidification. Furthermore, acetazolamide and ouabain in the bath solution (0.1 mM) also inhibited acidification. Conductive properties of the epithelium and of individual cell membranes were determined by means of cable analysis of the tubule and intracellular voltage recordings. The transepithelial voltage and resistance averaged -0.4 +\/- 0.4 mV, lumen negative, and 7,147 +\/- 845 omega X cm, respectively. Two functionally different cell types were identified by intracellular microelectrodes. Type I cells had a basolateral membrane voltage (Vbl) of -67.7 mV. As determined by ion substitution experiments, the basolateral membrane was conductive to K+ and Cl-. This cell also had a 4-acetamido-4'-isothiocyanostilbene-2-2'-disulfonic acid (SITS)-sensitive Na+-dependent HCO3- exit pathway in the basolateral membrane. Type II cells had a Vbl of -76.1 mV (P less than 0.05 vs. type I) and the basolateral membrane was conductive to K+ and Cl- but not to HCO3-. HCO3- movement across the basolateral membrane in this cell may occur by electroneutral Cl- -HCO3- exchange. The apical cell membrane of both cell types did not contain measurable ionic conductances, as evidenced by a high value of apical membrane fractional resistance (0.98 +\/- 0.01).(ABSTRACT TRUNCATED AT 250 WORDS) <\/jats:p>","DOI":"10.1152\/ajprenal.1987.252.4.f691","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T02:13:31Z","timestamp":1513995211000},"page":"F691-F699","source":"Crossref","is-referenced-by-count":2,"title":["Electroneutral H+ secretion in distal tubule of Amphiuma"],"prefix":"10.1152","volume":"252","author":[{"given":"B.","family":"Stanton","sequence":"first","affiliation":[]},{"given":"A.","family":"Omerovic","sequence":"additional","affiliation":[]},{"given":"B.","family":"Koeppen","sequence":"additional","affiliation":[]},{"given":"G.","family":"Giebisch","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1987.252.4.F691","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:44:45Z","timestamp":1567971885000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1987.252.4.F691"}},"issued":{"date-parts":[[1987,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1987,4,1]]}},"alternative-id":["10.1152\/ajprenal.1987.252.4.F691"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1987.252.4.f691","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1987,4,1]]}},{"indexed":{"date-parts":[[2022,4,3]],"date-time":"2022-04-03T10:35:44Z","timestamp":1648982144506},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1983,3,1]]},"abstract":"<jats:p> Recent technological advances allowing direct in vivo measurements of the determinants of glomerular ultrafiltration have greatly expanded our understanding of that process. In addition, these in vivo studies have clarified the dynamics of glomerular ultrafiltration in a number of physiologic and pathophysiologic conditions. Despite this progress, important issues remain unresolved and beyond the scrutiny of in vivo techniques. We have therefore devised a technique for in vitro glomerular perfusion of the isolated dog glomerulus. In eight glomeruli perfused at physiologic rates, the glomerular filtration rate averaged 39 nl\/min and the filtration fraction was 0.19. Filtration pressure disequilibrium was observed in all studies and thus allowed calculation of a unique value for the ultrafiltration coefficient. That parameter averaged 2.34 nl\/(min X mmHg). Morphologic studies employing transmission electron microscopy indicate that isolated perfused glomeruli remain ultrastructurally intact. The method for glomerular isolation and in vitro perfusion is presented in detail, the results obtained are compared with published in vivo results, and the advantages offered by the technique are discussed. <\/jats:p>","DOI":"10.1152\/ajprenal.1983.244.3.f349","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T15:34:14Z","timestamp":1513956854000},"page":"F349-F354","source":"Crossref","is-referenced-by-count":0,"title":["In vitro perfusion of the isolated dog glomerulus"],"prefix":"10.1152","volume":"244","author":[{"given":"R. W.","family":"Osgood","sequence":"first","affiliation":[]},{"given":"M.","family":"Patton","sequence":"additional","affiliation":[]},{"given":"M. J.","family":"Hanley","sequence":"additional","affiliation":[]},{"given":"M.","family":"Venkatachalam","sequence":"additional","affiliation":[]},{"given":"H. J.","family":"Reineck","sequence":"additional","affiliation":[]},{"given":"J. H.","family":"Stein","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1983.244.3.F349","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:25:56Z","timestamp":1567967156000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1983.244.3.F349"}},"issued":{"date-parts":[[1983,3,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1983,3,1]]}},"alternative-id":["10.1152\/ajprenal.1983.244.3.F349"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1983.244.3.f349","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1983,3,1]]}},{"indexed":{"date-parts":[[2022,4,2]],"date-time":"2022-04-02T07:05:10Z","timestamp":1648883110912},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1984,12,1]]},"abstract":"<jats:p> Contents: the correct title for the article on page F82 by J. I. Mertz, J. A. Haas, T. J. Berndt, J. C. Burnett, Jr., and F. G. Knox is \u201cEffects of bradykinin on renal interstitial pressures and proximal tubule reabsorption.\u201d <\/jats:p>","DOI":"10.1152\/ajprenal.1984.247.6.f981-r","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T15:59:02Z","timestamp":1513958342000},"page":"F981-F981","source":"Crossref","is-referenced-by-count":0,"title":["Effects of bradykinin on renal interstitial pressures and proximal tubule reabsorption"],"prefix":"10.1152","volume":"247","author":[{"given":"J. I.","family":"Mertz","sequence":"first","affiliation":[]},{"given":"J. A.","family":"Haas","sequence":"additional","affiliation":[]},{"given":"T. J.","family":"Berndt","sequence":"additional","affiliation":[]},{"suffix":"Jr.","given":"J. C.","family":"Burnett","sequence":"additional","affiliation":[]},{"given":"F. G.","family":"Knox","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1984.247.6.F981-r","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:29:27Z","timestamp":1567967367000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1984.247.6.F981-r"}},"issued":{"date-parts":[[1984,12,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1984,12,1]]}},"alternative-id":["10.1152\/ajprenal.1984.247.6.F981-r"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1984.247.6.f981-r","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1984,12,1]]}},{"indexed":{"date-parts":[[2022,4,3]],"date-time":"2022-04-03T02:38:14Z","timestamp":1648953494024},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1985,1,1]]},"abstract":"<jats:p> Prostaglandin E2 (PGE2) inhibits the action of the antidiuretic hormone (ADH) in isolated collecting tubules. A negative feedback loop has been postulated whereby ADH stimulates PGE2 synthesis. Furthermore, lysyl-bradykinin (LBK) inhibits the antidiuretic effect of ADH, probably via PGE2. Enhanced PGE2 synthesis has also been implicated as contributing to the inability to maximally concentrate urine during the neonatal period. We investigated PGE2 synthesis in microdissected cortical (CCT), medullary (MCT), and branched cortical (BCT) collecting tubules from adult and in corticomedullary collecting tubules (CT) from newborn rabbits. Isolated BCT produced significantly less PGE2 (12 +\/- 2 pg X mm-1 X 20 min-1) than CCT (65 +\/- 9) or MCT (76 +\/- 8) from kidneys of adult rabbits. CT from newborn rabbits produced only 19 +\/- 3 pg\/mm, significantly less than either CCT or MCT from adults. A large variability in basal PGE2 production and hormonal response was observed from tubule to tubule. Under either basal conditions or in the presence of 2 microM arachidonic acid, LBK enhanced PGE2 synthesis in CCT and MCT from adults. ADH enhanced PGE2 production in MCT under basal conditions and in CCT in the presence of arachidonic acid. Neither LBK nor ADH stimulated PGE2 synthesis in neonatal CT. A23187 consistently stimulated PGE2 synthesis in CCT and MCT from adults and, to a lesser extent, in CT from newborn rabbits. Our results support the hypothesis that ADH and LBK enhance PGE2 synthesis in the collecting tubule. This response is, however, subject to large variations from tubule to tubule and depends on the in vitro incubation conditions. <\/jats:p>","DOI":"10.1152\/ajprenal.1985.248.1.f134","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T00:42:15Z","timestamp":1513989735000},"page":"F134-F144","source":"Crossref","is-referenced-by-count":5,"title":["Synthesis of prostaglandin E2 in different segments of isolated collecting tubules from adult and neonatal rabbits"],"prefix":"10.1152","volume":"248","author":[{"given":"D.","family":"Schlondorff","sequence":"first","affiliation":[]},{"given":"J. A.","family":"Satriano","sequence":"additional","affiliation":[]},{"given":"G. J.","family":"Schwartz","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1985.248.1.F134","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:33:12Z","timestamp":1567971192000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1985.248.1.F134"}},"issued":{"date-parts":[[1985,1,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1985,1,1]]}},"alternative-id":["10.1152\/ajprenal.1985.248.1.F134"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1985.248.1.f134","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1985,1,1]]}},{"indexed":{"date-parts":[[2022,4,5]],"date-time":"2022-04-05T19:04:24Z","timestamp":1649185464604},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1987,11,1]]},"abstract":"<jats:p> The effect of glucose on renal responses to alpha 1-adrenergic stimulation was examined in isolated rat kidneys perfused with 5 mM lactate, 5 mM alanine, 0.5 mM pyruvate, and 0.2 mM mercaptopicolinic acid. Adding 5 mM glucose to this perfusate vasodilated the kidneys and raised the glomerular filtration rate (GFR) and free water clearance without altering fractional sodium excretion. alpha 1-Adrenergic actions were evaluated with norepinephrine (NE, 60 nM), methoxamine (600 nM), and prazosin (1 microM). Glucose altered neither the vasoconstriction nor the reduction in GFR produced by NE and methoxamine but increased the antinatriuretic responses (P less than 0.001). Glucose was required for prazosin to inhibit the effect of NE on sodium and lithium excretion. The nonmetabolized glucose analogue, alpha-methyl-D-glucoside (5 mM), did not increase the antinatriuretic response to NE, therefore glucose metabolism and not Na cotransport stimulated the alpha 1-adrenergic response. Glucose did not alter alpha 1-adrenoceptor number or binding affinity for prazosin in renal cortical homogenates. We conclude that glucose metabolism in the proximal tubule is involved in the stimulation of sodium reabsorption by alpha 1-adrenoceptor agonists. <\/jats:p>","DOI":"10.1152\/ajprenal.1987.253.5.f810","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T04:14:24Z","timestamp":1514002464000},"page":"F810-F815","source":"Crossref","is-referenced-by-count":1,"title":["Alpha 1-adrenergic stimulation of renal Na reabsorption requires glucose metabolism"],"prefix":"10.1152","volume":"253","author":[{"given":"A. D.","family":"Baines","sequence":"first","affiliation":[{"name":"Department of Clinical Biochemistry, University of Toronto, Ontario,Canada."}]},{"given":"R.","family":"Drangova","sequence":"additional","affiliation":[{"name":"Department of Clinical Biochemistry, University of Toronto, Ontario,Canada."}]},{"given":"P.","family":"Ho","sequence":"additional","affiliation":[{"name":"Department of Clinical Biochemistry, University of Toronto, Ontario,Canada."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1987.253.5.F810","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:54:29Z","timestamp":1567972469000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1987.253.5.F810"}},"issued":{"date-parts":[[1987,11,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1987,11,1]]}},"alternative-id":["10.1152\/ajprenal.1987.253.5.F810"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1987.253.5.f810","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1987,11,1]]}},{"indexed":{"date-parts":[[2022,4,4]],"date-time":"2022-04-04T23:35:59Z","timestamp":1649115359254},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1982,4,1]]},"abstract":"<jats:p> The renal handling of inorganic phosphate (Pi) is in part under the control of a powerful mechanism that is independent of parathyroid hormone and has the ability to enhance net tubular Pi reabsorption in response to a reduction in the Pi supply. The decreased renal reabsorption of Pi, the salient feature of the human disease X-linked hypophosphatemia, could be due to a loss of this adaptive capability of the tubular Pi transport system. To investigate this hypothesis, mutant hypophosphatemic (HYP) mice were used as a model of the human disease. Male HYP mice and normal littermates were subjected to high (0.75 g\/100 g), low (0.25 g\/100 g), or very low (0.03 g\/100 g) phosphorus diets for periods varying between 1 and 20 days. Then the overall tubular Pi transport capacity was assessed by determining the maximal net Pi reabsorption per unit volume of glomerular filtrate (max TRPi\/ml GF). The results indicate that the marked enhancement of max TRPi\/ml GF, which is observed in normal mice after the first day of Pi restriction, is completely absent in HYP mice. In chronically thyroparathyroidectomized animals, 10 days of low phosphorus diet stimulated conspicuous max TRPi\/ml GF in normal mice, whereas the same regimen did not significantly change the Pi reabsorptive capacity of HYP counterparts. The results of this study suggest that X-linked hypophosphatemia is a disease with a defect in the mechanism responsible for the adaptation of the tubular Pi transport system to Pi restriction. <\/jats:p>","DOI":"10.1152\/ajprenal.1982.242.4.f353","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T08:48:59Z","timestamp":1513932539000},"page":"F353-F359","source":"Crossref","is-referenced-by-count":1,"title":["Abnormal tubular adaptation to dietary Pi restriction in X-linked hypophosphatemic mice"],"prefix":"10.1152","volume":"242","author":[{"given":"R. C.","family":"Muhlbauer","sequence":"first","affiliation":[]},{"given":"J. P.","family":"Bonjour","sequence":"additional","affiliation":[]},{"given":"H.","family":"Fleisch","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1982.242.4.F353","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T14:18:50Z","timestamp":1567952330000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1982.242.4.F353"}},"issued":{"date-parts":[[1982,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1982,4,1]]}},"alternative-id":["10.1152\/ajprenal.1982.242.4.F353"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1982.242.4.f353","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1982,4,1]]}},{"indexed":{"date-parts":[[2022,4,5]],"date-time":"2022-04-05T02:11:41Z","timestamp":1649124701961},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1994,3,1]]},"abstract":"<jats:p> The pH of the isolated frog skin epithelium was determined on a cellular and subcellular level based on the distribution of a weak organic acid, 4-bromobenzoic acid. The indicator is detectable by X-ray microanalysis due to the presence of an element label. The results show that the pH of principal cells, but not the Na concentration, is closely correlated with the rate of transepithelial Na transport. Acidification leads to an inhibition of Na transport, regardless of whether the change was spontaneous or experimentally induced. Under the conditions of this study, the pH of principal cells was not well regulated. At a bath pH of 7.0, large pH differences between the cell layers were detectable. In mitochondria-rich cells, the pH was a function of the intracellular Cl concentration but not the Na transport rate. The cytoplasmic pH consistently exceeded the nuclear pH. The nuclear-cytoplasmic pH differential in principal cells amounted to 0.3 pH units, which is equivalent to a nuclear potential of -17 mV. The results support the view that the intracellular pH (pHi) is an important regulator of transepithelial Na transport. Regulation is primarily achieved at the level of the apical Na channel, making the Na influx the rate-limiting step in Na reabsorption. <\/jats:p>","DOI":"10.1152\/ajprenal.1994.266.3.f367","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T06:02:48Z","timestamp":1514008968000},"page":"F367-F374","source":"Crossref","is-referenced-by-count":1,"title":["pHi determines rate of sodium transport in frog skin: results of a new method to determine pHi"],"prefix":"10.1152","volume":"266","author":[{"given":"R.","family":"Rick","sequence":"first","affiliation":[{"name":"Department of Physiology and Biophysics, University of Alabama atBirmingham 35294."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1994.266.3.F367","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:31:35Z","timestamp":1567960295000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1994.266.3.F367"}},"issued":{"date-parts":[[1994,3,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1994,3,1]]}},"alternative-id":["10.1152\/ajprenal.1994.266.3.F367"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1994.266.3.f367","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1994,3,1]]}},{"indexed":{"date-parts":[[2022,4,5]],"date-time":"2022-04-05T01:38:28Z","timestamp":1649122708097},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1990,6,1]]},"abstract":"<jats:p> The present study tested the hypothesis that the influence of dietary phosphate (Pi) on the renal handling of Pi changes during development. We evaluated whether variations in the dietary Pi content would alter the tubular capacity of Pi reabsorption [Max RPi\/glomerular filtration rate (GFR)] in immature rats, which have a relatively greater Max RPi\/GFR compared with adult rats. Then we examined the response of immature and adult Pi-deprived rats to dietary Pi replenishment. Studies were performed in acutely thyroparathyroidectomized Wistar rats at three different stages of development: immature (3- to 4-wk old), young (6- to 7-wk old), and adult (12- to 13-wk old). Animals were fed either low (0.07%)-, normal (0.7%), or high (1.8%)-phosphate diet (LPD, NPD, and HPD, respectively) for 4 days and were then prepared for renal clearance experiments to determine the Max RPi\/GFR. On all dietary regimens, the Max RPi\/GFR was highest in immature rats and decreased progressively with age. When fed LPD, immature rats, with an already elevated rate of phosphate transport, displayed a remarkable 68 +\/- 13% increase in the Max RPi\/GFR (from 5.58 +\/- 0.29 to 9.47 +\/- 0.76 mumol\/ml, P less than 0.01). This was significantly greater than the 38 +\/- 3% increase observed in adult rats (from 3.50 +\/- 0.18 to 4.81 +\/- 0.09 mumol\/ml). Conversely, in response to HPD, the decrease in the Max RPi\/GFR was smallest in immature rats (-42 +\/- 2%) compared with the decrement in either young (-54 +\/- 3%) or adult (-61 +\/- 6%) rats.(ABSTRACT TRUNCATED AT 250 WORDS) <\/jats:p>","DOI":"10.1152\/ajprenal.1990.258.6.f1650","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T18:11:03Z","timestamp":1513966263000},"page":"F1650-F1656","source":"Crossref","is-referenced-by-count":2,"title":["Renal adaptation to changes in dietary phosphate during development"],"prefix":"10.1152","volume":"258","author":[{"given":"S. E.","family":"Mulroney","sequence":"first","affiliation":[{"name":"Department of Physiology and Biophysics, Georgetown University School of Medicine, Washington, DC 20007."}]},{"given":"A.","family":"Haramati","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, Georgetown University School of Medicine, Washington, DC 20007."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1990.258.6.F1650","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:20:52Z","timestamp":1567956052000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1990.258.6.F1650"}},"issued":{"date-parts":[[1990,6,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1990,6,1]]}},"alternative-id":["10.1152\/ajprenal.1990.258.6.F1650"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1990.258.6.f1650","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1990,6,1]]}},{"indexed":{"date-parts":[[2022,4,5]],"date-time":"2022-04-05T01:50:39Z","timestamp":1649123439369},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1994,12,1]]},"abstract":"<jats:p> The direct tubular natriuretic effect of calcium channel blockers (CCBs) may be due to an interaction between CCBs and a renal tubular dopamine receptor. We therefore studied the effects of two chemically unrelated CCBs, diltiazem and isradipine, infused into the right renal artery of 5% saline-loaded anesthetized rats alone or in the presence of a D1 antagonist, SKF-83742. Isradipine (0.03 microgram.kg-1.min-1) or diltiazem (20 but not 10 micrograms.kg-1.min-1) alone produced an increase in urine flow and an approximate doubling of absolute and fractional sodium excretion, which was not seen in the left kidney or in the control animals (analysis of variance, Scheffe's test, P &lt; 0.05). SKF-83742 alone given systemically or into the right renal artery did not affect these parameters but did block the actions of diltiazem or isradipine. There was no change in mean arterial pressure, renal blood flow, or glomerular filtration rate in any of the experiments. In additional studies, we found that a combined infusion of dopamine (0.1 microgram.kg-1.min-1) and diltiazem (10 micrograms.kg-1.min-1) (doses that by themselves did not alter renal function) produced a twofold or greater increase in urine flow and absolute and fractional sodium excretion; glomerular filtration rate was not significantly changed. Intrarenal arterial CCBs, without a change in renal hemodynamics, produce a natriuresis that is blocked by a D1 antagonist. Concomitant administration of diltiazem and dopamine (each in subeffective doses when used alone) produces a synergistic effect.(ABSTRACT TRUNCATED AT 250 WORDS) <\/jats:p>","DOI":"10.1152\/ajprenal.1994.267.6.f965","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T23:54:01Z","timestamp":1513986841000},"page":"F965-F970","source":"Crossref","is-referenced-by-count":0,"title":["Role of renal dopamine D1 receptors in natriuresis induced by calcium channel blockers"],"prefix":"10.1152","volume":"267","author":[{"given":"G. M.","family":"Eisner","sequence":"first","affiliation":[{"name":"Department of Medicine and Physiology and Biophysics, Georgetown University Medical Center, Washington, District of Columbia 20007."}]},{"given":"I.","family":"Yamaguchi","sequence":"additional","affiliation":[{"name":"Department of Medicine and Physiology and Biophysics, Georgetown University Medical Center, Washington, District of Columbia 20007."}]},{"given":"R. A.","family":"Felder","sequence":"additional","affiliation":[{"name":"Department of Medicine and Physiology and Biophysics, Georgetown University Medical Center, Washington, District of Columbia 20007."}]},{"given":"L. D.","family":"Asico","sequence":"additional","affiliation":[{"name":"Department of Medicine and Physiology and Biophysics, Georgetown University Medical Center, Washington, District of Columbia 20007."}]},{"given":"P. A.","family":"Jose","sequence":"additional","affiliation":[{"name":"Department of Medicine and Physiology and Biophysics, Georgetown University Medical Center, Washington, District of Columbia 20007."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1994.267.6.F965","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:55:43Z","timestamp":1567958143000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1994.267.6.F965"}},"issued":{"date-parts":[[1994,12,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1994,12,1]]}},"alternative-id":["10.1152\/ajprenal.1994.267.6.F965"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1994.267.6.f965","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1994,12,1]]}},{"indexed":{"date-parts":[[2022,4,1]],"date-time":"2022-04-01T19:44:11Z","timestamp":1648842251556},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1989,1,1]]},"abstract":"<jats:p> Potassium chloride permeability and relative ionic conductances of rat renal cortical brush-border (BBMV) and basolateral (BLMV) membrane vesicles were examined using the fluorescent probe 3,3'-dipropylthiadicarbocyanine iodide [diS-C3-(5)]. Vesicles were simultaneously isolated and separated by free-flow electrophoresis. These studies demonstrated that neither BBMV nor BLMV equilibrated in 100 mM KCl despite prolonged incubation. In both, an inwardly directed KCl gradient was sustained for 3 h. The low intravesicular KCl concentration of BLMV was confirmed utilizing the response of electrogenic Na+-dependent [3H]glutamine transport to variations in the membrane potential. Chloride conductance was significantly less than potassium conductance in BBMV and BLMV. Consequently, an inside-positive potential was maintained across both membranes. BLMV were significantly more fluid, less permeable, had a lower relative chloride conductance, and maintained a greater inside-positive potential than BBMV. The KCl permeabilities of BBMV and BLMV were inversely related to endogenous membrane copper content and were significantly reduced by exogenous copper. Permeability did not correlate with membrane magnesium content, nor was it affected by exogenous magnesium. These studies suggest that endogenous copper as well as intracellular factors may regulate the permeabilities of the brush-border and basolateral membranes of proximal tubule cells in vivo. <\/jats:p>","DOI":"10.1152\/ajprenal.1989.256.1.f18","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T21:05:54Z","timestamp":1513976754000},"page":"F18-F28","source":"Crossref","is-referenced-by-count":4,"title":["Differential permeabilities of rat renal brush-border and basolateral membrane vesicles"],"prefix":"10.1152","volume":"256","author":[{"given":"M. S.","family":"Lipkowitz","sequence":"first","affiliation":[{"name":"Department of Medicine, Mount Sinai School of Medicine, New York, NewYork 10029."}]},{"given":"R. G.","family":"Abramson","sequence":"additional","affiliation":[{"name":"Department of Medicine, Mount Sinai School of Medicine, New York, NewYork 10029."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1989.256.1.F18","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:07:52Z","timestamp":1567969672000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1989.256.1.F18"}},"issued":{"date-parts":[[1989,1,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1989,1,1]]}},"alternative-id":["10.1152\/ajprenal.1989.256.1.F18"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1989.256.1.f18","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1989,1,1]]}},{"indexed":{"date-parts":[[2022,4,5]],"date-time":"2022-04-05T02:22:47Z","timestamp":1649125367621},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1996,4,1]]},"abstract":"<jats:p> The spatial relationship between vitamin D receptor (VDR) and calbindin D28k [calcium binding protein D28k (CaBP-D28k)] gene expression within the murine kidney was studied by localizing their mRNAs in discrete nephron structures using reverse transcription-polymerase chain reaction (RT-PCR). Primers for beta-actin mRNA were used as a control for the presence of tissue during RT-PCR for CaBP-D28k mRNA. mRNA for CaBP-D28k was found only in distal convoluted tubules (DCTs), connecting tubules (CNTs), and cortical collecting ducts (CCDs). In contrast, VDR mRNA was detected in glomeruli, S2 proximal convoluted tubules, cortical thick ascending limbs of Henle's loop, DCTs, CNTs, and initial CCDs. The presence of both VDR and CaBP-D28k mRNA in DCTs, CNTs, and CCDs is consistent with the hypothesis that cacitriol acts via the VDR to stimulate CaBP-D28k synthesis. Conversely, the presence of VDR mRNA in other parts of the nephron suggests that calcitriol has genomically mediated actions within the kidney in addition to stimulation of CaBP-D28k synthesis. <\/jats:p>","DOI":"10.1152\/ajprenal.1996.270.4.f677","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T02:32:56Z","timestamp":1513996376000},"page":"F677-F681","source":"Crossref","is-referenced-by-count":2,"title":["RT-PCR microlocalization of mRNAs for calbindin D28k and vitamin D receptor in the murine nephron"],"prefix":"10.1152","volume":"270","author":[{"given":"L.","family":"Liu","sequence":"first","affiliation":[{"name":"Department of Medicine, University of Oklahoma Health Sciences Center,Oklahoma City, USA."}]},{"given":"A.","family":"Khastgir","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Oklahoma Health Sciences Center,Oklahoma City, USA."}]},{"given":"J. M.","family":"McCauley","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Oklahoma Health Sciences Center,Oklahoma City, USA."}]},{"given":"S. T.","family":"Dunn","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Oklahoma Health Sciences Center,Oklahoma City, USA."}]},{"given":"J. H.","family":"Morrissey","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Oklahoma Health Sciences Center,Oklahoma City, USA."}]},{"given":"S.","family":"Christakos","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Oklahoma Health Sciences Center,Oklahoma City, USA."}]},{"given":"M. R.","family":"Hughes","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Oklahoma Health Sciences Center,Oklahoma City, USA."}]},{"given":"J. E.","family":"Bourdeau","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Oklahoma Health Sciences Center,Oklahoma City, USA."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1996.270.4.F677","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:07:47Z","timestamp":1567958867000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1996.270.4.F677"}},"issued":{"date-parts":[[1996,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1996,4,1]]}},"alternative-id":["10.1152\/ajprenal.1996.270.4.F677"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1996.270.4.f677","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1996,4,1]]}},{"indexed":{"date-parts":[[2022,4,4]],"date-time":"2022-04-04T00:23:34Z","timestamp":1649031814924},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1990,11,1]]},"abstract":"<jats:p> We have previously shown that the isolated perfused cortical collecting duct (CCD) from chloride-depleted alkalotic (CDA) rats continues to secrete HCO3 for up to 3 h. To determine whether the sustained alteration in transport was associated with changes in intracellular ion concentrations, we performed energy-dispersive X-ray microanalysis in microdissected tubule bundles obtained from CDA rats and rats with normal acid-base status (CON). Before analysis, the bundles from both groups were incubated for 1 h in vitro in a modified Ringer solution (pH 7.4, 105 mM Cl). Principal (PC) and intercalated cells (IC) of the CCD from CON animals differed in the nuclear concentration of Na (17.0 vs. 24.7 mmol\/l cell water), K (192.5 vs. 177.0 mmol\/l cell water), and Cl (17.8 vs. 47.8 mmol\/l cell water). Cells of the cortical thick ascending limb of Henle (CTAL) had the lowest Na and Cl values (11.5 and 14.8 mmol\/l cell water, respectively). CDA resulted in no systematic Cl changes. In the IC the nuclear Na concentration was significantly increased (32.0 vs. 24.7 mmol\/l cell water) and in all cells a small reduction in K concentration was detectable. These findings suggest that 1) the different transport functions of IC, PC, and CTAL are associated with differences in the intracellular ion composition, and 2) the sustained HCO3 secretion seen in CCD from CDA rats cannot be explained as the result of intracellular Cl depletion. <\/jats:p>","DOI":"10.1152\/ajprenal.1990.259.5.f778","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T23:44:53Z","timestamp":1513986293000},"page":"F778-F782","source":"Crossref","is-referenced-by-count":2,"title":["Ion concentrations in the rat CCD: differences between cell types and effect of alkalosis"],"prefix":"10.1152","volume":"259","author":[{"given":"J. D.","family":"Gifford","sequence":"first","affiliation":[{"name":"Department of Physiology and Biophysics, University of Alabama,Birmingham 35294."}]},{"given":"J. H.","family":"Galla","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, University of Alabama,Birmingham 35294."}]},{"given":"R. G.","family":"Luke","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, University of Alabama,Birmingham 35294."}]},{"given":"R.","family":"Rick","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, University of Alabama,Birmingham 35294."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1990.259.5.F778","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:27:03Z","timestamp":1567970823000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1990.259.5.F778"}},"issued":{"date-parts":[[1990,11,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1990,11,1]]}},"alternative-id":["10.1152\/ajprenal.1990.259.5.F778"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1990.259.5.f778","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1990,11,1]]}},{"indexed":{"date-parts":[[2022,4,3]],"date-time":"2022-04-03T00:11:28Z","timestamp":1648944688810},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1980,4,1]]},"abstract":"<jats:p> Lactate is absorbed in the proximal tubule and also enters tubular cells at the peritubular membrane. To characterize peritubular lactate entry, lactate uptake was measured in isolated nonperfused proximal tubules. Tubules were dissected and incubated in Ringer solution with L(+)-[U-14C]lactate and 3H2O. After incubation, the tubules were extracted, and the extracts were assayed for 14C and 3H or were chromatographed to determine the percentage of tubule 14C identifiable as lactate. Maximal steady-state tubular fluid-to-bath lactate concentration ratios (TF\/B lactate) occurred by 30-60 min incubation at 25 degrees C. In 30 min, one-third of the tubules established a TF\/B lactate ratio greater than 1.00, and 61.4 +\/- 18.6% of tubule 14C was lactate. There was no difference in TF\/B lactate ratio in proximal and distal proximal segments. Uptake was depressed at 5 degrees C. Mersalyl at 10(-4) M increased the TF\/B lactate ratio and tubule water content. Probenecid at 7.5-30 x 10(-4) M also increased the TF\/B lactate ratio. Distal proximal tubules incubated with [3H]PAH showed a control TF\/B para-aminohippurate (PAH) ratio of approximately 30, but with 10(-4) M mersalyl the TF\/B PAH ratio was approximately 1.00. Lactate uptake at the peritubular membrane occurs against an electrochemical gradient, independently from the PAH transport mechanism. <\/jats:p>","DOI":"10.1152\/ajprenal.1980.238.4.f296","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T08:22:56Z","timestamp":1513930976000},"page":"F296-F304","source":"Crossref","is-referenced-by-count":1,"title":["Peritubular uptake of lactate by Thamnophis proximal tubule"],"prefix":"10.1152","volume":"238","author":[{"given":"P. H.","family":"Brand","sequence":"first","affiliation":[]},{"given":"R.","family":"Stansbury","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1980.238.4.F296","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T14:17:40Z","timestamp":1567952260000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1980.238.4.F296"}},"issued":{"date-parts":[[1980,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1980,4,1]]}},"alternative-id":["10.1152\/ajprenal.1980.238.4.F296"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1980.238.4.f296","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1980,4,1]]}},{"indexed":{"date-parts":[[2022,4,3]],"date-time":"2022-04-03T00:15:37Z","timestamp":1648944937957},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1985,5,1]]},"abstract":"<jats:p> Prostaglandin synthesis inhibition antagonizes the chloruretic effect of furosemide. To identify the site of this interaction, cortical micropuncture was performed in furosemide-treated rats during meclofenamate or indomethacin infusion. Control rats received the vehicle for prostaglandin synthesis inhibition. The fractional excretion of chloride decreased from 10.6 +\/- 1.0% in control rats to 6.5 +\/- 0.93% in indomethacin-treated rats (P less than 0.01) and to 5.7 +\/- 0.7% in meclofenamate-treated rats (P less than 0.001). Mean arterial pressure, inulin clearance, renal blood flow, and single nephron glomerular filtration rate were not different among the groups. Chloride delivery out of the late proximal tubule was also not different among the groups. Early distal tubule chloride delivery was greater (P less than 0.001) in control rats than in either prostaglandin-inhibited group. Late distal chloride delivery was also greater in control rats. Calculated loop segment chloride uptake was 9 +\/- 2% in furosemide-treated control rats but 18 +\/- 2% in both indomethacin- and meclofenamate-treated rats (P less than 0.05). Distal tubule chloride uptake was greater in control than in prostaglandin-inhibited rats. Thus, the attenuated chloruretic response to furosemide observed in indomethacin- or meclofenamate-treated animals may in part result from increased chloride uptake in the loop segment of superficial nephrons. <\/jats:p>","DOI":"10.1152\/ajprenal.1985.248.5.f698","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T19:32:13Z","timestamp":1513971133000},"page":"F698-F704","source":"Crossref","is-referenced-by-count":0,"title":["Prostaglandin inhibitors alter loop segment chloride uptake during furosemide diuresis"],"prefix":"10.1152","volume":"248","author":[{"given":"K. A.","family":"Kirchner","sequence":"first","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1985.248.5.F698","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:32:08Z","timestamp":1567956728000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1985.248.5.F698"}},"issued":{"date-parts":[[1985,5,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1985,5,1]]}},"alternative-id":["10.1152\/ajprenal.1985.248.5.F698"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1985.248.5.f698","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1985,5,1]]}},{"indexed":{"date-parts":[[2022,4,3]],"date-time":"2022-04-03T09:58:21Z","timestamp":1648979901999},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2022,2,1]]},"DOI":"10.1152\/ajprenal.2022.322.2.au","type":"journal-article","created":{"date-parts":[[2022,2,14]],"date-time":"2022-02-14T15:46:58Z","timestamp":1644853618000},"page":"i-iii","update-policy":"http:\/\/dx.doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["First Author Spotlight"],"prefix":"10.1152","volume":"322","member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.2022.322.2.AU","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,2,14]],"date-time":"2022-02-14T15:46:59Z","timestamp":1644853619000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.2022.322.2.AU"}},"issued":{"date-parts":[[2022,2,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2022,2,1]]}},"alternative-id":["10.1152\/ajprenal.2022.322.2.AU"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.2022.322.2.au","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2022,2,1]]},"assertion":[{"value":"2021-12-28","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2022-01-10","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2022-01-10","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2022-02-14","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2022,3,30]],"date-time":"2022-03-30T05:59:10Z","timestamp":1648619950643},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1984,5,1]]},"abstract":"<jats:p> We assessed the vascular, phosphaturic, and calcemic responses to several synthetic parathyroid hormone (PTH) analogues. Bovine (b) PTH (1-34), human (h) PTH (1-34), hPTH (53-84), [ Nle8 , Nle18 , Tyr34 ]bPTH (1-34), and [ Nle8 , Nle18 , Tyr34 ]bPTH (3-34) were administered in doses between 1 and 500 micrograms\/kg as bolus intravenous injections to male Wistar-Kyoto rats aged 18-26 wk. Antagonism of the action of PTH was assessed in rats pretreated with 10 or 100 micrograms\/kg [ Nle8 , Nle18 , Tyr34 ]bPTH (3-34) followed by 10 micrograms\/kg of bPTH (1-34), or with 10 micrograms\/kg hPTH (53-84) followed by 10 micrograms\/kg hPTH (1-34). Bovine PTH (1-34), hPTH (1-34), and [ Nle8 , Nle18 , Tyr34 ]bPTH (1-34) produced virtually identical log dose-dependent hypotension, with 100 micrograms\/kg of each analogue producing a 56% reduction in mean arterial pressure. Neither hPTH (53-84) nor [ Nle8 , Nle18 , Tyr34 ]bPTH (3-34) demonstrated any effect on mean arterial pressure at doses up to 500 micrograms\/kg. Pretreatment with the inactive analogues failed to antagonize the vasodilating response to either bPTH (1-34) or hPTH (1-34). The vasoactive analogues significantly increased urinary phosphorus excretion while the inactive analogues did not modify it. hPTH (1-34) produced a modest decrease in serum Ca2+ at 1 min after injection. The results document that the vasodilating effect of PTH is a specific action of the peptide. Deletion of the first two amino acid residues abolishes both the phosphaturic and hypotensive effects of the peptide. Acute changes in serum Ca2+ do not appear to be a prerequisite for the vasodilatory response. Inactive analogues of PTH do not antagonize the vascular actions of the peptide. <\/jats:p>","DOI":"10.1152\/ajprenal.1984.246.5.f551","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T11:46:51Z","timestamp":1513943211000},"page":"F551-F556","source":"Crossref","is-referenced-by-count":2,"title":["Structural prerequisites for the hypotensive action of parathyroid hormone"],"prefix":"10.1152","volume":"246","author":[{"given":"D. H.","family":"Ellison","sequence":"first","affiliation":[]},{"given":"D. A.","family":"McCarron","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1984.246.5.F551","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T14:34:45Z","timestamp":1567953285000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1984.246.5.F551"}},"issued":{"date-parts":[[1984,5,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1984,5,1]]}},"alternative-id":["10.1152\/ajprenal.1984.246.5.F551"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1984.246.5.f551","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1984,5,1]]}},{"indexed":{"date-parts":[[2022,4,3]],"date-time":"2022-04-03T15:32:03Z","timestamp":1648999923907},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1984,6,1]]},"abstract":"<jats:p> We studied the excretion of electrolytes and adenosine 3',5'-cyclic monophosphate (cAMP) by rat kidneys perfused for 2 or 3 h at several concentrations of phosphate (Pi). Fractional phosphate excretion increased with higher perfusate Pi concentrations (up to 4.0 mM Pi) without parathyroid hormone (PTH), but no tubular maximum for phosphate reabsorption was reached. The addition of synthetic bovine 1-34 PTH (bPTH) gave a dose-related phosphaturia that depended on the perfusate Pi level. The urinary cAMP response to doses of bPTH was highly dependent on perfusate Pi concentration: with 20 nM bPTH, urinary cAMP was 211 +\/- 94 pmol\/ml glomerular filtration rate at 1.2 mM Pi and was 3,998 +\/- 711 at 4.0 mM Pi (P less than 0.001). Without bPTH, cAMP excretion did not differ among Pi levels. Calcium-to-sodium clearance ratio rose with time in kidneys perfused without bPTH but fell with the addition of as little as 0.02 nM bPTH, regardless of Pi concentration. Variations in Pi or bPTH did not affect fractional magnesium excretion, which fell by 68% through 3 h of perfusion (P less than 0.001). These data suggest that the effects of Pi concentration on renal electrolyte excretion are consistent with changes in the filtered Pi load but that extracellular Pi concentrations dramatically alter the renal cAMP response to bPTH in the isolated perfused kidney. <\/jats:p>","DOI":"10.1152\/ajprenal.1984.246.6.f907","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T11:45:27Z","timestamp":1513943127000},"page":"F907-F915","source":"Crossref","is-referenced-by-count":0,"title":["Effect of perfusate phosphate concentration on responses to PTH in isolated rat kidney"],"prefix":"10.1152","volume":"246","author":[{"given":"S. J.","family":"Scheinman","sequence":"first","affiliation":[]},{"given":"R.","family":"Coulson","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1984.246.6.F907","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T14:34:59Z","timestamp":1567953299000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1984.246.6.F907"}},"issued":{"date-parts":[[1984,6,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1984,6,1]]}},"alternative-id":["10.1152\/ajprenal.1984.246.6.F907"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1984.246.6.f907","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1984,6,1]]}},{"indexed":{"date-parts":[[2022,4,1]],"date-time":"2022-04-01T00:50:41Z","timestamp":1648774241797},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1996,5,1]]},"abstract":"<jats:p> Ten patients (18 +\/- 1 yr) on chronic hemodialysis (HD) with anemia were studied before and after treatment with erythropoietin (EPO) for 9 mo. Six patients had evidence of iron overload (serum ferritin over 300 ng\/ml; group I) and the other four patients (serum ferritin below 300 ng\/ml; group II) did not. Before treatment, both groups of patients were glucose tolerant but insulin resistant and hyperinsulinemic. There was equal correction of anemia but no significant changes in serum biochemistry (apart from iron studies) or anthropometric measurements in both groups. With amelioration of anemia and iron overload in group I, insulin sensitivity increased by 53% to within normal values. Insulin secretion also normalized. With amelioration of anemia but no change in iron status in group II, insulin sensitivity (increased by 60%) and insulin secretion also normalized. Thus correction of anemia by EPO reversed insulin resistance and hyperinsulinemia in HD patients with or without iron overload. The effects of correction of anemia rather than iron overload may be more important in the pathogenesis of insulin abnormalities in end-stage renal disease. <\/jats:p>","DOI":"10.1152\/ajprenal.1996.270.5.f839","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T06:59:33Z","timestamp":1514012373000},"page":"F839-F844","source":"Crossref","is-referenced-by-count":6,"title":["Correction of anemia by erythropoietin reverses insulin resistance and hyperinsulinemia in uremia"],"prefix":"10.1152","volume":"270","author":[{"given":"R. H.","family":"Mak","sequence":"first","affiliation":[{"name":"Department of Pediatrics, Stanford University School of Medicine,California 94305-5119, USA."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1996.270.5.F839","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:08:26Z","timestamp":1567973306000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1996.270.5.F839"}},"issued":{"date-parts":[[1996,5,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1996,5,1]]}},"alternative-id":["10.1152\/ajprenal.1996.270.5.F839"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1996.270.5.f839","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1996,5,1]]}},{"indexed":{"date-parts":[[2022,3,30]],"date-time":"2022-03-30T08:37:08Z","timestamp":1648629428237},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1982,7,1]]},"abstract":"<jats:p> The Na, K, and Cl conductive properties and the electrophysiological variability of the rabbit isolated cortical collecting tubule were assessed by evaluating the effect of single-ion substitutions on the transepithelial potential difference, Vte, and the transepithelial conductance, Gte. The Na permeability (and conductance) of the tight junction and basolateral cell membrane appeared to be low. However, a significant but variable amiloride-sensitive Na conductance was identified at the apical cell membrane. Although this Na conductance accounts for less than 10% of the Gte, variations in this conductance caused major alterations in the active transepithelial Na current and the Vte. A highly variable K permeability (and conductance) was also identified at the apical cell border and may account for some of the variability in Vte and Gte. This probably provides a pathway for K secretion from cell to lumen. The K permeability of the tight junction and basolateral cell membrane appeared to be relatively low. In contrast, the Cl permeability (and conductance) of the tight junction, and perhaps of the basolateral cell membrane, appeared to be high but variable and to account for the major fraction of the Gte and its variability. It is concluded that variations in the Na and K conductance of the apical cell membrane and the Cl conductance of the tight junction and basolateral cell membrane predominantly account for the variations in the electrophysiological properties of the cortical collecting tubule. <\/jats:p>","DOI":"10.1152\/ajprenal.1982.243.1.f81","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T13:49:57Z","timestamp":1513950597000},"page":"F81-F95","source":"Crossref","is-referenced-by-count":6,"title":["Ionic conductive properties and electrophysiology of the rabbit cortical collecting tubule"],"prefix":"10.1152","volume":"243","author":[{"given":"R. G.","family":"O'Neil","sequence":"first","affiliation":[]},{"given":"E. L.","family":"Boulpaep","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1982.243.1.F81","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:15:49Z","timestamp":1567966549000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1982.243.1.F81"}},"issued":{"date-parts":[[1982,7,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1982,7,1]]}},"alternative-id":["10.1152\/ajprenal.1982.243.1.F81"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1982.243.1.f81","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1982,7,1]]}},{"indexed":{"date-parts":[[2024,1,22]],"date-time":"2024-01-22T22:00:09Z","timestamp":1705960809471},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1986,10,1]]},"abstract":"<jats:p> Lysine uptake by isolated rat renal brush-border membrane vesicles occurs via a single saturable system plus a significant diffusion component with indication of a single energy of activation on an Arrhenius plot. Initial uptake is not sodium dependent, and intravesicular accumulation of lysine at longer time points is greatest in the absence of sodium. Accumulation levels differ in the presence or absence of NaCl or choline chloride and are specific for the cation used. Lysine uptake is membrane potential sensitive and inhibitable by cystine, dibasic amino acids, and cycloleucine. Heteroexchange diffusion of lysine with cystine and lysine with arginine occurs, but no heteroexchange occurs with cycloleucine, indicating that lysine shares a transport system with cystine and dibasic amino acids but not with cycloleucine. <\/jats:p>","DOI":"10.1152\/ajprenal.1986.251.4.f734","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T00:55:07Z","timestamp":1513990507000},"page":"F734-F742","source":"Crossref","is-referenced-by-count":3,"title":["Lysine uptake by rat renal brush-border membrane vesicles"],"prefix":"10.1152","volume":"251","author":[{"given":"P. D.","family":"McNamara","sequence":"first","affiliation":[]},{"given":"C. T.","family":"Rea","sequence":"additional","affiliation":[]},{"given":"S.","family":"Segal","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1986.251.4.F734","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:34:18Z","timestamp":1567971258000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1986.251.4.F734"}},"issued":{"date-parts":[[1986,10,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1986,10,1]]}},"alternative-id":["10.1152\/ajprenal.1986.251.4.F734"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1986.251.4.f734","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1986,10,1]]}},{"indexed":{"date-parts":[[2023,5,11]],"date-time":"2023-05-11T15:10:07Z","timestamp":1683817807008},"reference-count":53,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2007,7]]},"abstract":"<jats:p>The renin-angiotensin system is activated in the developing kidney and is necessary for normal renal development, but is further activated by unilateral ureteral obstruction (UUO). During nephrogenesis, there is a switch from a preponderance of angiotensin AT<jats:sub>2<\/jats:sub>to AT<jats:sub>1<\/jats:sub>receptors in the rat. We examined the renal cellular response to angiotensin II receptor inhibition in the neonatal rat subjected to partial UUO under anesthesia within 48 h of birth. Group I (\u201cearly\u201d) received saline vehicle, losartan (AT<jats:sub>1<\/jats:sub>inhibitor), or PD-123319 (AT<jats:sub>2<\/jats:sub>inhibitor) during the completion of nephrogenesis in the first 10 days of life. Group II (\u201clate\u201d) received each of the three treatments throughout the subsequent 10 days of life. Kidneys were harvested at 21 days, and the distribution of renin, apoptosis, macrophages, \u03b1-smooth muscle actin, and collagen was determined. Losartan and PD-123319 each increased vascular renin distribution in both kidneys. Partial UUO reduced growth and increased apoptosis, macrophages, \u03b1-smooth muscle actin, and collagen in the obstructed kidney. Early losartan treatment further increased \u03b1-smooth muscle actin and collagen in the obstructed kidney and induced apoptosis, macrophages, and collagen in the contralateral kidney. Late losartan treatment had no effect on any of the parameters in either kidney, and PD-123319 had no effect on either kidney. We conclude that selective inhibition of AT<jats:sub>1<\/jats:sub>receptors during nephrogenesis (but not during subsequent renal maturation) exacerbates injury to the obstructed kidney and also injures the contralateral kidney. These results suggest that angiotensin II receptor blockers should be avoided in the developing hydronephrotic kidney.<\/jats:p>","DOI":"10.1152\/ajprenal.00071.2007","type":"journal-article","created":{"date-parts":[[2007,4,19]],"date-time":"2007-04-19T00:38:47Z","timestamp":1176943127000},"page":"F262-F268","source":"Crossref","is-referenced-by-count":16,"title":["Angiotensin AT<sub>1<\/sub>-receptor inhibition exacerbates renal injury resulting from partial unilateral ureteral obstruction in the neonatal rat"],"prefix":"10.1152","volume":"293","author":[{"given":"Christopher M.","family":"Coleman","sequence":"first","affiliation":[]},{"given":"Jordan J.","family":"Minor","sequence":"additional","affiliation":[]},{"given":"Laura E.","family":"Burt","sequence":"additional","affiliation":[]},{"given":"Barbara A.","family":"Thornhill","sequence":"additional","affiliation":[]},{"given":"Michael S.","family":"Forbes","sequence":"additional","affiliation":[]},{"given":"Robert L.","family":"Chevalier","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.356"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00488.x"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00427.x"},{"key":"R4","doi-asserted-by":"crossref","unstructured":"Chen CO, Park MH, Forbes MS, Thornhill BA, Kiley SC, Yoo KH, Chevalier RL.Angiotensin converting enzyme inhibition aggravates renal interstitial injury resulting from partial unilateral ureteral obstruction in the neonatal rat.Am J Physiol Renal Physiol292: F946\u2013F955, 2007.","DOI":"10.1152\/ajprenal.00287.2006"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00533.x"},{"key":"R6","unstructured":"Chevalier RL, Cachat F.Role of angiotensin II in chronic ureteral obstruction. In:The Renin-Angiotensin System and Progression of Renal Diseases, edited by Wolf G. Basel: Karger, 2001, p. 250\u2013260."},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1996.270.2.R393"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.1.F41"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(01)62137-2"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1097\/01.ju.0000082964.24635.15"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(01)66407-3"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-006-0070-1"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1097\/01.LAB.0000101911.53973.90"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1177\/41.3.7679127"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1002\/path.1417"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000130564.75008.F5"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1172\/JCI4236"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2000.00374.x"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-200018020-00001"},{"key":"R20","doi-asserted-by":"crossref","unstructured":"Guron G, Marcussen N, Nilsson A, Sundelin B, Friberg P.Postnatal time frame for renal vulnerability to enalapril in rats.J Am Soc Nephol10: 1550\u20131560, 1999.","DOI":"10.1681\/ASN.V1071550"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00294.2003"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.183"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00387.2005"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1993.246"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.215"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00162.x"},{"key":"R27","doi-asserted-by":"crossref","unstructured":"Lange-Sperandio B, Fulda S, Vandewalle A, Chevalier RL.Macrophages induce apoptosis in proximal tubule cells.Pediatr Nephrol18: 335\u2013341, 2003.","DOI":"10.1007\/s00467-003-1123-3"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00236.2003"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.1998.00893.x"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00643.x"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1007\/s004290050126"},{"key":"R32","unstructured":"McCausland JE, Bertram JF, Ryan GB, Alcorn D.Glomerular number and size following chronic angiotensin II blockade in the postnatal rat.Exp Nephrol5: 201\u2013209, 1997."},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(05)65933-2"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1172\/JCI4401"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.414"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.1.F39"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1254\/jjp.90.361"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1172\/JCI200215045"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00059.2006"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.30.5.1238"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006040356"},{"key":"R42","doi-asserted-by":"crossref","unstructured":"Satoh M, Kashihara N, Yamasaki Y, Maruyama K, Okamoto K, Maeshima Y, Sugiyama H, Sugaya T, Murakami K, Makino H.Renal interstitial fibrosis is reduced in angiotensin II type 1a receptor-deficient mice.J Am Soc Nephol12: 317\u2013325, 2001.","DOI":"10.1681\/ASN.V122317"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-003-1158-5"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1038\/sj.cdd.4401779"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00721.x"},{"key":"R46","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000149105.75125.2a"},{"key":"R47","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(01)62699-5"},{"key":"R48","unstructured":"Takese O, Cunnigham PN, Guo R, Hack BK, Quigg RJ.Clusterin induces apoptosis in proximal tubular epithelial cells exposed to LPS by preventing NF-kB-dependent Bcl-xL production (Abstract).J Am Soc Nephol17: 781A, 2006."},{"key":"R49","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00052.x"},{"key":"R50","doi-asserted-by":"crossref","unstructured":"Topcu SO, Pedersen M, Norregard R, Wang G, Knepper M, Djurhuus JC, Nielsen S, Jorgensen TM, Frokiaer J.Candesartan prevents long-term impairment of renal function in response to neonatal partial unilateral ureteral obstruction.Am J Physiol Renal Physiol292: F736\u2013F748, 2007.","DOI":"10.1152\/ajprenal.00241.2006"},{"key":"R51","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-3476(05)81916-X"},{"key":"R52","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)62533-3"},{"key":"R53","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.2000.278.3.R640"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00071.2007","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,5,11]],"date-time":"2023-05-11T14:28:08Z","timestamp":1683815288000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00071.2007"}},"issued":{"date-parts":[[2007,7]]},"references-count":53,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2007,7]]}},"alternative-id":["10.1152\/ajprenal.00071.2007"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00071.2007","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2007,7]]}},{"indexed":{"date-parts":[[2023,2,20]],"date-time":"2023-02-20T09:52:06Z","timestamp":1676886726331},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1985,9,1]]},"abstract":"<jats:p> Renal blood flow and hemodynamic autoregulation were assessed in seven chronically instrumented canines studied in the conscious state and after pentobarbital anesthesia administration (30 mg\/kg). The effects of acute arterial hemorrhage (10 and 15 ml\/kg) were also studied. In the conscious state, no significant changes in autoregulation were observed following 10 mg\/kg hemorrhage. With pentobarbital and 10 ml\/kg hemorrhage, a significant change in the limits of autoregulation was noted (autoregulatory limit 78.5 +\/- 16.6 vs. 88.4 +\/- 25.3 mmHg, P less than 0.05). Four animals were also studied in the conscious state following 15 ml\/kg acute arterial hemorrhage. In these animals, mean arterial pressure decreased (from 105.0 +\/- 11.4 to 87.8 +\/- 7.2 mmHg, P less than 0.025) but renal blood flow (from 293 +\/- 38 to 272 +\/- 65 ml\/min) and autoregulatory limit did not change. We conclude that renal blood flow is unaffected by hemorrhage or pentobarbital alone. In the conscious state, renal pressure-flow autoregulation is maintained despite moderate hemorrhage and systemic hypotension. The lower limit of autoregulation is significantly changed by even minor hemorrhage in the pentobarbital-anesthetized state. <\/jats:p>","DOI":"10.1152\/ajprenal.1985.249.3.f356","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T00:12:48Z","timestamp":1513987968000},"page":"F356-F360","source":"Crossref","is-referenced-by-count":1,"title":["Effect of pentobarbital and hemorrhage on renal autoregulation"],"prefix":"10.1152","volume":"249","author":[{"given":"P. C.","family":"Kremser","sequence":"first","affiliation":[]},{"given":"B. L.","family":"Gewertz","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1985.249.3.F356","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:31:06Z","timestamp":1567971066000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1985.249.3.F356"}},"issued":{"date-parts":[[1985,9,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1985,9,1]]}},"alternative-id":["10.1152\/ajprenal.1985.249.3.F356"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1985.249.3.f356","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1985,9,1]]}},{"indexed":{"date-parts":[[2024,8,8]],"date-time":"2024-08-08T22:33:38Z","timestamp":1723156418287},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1988,1,1]]},"abstract":"<jats:p> The concentration of atrial natriuretic factor (ANF) in atria and plasma was investigated in relation to the regulation of renal glomerular ANF receptors in the rat during changes in water and sodium intake. A decrease in plasma immunoreactive ANF (IR-ANF) was observed after 4 days of water deprivation or after 1 wk on a low-sodium diet, whereas animals offered 1% NaCl in their drinking water had elevated plasma ANF values. Atrial IR-ANF was lower in water-deprived and higher in sodium-restricted rats than in their respective controls. A low-sodium intake or water deprivation increased the density of glomerular ANF receptors, whereas the inverse occurred with a high-salt consumption. It is concluded that an inverse correlation exists between ANF plasma concentration and renal glomerular ANF receptor sites. <\/jats:p>","DOI":"10.1152\/ajprenal.1988.254.1.f51","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T03:33:38Z","timestamp":1514000018000},"page":"F51-F55","source":"Crossref","is-referenced-by-count":3,"title":["Glomerular ANF receptor regulation during changes in sodium and water metabolism"],"prefix":"10.1152","volume":"254","author":[{"given":"G.","family":"Gauquelin","sequence":"first","affiliation":[{"name":"Laboratory of Experimental Hypertension and Vasoactive Peptides, Clinical Research Institute of Montreal, Quebec, Canada."}]},{"given":"R.","family":"Garcia","sequence":"additional","affiliation":[{"name":"Laboratory of Experimental Hypertension and Vasoactive Peptides, Clinical Research Institute of Montreal, Quebec, Canada."}]},{"given":"F.","family":"Carrier","sequence":"additional","affiliation":[{"name":"Laboratory of Experimental Hypertension and Vasoactive Peptides, Clinical Research Institute of Montreal, Quebec, Canada."}]},{"given":"M.","family":"Cantin","sequence":"additional","affiliation":[{"name":"Laboratory of Experimental Hypertension and Vasoactive Peptides, Clinical Research Institute of Montreal, Quebec, Canada."}]},{"given":"J.","family":"Gutkowska","sequence":"additional","affiliation":[{"name":"Laboratory of Experimental Hypertension and Vasoactive Peptides, Clinical Research Institute of Montreal, Quebec, Canada."}]},{"given":"G.","family":"Thibault","sequence":"additional","affiliation":[{"name":"Laboratory of Experimental Hypertension and Vasoactive Peptides, Clinical Research Institute of Montreal, Quebec, Canada."}]},{"given":"E. L.","family":"Schiffrin","sequence":"additional","affiliation":[{"name":"Laboratory of Experimental Hypertension and Vasoactive Peptides, Clinical Research Institute of Montreal, Quebec, Canada."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1988.254.1.F51","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:51:21Z","timestamp":1567972281000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1988.254.1.F51"}},"issued":{"date-parts":[[1988,1,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1988,1,1]]}},"alternative-id":["10.1152\/ajprenal.1988.254.1.F51"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1988.254.1.f51","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1988,1,1]]}},{"indexed":{"date-parts":[[2023,6,1]],"date-time":"2023-06-01T21:05:47Z","timestamp":1685653547039},"reference-count":30,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,8,1]]},"abstract":"<jats:p>Renin-expressing cells in the kidney normally appear as mural cells of developing preglomerular vessels and finally impose as granulated juxtaglomerular cells in adult kidneys. The differentiation of renin-expressing cells from the metanephric mesenchyme in general and the potential role of special precursor stages in particular is not well understood. Therefore, it was the aim of this study to search for renin cell precursors in the kidney. As an experimental model, we used kidneys of aldosterone synthase-deficient mice, which display a prominent compensatory overproduction of renin cells that are arranged in multilayered perivascular cell clusters. We found that the perivascular cell clusters contained two apparently distinct cell types, one staining positive for renin and another one staining positive for type I procollagen (PC1). It appeared as if PC1 and renin expression were inversely related at the cellular level. The proportion of renin-positive to PC1-positive cells in the clusters was inversely linked to the rate of salt intake, as was overall renin expression. Our findings suggest that the cells in the perivascular cell clusters can reversibly switch between PC1 and renin expression and that PC1-expressing cells might be precursors of renin cells. A few of those PC1-positive cells were found also in adult wild-type kidneys in the juxtaglomerular lacis cell area, in which renin expression can be induced on demand.<\/jats:p>","DOI":"10.1152\/ajprenal.00079.2013","type":"journal-article","created":{"date-parts":[[2013,6,13]],"date-time":"2013-06-13T03:14:41Z","timestamp":1371093281000},"page":"F355-F361","source":"Crossref","is-referenced-by-count":7,"title":["Procollagen I-expressing renin cell precursors"],"prefix":"10.1152","volume":"305","author":[{"given":"Christian","family":"Karger","sequence":"first","affiliation":[{"name":"Institut f\u00fcr Physiologie der Universit\u00e4t Regensburg, Regensburg, Germany;"}]},{"given":"Felix","family":"Kurtz","sequence":"additional","affiliation":[{"name":"Klinik und Poliklinik f\u00fcr Innere Medizin II, Universit\u00e4t Regensburg, Regensburg, Germany;"}]},{"given":"Dominik","family":"Steppan","sequence":"additional","affiliation":[{"name":"Institut f\u00fcr Physiologie der Universit\u00e4t Regensburg, Regensburg, Germany;"}]},{"given":"Ilona","family":"Schwarzensteiner","sequence":"additional","affiliation":[{"name":"Institut f\u00fcr Physiologie der Universit\u00e4t Regensburg, Regensburg, Germany;"}]},{"given":"Katharina","family":"Machura","sequence":"additional","affiliation":[{"name":"Institut f\u00fcr Physiologie der Universit\u00e4t Regensburg, Regensburg, Germany;"}]},{"given":"Peter","family":"Angel","sequence":"additional","affiliation":[{"name":"Division of Signal Transduction and Growth Control, Deutsches Krebsforschungszentrum, Heidelberg, Germany; and"}]},{"given":"Bernhard","family":"Banas","sequence":"additional","affiliation":[{"name":"Klinik und Poliklinik f\u00fcr Innere Medizin II, Universit\u00e4t Regensburg, Regensburg, Germany;"}]},{"given":"Juha","family":"Risteli","sequence":"additional","affiliation":[{"name":"Institute of Diagnostics, Department of Clinical Chemistry, University of Oulu and NordLab Oulu, Oulu University Hospital, Oulu, Finland"}]},{"given":"Armin","family":"Kurtz","sequence":"additional","affiliation":[{"name":"Institut f\u00fcr Physiologie der Universit\u00e4t Regensburg, Regensburg, Germany;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/j.devcel.2011.07.001"},{"key":"B2","doi-asserted-by":"crossref","first-page":"516","DOI":"10.1681\/ASN.V93516","volume":"9","author":"Bartter FC","year":"1998","journal-title":"J Am Soc Nephrol"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2011040401"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00011.2009"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/0145-2126(86)90021-4"},{"key":"B6","doi-asserted-by":"crossref","first-page":"149","DOI":"10.1007\/BF00229076","volume":"255","author":"Christensen JA","year":"1989","journal-title":"Cell Tissue Res"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1002\/gene.20004"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.259.4.F660"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2009.423"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.29.1.216"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1006\/jsbi.2002.4450"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/j.humpath.2006.07.001"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.2011.05531.x"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00647.2010"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2012080791"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1146\/annurev-physiol-012110-142238"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1210\/en.2004-1102"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0b013e32833aff32"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00257.2005"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000249902.09036.e7"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.272.4.F515"},{"key":"B22","first-page":"543","volume":"71","author":"Owen RA","year":"1994","journal-title":"Lab Invest"},{"key":"B23","doi-asserted-by":"crossref","first-page":"63","DOI":"10.1681\/ASN.V9163","volume":"9","author":"Reddi V","year":"1998","journal-title":"J Am Soc Nephrol"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1038\/labinvest.2012.57"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002571"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2011080818"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/S1534-5807(04)00134-0"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1007\/BF00305480"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1007\/BF00750580"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1164\/rccm.200406-698OC"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00079.2013","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,2,25]],"date-time":"2022-02-25T00:22:01Z","timestamp":1645748521000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00079.2013"}},"issued":{"date-parts":[[2013,8,1]]},"references-count":30,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2013,8,1]]}},"alternative-id":["10.1152\/ajprenal.00079.2013"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00079.2013","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2013,8,1]]}},{"indexed":{"date-parts":[[2023,3,27]],"date-time":"2023-03-27T17:51:54Z","timestamp":1679939514695},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1994,8,1]]},"abstract":"<jats:p> The mechanism(s) whereby a denuded renal tubular epithelial cell surface becomes reestablished remains unknown. We therefore measured the rate of renewal of mechanical wounds made in confluent monolayers of two established renal tubular epithelial cell lines. We found that wounds of MDCK cells heal at a faster rate than wounds of LLC-PK1 cells. The magnitude of wound healing did not differ when cells grown on plastic were compared with cells grown on fibronectin, laminin, or collagen. Irradiation (4,000 rads) of MDCK and LLC-PK1 cells significantly reduced indexes of proliferation (5-bromo-2'-deoxyuridine and thymidine uptake) without affecting wound healing. Serum and epidermal growth factor (EGF) enhance whereas transforming growth factor-beta 1 (TGF-beta 1) impairs wound healing. Hepatocyte growth factor (HGF) stimulates wound healing at low concentrations and inhibits healing at high concentrations in MDCK cells while not affecting healing of LLC-PK1 cell wounds at any concentration. Several interleukins (IL-1, IL-2, IL-3, and IL-6) did not affect wound healing in either cell type. Healing of LLC-PK1 but not MDCK cells was impaired by exposure to a peptide containing a RGD sequence. Conversely, healing of MDCK but not LLC-PK1 cells was impaired by the REDV tetrapeptide. Healing of both LLC-PK1 and MDCK was impaired by heparin but not by the LDVPS peptide. These results demonstrate that mechanical wounds of LLC-PK1 and MDCK cells heal, at least in part, by migration. Healing is regulated by serum and growth factors including EGF, HGF, and TGF-beta 1.(ABSTRACT TRUNCATED AT 250 WORDS) <\/jats:p>","DOI":"10.1152\/ajprenal.1994.267.2.f257","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T05:02:00Z","timestamp":1514005320000},"page":"F257-F264","source":"Crossref","is-referenced-by-count":9,"title":["Mechanisms of recovery from mechanical injury of renal tubular epithelial cells"],"prefix":"10.1152","volume":"267","author":[{"given":"H. T.","family":"Sponsel","sequence":"first","affiliation":[{"name":"Department of Medicine, Denver Veterans Affairs Medical Center,Colorado."}]},{"given":"R.","family":"Breckon","sequence":"additional","affiliation":[{"name":"Department of Medicine, Denver Veterans Affairs Medical Center,Colorado."}]},{"given":"W.","family":"Hammond","sequence":"additional","affiliation":[{"name":"Department of Medicine, Denver Veterans Affairs Medical Center,Colorado."}]},{"given":"R. J.","family":"Anderson","sequence":"additional","affiliation":[{"name":"Department of Medicine, Denver Veterans Affairs Medical Center,Colorado."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1994.267.2.F257","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:56:20Z","timestamp":1567972580000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1994.267.2.F257"}},"issued":{"date-parts":[[1994,8,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1994,8,1]]}},"alternative-id":["10.1152\/ajprenal.1994.267.2.F257"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1994.267.2.f257","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1994,8,1]]}},{"indexed":{"date-parts":[[2024,6,16]],"date-time":"2024-06-16T02:52:41Z","timestamp":1718506361991},"reference-count":9,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2010,5]]},"DOI":"10.1152\/ajprenal.00095.2010","type":"journal-article","created":{"date-parts":[[2010,3,3]],"date-time":"2010-03-03T20:51:05Z","timestamp":1267649465000},"page":"F1103-F1104","source":"Crossref","is-referenced-by-count":4,"title":["Compelling \u201cmetabolomic\u201d biomarkers may signal PKD pathogenesis"],"prefix":"10.1152","volume":"298","author":[{"given":"Erik M.","family":"Schwiebert","sequence":"first","affiliation":[]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbadis.2006.11.006"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.2337\/db06-1593"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1007\/s11302-008-9102-6"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00108.2004"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00291.2006"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.0337.2000"},{"key":"B7","author":"Taylor SL","journal-title":"Am J Physiol Renal Physiol"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00103.2006"},{"key":"B9","doi-asserted-by":"crossref","first-page":"218","DOI":"10.1681\/ASN.V102218","volume":"10","author":"Wilson PD","year":"1999","journal-title":"J Am Soc Nephrol"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00095.2010","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,10,24]],"date-time":"2021-10-24T05:08:21Z","timestamp":1635052101000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00095.2010"}},"issued":{"date-parts":[[2010,5]]},"references-count":9,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2010,5]]}},"alternative-id":["10.1152\/ajprenal.00095.2010"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00095.2010","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2010,5]]}},{"indexed":{"date-parts":[[2022,4,2]],"date-time":"2022-04-02T21:05:09Z","timestamp":1648933509037},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1988,10,1]]},"abstract":"<jats:p> It has been suggested that the glomerular basement membrane heparan sulfate proteoglycan (HSPG) is an important determinant of the glomerular permselectivity barrier. Derangements in the content of basement membrane heparan sulfate have been implicated in alterations in glomerular permselectivity seen in many glomerular diseases such as aminonucleoside nephrosis. The cellular origin and metabolism of the glomerular basement membrane HSPG have not been studied in detail. We have detected the expression of the proteoglycan by cloned glomerular visceral epithelial cells of the rat by employing a specific antibody against the core protein of HSPG isolated from the rat glomerular basement membrane. These findings suggest that in the rat in vivo glomerular visceral epithelial cells are one source of heparan sulfate present in the glomerular basement membrane. The effect of puromycin aminonucleoside (PAN) on the HSPG core protein content of the cloned glomerular epithelial cells was studied. By a quantitative immunoperoxidase method, the aminonucleoside caused a 28% reduction in the core protein content of the epithelial cells (P less than 0.01) following 72 h of incubation. However, the content of Heymann nephritis-related antigen, Fx1A was unchanged. Studies employing [3H]leucine incorporation showed that PAN was a weak inhibitor of de novo protein synthesis at 24 h of incubation, with complete recovery at 48 and 72 h. These data suggest that PAN effect on heparan sulfate core protein cannot be attributed to generalized inhibition of protein synthesis. The precise mechanism underlying the aminonucleoside effect on heparan sulfate core protein remains to be elucidated. <\/jats:p>","DOI":"10.1152\/ajprenal.1988.255.4.f590","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T16:24:38Z","timestamp":1513959878000},"page":"F590-F596","source":"Crossref","is-referenced-by-count":5,"title":["Effect of puromycin aminonucleoside on HSPG core protein content of glomerular epithelial cells"],"prefix":"10.1152","volume":"255","author":[{"given":"B. S.","family":"Kasinath","sequence":"first","affiliation":[{"name":"Department of Medicine, Rush Medical College, Illinois 60612."}]},{"given":"A. K.","family":"Singh","sequence":"additional","affiliation":[{"name":"Department of Medicine, Rush Medical College, Illinois 60612."}]},{"given":"Y. S.","family":"Kanwar","sequence":"additional","affiliation":[{"name":"Department of Medicine, Rush Medical College, Illinois 60612."}]},{"given":"E. J.","family":"Lewis","sequence":"additional","affiliation":[{"name":"Department of Medicine, Rush Medical College, Illinois 60612."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1988.255.4.F590","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:10:47Z","timestamp":1567955447000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1988.255.4.F590"}},"issued":{"date-parts":[[1988,10,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1988,10,1]]}},"alternative-id":["10.1152\/ajprenal.1988.255.4.F590"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1988.255.4.f590","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1988,10,1]]}},{"indexed":{"date-parts":[[2022,4,5]],"date-time":"2022-04-05T07:49:51Z","timestamp":1649144991472},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1995,6,1]]},"abstract":"<jats:p> After sublethal injury, proximal tubular cells acquire resistance to further attack. This study evaluated whether this could be a possible consequence of decreased protein synthesis, a potential correlate of cell damage. To this end, cultured human proximal tubular cells (HK-2) were subjected to 0\u201324 h of protein synthesis inhibition (&gt; 98%), either by adding protein synthesis inhibitors [cycloheximide (CH) or verrucarin A] or by inducing sublethal ATP depletion (antimycin A + 2-deoxyglucose). After 24 h of these treatments, significant resistance to Ca2+ ionophore\/ATP depletion-induced attack was noted (assessed by vital dye exclusion, compared with normal cells). That &lt; or = 6 h of protein synthesis inhibition caused no cytoresistance implied the importance of evolving protein depletion rather than nonspecific drug effects or protein synthesis inhibition per se. CH plus ATP depletion did not induce additive benefits, suggesting a common mechanism. Cytoresistance was dissociated from the extent of free Ca2+ loading and ATP depletion but was associated with a decrease in membrane deacylation. CH removal promptly restored protein synthesis and cytoresistance was lost; conversely, ATP recovery did not restore protein synthesis and cytoresistance persisted. The emergence of cytoresistance correlated with the disappearance\/dephosphorylation of an unidentified 130-kDa tyrosine-phosphorylated protein\/protein complex (denoted pp-130). The functional significance of this change was suggested by the fact that tyrosine phosphatase inhibition with orthovanadate maintained pp-130 expression and prevented the cytoresistant state. We conclude that protein synthesis inhibition in HK-2 cells can induce a cytoresistant state. Suppression in phospholipase activity and altered tyrosine phosphorylation events may have functional significance in this regard. <\/jats:p>","DOI":"10.1152\/ajprenal.1995.268.6.f1154","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T05:34:24Z","timestamp":1514007264000},"page":"F1154-F1163","source":"Crossref","is-referenced-by-count":8,"title":["Protein synthesis inhibition induces cytoresistance in cultured human proximal tubular (HK-2) cells"],"prefix":"10.1152","volume":"268","author":[{"given":"M.","family":"Iwata","sequence":"first","affiliation":[{"name":"Fred Hutchinson Cancer Research Center, University of Washington, Seattle 98104, USA."}]},{"given":"J.","family":"Herrington","sequence":"additional","affiliation":[{"name":"Fred Hutchinson Cancer Research Center, University of Washington, Seattle 98104, USA."}]},{"given":"R. A.","family":"Zager","sequence":"additional","affiliation":[{"name":"Fred Hutchinson Cancer Research Center, University of Washington, Seattle 98104, USA."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1995.268.6.F1154","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:01:02Z","timestamp":1567972862000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1995.268.6.F1154"}},"issued":{"date-parts":[[1995,6,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1995,6,1]]}},"alternative-id":["10.1152\/ajprenal.1995.268.6.F1154"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1995.268.6.f1154","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1995,6,1]]}},{"indexed":{"date-parts":[[2023,10,13]],"date-time":"2023-10-13T08:20:42Z","timestamp":1697185242909},"reference-count":48,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1999,6,1]]},"abstract":"<jats:p>Uroguanylin, guanylin, and lymphoguanylin are small peptides that activate renal and intestinal receptor guanylate cyclases (GC). They are structurally similar to bacterial heat-stable enterotoxins (ST) that cause secretory diarrhea. Uroguanylin, guanylin, and ST elicit natriuresis, kaliuresis, and diuresis by direct actions on kidney GC receptors. A 3,762-bp cDNA characterizing a uroguanylin\/guanylin\/ST receptor was isolated from opossum kidney (OK) cell RNA\/cDNA. This kidney cDNA (OK-GC) encodes a mature protein containing 1,049 residues sharing 72.4\u201375.8% identity with rat, human, and porcine forms of intestinal GC-C receptors. COS or HEK-293 cells expressing OK-GC receptor protein were activated by uroguanylin, guanylin, or ST<jats:sub>13<\/jats:sub>peptides. The 3.8-kb OK-GC mRNA transcript is most abundant in the kidney cortex and intestinal mucosa, with lower mRNA levels observed in urinary bladder, adrenal gland, and myocardium and with no detectable transcripts in skin or stomach mucosa. We propose that OK-GC receptor GC participates in a renal mechanism of action for uroguanylin and\/or guanylin in the physiological regulation of urinary sodium, potassium, and water excretion. This renal tubular receptor GC may be a target for circulating uroguanylin in an endocrine link between the intestine and kidney and\/or participate in an intrarenal paracrine mechanism for regulation of kidney function via the intracellular second messenger, cGMP.<\/jats:p>","DOI":"10.1152\/ajprenal.1999.276.6.f882","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T18:00:01Z","timestamp":1514052001000},"page":"F882-F891","source":"Crossref","is-referenced-by-count":14,"title":["Structure and activity of OK-GC: a kidney receptor guanylate cyclase activated by guanylin peptides"],"prefix":"10.1152","volume":"276","author":[{"given":"Roslyn M.","family":"London","sequence":"first","affiliation":[{"name":"Pharmacology, and"}]},{"given":"Sammy L.","family":"Eber","sequence":"additional","affiliation":[{"name":"Harry S. Truman Memorial Veterans Hospital and Departments of"},{"name":"Pharmacology, and"}]},{"given":"Sandhya S.","family":"Visweswariah","sequence":"additional","affiliation":[{"name":"Department of Molecular Reproduction, Development and Genetics, Indian Institute of Science, Bangalore 560012, India"}]},{"given":"William J.","family":"Krause","sequence":"additional","affiliation":[{"name":"Pathology and Anatomical Sciences, School of Medicine, Missouri University, Columbia, Missouri 65212; and"}]},{"given":"Leonard R.","family":"Forte","sequence":"additional","affiliation":[{"name":"Harry S. Truman Memorial Veterans Hospital and Departments of"},{"name":"Pharmacology, and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2736(81)90243-1"},{"issue":"35","key":"B2","first-page":"G972","volume":"272","author":"Blanchard R. K.","year":"1997","journal-title":"Am. J. Physiol."},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/0003-2697(76)90527-3"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.89.3.947"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1210\/edrv-15-2-135"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1996.0255"},{"issue":"36","key":"B7","first-page":"E957","volume":"273","author":"Fan X.","year":"1997","journal-title":"Am. J. Physiol."},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1210\/endo.138.11.5539"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.75.6.2800"},{"issue":"44","key":"B10","first-page":"F191","volume":"275","author":"Fonteles M. C.","year":"1998","journal-title":"Am. J. Physiol."},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1210\/endo.140.4.6630"},{"key":"B12","first-page":"17","volume":"11","author":"Forte L. R.","year":"1996","journal-title":"News Physiol. Sci."},{"issue":"24","key":"B13","first-page":"F1040","volume":"255","author":"Forte L. R.","year":"1988","journal-title":"Am. J. Physiol."},{"issue":"26","key":"B14","first-page":"F874","volume":"257","author":"Forte L. R.","year":"1989","journal-title":"Am. J. Physiol."},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1992.263.3.C607"},{"key":"B16","first-page":"173","volume":"125","author":"Giannella R. A.","year":"1995","journal-title":"J. Lab. Clin. Med."},{"key":"B17","first-page":"276","volume":"45","author":"Greenberg R. N.","year":"1997","journal-title":"J. Investig. Med."},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/S0016-5085(96)70018-5"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1093\/infdis\/142.2.220"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.94.6.2705"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.90.22.10464"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/0167-4838(95)00204-4"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1038\/271755a0"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.94.4.1276"},{"issue":"37","key":"B25","first-page":"G633","volume":"274","author":"Joo N. S.","year":"1998","journal-title":"Am. J. Physiol."},{"issue":"35","key":"B26","first-page":"F342","volume":"266","author":"Kita T.","year":"1994","journal-title":"Am. J. Physiol."},{"key":"B27","first-page":"407","volume":"184","author":"Krause W. J.","year":"1994","journal-title":"J. Anat."},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1006\/gcen.1997.6921"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1159\/000147735"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1007\/BF00318641"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1994.sp020307"},{"key":"B32","doi-asserted-by":"crossref","first-page":"1470","DOI":"10.1016\/S0021-9258(17)36116-1","volume":"261","author":"Kuno T.","year":"1986","journal-title":"J. Biol. Chem."},{"key":"B33","first-page":"433","volume":"49","author":"Lennane R. J.","year":"1975","journal-title":"Clin. Sci. Mol. Med."},{"issue":"28","key":"B34","first-page":"G394","volume":"265","author":"Li Z.","year":"1993","journal-title":"Am. J. Physiol."},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-0773.1992.tb00449.x"},{"issue":"36","key":"B36","first-page":"G93","volume":"273","author":"London R. M.","year":"1997","journal-title":"Am. J. Physiol."},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1997.7487"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1996.0447"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1097-4644(19970915)66:4<500::AID-JCB9>3.0.CO;2-P"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1126\/science.274.5295.2082"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(90)90497-3"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119683"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1016\/0006-291X(91)91736-V"},{"key":"B44","doi-asserted-by":"crossref","first-page":"2174","DOI":"10.1016\/S0021-9258(18)53978-8","volume":"268","author":"Vaandrager A. B.","year":"1993","journal-title":"J. Biol. Chem."},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1111\/j.1348-0421.1994.tb01819.x"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1016\/S0016-5085(97)70197-5"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1016\/0006-291X(89)92447-9"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1016\/0006-291X(92)91699-Q"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1999.276.6.F882","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:54:38Z","timestamp":1660190078000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1999.276.6.F882"}},"issued":{"date-parts":[[1999,6,1]]},"references-count":48,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1999,6,1]]}},"alternative-id":["10.1152\/ajprenal.1999.276.6.F882"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1999.276.6.f882","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1999,6,1]]}},{"indexed":{"date-parts":[[2022,4,2]],"date-time":"2022-04-02T23:06:21Z","timestamp":1648940781936},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1988,3,1]]},"abstract":"<jats:p> The mechanisms responsible for the large increases of intracellular ATP levels seen after isolated rabbit proximal tubules are treated with exogenous adenine nucleotides were studied. Exogenous ATP was rapidly degraded via adenosine as far as hypoxanthine. Degradation of AMP to adenosine was substantially inhibited by beta-glycerol phosphate. In studies of the ability of individual exogenous purines to increase intracellular ATP levels, single large doses of adenosine were less effective than equimolar doses of exogenous ATP but were substantially more effective than exogenous inosine or hypoxanthine. Exogenous guanine derived compounds increased only cell GTP. Incremental delivery of smaller doses of adenosine to maintain medium levels greater than 5 microM or inhibition of adenosine deaminase with erythro-9-[3-(2-hydroxynonyl)]adenine or 2'-deoxycoformicin enhanced the nucleoside's effectiveness. However, the initial increase of cell ATP was still greater after treatment with exogenous ATP than after adenosine and, in the presence of adenosine deaminase inhibition, larger increases of cell ATP were produced by 50 microM adenosine than by 250 microM adenosine. These observations are most consistent with substrate inhibition of adenosine kinase by adenosine. Furthermore, the adenosine kinase inhibitor, 5-iodotubercidin, prevented the increases of cell ATP resulting from exogenous adenosine or exogenous ATP. These studies demonstrate how the differential uptake and utilization characteristics of nucleosides and bases can fully account for the increases of intracellular nucleotides produced in isolated tubules by exogenous purines. <\/jats:p>","DOI":"10.1152\/ajprenal.1988.254.3.f311","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T03:20:04Z","timestamp":1513999204000},"page":"F311-F322","source":"Crossref","is-referenced-by-count":2,"title":["Modulation of cell nucleotide levels of isolated kidney tubules"],"prefix":"10.1152","volume":"254","author":[{"given":"J. M.","family":"Weinberg","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, Veterans Administration Medical Center, Ann Arbor, Michigan."}]},{"given":"J. A.","family":"Davis","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Veterans Administration Medical Center, Ann Arbor, Michigan."}]},{"given":"A.","family":"Lawton","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Veterans Administration Medical Center, Ann Arbor, Michigan."}]},{"given":"M.","family":"Abarzua","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Veterans Administration Medical Center, Ann Arbor, Michigan."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1988.254.3.F311","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:48:44Z","timestamp":1567972124000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1988.254.3.F311"}},"issued":{"date-parts":[[1988,3,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1988,3,1]]}},"alternative-id":["10.1152\/ajprenal.1988.254.3.F311"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1988.254.3.f311","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1988,3,1]]}},{"indexed":{"date-parts":[[2023,10,12]],"date-time":"2023-10-12T19:27:20Z","timestamp":1697138840712},"reference-count":28,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1997,12,1]]},"abstract":"<jats:p>Sites of renal Mg transport were identified in seawater killifish ( Fundulus heteroclitus) using a Cameca model IMS-3f ion microscope. Killifish were given an intraperitoneal injection of the stable isotope<jats:sup>26<\/jats:sup>Mg (99.5% enrichment) to stimulate and trace renal Mg excretion. We identified two sites of<jats:sup>26<\/jats:sup>Mg transport in frozen freeze-dried cryosections of kidney: the proximal tubule, known to secrete Mg, and the collecting duct, heretofore not known to handle Mg. In epithelial cells of the proximal tubule, the punctate distribution of injected<jats:sup>26<\/jats:sup>Mg suggests transcytotic excretion of Mg in bound form. In collecting ducts, a subpopulation of Mg\/Ca-rich cells was identified with high accumulations of injected<jats:sup>26<\/jats:sup>Mg. Here, the punctate distribution of<jats:sup>26<\/jats:sup>Mg decreased from the apical to the basal region of the cells, revealing a transcytotic gradient of apparently bound Mg. Since proximal tubules of fish are implicated with Mg secretion, Mg\/Ca-rich cells in the collecting duct may reabsorb Mg, thereby providing the usual two-step of renal regulation, now also for Mg.<\/jats:p>","DOI":"10.1152\/ajprenal.1997.273.6.f939","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T14:32:50Z","timestamp":1514039570000},"page":"F939-F948","source":"Crossref","is-referenced-by-count":13,"title":["Identification of Mg-transporting renal tubules and cells by ion microscopy imaging of stable isotopes"],"prefix":"10.1152","volume":"273","author":[{"given":"Subhash","family":"Chandra","sequence":"first","affiliation":[{"name":"Ion Microscopy Laboratory, Department of Chemistry, and"}]},{"given":"George H.","family":"Morrison","sequence":"additional","affiliation":[{"name":"Ion Microscopy Laboratory, Department of Chemistry, and"}]},{"given":"Klaus W.","family":"Beyenbach","sequence":"additional","affiliation":[{"name":"Section of Physiology, Cornell University, Ithaca, New York 14853"}]}],"member":"24","reference":[{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1021\/ac00199a002"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1007\/s003600050048"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/299054a0"},{"key":"B5","first-page":"241","volume":"19","author":"Beyenbach K. W.","year":"1993","journal-title":"Miner. Electrolyte Metab."},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1113\/expphysiol.1993.sp003682"},{"key":"B7","first-page":"395","volume":"1","author":"Castaing R.","year":"1962","journal-title":"J. Microsc."},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2818.1987.tb02869.x"},{"key":"B9","doi-asserted-by":"crossref","first-page":"15186","DOI":"10.1016\/S0021-9258(17)36590-0","volume":"269","author":"Chandra S.","year":"1994","journal-title":"J. Biol. Chem."},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.87.15.5715"},{"key":"B11","first-page":"158","volume":"158","author":"Chandra S.","year":"1988","journal-title":"Methods Enzymol."},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2818.1986.tb04670.x"},{"issue":"31","key":"B13","first-page":"F108","volume":"262","author":"Cliff W. H.","year":"1992","journal-title":"Am. J. Physiol."},{"issue":"19","key":"B14","first-page":"R616","volume":"250","author":"Cliff W. H.","year":"1986","journal-title":"Am. J. Physiol."},{"issue":"31","key":"B15","first-page":"F1100","volume":"262","author":"Dai L. J.","year":"1992","journal-title":"Am. J. Physiol."},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1994.74.2.305"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1002\/aja.1000530103"},{"key":"B18","first-page":"32","volume":"63","author":"Hentschel H.","year":"1994","journal-title":"Eur. J. Cell Biol."},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/S1546-5098(08)60083-7"},{"key":"B20","doi-asserted-by":"crossref","first-page":"1305","DOI":"10.1681\/ASN.V1121305","volume":"1","author":"LeFurgey A.","year":"1991","journal-title":"J. Am. Soc. Nephrol."},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1002\/aja.1001550108"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/0248-4900(92)90021-R"},{"issue":"40","key":"B23","first-page":"F508","volume":"271","author":"Miller D. S.","year":"1996","journal-title":"Am. J. Physiol."},{"issue":"36","key":"B24","first-page":"R695","volume":"267","author":"Miller D. S.","year":"1994","journal-title":"Am. J. Physiol."},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1989.256.3.C540"},{"issue":"18","key":"B26","first-page":"F497","volume":"249","author":"Renfro J. L.","year":"1985","journal-title":"Am. J. Physiol."},{"key":"B27","first-page":"282","volume":"19","author":"Romani A.","year":"1993","journal-title":"Miner. Electrolyte Metab."},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2818.1990.tb03047.x"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/0143-4160(92)90039-U"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1997.273.6.F939","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:47:00Z","timestamp":1660189620000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1997.273.6.F939"}},"issued":{"date-parts":[[1997,12,1]]},"references-count":28,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1997,12,1]]}},"alternative-id":["10.1152\/ajprenal.1997.273.6.F939"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1997.273.6.f939","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1997,12,1]]}},{"indexed":{"date-parts":[[2023,12,15]],"date-time":"2023-12-15T10:55:54Z","timestamp":1702637754475},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1986,10,1]]},"abstract":"<jats:p> Fasting in rats decreases plasma citrate levels and reduces urinary citrate excretion by the kidney. After 72 h of fasting, the endogenous renal citrate clearance was decreased and the fractional citrate excretion was 0.026 +\/- 0.008 compared with 0.218 +\/- 0.030 in control fed rats. To determine whether these findings result from an adaptation in citrate transport across the plasma membrane of the renal tubular cell, Na+ gradient-dependent [14C]citrate uptake was examined in brush-border membrane vesicles (BBMW) prepared from kidneys of fed and 72-h fasted rats. The initial rate (10 s) of Na+ gradient-stimulated uptake of 100 microM citrate was significantly increased in BBMW from kidneys of fasted rats (380 +\/- 24.9 pmol\/mg prot) compared with fed rats (255 +\/- 24.9 pmol\/mg prot). Arterial acid-base parameters from conscious animals were similar between the two groups. There was no significant difference in Na+-independent citrate uptake or in L-glutamine uptake measured at 20 s in BBMV from the kidneys of fasted compared with fed rats. An adaptation occurs in the brush-border membrane of the renal tubular cell of fasting rats, unrelated to systemic acidosis, that may result in increased reabsorption of citrate. <\/jats:p>","DOI":"10.1152\/ajprenal.1986.251.4.f678","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T00:55:07Z","timestamp":1513990507000},"page":"F678-F682","source":"Crossref","is-referenced-by-count":3,"title":["Effects of fasting on citrate transport by the brush-border membrane of rat kidney"],"prefix":"10.1152","volume":"251","author":[{"given":"D. W.","family":"Windus","sequence":"first","affiliation":[]},{"given":"D. E.","family":"Cohn","sequence":"additional","affiliation":[]},{"given":"M.","family":"Heifets","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1986.251.4.F678","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:34:15Z","timestamp":1567971255000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1986.251.4.F678"}},"issued":{"date-parts":[[1986,10,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1986,10,1]]}},"alternative-id":["10.1152\/ajprenal.1986.251.4.F678"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1986.251.4.f678","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1986,10,1]]}},{"indexed":{"date-parts":[[2024,5,28]],"date-time":"2024-05-28T01:31:00Z","timestamp":1716859860474},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1990,2,1]]},"abstract":"<jats:p> Purified brush-border membrane vesicles (BBMV) of lobster antennal gland labyrinth and bladder were separately formed by a magnesium precipitation technique. L-[3H]proline uptake was stimulated by a transmembrane NaCl gradient [outside (o) greater than inside (i)] to a greater extent in BBMV from labyrinth than those from the bladder. Detailed study of the labyrinth proline-transport processes revealed a specific dependence on NaCl, with negligible stimulatory effects by NaSCN, Na-gluconate, or KCl. A transmembrane proton gradient (o greater than i) was without stimulatory effect on proline transport. A transmembrane potential difference alone, in the presence of equilibrated NaCl and L-[3H]proline, led to net influx of the labeled amino acid, suggesting that the uptake process was electrogenic and capable of bringing about the net transfer of positive charge to the vesicle interior. Although a transmembrane Na gradient alone, in the presence of equilibrated Cl and L-[3H]proline, was able to bring about the net influx of the amino acid, a transmembrane Cl gradient alone under Na- and L-[3H]proline-equilibrated conditions was not, suggesting that only the Na gradient could energize the carrier process through cotransport, while the anion served an essential activating role. Proline influx by these vesicles occurred by the combination of at least one saturable Michaelis-Menten carrier system (apparent Kt = 0.37 mM; apparent JM = 1.19 nmol.mg protein-1.10 s-1) and apparent diffusion (P = 0.33 nmol.mg protein-1.10 s-1.mM-1). Static head analysis of the transport process suggested a cotransport stoichiometry of 2 Na:1 proline with essential activation by Cl ion. <\/jats:p>","DOI":"10.1152\/ajprenal.1990.258.2.f311","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T16:33:17Z","timestamp":1513960397000},"page":"F311-F320","source":"Crossref","is-referenced-by-count":2,"title":["Proline transport by brush-border membrane vesicles of lobster antennal glands"],"prefix":"10.1152","volume":"258","author":[{"given":"R. D.","family":"Behnke","sequence":"first","affiliation":[{"name":"Department of Zoology, University of Hawaii, Manoa, Honolulu96822."}]},{"given":"R. K.","family":"Wong","sequence":"additional","affiliation":[{"name":"Department of Zoology, University of Hawaii, Manoa, Honolulu96822."}]},{"given":"S. M.","family":"Huse","sequence":"additional","affiliation":[{"name":"Department of Zoology, University of Hawaii, Manoa, Honolulu96822."}]},{"given":"S. J.","family":"Reshkin","sequence":"additional","affiliation":[{"name":"Department of Zoology, University of Hawaii, Manoa, Honolulu96822."}]},{"given":"G. A.","family":"Ahearn","sequence":"additional","affiliation":[{"name":"Department of Zoology, University of Hawaii, Manoa, Honolulu96822."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1990.258.2.F311","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:11:50Z","timestamp":1567955510000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1990.258.2.F311"}},"issued":{"date-parts":[[1990,2,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1990,2,1]]}},"alternative-id":["10.1152\/ajprenal.1990.258.2.F311"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1990.258.2.f311","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1990,2,1]]}},{"indexed":{"date-parts":[[2022,4,3]],"date-time":"2022-04-03T16:05:49Z","timestamp":1649001949966},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1987,4,1]]},"abstract":"<jats:p> Bone mineral buffers protons during acute metabolic acidosis; whether parathyroid hormone (PTH) augments proton buffering is controversial. To determine whether PTH augments proton buffering by bone, we cultured neonatal mouse calvariae with or without PTH (10(-8) M) for 3 h in medium that was physiologically acid (pH approximately 7.20), neutral (pH approximately 7.40), or alkaline (pH approximately 7.60). Over the entire pH range studied there was less influx of protons into calvariae treated with PTH than into control calvariae, indicating that PTH does not augment but instead inhibits proton buffering by bone. To determine whether chronic exposure to PTH is necessary to augment proton buffering, calvariae were incubated with PTH for 24 h before a 3-h culture. Calcium efflux from calvariae exposed to PTH (10(-8) M) for 24 h exceeded that of controls. When these same calvariae were recultured for 3 h in fresh medium, PTH-treated and control calvariae behaved similarly, with net efflux of protons into acid, neutral, and alkaline media. Regardless of whether PTH is added at the time of exposure to acid medium or 24 h before calvariae cultured with PTH do not buffer protons to a greater extent than controls. <\/jats:p>","DOI":"10.1152\/ajprenal.1987.252.4.f585","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T21:13:31Z","timestamp":1513977211000},"page":"F585-F589","source":"Crossref","is-referenced-by-count":7,"title":["Effects of parathyroid hormone on net proton flux from neonatal mouse calvariae"],"prefix":"10.1152","volume":"252","author":[{"given":"D. A.","family":"Bushinsky","sequence":"first","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1987.252.4.F585","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:44:38Z","timestamp":1567957478000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1987.252.4.F585"}},"issued":{"date-parts":[[1987,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1987,4,1]]}},"alternative-id":["10.1152\/ajprenal.1987.252.4.F585"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1987.252.4.f585","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1987,4,1]]}},{"indexed":{"date-parts":[[2022,3,30]],"date-time":"2022-03-30T18:15:05Z","timestamp":1648664105152},"reference-count":0,"publisher":"American Physiological Society","issue":"8","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2012,4,15]]},"DOI":"10.1152\/ajprenal.00040.2012","type":"journal-article","created":{"date-parts":[[2012,1,26]],"date-time":"2012-01-26T05:45:07Z","timestamp":1327556707000},"page":"F1063-F1063","source":"Crossref","is-referenced-by-count":0,"title":["2012 Robert W. Berliner Award for Excellence in Renal Physiology"],"prefix":"10.1152","volume":"302","member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00040.2012","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T00:17:54Z","timestamp":1567988274000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00040.2012"}},"issued":{"date-parts":[[2012,4,15]]},"references-count":0,"journal-issue":{"issue":"8","published-print":{"date-parts":[[2012,4,15]]}},"alternative-id":["10.1152\/ajprenal.00040.2012"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00040.2012","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2012,4,15]]}},{"indexed":{"date-parts":[[2022,3,30]],"date-time":"2022-03-30T17:40:39Z","timestamp":1648662039620},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1988,4,1]]},"abstract":"<jats:p> The secretory and reabsorptive transport of salicylate was studied in the isolated and perfused rabbit proximal tubule (S2 segment). Salicylate secretion (Jb----lsal) fulfilled the criteria for a carrier-mediated transport system: Jb----lsal was saturable, was reversibly inhibited by probenecid, and occurred against a concentration gradient. The Km and Vmax for this secretory transport were 80 microM and 3,200 fmol.min-1.mm-1, respectively. At luminal pH of 7.4 and 6.6, salicylate reabsorption (Jl----bsal) was low (100 fmol.min-1.mm-1). Jl----bsal was stimulated by increasing the bath PCO2 or by removing basolateral HCO3-; Jl----bsal was inhibited by ethoxyzolamide and by SITS in the bath. Our results indicate that salicylate reabsorption depends on H+ secretion, consistent with reabsorption by simple nonionic diffusion. When salicylate was present in the lumen only, Jl----bsal increased after inhibition of the secretory transport by adding ouabain or probenecid in the bath or by lowering the bath temperature. These results are compatible with luminal recycling of salicylate, and suggest the presence of a mediated secretory transporter located at the luminal membrane. <\/jats:p>","DOI":"10.1152\/ajprenal.1988.254.4.f554","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T03:22:12Z","timestamp":1513999332000},"page":"F554-F561","source":"Crossref","is-referenced-by-count":0,"title":["Transport of salicylate in proximal tubule (S2 segment) isolated from rabbit kidney"],"prefix":"10.1152","volume":"254","author":[{"given":"L.","family":"Schild","sequence":"first","affiliation":[{"name":"Institut de Pharmacologie de l'Universite de Lausanne,Switzerland."}]},{"given":"F.","family":"Roch-Ramel","sequence":"additional","affiliation":[{"name":"Institut de Pharmacologie de l'Universite de Lausanne,Switzerland."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1988.254.4.F554","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:50:08Z","timestamp":1567972208000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1988.254.4.F554"}},"issued":{"date-parts":[[1988,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1988,4,1]]}},"alternative-id":["10.1152\/ajprenal.1988.254.4.F554"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1988.254.4.f554","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1988,4,1]]}},{"indexed":{"date-parts":[[2022,3,30]],"date-time":"2022-03-30T21:40:31Z","timestamp":1648676431433},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1983,10,1]]},"abstract":"<jats:p> Urinary bladders from freshwater turtles, mounted as sacs, were stripped of their serosa and submucosa. This did not alter conductance. They were maintained in open circuit except for brief observation of short-circuit current (SCC) every 15 min. Potential difference (PD) averaged 68 +\/- 14 mV and SCC 485 +\/- 100 microA. Acetazolamide 10(-3) M increased SCC by 46 +\/- 27 microA. Aldosterone 10(-7) M following acetazolamide resulted in a rise in SCC that began at about 75 min and reached a plateau between 3 and 5 h. SCC rose 127 +\/- 15% compared with control bladder halves. ATP measured in perchloric acid extracts 5 h after addition of aldosterone increased by 33% (P less than 0.01) and (ATP)\/(ADP) X (Pi) by 81% (P less than 0.01). These results support the view that the stimulatory effects of aldosterone on active sodium transport involve an increase in ATP and (ATP)\/(ADP) X (Pi). <\/jats:p>","DOI":"10.1152\/ajprenal.1983.245.4.f512","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T14:43:17Z","timestamp":1513953797000},"page":"F512-F514","source":"Crossref","is-referenced-by-count":0,"title":["Aldosterone response in the turtle bladder is associated with an increase in ATP"],"prefix":"10.1152","volume":"245","author":[{"given":"N.","family":"Cortas","sequence":"first","affiliation":[]},{"given":"E.","family":"Abras","sequence":"additional","affiliation":[]},{"given":"M.","family":"Walser","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1983.245.4.F512","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:24:38Z","timestamp":1567967078000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1983.245.4.F512"}},"issued":{"date-parts":[[1983,10,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1983,10,1]]}},"alternative-id":["10.1152\/ajprenal.1983.245.4.F512"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1983.245.4.f512","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1983,10,1]]}},{"indexed":{"date-parts":[[2022,3,31]],"date-time":"2022-03-31T20:23:10Z","timestamp":1648758190922},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1997,2,1]]},"abstract":"<jats:p> The growth factor\/receptor combination of hepatocyte growth factor (HGF)\/c-met has been postulated to be critical for mesenchymal-to-epithelial conversion and tubule formation in the developing kidney. We therefore isolated and immortalized cells from embryonic kidneys of met -\/- transgenic mice to determine whether these cells were epithelial and able to chemotax and form tubules in vitro. The cells were immortalized with retrovirus expressing human papillomavirus 16 (HPV 16) E6\/E7 genes. Two rapidly dividing clones were isolated and found to express the epithelial cell markers cytokeratin, zonula occludens-1, and E-cadherin but not to express the fibroblast marker vimentin. The met -\/- cells were able to chemotax in response to epidermal growth factor and transforming growth factor-alpha (TGF-alpha) and form tubules in vitro in response to TGF-alpha but not HGF. These experiments suggest that the HGF\/c-met axis is not essential for epithelial cell development in the embryonic kidney and demonstrate that other growth factors are capable of supporting early tubulogenesis. <\/jats:p>","DOI":"10.1152\/ajprenal.1997.272.2.f222","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T03:43:57Z","timestamp":1514000637000},"page":"F222-F228","source":"Crossref","is-referenced-by-count":1,"title":["Met -\/- kidneys express epithelial cells that chemotax and form tubules in response to EGF receptor ligands"],"prefix":"10.1152","volume":"272","author":[{"given":"C.","family":"Kjelsberg","sequence":"first","affiliation":[{"name":"Division of Nephrology, Beth Israel Hospital, Boston, Massachusetts02215, USA."}]},{"given":"H.","family":"Sakurai","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Beth Israel Hospital, Boston, Massachusetts02215, USA."}]},{"given":"K.","family":"Spokes","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Beth Israel Hospital, Boston, Massachusetts02215, USA."}]},{"given":"C.","family":"Birchmeier","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Beth Israel Hospital, Boston, Massachusetts02215, USA."}]},{"given":"I.","family":"Drummond","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Beth Israel Hospital, Boston, Massachusetts02215, USA."}]},{"given":"S.","family":"Nigam","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Beth Israel Hospital, Boston, Massachusetts02215, USA."}]},{"given":"L. G.","family":"Cantley","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Beth Israel Hospital, Boston, Massachusetts02215, USA."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1997.272.2.F222","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:16:27Z","timestamp":1567959387000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1997.272.2.F222"}},"issued":{"date-parts":[[1997,2,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1997,2,1]]}},"alternative-id":["10.1152\/ajprenal.1997.272.2.F222"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1997.272.2.f222","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1997,2,1]]}},{"indexed":{"date-parts":[[2022,3,31]],"date-time":"2022-03-31T06:51:40Z","timestamp":1648709500237},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1988,10,1]]},"abstract":"<jats:p> Atrial natriuretic factor (ANF) concentration in atria and plasma was investigated in relation to the density and affinity of renal glomerular ANF receptors during water deprivation and rehydration in the rat. Immunoreactive (IR) ANF-(99-126) was lower during water deprivation (4.2 +\/- 0.5 fmol\/ml) than in normally hydrated animals (10 +\/- 1.5 fmol\/ml); NH2-terminal IR ANF-(1-98) was also lower in water-deprived rats (75 +\/- 2.4 fmol\/ml) than in the controls (708 +\/- 105 fmol\/ml). These decreased plasma COOH- and NH2-terminal ANF concentrations were accompanied by significantly higher hematocrit, serum osmolality, and Na+ values. The renal glomerular ANF receptor population was greater in water-deprived animals than a control animals. After rehydration, IR ANF was elevated within 1 h and reached control values after 6 h. Hematocrit, serum osmolality, and Na+ did not normalize until 48, 6, and 24 h, respectively. The renal glomerular ANF receptor population, which was markedly higher in water-deprived rats, gradually declined after rehydration, so that no difference was observed with the control group 24 h later. <\/jats:p>","DOI":"10.1152\/ajprenal.1988.255.4.f621","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T21:24:38Z","timestamp":1513977878000},"page":"F621-F625","source":"Crossref","is-referenced-by-count":0,"title":["Glomerular atrial natriuretic factor receptors during rehydration: plasma NH2- and COOH-terminal levels"],"prefix":"10.1152","volume":"255","author":[{"given":"G.","family":"Gauquelin","sequence":"first","affiliation":[{"name":"Laboratory of Experimental Hypertension and Vasoactive Peptides,Clinical Research Institute of Montreal, Canada."}]},{"given":"G.","family":"Thibault","sequence":"additional","affiliation":[{"name":"Laboratory of Experimental Hypertension and Vasoactive Peptides,Clinical Research Institute of Montreal, Canada."}]},{"given":"M.","family":"Cantin","sequence":"additional","affiliation":[{"name":"Laboratory of Experimental Hypertension and Vasoactive Peptides,Clinical Research Institute of Montreal, Canada."}]},{"given":"E. L.","family":"Schiffrin","sequence":"additional","affiliation":[{"name":"Laboratory of Experimental Hypertension and Vasoactive Peptides,Clinical Research Institute of Montreal, Canada."}]},{"given":"R.","family":"Garcia","sequence":"additional","affiliation":[{"name":"Laboratory of Experimental Hypertension and Vasoactive Peptides,Clinical Research Institute of Montreal, Canada."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1988.255.4.F621","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:10:49Z","timestamp":1567969849000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1988.255.4.F621"}},"issued":{"date-parts":[[1988,10,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1988,10,1]]}},"alternative-id":["10.1152\/ajprenal.1988.255.4.F621"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1988.255.4.f621","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1988,10,1]]}},{"indexed":{"date-parts":[[2022,4,1]],"date-time":"2022-04-01T08:13:27Z","timestamp":1648800807685},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1995,2,1]]},"abstract":"<jats:p> The cells of the inner medulla of the mammalian kidney accumulate high concentrations of nonurea organic osmolytes. The organic osmolytes found in the kidney include glycine betaine and sorbitol. This study was designed to measure changes in the urinary excretion of glycine betaine and sorbitol and the plasma concentration of glycine betaine in response to an acute water load (20 ml\/kg) or acute water deprivation in young healthy males. In response to a water load the urinary excretion of glycine betaine and sorbitol increased parallel with or shortly after urinary urea excretion. The increase in urinary urea and sorbitol excretions preceded maximum minute volume, whereas peak glycine betaine excretion was closely related to maximum urine minute volume. Subsequently, urea, sorbitol, and glycine betaine excretion rates returned to baseline. In contrast, during water deprivation no change in glycine betaine, sorbitol, and urea urinary excretions occurred during the study period. Plasma glycine betaine concentration was stable during both diuresis and antidiuresis. We conclude that the organic osmolytes glycine betaine and sorbitol are components of a physiological and dynamic system in response to an acute water diuresis. <\/jats:p>","DOI":"10.1152\/ajprenal.1995.268.2.f227","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T04:32:24Z","timestamp":1514003544000},"page":"F227-F233","source":"Crossref","is-referenced-by-count":3,"title":["Short-term response of nonurea organic osmolytes in human kidney to a water load and water deprivation"],"prefix":"10.1152","volume":"268","author":[{"given":"P. C.","family":"Sizeland","sequence":"first","affiliation":[{"name":"Department of Nephrology, Christchurch Hospital, New Zealand."}]},{"given":"S. T.","family":"Chambers","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Christchurch Hospital, New Zealand."}]},{"given":"M.","family":"Lever","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Christchurch Hospital, New Zealand."}]},{"given":"L. M.","family":"Bason","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Christchurch Hospital, New Zealand."}]},{"given":"R. A.","family":"Robson","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Christchurch Hospital, New Zealand."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1995.268.2.F227","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:55:22Z","timestamp":1567972522000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1995.268.2.F227"}},"issued":{"date-parts":[[1995,2,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1995,2,1]]}},"alternative-id":["10.1152\/ajprenal.1995.268.2.F227"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1995.268.2.f227","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1995,2,1]]}},{"indexed":{"date-parts":[[2022,4,5]],"date-time":"2022-04-05T16:52:48Z","timestamp":1649177568339},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1987,7,1]]},"abstract":"<jats:p> Acidic intracellular compartments were identified in cells of isolated perfused rabbit proximal convoluted tubules (PCT) with the weak base, N-(3-[(2,4-dinitrophenyl)amino]propyl)-N-(3-aminopropyl)methylamine, dihydrochloride (DAMP), a congener of dinitrophenol (DNP) and immunogold staining at the ultrastructural level in Lowicryl-embedded tissue. DAMP is protonated upon entrance into an acidic compartment and binds to protein. Glutaraldehyde fixation cross-links the DAMP-protein complex to maintain the complex in its original environment. Monoclonal antibodies directed against DNP cross-react with DAMP to identify its location in tissue sections. Accumulation of colloidal gold-conjugated antibodies to the monoclonal anti-DNP antibodies, indicating the presence of an acidic environment, was found in large endocytic vacuoles (diam greater than 0.5 micron) and lysosomes, and to a lesser extent in endocytic vesicles. Qualitatively, activity greater than background was not found in other organelles, including the Golgi apparatus and the cell nuclei. The specificity of the technique was tested by treating tubules with the ionophore, monensin, to collapse the intracellular pH gradient. This treatment resulted in the complete disappearance of the specific localization of colloidal gold particles. Quantitative analysis of the number of colloidal gold particles per area of cross-sectioned cell organelle demonstrated that monensin especially affected those counts obtained over large endocytic vacuoles and lysosomes. The present ultrastructural observations, therefore, identify endocytic vesicles, endocytic vacuoles, and lysosomes as acidic intracellular compartments in isolated rabbit PCT. This technique affords the opportunity to identify the location of acidic compartments along the entire nephron at the ultrastructural level. <\/jats:p>","DOI":"10.1152\/ajprenal.1987.253.1.f95","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T21:11:34Z","timestamp":1513977094000},"page":"F95-F103","source":"Crossref","is-referenced-by-count":0,"title":["Ultrastructural localization of acidic compartments in cells of isolated rabbit PCT"],"prefix":"10.1152","volume":"253","author":[{"given":"L.","family":"Larsson","sequence":"first","affiliation":[]},{"suffix":"3rd","given":"W. L.","family":"Clapp","sequence":"additional","affiliation":[]},{"given":"C. H.","family":"Park","sequence":"additional","affiliation":[]},{"given":"J. K.","family":"Cannon","sequence":"additional","affiliation":[]},{"given":"C. C.","family":"Tisher","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1987.253.1.F95","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:42:48Z","timestamp":1567957368000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1987.253.1.F95"}},"issued":{"date-parts":[[1987,7,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1987,7,1]]}},"alternative-id":["10.1152\/ajprenal.1987.253.1.F95"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1987.253.1.f95","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1987,7,1]]}},{"indexed":{"date-parts":[[2022,4,2]],"date-time":"2022-04-02T12:54:08Z","timestamp":1648904048947},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1989,11,1]]},"abstract":"<jats:p> Glomerular filtration rate (GFR; creatinine clearance) and renal excretion rates of active kallikrein, prokallikrein, and kinins were measured in seven normal male subjects after a week on a constant low (40 g\/day)-protein diet (LP) and during a subsequent week when only protein content was increased to 140 g\/day (HP). Renal kinin excretion increased from 19.7 +\/- 1.2 micrograms\/day on day 7 of LP to 26.0 +\/- 2.5 on day 1 of HP (P less than 0.002), and this higher rate persisted during HP. Active kallikrein excretion increased from 105 +\/- 16 to 171 +\/- 40 micrograms\/day on day 2 of HP (P less than 0.006). Prokallikrein excretion did not increase significantly until day 4 of HP, 52 +\/- 16 vs. 96 +\/- 38 micrograms\/day (P less than 0.03). The increases in active kallikrein and kinin excretion preceded an increase in GFR, which went from 117 +\/- 6.8 ml\/min on LP to 130 +\/- 10 ml\/min on day 5 of HP (P less than 0.003). At the end of the LP diet, acute ingestion of 40 g of a casein solution produced an increase in kinin excretion after 2 h (586 +\/- 64 vs. 402 +\/- 33 pg\/min, P less than 0.001) and further to 640 +\/- 74 pg\/min at 3 h (P less than 0.001). This was accompanied by an increase in GFR at 3 h (154 +\/- 18 vs. 132 +\/- 10 ml\/min, P less than 0.05). Kinin excretion rate correlated directly with GFR during both chronic (r = 0.87) and acute (r = 0.77) studies.(ABSTRACT TRUNCATED AT 250 WORDS) <\/jats:p>","DOI":"10.1152\/ajprenal.1989.257.5.f718","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T17:07:26Z","timestamp":1513962446000},"page":"F718-F723","source":"Crossref","is-referenced-by-count":0,"title":["Acute and chronic responses of human renal kallikrein and kinins to dietary protein"],"prefix":"10.1152","volume":"257","author":[{"given":"P.","family":"Bolin","sequence":"first","affiliation":[{"name":"Department of Medicine, Medical University of South Carolina,Charleston 29425."}]},{"given":"A. A.","family":"Jaffa","sequence":"additional","affiliation":[{"name":"Department of Medicine, Medical University of South Carolina,Charleston 29425."}]},{"given":"P. F.","family":"Rust","sequence":"additional","affiliation":[{"name":"Department of Medicine, Medical University of South Carolina,Charleston 29425."}]},{"given":"R. K.","family":"Mayfield","sequence":"additional","affiliation":[{"name":"Department of Medicine, Medical University of South Carolina,Charleston 29425."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1989.257.5.F718","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:14:55Z","timestamp":1567955695000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1989.257.5.F718"}},"issued":{"date-parts":[[1989,11,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1989,11,1]]}},"alternative-id":["10.1152\/ajprenal.1989.257.5.F718"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1989.257.5.f718","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1989,11,1]]}},{"indexed":{"date-parts":[[2022,3,31]],"date-time":"2022-03-31T05:51:38Z","timestamp":1648705898821},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1977,11,1]]},"abstract":"<jats:p> Uptake of p-aminohippurate (PAH) by rat kidney slices was optimal at a pH of around 7.3 when incubation temperature was 37 degrees C. At 25 degrees C, however, optimal pH was increased to about 7.5. When the uptake was evaluated as a function of the OH\/H ratio of the medium, it was found that optimal uptake is at a constant OH\/H. Data showing the same characteristics of OH\/H dependence were also observed for phenol red. Passive uptake of PAH was pH independent. Efflux rates for PAH also showed the pH optimal which was identical to that of uptake. At both 25 and 37 degrees C the Km appeared to be independent of pH while the maximum rate of active influx. An optimal OH\/H ratio determines maximal velocity and this ratio is fixed and independent of temperature. <\/jats:p>","DOI":"10.1152\/ajprenal.1977.233.5.f382","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T20:08:13Z","timestamp":1513973293000},"page":"F382-F387","source":"Crossref","is-referenced-by-count":0,"title":["pH-temperature dependence of organic acid transport in rat kidney slices"],"prefix":"10.1152","volume":"233","author":[{"given":"Y. S.","family":"Park","sequence":"first","affiliation":[]},{"given":"S.","family":"Solomon","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1977.233.5.F382","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:56:04Z","timestamp":1567968964000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1977.233.5.F382"}},"issued":{"date-parts":[[1977,11,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1977,11,1]]}},"alternative-id":["10.1152\/ajprenal.1977.233.5.F382"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1977.233.5.f382","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1977,11,1]]}},{"indexed":{"date-parts":[[2022,3,31]],"date-time":"2022-03-31T06:18:26Z","timestamp":1648707506370},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1985,9,1]]},"DOI":"10.1152\/ajprenal.1985.249.3.f323","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T19:12:48Z","timestamp":1513969968000},"page":"F323-F323","source":"Crossref","is-referenced-by-count":0,"title":["Introduction"],"prefix":"10.1152","volume":"249","member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1985.249.3.F323","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:31:04Z","timestamp":1567956664000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1985.249.3.F323"}},"issued":{"date-parts":[[1985,9,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1985,9,1]]}},"alternative-id":["10.1152\/ajprenal.1985.249.3.F323"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1985.249.3.f323","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1985,9,1]]}},{"indexed":{"date-parts":[[2022,4,2]],"date-time":"2022-04-02T13:40:46Z","timestamp":1648906846543},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1997,1,1]]},"abstract":"<jats:p> The influence of hydronephrosis (6-10 wk) on the renal vascular response to arginine vasopressin (AVP) was assessed, using isolated perfused normal and hydronephrotic rat kidneys. In normal kidneys, AVP (0.3 nM) reduced renal perfusate flow (RPF) by 55 +\/- 7% (P &lt; 0.01). AVP-induced decrements in RPF were reversed partially by diltiazem (10 microM) and completely by 10 nM of an AVP (V1)-receptor antagonist (AVPX). In hydronephrotic kidneys, AVP reduced RPF by 81 +\/- 2% (P &lt; 0.01) and constricted afferent (AA) and efferent arterioles (EA) by 33 +\/- 3 (P &lt; 0.01) and 33 +\/- 5% (P &lt; 0.01), respectively. The addition of diltiazem altered neither RPF nor vessel diameters. Administration of AVPX recovered RPF, AA, and EA diameters. When hydronephrotic kidneys were pretreated with thromboxane (Tx) inhibitors, AVP reduced RPF by 62 +\/- 5% (P &lt; 0.01) and constricted AAs and EAs by 26 +\/- 2 (P &lt; 0.01) and 17 +\/- 3% (P &lt; 0.05), respectively. Under Tx blockade, diltiazem partially reversed the AVP-induced reduction in RPF and restored the decrements in AA diameter. Subsequent addition of AVPX returned RPF and EA diameter. Our data indicate that AVP elicits substantial renal microvascular constriction and suggest that AVP stimulates Tx production in hydronephrotic kidneys, thereby altering renal vascular responsiveness to this peptide. <\/jats:p>","DOI":"10.1152\/ajprenal.1997.272.1.f40","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T03:32:04Z","timestamp":1513999924000},"page":"F40-F47","source":"Crossref","is-referenced-by-count":1,"title":["Arginine vasopressin interacts with thromboxane in hydronephrosis"],"prefix":"10.1152","volume":"272","author":[{"given":"T.","family":"Takenaka","sequence":"first","affiliation":[{"name":"Shinjuku Suimei Clinic, Tokyo, Japan."}]},{"given":"H.","family":"Forster","sequence":"additional","affiliation":[{"name":"Shinjuku Suimei Clinic, Tokyo, Japan."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1997.272.1.F40","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:15:37Z","timestamp":1567959337000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1997.272.1.F40"}},"issued":{"date-parts":[[1997,1,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1997,1,1]]}},"alternative-id":["10.1152\/ajprenal.1997.272.1.F40"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1997.272.1.f40","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1997,1,1]]}},{"indexed":{"date-parts":[[2022,4,1]],"date-time":"2022-04-01T05:14:27Z","timestamp":1648790067332},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1992,7,1]]},"abstract":"<jats:p> We have studied localization of mRNAs coding isozymes of rat plasma membrane Ca(2+)-adenosinetriphosphatase pump (rPMCA) in the rat kidney, with use of reverse transcription (RT) with subsequent amplification by polymerase chain reaction (PCR). When zones of the kidney were separated by macrodissection, a large amount of mRNA coding isozyme rPMCA1 was found in all zones; mRNA for isozyme rPMCA2 was abundant in cortex and in outer medulla, and mRNA for isozyme rPMCA3 was prominent in outer medulla. The mRNAs were analyzed in microdissected cortical nephron segments by use of RT-PCR approach described previously [T. Moriyama, H. R. Murphy, B. M. Martin, and A. Garcia-Perez. Am. J. Physiol. 258 (Renal Fluid Electrolyte Physiol. 27): F1470-F1474, 1990]. We detected mRNA for isozyme rPMCA2 in microdissected distal convoluted tubules (DCT) and in cortical thick ascending limbs (CTAL) and, less consistently, also in proximal convoluted tubule and in glomeruli. The mRNA for isozyme rPMCA1 was abundant in glomeruli but was absent in all examined cortical tubular segments. Our results document that mRNAs for all three major isozymes of rPMCA are present and show a unique distribution in the three major zones of rat renal parenchyma. Specific mRNA coding for rPMCA2 was detected in cortical tubules, namely in CTAL and DCT, whereas mRNA coding isozyme rPMCA1 was found in glomeruli. We suggest that isozyme rPMCA2 might be specifically related to epithelial cells and their function, whereas rPMCA1 is probably a component of nonepithelial cells including these in glomeruli. <\/jats:p>","DOI":"10.1152\/ajprenal.1992.263.1.f7","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T10:12:07Z","timestamp":1514023927000},"page":"F7-F14","source":"Crossref","is-referenced-by-count":10,"title":["Localization of mRNAs coding for isozymes of plasma membrane Ca(2+)-ATPase pump in rat kidney"],"prefix":"10.1152","volume":"263","author":[{"given":"M.","family":"Magosci","sequence":"first","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, Mayo Clinic, Mayo Medical School, Rochester, Minnesota 55905."}]},{"given":"M.","family":"Yamaki","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, Mayo Clinic, Mayo Medical School, Rochester, Minnesota 55905."}]},{"given":"J. T.","family":"Penniston","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, Mayo Clinic, Mayo Medical School, Rochester, Minnesota 55905."}]},{"given":"T. P.","family":"Dousa","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, Mayo Clinic, Mayo Medical School, Rochester, Minnesota 55905."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1992.263.1.F7","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:26:27Z","timestamp":1567974387000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1992.263.1.F7"}},"issued":{"date-parts":[[1992,7,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1992,7,1]]}},"alternative-id":["10.1152\/ajprenal.1992.263.1.F7"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1992.263.1.f7","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1992,7,1]]}},{"indexed":{"date-parts":[[2023,10,6]],"date-time":"2023-10-06T13:54:45Z","timestamp":1696600485069},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1987,6,1]]},"abstract":"<jats:p> Reduction of renal mass in the rat results in an increased glomerular prostaglandin (PG) and thromboxane (TX) formation that modulates renal hemodynamics. To evaluate whether dietary protein intake could exert effects on renal PG and TX formation after reduction of approximately 70% of renal mass, rats with remnant kidneys were placed on either a high-protein (HP) or a low-protein (LP) diet. After 2 wk on the diet, proteinuria, glomerular filtration rate (GFR), urinary PGE2 excretion, and glomerular PGE2, 6-keto PGF1 alpha, and TxB2 biosynthesis were significantly greater in the rats on HP diets. Two-wk administration of the thromboxane synthesis inhibitor UK 38485 reduced renal TxB2 formation by approximately 70%. In addition, chronic UK 38485 treatment significantly inhibited papillary PGE2 production. Neither chronic nor bolus administration of UK 38485 had an effect on proteinuria or GFR in rats on HP diets. Chronic UK 38485 treatment, however, reduced GFR and proteinuria in rats on LP diets. The bolus administration of UK 38485 did not alter GFR in animals receiving a LP diet. The cyclooxygenase inhibitor indomethacin reduced GFR only in rats on HP diets. The data demonstrate that HP intake stimulates renal prostanoid formation. The increased prostaglandin formation on HP intake modulates GFR in these rats. <\/jats:p>","DOI":"10.1152\/ajprenal.1987.252.6.f1088","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T02:04:41Z","timestamp":1513994681000},"page":"F1088-F1094","source":"Crossref","is-referenced-by-count":2,"title":["High protein intake stimulates glomerular prostaglandin formation in remnant kidneys"],"prefix":"10.1152","volume":"252","author":[{"given":"R. A.","family":"Stahl","sequence":"first","affiliation":[]},{"given":"S.","family":"Kudelka","sequence":"additional","affiliation":[]},{"given":"U.","family":"Helmchen","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1987.252.6.F1088","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:42:06Z","timestamp":1567971726000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1987.252.6.F1088"}},"issued":{"date-parts":[[1987,6,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1987,6,1]]}},"alternative-id":["10.1152\/ajprenal.1987.252.6.F1088"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1987.252.6.f1088","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1987,6,1]]}},{"indexed":{"date-parts":[[2022,4,4]],"date-time":"2022-04-04T06:45:32Z","timestamp":1649054732994},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,7,1]]},"DOI":"10.1152\/ajprenal.00267.2013","type":"journal-article","created":{"date-parts":[[2013,5,16]],"date-time":"2013-05-16T04:22:37Z","timestamp":1368678157000},"page":"F1-F2","source":"Crossref","is-referenced-by-count":0,"title":["Meet your new <i>AJP-Renal Physiology<\/i> editors"],"prefix":"10.1152","volume":"305","author":[{"given":"P.","family":"Darwin Bell","sequence":"first","affiliation":[{"name":"Department of Medicine, Medical University of South Caroline, Charleston, South Carolina"}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00267.2013","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T23:34:49Z","timestamp":1567985689000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00267.2013"}},"issued":{"date-parts":[[2013,7,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2013,7,1]]}},"alternative-id":["10.1152\/ajprenal.00267.2013"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00267.2013","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2013,7,1]]}},{"indexed":{"date-parts":[[2022,4,1]],"date-time":"2022-04-01T17:01:01Z","timestamp":1648832461748},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1986,9,1]]},"abstract":"<jats:p> Administration of nicotinamide to rats produces a dose-dependent increase in nicotinamide adenine dinucleotide (NAD) content in the renal cortex and specific inhibition of sodium gradient-dependent phosphate transport across the renal brush-border membrane (BBM). Nicotinamide acts both as a precursor for NAD synthesis and as an inhibitor of NAD hydrolysis. To determine if the latter effect contributes to the change in phosphate transport, a nicotinamide analogue was used in the present study. 5-Methylnicotinamide (5MN) cannot support NAD synthesis, but it is an equipotent inhibitor of NAD-hydrolyzing enzymes. The characteristics of the specific inhibitory effect of nicotinamide on sodium gradient-dependent phosphate transport were reproduced by an equimolar dose (4 mmol\/kg body wt) of 5MN. Unlike nicotinamide, the action of 5MN did not involve a change in renal cortical NAD content. These data indicate that inhibition of NAD hydrolyzing enzymes may be associated with inhibition of BBM phosphate transport, and this effect occurs independently of changes in NAD levels. These conclusions are supported by the finding that BBM phosphate transport was not inhibited by administration of nicotinic acid, an analogue that does not inhibit NAD hydrolysis. <\/jats:p>","DOI":"10.1152\/ajprenal.1986.251.3.f520","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T01:03:31Z","timestamp":1513991011000},"page":"F520-F527","source":"Crossref","is-referenced-by-count":0,"title":["5-Methylnicotinamide inhibits renal brush-border phosphate transport with no change in NAD"],"prefix":"10.1152","volume":"251","author":[{"given":"S. A.","family":"Kempson","sequence":"first","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1986.251.3.F520","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:36:40Z","timestamp":1567971400000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1986.251.3.F520"}},"issued":{"date-parts":[[1986,9,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1986,9,1]]}},"alternative-id":["10.1152\/ajprenal.1986.251.3.F520"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1986.251.3.f520","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1986,9,1]]}},{"indexed":{"date-parts":[[2022,4,5]],"date-time":"2022-04-05T22:41:25Z","timestamp":1649198485735},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2001,6,1]]},"DOI":"10.1152\/ajprenal.2001.280.6.fa2","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T14:14:11Z","timestamp":1514038451000},"page":"Fa2-Fa2","source":"Crossref","is-referenced-by-count":0,"title":["Corrigendum"],"prefix":"10.1152","volume":"280","member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.2001.280.6.Fa2","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:57:26Z","timestamp":1567976246000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.2001.280.6.Fa2"}},"issued":{"date-parts":[[2001,6,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2001,6,1]]}},"alternative-id":["10.1152\/ajprenal.2001.280.6.Fa2"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.2001.280.6.fa2","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2001,6,1]]}},{"indexed":{"date-parts":[[2022,4,1]],"date-time":"2022-04-01T14:40:16Z","timestamp":1648824016114},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1985,8,1]]},"abstract":"<jats:p> Previous uncertainty regarding glomerular ultrafilterability (UF) of aluminum has limited the definition of renal Al handling. Glomerular micropuncture was therefore performed in hydropenic Munich-Wistar rats infused with AlCl3 to achieve plasma (P) Al levels between 2 and 10 mg\/liter. Glomerular fluid, P, and urine Al concentrations were measured by flameless atomic-absorption spectrophotometry. UFA1 was inversely correlated with PA1 [%UFA1 = 10.3 - 8.4 (log PA1), r = -0.90, P less than 0.01]. When this equation was used to calculate the filtered load (FLA1), A1 excretion (UA1V, ng\/min) in simultaneously collected samples was found to be a direct function of FLA1 [UA1V = 5.7 + 0.37 (FLA1), r = 0.93, P less than 0.01]. Fractional excretion (FE) of A1 was 39.4 +\/- 4.2% in these hydropenic experiments (FENa = 0.3 +\/- 0.1%). We next evaluated the tubular handling of A1 (using these UF data) during step-wise extracellular fluid volume expansion with isotonic saline (2.5, 5.0, 7.0, and 7.0% body wt) and during the infusion of increasing doses (2.7, 5.3, 8.0, and 8.0 mg X kg-1 X h-1) of furosemide as urinary losses were quantitatively replaced. The natriuresis produced by volume expansion (FENa = 1.0, 3.0, 8.4, and 7.9%) and furosemide (FENa = 4.2, 6.0, 6.6, and 6.7%) were comparable. At similar FLA1, 7% volume expansion but not furosemide (at any dose) increased UA1V (240 and 95 ng\/min, respectively, vs. 116 ng\/min in hydropenia) and FEA1 (84.5 and 29.4 vs. 37.4%, respectively). These data indicate that at pharmacological PA1 levels, less than 8.4% of PA1 is ultrafilterable, suggesting extensive plasma protein binding.(ABSTRACT TRUNCATED AT 250 WORDS) <\/jats:p>","DOI":"10.1152\/ajprenal.1985.249.2.f192","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T19:15:14Z","timestamp":1513970114000},"page":"F192-F197","source":"Crossref","is-referenced-by-count":0,"title":["Renal handling of aluminum in the rat: clearance and micropuncture studies"],"prefix":"10.1152","volume":"249","author":[{"given":"M. A.","family":"Burnatowska-Hledin","sequence":"first","affiliation":[]},{"given":"G. H.","family":"Mayor","sequence":"additional","affiliation":[]},{"given":"K.","family":"Lau","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1985.249.2.F192","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:29:38Z","timestamp":1567956578000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1985.249.2.F192"}},"issued":{"date-parts":[[1985,8,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1985,8,1]]}},"alternative-id":["10.1152\/ajprenal.1985.249.2.F192"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1985.249.2.f192","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1985,8,1]]}},{"indexed":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T04:11:16Z","timestamp":1660191076609},"reference-count":24,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1998,7,1]]},"abstract":"<jats:p>Developmental expression of ion channels possibly participating in regulatory volume decrease was studied in rat embryonic ( day E17) and perinatal ( days P1\u20136) ureteric bud and in postnatal ( P9\u201314) cortical collecting duct cells in primary monolayer culture. In isotonic bath solution, whole cell conductance (in nS\/10 pF) was highest in E17 (4.0 \u00b1 0.5, n = 31) compared with P1\u20136 (2.0 \u00b1 0.1, n = 16) and P9\u201314 (1.3 \u00b1 0.2, n = 12) due to a decreasing contribution of a DIDS-sensitive Cl conductance, from E17 (2.8 \u00b1 0.7, n = 12) to P1\u20136 (0.53 \u00b1 0.07, n = 9) and P9\u201314 (0.05 \u00b1 0.1, n = 7). Cl conductance in E17 exhibited a permselectivity of I \u2248 Cl \u2248 Br \u226b gluconate, and it activated time dependently. Hypotonic bath solution induced a large increase of whole cell conductance in P1\u20136 and in P9\u201314 but not in E17 (by 20.0 \u00b1 3.7, 21.5 \u00b1 5.5, and 4.9 \u00b1 1.7; n = 11, 12, and 25, respectively) due to the activation of a time-dependently inactivating Cl conductance with a permselectivity of I \u2265 Br &gt; Cl \u226b gluconate. In conclusion, the expression of Cl channels, as studied in vitro, appears to shift from an apparently constitutively active embryonic to a hypotonic swelling-activated type during late embryonic development of the collecting duct.<\/jats:p>","DOI":"10.1152\/ajprenal.1998.275.1.f25","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T15:28:40Z","timestamp":1514042920000},"page":"F25-F32","source":"Crossref","is-referenced-by-count":2,"title":["Expression of a hypotonic swelling-activated Cl conductance during ontogeny of collecting duct epithelium"],"prefix":"10.1152","volume":"275","author":[{"given":"Stephan M.","family":"Huber","sequence":"first","affiliation":[{"name":"Physiologisches Institut, Ludwig-Maximilians-Universit\u00e4t, 80336 Munich, Germany"}]},{"given":"Michael F.","family":"Horster","sequence":"additional","affiliation":[{"name":"Physiologisches Institut, Ludwig-Maximilians-Universit\u00e4t, 80336 Munich, Germany"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.88.14.6003"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1126\/science.1712984"},{"issue":"7","key":"B3","first-page":"L1","volume":"263","author":"Anderson M. P.","year":"1992","journal-title":"Am. J. Physiol."},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1007\/BF01870526"},{"issue":"40","key":"B5","first-page":"C1224","volume":"271","author":"Boese S. H.","year":"1996","journal-title":"Am. J. Physiol."},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.87.13.4956"},{"issue":"30","key":"B7","first-page":"F91","volume":"261","author":"Evan A. P.","year":"1991","journal-title":"Am. J. Physiol."},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.387"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/0076-6879(90)91026-3"},{"issue":"40","key":"B10","first-page":"F698","volume":"271","author":"Huber S. M.","year":"1996","journal-title":"Am. J. Physiol."},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1995.sp020560"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1007\/BF00370589"},{"key":"B14","first-page":"48","volume":"16","author":"Lang F.","year":"1993","journal-title":"Renal Physiol. Biochem."},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.108.3.177"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1987.115"},{"key":"B17","doi-asserted-by":"crossref","first-page":"5575","DOI":"10.1016\/S0021-9258(18)42804-9","volume":"267","author":"Morris A. P.","year":"1992","journal-title":"J. Biol. Chem."},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1165\/ajrcmb.12.6.7766424"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1038\/356238a0"},{"issue":"39","key":"B20","first-page":"F391","volume":"270","author":"Satlin L. M.","year":"1996","journal-title":"Am. J. Physiol."},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1007\/BF00370998"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1996.270.3.C711"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1038\/356057a0"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1093\/biomet\/38.3-4.330"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1989.256.6.C1111"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1998.275.1.F25","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:48:33Z","timestamp":1660189713000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1998.275.1.F25"}},"issued":{"date-parts":[[1998,7,1]]},"references-count":24,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1998,7,1]]}},"alternative-id":["10.1152\/ajprenal.1998.275.1.F25"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1998.275.1.f25","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1998,7,1]]}},{"indexed":{"date-parts":[[2024,8,14]],"date-time":"2024-08-14T15:55:13Z","timestamp":1723650913210},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1995,8,1]]},"abstract":"<jats:p> The effects of anisosmotic media on intracellular Ca2+ and H+ concentrations ([Ca2+]i and pHi, respectively) were studied to investigate whether these changes play a role in epithelial cell volume regulation. [Ca2+]i and pHi were measured in rabbit proximal tubular cells in primary culture using the fluorescent ratio probes fura 2 and 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein. Changing medium osmolarity from 300 to 150 mosmol resulted in a rapid transient increase in fura 2 ratio from 0.89 +\/- 0.02 to 1.15 +\/- 0.03, which lasted for several minutes and returned to base line within 10 min. The source of Ca2+ was extracellular as well as intracellular. Simultaneous with this increase in [Ca2+]i, cells slowly acidified from pHi of 7.51 +\/- 0.03 to 6.86 +\/- 0.02. This osmotic swelling-induced acidification could not be explained by a decrease in the rate of Na+\/H+ exchange or increase in the rate of Cl-\/HCO3- exchange. Subsequently increasing medium osmolarity from 150 to 500 mosmol decreased the fura 2 ratio below the initial level observed in isotonic media, while pHi increased from 6.96 +\/- 0.02 to 7.37 +\/- 0.03. This decrease in [Ca2+]i was due to inhibition of Ca2+ influx and to an increase in Ca2+ efflux. The osmotic shrinkage-induced alkalinization was slightly inhibited by ethylisopropylamiloride, indicative of activation of Na+\/H+ exchange. To test whether an increase in [Ca2+]i causes a decrease in pHi or vice versa, pHi and [Ca2+]i were manipulated at isotonic conditions. Surprisingly, a decrease in [Ca2+]i was accompanied by a decrease in pHi, and an increase in pHi resulted in an increase in [Ca2+]i, in the absence of osmotic perturbation.(ABSTRACT TRUNCATED AT 250 WORDS) <\/jats:p>","DOI":"10.1152\/ajprenal.1995.269.2.f205","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T06:13:31Z","timestamp":1514009611000},"page":"F205-F211","source":"Crossref","is-referenced-by-count":2,"title":["Effects of osmotic perturbation on [Ca2+]i and pHi in rabbit proximal tubular cells in primary culture"],"prefix":"10.1152","volume":"269","author":[{"given":"N. J.","family":"Raat","sequence":"first","affiliation":[{"name":"Department of Cell Physiology, University of Nijmegen, TheNetherlands."}]},{"given":"C. H.","family":"van Os","sequence":"additional","affiliation":[{"name":"Department of Cell Physiology, University of Nijmegen, TheNetherlands."}]},{"given":"R. J.","family":"Bindels","sequence":"additional","affiliation":[{"name":"Department of Cell Physiology, University of Nijmegen, TheNetherlands."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1995.269.2.F205","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:02:59Z","timestamp":1567972979000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1995.269.2.F205"}},"issued":{"date-parts":[[1995,8,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1995,8,1]]}},"alternative-id":["10.1152\/ajprenal.1995.269.2.F205"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1995.269.2.f205","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1995,8,1]]}},{"indexed":{"date-parts":[[2024,5,12]],"date-time":"2024-05-12T19:59:43Z","timestamp":1715543983083},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1981,10,1]]},"abstract":"<jats:p> Fractional lithium clearance (CLi\/CIn), transit time-occlusion time (e-TT\/OT), and late proximal tubular fluid-to-plasma inulin ratio [1\/(TF\/P)In] collected by micropuncture were determined successively in the same rat during Amytal anesthesia. The rats were examined during hydropenia, after partial aortic constriction, or during saline diuresis. There was a linear relationship (r = 0.80) between CLi\/CIn and e-TT\/OT. The 1\/(TF\/P)In ratio correlated closely with both CLi\/CIn (r = 0.88) and e-TT\/OT (r = 0.91) when intraluminal pressure was maintained at the free-flow level during fluid collection. If fluid collection was guided merely by the position of an oil droplet and the luminal diameter, the 1\/(TF\/P)In data were not correlated with either CLi\/CIn or e-TT\/OT. Over a wide range of proximal absolute and fractional reabsorption rates the technically simpler lithium clearance and TT\/OT methods may provide data on proximal fractional reabsorption that are as accurate and reliable as data obtained by pressure-controlled micropuncture collection. Micropuncture carried out without pressure control provides highly inaccurate data and is clearly inferior to the other methods. These results are consistent with the possibility that lithium is reabsorbed exclusively by the proximal tubules, 17-20% being reabsorbed by the pars recta. <\/jats:p>","DOI":"10.1152\/ajprenal.1981.241.4.f348","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T09:05:17Z","timestamp":1513933517000},"page":"F348-F355","source":"Crossref","is-referenced-by-count":9,"title":["Comparison of three measures of proximal tubular reabsorption: lithium clearance, occlusion time, and micropuncture"],"prefix":"10.1152","volume":"241","author":[{"given":"K.","family":"Thomsen","sequence":"first","affiliation":[]},{"given":"N. H.","family":"Holstein-Rathlou","sequence":"additional","affiliation":[]},{"given":"P. P.","family":"Leyssac","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1981.241.4.F348","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T14:19:13Z","timestamp":1567952353000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1981.241.4.F348"}},"issued":{"date-parts":[[1981,10,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1981,10,1]]}},"alternative-id":["10.1152\/ajprenal.1981.241.4.F348"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1981.241.4.f348","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1981,10,1]]}},{"indexed":{"date-parts":[[2024,5,12]],"date-time":"2024-05-12T19:18:11Z","timestamp":1715541491296},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1977,3,1]]},"abstract":"<jats:p> During the onset of malignant hypertension (MH) in rats treated with deoxycorticosterone trimethylacetate (DOC), plasma arginine vasopressin (AVP) concentrations increase tenfold as a consequence of hypovolemia and hyperosmolality. In benign hypertensive (BH) rats, plasma AVP is increased threefold in comparison with control animals. Plasma renin is markedly suppressed in both BH and MH animals. In MH rats, biologically active AVP antiserum lowers blood pressure (BP) transiently to normal or subnormal levels; in BH rats, a small BP-lowering effect of the AVP antiserum is seen. (Biologically active angiotensin II antiserum does not lower BP in MH rats.) The relationship between the height of BP and plasma AVP concentration in DOC hypertensive rats indicates, when compared with that relationship in diabetes insipidus rats infused with AVP, a marked enhancement of the vasopressor effect of AVP. These findings and the earlier observation of vasopressin-induced vascular damage by Byrom (F. B. Byrom, The Hypertensive Vascular Crisis. London: Heinemann, 1969) strongly suggest that ADH is involved as a vasopressor hormone in the pathogenesis of malignant DOC hypertension. <\/jats:p>","DOI":"10.1152\/ajprenal.1977.232.3.f260","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T20:24:50Z","timestamp":1513974290000},"page":"F260-F269","source":"Crossref","is-referenced-by-count":8,"title":["Vasopressor role of ADH in the pathogenesis of malignant DOC hypertension"],"prefix":"10.1152","volume":"232","author":[{"given":"J.","family":"Mohring","sequence":"first","affiliation":[]},{"given":"B.","family":"Mohring","sequence":"additional","affiliation":[]},{"given":"M.","family":"Petri","sequence":"additional","affiliation":[]},{"given":"D.","family":"Haack","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1977.232.3.F260","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:59:15Z","timestamp":1567969155000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1977.232.3.F260"}},"issued":{"date-parts":[[1977,3,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1977,3,1]]}},"alternative-id":["10.1152\/ajprenal.1977.232.3.F260"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1977.232.3.f260","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1977,3,1]]}},{"indexed":{"date-parts":[[2024,1,10]],"date-time":"2024-01-10T00:10:31Z","timestamp":1704845431257},"reference-count":20,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2006,12]]},"abstract":"<jats:p>The \u03b3-subunit of Na-K-ATPase is robustly expressed in inner medullary collecting duct (IMCD)3 cells either acutely challenged or adapted to hypertonicity but not under isotonic conditions. Circumstantial evidence suggests that this protein may be important for the survival of renal cells in a hypertonic environment. However, no direct proof for such a contention has been forthcoming. The complete mRNA sequences of either \u03b3-subunit isoforms were spliced into an expression vector and transfected into IMCD3 cells. Multiple clones stably expressed \u03b3-subunit protein under isotonic conditions. Clones expressing the \u03b3<jats:sub>b<\/jats:sub>isoform showed enhanced survival at lethal acute hypertonicity compared with either \u03b3<jats:sub>a<\/jats:sub>isoform or empty vector (control) expressing clones. We also evaluated the loss of \u03b3-subunit expression on the survival of IMCD3 cells exposed to hypertonicity employing silencing RNA techniques. Multiple stable \u03b3-subunit-specific siRNA clones were obtained and exposed to sublethal hypertonicity. Under these conditions, both the level of \u03b3 mRNA and protein was essentially undetectable. The impact of silencing \u03b3-subunit expression resulted in a 70% reduction at 48 h ( P &lt; 0.01) in cell survival compared with empty vector (control) clones. \u03b3 siRNA clones showed a 45% decrease in myo-inositol uptake compared with controls after an 18-h exposure to sublethal hypertonicity. Taken together, these data demonstrate a direct and critical role of the \u03b3-subunit on IMCD3 cell survival and\/or adaptation in response to ionic hypertonic stress.<\/jats:p>","DOI":"10.1152\/ajprenal.00077.2006","type":"journal-article","created":{"date-parts":[[2006,6,28]],"date-time":"2006-06-28T01:49:49Z","timestamp":1151459389000},"page":"F1142-F1147","source":"Crossref","is-referenced-by-count":6,"title":["Silencing and overexpression of the \u03b3-subunit of Na-K-ATPase directly affect survival of IMCD3 cells in response to hypertonic stress"],"prefix":"10.1152","volume":"291","author":[{"given":"Juan M.","family":"Capasso","sequence":"first","affiliation":[]},{"given":"Christopher J.","family":"Rivard","sequence":"additional","affiliation":[]},{"given":"Tomas","family":"Berl","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00146.2001"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1016\/S1095-6433(02)00203-9"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.59.1.437"},{"key":"R4","doi-asserted-by":"crossref","unstructured":"Capasso JM, Keenan TW, Abeijon C, and Hirschberg CB.Mechanism of phosphorylation in the lumen of the Golgi apparatus. Translocation of adenosine 5\u2032-triphosphate into Golgi vesicles from rat liver and mammary gland.J Biol Chem264: 5233\u20135240, 1989.","DOI":"10.1016\/S0021-9258(18)83723-1"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.5.F768"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.231309198"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00026.2004"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1130871100"},{"key":"R9","unstructured":"Chamberlin MEand Strange K.Anisosmotic cell volume regulation: a comparative view.Am J Physiol Cell Physiol257: C159\u2013C173, 1989."},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.2003.tb07225.x"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M500080200"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1991.71.4.1081"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.68.040104.131852"},{"key":"R14","doi-asserted-by":"crossref","unstructured":"Pihakaski-Maunsbach K, Tokonabe S, Vorum H, Rivard CJ, Capasso JM, Berl T, and Maunsbach AB.The \u03b3-subunit of Na-K-ATPase is incorporated into plasma membranes of mouse IMCD3 cells in response to hypertonicity.Am J Physiol Renal Physiol288: F650\u2013F657, 2005.","DOI":"10.1152\/ajprenal.00162.2004"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.2003.tb07221.x"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000077413.41276.17"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00031.2002"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.260.5.F619"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M405622200"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.2.800"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00077.2006","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,7,28]],"date-time":"2021-07-28T23:05:03Z","timestamp":1627513503000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00077.2006"}},"issued":{"date-parts":[[2006,12]]},"references-count":20,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2006,12]]}},"alternative-id":["10.1152\/ajprenal.00077.2006"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00077.2006","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2006,12]]}},{"indexed":{"date-parts":[[2025,9,10]],"date-time":"2025-09-10T21:57:20Z","timestamp":1757541440188},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1984,5,1]]},"abstract":"<jats:p> To ascertain whether Na+ gradient-stimulated 32Pi uptake was demonstrable in renal basolateral membrane vesicles, we measured 32Pi uptake in basolateral membrane suspensions isolated from canine renal cortex and compared solute uptake in basolateral suspensions with that measured in brush border suspensions. Measurements revealed Na+ gradient-dependent 32Pi transport in basolateral preparations. D-[3H] Glucose uptakes in basolateral suspensions were not stimulated by the Na+ gradient in contrast to findings in brush border suspensions. Na+ gradient-dependent 32Pi transport in basolateral suspensions was electrogenic in contrast to that measured in brush border preparations. Unlike 32Pi uptake in brush border preparations, Na+ gradient-dependent 32Pi uptake in basolateral suspensions did not increase as extravesicular pH was increased from 6.5 to 7.5. Na+ gradient-dependent 32Pi uptake in basolateral membranes showed saturation over the range of [Pi] from 5 to 100 microM (apparent Km, 14 +\/- 2 microM; apparent Vmax, 34 +\/- 2 pmol Pi X mg protein-1 X 30s-1). Our findings are compatible with the presence of an electrogenic Na+-Pi cotransporter in the canine proximal tubular basolateral membrane. <\/jats:p>","DOI":"10.1152\/ajprenal.1984.246.5.f663","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T16:46:51Z","timestamp":1513961211000},"page":"F663-F669","source":"Crossref","is-referenced-by-count":2,"title":["Na+ gradient-dependent Pi uptake in basolateral membrane vesicles from dog kidney"],"prefix":"10.1152","volume":"246","author":[{"given":"S. J.","family":"Schwab","sequence":"first","affiliation":[]},{"given":"S.","family":"Klahr","sequence":"additional","affiliation":[]},{"given":"M. R.","family":"Hammerman","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1984.246.5.F663","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:34:53Z","timestamp":1567967693000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1984.246.5.F663"}},"issued":{"date-parts":[[1984,5,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1984,5,1]]}},"alternative-id":["10.1152\/ajprenal.1984.246.5.F663"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1984.246.5.f663","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1984,5,1]]}},{"indexed":{"date-parts":[[2025,9,10]],"date-time":"2025-09-10T22:21:04Z","timestamp":1757542864614},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1986,3,1]]},"abstract":"<jats:p> The stoichiometry of the sodium chloride cotransport system was examined in isolated perfused rectal glands of Squalus acanthias by kinetic analysis of the effect on chloride secretion of progressive substitutions of other ions for sodium and chloride in the perfusate. Secretion was stimulated by a constant infusion of dibutyryl cyclic AMP (5 X 10(-5) M) and theophylline (2.5 X 10(-4) M). Sodium was replaced by N-methyl-D-glucamine, whereas chloride was replaced by gluconate. The Km values for sodium, obtained using three different graphic methods, were close to or at the normal concentration of sodium in the plasma of the shark, suggesting that plasma sodium concentration regulates transport by the gland. The Km values for chloride were far below the normal concentration of chloride in the plasma, indicating that the chloride sites are normally saturated and therefore plasma chloride concentration cannot control transport by the gland. Hill plots revealed slopes of 1.06 for sodium and 1.6 for chloride, consistent with the hypothesis that 2 Cl- and 1 Na+ interact in the cotransport process. The cotransport linkage of 2 Cl- with 1 Na+ in the initial step of entry into the cell can be viewed as a device that doubles the energetic efficiency of salt transport, allowing 2 NaCl to be secreted for every 1 Na+ actively pumped. <\/jats:p>","DOI":"10.1152\/ajprenal.1986.250.3.f516","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T01:24:13Z","timestamp":1513992253000},"page":"F516-F519","source":"Crossref","is-referenced-by-count":1,"title":["Stoichiometry of sodium chloride transport by rectal gland of Squalus acanthias"],"prefix":"10.1152","volume":"250","author":[{"given":"P.","family":"Silva","sequence":"first","affiliation":[]},{"given":"M. A.","family":"Myers","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1986.250.3.F516","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:37:06Z","timestamp":1567971426000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1986.250.3.F516"}},"issued":{"date-parts":[[1986,3,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1986,3,1]]}},"alternative-id":["10.1152\/ajprenal.1986.250.3.F516"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1986.250.3.f516","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1986,3,1]]}},{"indexed":{"date-parts":[[2025,9,10]],"date-time":"2025-09-10T22:35:15Z","timestamp":1757543715471},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1992,3,1]]},"abstract":"<jats:p> This study was designed to identify the subtypes of angiotensin II (ANG II) receptors present on glomeruli and glomerular mesangial cells and establish their functional significance. Dup 753 and its metabolite EXP 3174, two nonpeptide ANG II-1 receptor (AT1) antagonists, displaced 125I-ANG II and its analogue 125I-[Sar1,Ala8]ANG II from their binding sites in rat and human glomeruli and cultured human mesangial cells, whereas CGP 42112 A and PD 123177, two ANG II-2 receptor (AT2) antagonists, exhibited little displacing activity. Dup 753 and EXP 3174 did not modify the dissociation constant (Kd) value but markedly decreased the number of sites of 125I-[Sar1,Ala8]ANG II binding. The addition of PD 123177 did not further inhibit binding when all AT1 sites were occupied by Dup 753. Binding was markedly reduced by dithiothreitol. EXP 3174 and Dup 753 inhibited the main biological functions of ANG II in mesangial cells including increases in intracellular calcium concentration, PGE2 production, and protein synthesis. PD 123177 was also active but at concentrations 1,000- to 10,000-fold greater than those of AT1 antagonists. These results indicate that 1) only AT1 receptors are present in glomeruli and glomerular mesangial cells; 2) these receptors mediate the functional responses to ANG II; 3) the nonpeptide AT1 antagonists behave as noncompetitive inhibitors; and 4) high concentrations of the nonpeptide AT2 antagonists can recognize AT1 sites. <\/jats:p>","DOI":"10.1152\/ajprenal.1992.262.3.f432","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T03:57:12Z","timestamp":1514001432000},"page":"F432-F441","source":"Crossref","is-referenced-by-count":2,"title":["Characterization of angiotensin II receptor subtypes in human glomeruli and mesangial cells"],"prefix":"10.1152","volume":"262","author":[{"given":"D.","family":"Chansel","sequence":"first","affiliation":[{"name":"Institut National de la Sante et de la Recherche Medicale 64, HopitalTenon, Paris, France."}]},{"given":"S.","family":"Czekalski","sequence":"additional","affiliation":[{"name":"Institut National de la Sante et de la Recherche Medicale 64, HopitalTenon, Paris, France."}]},{"given":"P.","family":"Pham","sequence":"additional","affiliation":[{"name":"Institut National de la Sante et de la Recherche Medicale 64, HopitalTenon, Paris, France."}]},{"given":"R.","family":"Ardaillou","sequence":"additional","affiliation":[{"name":"Institut National de la Sante et de la Recherche Medicale 64, HopitalTenon, Paris, France."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1992.262.3.F432","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:19:39Z","timestamp":1567959579000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1992.262.3.F432"}},"issued":{"date-parts":[[1992,3,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1992,3,1]]}},"alternative-id":["10.1152\/ajprenal.1992.262.3.F432"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1992.262.3.f432","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1992,3,1]]}},{"indexed":{"date-parts":[[2023,8,19]],"date-time":"2023-08-19T13:19:43Z","timestamp":1692451183792},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1981,8,1]]},"abstract":"<jats:p> Net calcium efflux (JCanet) was compared in isolated perfused cortical and medullary segments of the thick ascending limb of Henle of the rabbit kidney. In response to the addition of calcitonin to the bathing medium, cortical segments showed no change in JCanet, whereas in medullary segments JCanet increased significantly. Similar studies substituting 8-bromo-cyclic AMP (8-BrcAMP) in concentrations of 10(-4) M or lower in the bath showed no effect on JCanet in either segment. When the concentration of 8-BrcAMP in the bath was increased to 10(-3) M, JCanet rose significantly in both segments. These results indicate heterogeneity of response to calcitonin in the cortical and medullary segments of the thick ascending limb of Henle, but a similar response of calcium transport to cAMP. Because we have previously shown that parathyroid hormone stimulates net calcium efflux in the cortical but not in the medullary segments of the thick ascending limb of Henle, the present observations suggest that cAMP may be the mediator of the actions of both calcitonin and parathyroid hormone. <\/jats:p>","DOI":"10.1152\/ajprenal.1981.241.2.f171","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T09:34:40Z","timestamp":1513935280000},"page":"F171-F174","source":"Crossref","is-referenced-by-count":5,"title":["Hormonal regulation of calcium transport in thick ascending limb renal tubules"],"prefix":"10.1152","volume":"241","author":[{"given":"W. N.","family":"Suki","sequence":"first","affiliation":[]},{"given":"D.","family":"Rouse","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1981.241.2.F171","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T14:22:42Z","timestamp":1567952562000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1981.241.2.F171"}},"issued":{"date-parts":[[1981,8,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1981,8,1]]}},"alternative-id":["10.1152\/ajprenal.1981.241.2.F171"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1981.241.2.f171","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1981,8,1]]}},{"indexed":{"date-parts":[[2024,5,12]],"date-time":"2024-05-12T17:30:26Z","timestamp":1715535026254},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1986,7,1]]},"abstract":"<jats:p> A technique was designed to study renin release from superfused rat glomeruli with short attached arterioles (SAG), from single glomeruli with long attached arterioles (LAG), and from single afferent arterioles (AA). The preparations obtained by magnetic isolation and microdissection were superfused individually, and the renin release was measured by an ultramicroradioimmunoassay with a detection limit of 3 X 10(-9) Goldblatt units. The renin content of one SAG was about one-fifth of that contained in one AA. Isoprenaline (10(-5) M) did not change renin release from SAG, whereas renin release from AA and LAG increased threefold (P less than 0.01). A 30-mosmol\/kg reduction in medium sodium chloride concentration increased renin release from SAG 50% (P less than 0.01). This challenge caused no change in renin release from AA. It is concluded that the isoprenaline-sensitive juxtaglomerular (JG) cells are located in the afferent arteriole only at some distance from the glomerulus, whereas those cells sensitive to sodium chloride are located within and\/or close to the glomerulus. <\/jats:p>","DOI":"10.1152\/ajprenal.1986.251.1.f12","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T01:01:17Z","timestamp":1513990877000},"page":"F12-F16","source":"Crossref","is-referenced-by-count":3,"title":["Renin release from different parts of rat afferent arterioles in vitro"],"prefix":"10.1152","volume":"251","author":[{"given":"L.","family":"Baumbach","sequence":"first","affiliation":[]},{"given":"O.","family":"Skott","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1986.251.1.F12","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:34:59Z","timestamp":1567971299000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1986.251.1.F12"}},"issued":{"date-parts":[[1986,7,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1986,7,1]]}},"alternative-id":["10.1152\/ajprenal.1986.251.1.F12"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1986.251.1.f12","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1986,7,1]]}},{"indexed":{"date-parts":[[2024,2,7]],"date-time":"2024-02-07T17:54:45Z","timestamp":1707328485302},"reference-count":42,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1999,11,1]]},"abstract":"<jats:p> Clinically, a decrease in blood pH may be due to either a reduction in bicarbonate concentration ([H[Formula: see text]], metabolic acidosis) or an increase in[Formula: see text] (respiratory acidosis). In mammals, metabolic acidosis induces a far greater increase in urine calcium excretion than respiratory acidosis. In cultured bone, metabolic acidosis induces a marked increase in calcium efflux and a decrease in osteoblastic collagen synthesis, whereas isohydric respiratory acidosis has little effect on either parameter. We have shown that metabolic acidosis prevents the normal developmental increase in the expression of RNA for matrix Gla protein and osteopontin in chronic cultures of primary murine calvarial bone cells (predominantly osteoblasts) but does not alter expression of osteonectin. To compare the effects of isohydric metabolic and respiratory acidosis on expression of these genes, bone cell cultures were incubated in medium at pH \u223c7.2 to model metabolic ([H[Formula: see text]], \u223c13 mM) or respiratory ([Formula: see text], \u223c80 mmHg) acidosis or at pH \u223c7.4 as a control. Cells were sampled at weeks 4, 5, and 6 to assess specific RNA content. At all time periods studied, both metabolic and respiratory acidosis inhibited the expression of RNA for matrix Gla protein and osteopontin to a similar extent, whereas there was no change in osteonectin expression. In contrast to the significant difference in the effects of metabolic and respiratory acidosis on bone calcium efflux and osteoblastic collagen synthesis, these two forms of acidosis have a similar effect on osteoblastic RNA expression of both matrix Gla protein and osteopontin. Thus, although several aspects of bone cell function are dependent on the type of acidosis, expression of these two matrix genes appears to be regulated by extracellular pH, independently of the type of acidosis. <\/jats:p>","DOI":"10.1152\/ajprenal.1999.277.5.f750","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T07:05:33Z","timestamp":1514012733000},"page":"F750-F755","source":"Crossref","is-referenced-by-count":15,"title":["In vitro metabolic and respiratory acidosis selectively  inhibit osteoblastic matrix gene expression"],"prefix":"10.1152","volume":"277","author":[{"given":"Kevin K.","family":"Frick","sequence":"first","affiliation":[{"name":"Nephrology Unit, Department of Medicine, University of Rochester School of Medicine, Rochester, New York 14642"}]},{"given":"David A.","family":"Bushinsky","sequence":"additional","affiliation":[{"name":"Nephrology Unit, Department of Medicine, University of Rochester School of Medicine, Rochester, New York 14642"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/0169-6009(91)90100-E"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1007\/BF02556874"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/S0169-6009(08)80225-5"},{"issue":"23","key":"B4","first-page":"F306","volume":"254","author":"Bushinsky D. A.","year":"1988","journal-title":"Am. J. Physiol."},{"issue":"25","key":"B5","first-page":"F836","volume":"256","author":"Bushinsky D. A.","year":"1989","journal-title":"Am. J. Physiol."},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.251"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1995.268.1.C80"},{"issue":"12","key":"B9","first-page":"F570","volume":"243","author":"Bushinsky D. A.","year":"1982","journal-title":"Am. J. Physiol."},{"issue":"17","key":"B10","first-page":"F785","volume":"248","author":"Bushinsky D. A.","year":"1985","journal-title":"Am. J. Physiol."},{"issue":"14","key":"B11","first-page":"F204","volume":"245","author":"Bushinsky D. A.","year":"1983","journal-title":"Am. J. Physiol."},{"issue":"34","key":"B12","first-page":"F530","volume":"265","author":"Bushinsky D. A.","year":"1993","journal-title":"Am. J. Physiol."},{"issue":"22","key":"B13","first-page":"F998","volume":"253","author":"Bushinsky D. A.","year":"1987","journal-title":"Am. J. Physiol."},{"issue":"32","key":"B14","first-page":"F510","volume":"263","author":"Bushinsky D. A.","year":"1992","journal-title":"Am. J. Physiol."},{"issue":"31","key":"B15","first-page":"F425","volume":"262","author":"Bushinsky D. A.","year":"1992","journal-title":"Am. J. Physiol."},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1002\/jbmr.5650080112"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1990.220"},{"issue":"30","key":"B18","first-page":"F76","volume":"261","author":"Chabala J. M.","year":"1991","journal-title":"Am. J. Physiol."},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/0003-2697(87)90021-2"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.96.3.639"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/13.5.1431"},{"issue":"44","key":"B22","first-page":"F840","volume":"275","author":"Frick K. K.","year":"1998","journal-title":"Am. J. Physiol."},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1997.272.5.C1450"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1989.69.3.990"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1002\/jbmr.5650020607"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.90.18.8562"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1002\/jbmr.5650060916"},{"issue":"31","key":"B28","first-page":"F442","volume":"262","author":"Krieger N. S.","year":"1992","journal-title":"Am. J. Physiol."},{"key":"B29","first-page":"27","volume":"109","author":"Lau K.","year":"1987","journal-title":"J. Lab. Clin. Med."},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM197909063011008"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1172\/JCI105467"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1172\/JCI105624"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1172\/JCI2131"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1038\/386078a0"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.3109\/03008209609029192"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1210\/endo-127-1-185"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.247"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1152\/jappl.1963.18.6.1079"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1152\/jappl.1980.48.5.802"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199406233302502"},{"issue":"33","key":"B41","first-page":"F882","volume":"264","author":"Sprague S. M.","year":"1993","journal-title":"Am. J. Physiol."},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.385"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/14.11.4483"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1999.277.5.F750","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:39:33Z","timestamp":1567960773000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1999.277.5.F750"}},"issued":{"date-parts":[[1999,11,1]]},"references-count":42,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1999,11,1]]}},"alternative-id":["10.1152\/ajprenal.1999.277.5.F750"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1999.277.5.f750","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1999,11,1]]}},{"indexed":{"date-parts":[[2023,10,22]],"date-time":"2023-10-22T09:18:24Z","timestamp":1697966304661},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1987,7,1]]},"abstract":"<jats:p> Fractional lithium clearance (CLi\/CIn), transit time occlusion time (e-TT\/OT), and late proximal tubule fluid-to-plasma inulin ratio [1\/(TF\/P)In] determined by micropuncture were measured in the same kidney during 5-sec-butyl-5-ethyl-2-thiobarbituric acid (Inactin) anesthesia in rats fed either less than 2 mu eq sodium\/g diet, rodent chow containing 20 mu eq sodium\/g diet, or rodent chow and 0.5% NaCl to drink. Both CLi\/CIn vs. e-TT\/OT (r = 0.59) or 1(TF\/P)In (r = 0.65) were linearly correlated at all sodium intakes. Quantitative estimates of proximal delivery by 1\/(TF\/P)In and e-TT\/OT were similar (P = NS), whereas estimates from CLi\/CIn were lower (P less than 0.05 or less) than the direct methods even when corrected for pars recta reabsorption. After acetazolamide or amiloride, but not furosemide, all methods for proximal delivery correlated quantitatively (P = NS) in sodium-restricted rats. Between amiloride and nondiuretic sodium-restricted rats, 1\/(TF\/P)In was not different. Proximal delivery estimated by CLi\/CIn slightly (P = NS) underestimated direct measurements during 2% volume expansion [fractional sodium excretion (FeNa) 0.65 +\/- 0.08%]. Thus, in the rat, CLi\/CIn is not a quantitative estimate of proximal delivery if FeNa is less than 0.65% due to distal lithium reabsorption. CLi\/CIn determined after amiloride may provide a correct estimate of proximal delivery during sodium restriction. <\/jats:p>","DOI":"10.1152\/ajprenal.1987.253.1.f188","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T02:11:34Z","timestamp":1513995094000},"page":"F188-F196","source":"Crossref","is-referenced-by-count":6,"title":["Lithium as a marker for proximal tubular delivery during low salt intake and diuretic infusion"],"prefix":"10.1152","volume":"253","author":[{"given":"K. A.","family":"Kirchner","sequence":"first","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1987.253.1.F188","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:42:56Z","timestamp":1567971776000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1987.253.1.F188"}},"issued":{"date-parts":[[1987,7,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1987,7,1]]}},"alternative-id":["10.1152\/ajprenal.1987.253.1.F188"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1987.253.1.f188","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1987,7,1]]}},{"indexed":{"date-parts":[[2024,8,24]],"date-time":"2024-08-24T14:56:30Z","timestamp":1724511390245},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1988,10,1]]},"abstract":"<jats:p> Osmotically active organic solutes, osmolytes, exist at high concentrations in the renal inner medulla; however, their modulation during antidiuresis remains largely undefined. Renal osmolyte levels were measured by nuclear magnetic resonance spectroscopy and biochemical assays in perchloric acid extracts from normal and dehydrated (3 days) rats. Dehydration increased urine osmolality from 1,503 to 3,748 mosmol\/kg and inner medullary urea content from 2,036 to 4,405 nmol\/mg protein. In addition, inner medullary trimethylamines [glycerophosphorylcholine (GPC) and betaine] and polyhydric alcohols (inositol and sorbitol) significantly increased by 95 and 78%, respectively. Ninhydrin-positive substances (amino acids), although abundant, were unchanged. Renal cortex also contained GPC, betaine, and inositol but only inositol increased with dehydration. Analysis of correlations among inner medullary osmolytes showed that only GPC was consistently elevated by dehydration and was not directly correlated with the other osmolytes. In contrast, betaine and inositol contents were linearly related to each other and both tended to rise only when sorbitol content was unchanged. In conclusion, the major osmolytes in the rat renal inner medulla can increase during antidiuresis but they are regulated in a complex manner. <\/jats:p>","DOI":"10.1152\/ajprenal.1988.255.4.f626","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T21:24:38Z","timestamp":1513977878000},"page":"F626-F634","source":"Crossref","is-referenced-by-count":3,"title":["Accumulation of major organic osmolytes in rat renal inner medulla in dehydration"],"prefix":"10.1152","volume":"255","author":[{"given":"S. R.","family":"Gullans","sequence":"first","affiliation":[{"name":"Renal Division, Brigham and Women's Hospital, Boston,Massachusetts."}]},{"given":"J. D.","family":"Blumenfeld","sequence":"additional","affiliation":[{"name":"Renal Division, Brigham and Women's Hospital, Boston,Massachusetts."}]},{"given":"J. A.","family":"Balschi","sequence":"additional","affiliation":[{"name":"Renal Division, Brigham and Women's Hospital, Boston,Massachusetts."}]},{"given":"M.","family":"Kaleta","sequence":"additional","affiliation":[{"name":"Renal Division, Brigham and Women's Hospital, Boston,Massachusetts."}]},{"given":"R. M.","family":"Brenner","sequence":"additional","affiliation":[{"name":"Renal Division, Brigham and Women's Hospital, Boston,Massachusetts."}]},{"given":"C. W.","family":"Heilig","sequence":"additional","affiliation":[{"name":"Renal Division, Brigham and Women's Hospital, Boston,Massachusetts."}]},{"given":"S. C.","family":"Hebert","sequence":"additional","affiliation":[{"name":"Renal Division, Brigham and Women's Hospital, Boston,Massachusetts."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1988.255.4.F626","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:10:50Z","timestamp":1567969850000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1988.255.4.F626"}},"issued":{"date-parts":[[1988,10,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1988,10,1]]}},"alternative-id":["10.1152\/ajprenal.1988.255.4.F626"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1988.255.4.f626","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1988,10,1]]}},{"indexed":{"date-parts":[[2024,6,17]],"date-time":"2024-06-17T20:33:21Z","timestamp":1718656401477},"reference-count":35,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1999,8,1]]},"abstract":"<jats:p>Sodium butyrate and its derivatives are useful therapeutic agents for the treatment of genetic diseases including urea cycle disorders, sickle cell disease, thalassemias, and possibly cystic fibrosis (CF). Butyrate partially restores cAMP-activated Cl<jats:sup>\u2212<\/jats:sup>secretion in CF epithelial cells by stimulating \u0394F508 cystic fibrosis transmembrane conductance regulator (\u0394F508-CFTR) gene expression and increasing the amount of \u0394F508-CFTR in the plasma membrane. Because the effect of butyrate on Cl<jats:sup>\u2212<\/jats:sup>secretion by renal epithelial cells has not been reported, we examined the effects of chronic butyrate treatment (15\u201318 h) on the function, expression, and localization of CFTR fused to the green fluorescent protein (GFP-CFTR) in stably transfected MDCK cells. We report that sodium butyrate reduced Cl<jats:sup>\u2212<\/jats:sup>secretion across MDCK cells, yet increased apical membrane GFP-CFTR expression 25-fold and increased apical membrane Cl<jats:sup>\u2212<\/jats:sup>currents 30-fold. Although butyrate also increased Na-K-ATPase protein expression twofold, the drug reduced the activity of the Na-K-ATPase by 55%. Our findings suggest that butyrate inhibits cAMP-stimulated Cl<jats:sup>\u2212<\/jats:sup>secretion across MDCK cells in part by reducing the activity of the Na-K-ATPase.<\/jats:p>","DOI":"10.1152\/ajprenal.1999.277.2.f271","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T17:51:55Z","timestamp":1514051515000},"page":"F271-F276","source":"Crossref","is-referenced-by-count":14,"title":["Butyrate increases apical membrane CFTR but reduces chloride secretion in MDCK cells"],"prefix":"10.1152","volume":"277","author":[{"given":"Bryan D.","family":"Moyer","sequence":"first","affiliation":[{"name":"Department of Physiology, Dartmouth Medical School, Hanover, New Hampshire 03755"}]},{"given":"Dominique","family":"Loffing-Cueni","sequence":"additional","affiliation":[{"name":"Department of Physiology, Dartmouth Medical School, Hanover, New Hampshire 03755"}]},{"given":"Jan","family":"Loffing","sequence":"additional","affiliation":[{"name":"Department of Physiology, Dartmouth Medical School, Hanover, New Hampshire 03755"}]},{"given":"Donna","family":"Reynolds","sequence":"additional","affiliation":[{"name":"Department of Physiology, Dartmouth Medical School, Hanover, New Hampshire 03755"}]},{"given":"Bruce A.","family":"Stanton","sequence":"additional","affiliation":[{"name":"Department of Physiology, Dartmouth Medical School, Hanover, New Hampshire 03755"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/0014-4827(76)90036-7"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1097-4644(19980501)69:2<201::AID-JCB10>3.0.CO;2-H"},{"issue":"12","key":"B3","first-page":"L615","volume":"268","author":"Cheng S. H.","year":"1995","journal-title":"Am. J. Physiol."},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(90)90148-8"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.88.20.9262"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.39.24148"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1996.271.6.C1853"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115582"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1006\/excr.1997.3725"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1007\/BF00374853"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1996.270.1.C389"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117709"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1996.270.6.C1611"},{"issue":"37","key":"B14","first-page":"F347","volume":"268","author":"Kizer N. L.","year":"1995","journal-title":"Am. J. Physiol."},{"key":"B15","first-page":"65","volume":"42","author":"Kruh J.","year":"1982","journal-title":"Mol. Cell. Biochem."},{"key":"B16","first-page":"275","volume":"17","author":"Loffing J.","year":"1998","journal-title":"Ped. Pulmonol. Suppl."},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1995.269.6.C1496"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1172\/JCI1042"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1042\/bj3220259"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.34.21759"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1002\/jcb.240590831"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1126\/science.2475911"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1996.1102"},{"key":"B24","first-page":"509","volume":"37","author":"Rivero J. A.","year":"1996","journal-title":"Proc. Am. Assoc. Cancer Res."},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1996.270.2.C600"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119788"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1164\/ajrccm.157.2.9706088"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1997.6515"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.137.6.1211"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1113\/expphysiol.1993.sp003674"},{"key":"B31","first-page":"457","volume":"109","author":"Stanton B. A.","year":"1997","journal-title":"Wien Klin. Wochenschr."},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.biochem.67.1.509"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1995.269.3.C683"},{"key":"B34","doi-asserted-by":"crossref","first-page":"1453","DOI":"10.1242\/jcs.110.13.1453","volume":"110","author":"Wacker I.","year":"1997","journal-title":"J. Cell Sci."},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(93)90353-R"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1999.277.2.F271","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:54:04Z","timestamp":1660190044000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1999.277.2.F271"}},"issued":{"date-parts":[[1999,8,1]]},"references-count":35,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1999,8,1]]}},"alternative-id":["10.1152\/ajprenal.1999.277.2.F271"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1999.277.2.f271","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1999,8,1]]}},{"indexed":{"date-parts":[[2024,6,17]],"date-time":"2024-06-17T20:33:47Z","timestamp":1718656427936},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1997,4,1]]},"abstract":"<jats:p> To determine whether insulin-like growth factor I (IGF-I) stimulated apical sodium\/hydrogen exchange (NHE), confluent primary human proximal tubule cells (PTC) were incubated for 48 h in serum-free media in the presence or absence of 100 ng\/ml IGF-I. Cells incubated in IGF-I demonstrated significant increases in thymidine incorporation (181.2 +\/- 30.3% of control values; n = 12, P = 0.01) and in resting intracellular pH (pHi) (7.52 +\/- 0.08 vs. 7.30 +\/- 0.06; n = 20, P &lt; 0.05), as determined by 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein quantitative microspectrofluorometry. Following intracellular acid loading, ethylisopropylamiloride (EIPA)-inhibitable H+ efflux and 22Na+ influx after 1 min were both significantly enhanced in IGF-I-treated cells compared with controls (8.78 +\/- 1.69 vs. 3.03 +\/- 0.72 mM\/min and 3.47 +\/- 0.49 vs. 1.55 +\/- 0.35 nmol x mg protein(-1) x min(-1), respectively). 22Na+ uptake studies in PTC grown on permeable supports demonstrated preferential stimulation of apical vs. basolateral NHE. The 50% inhibitory concentrations (IC50) in IGF-I-treated and control cells for EIPA (0.5 and 1.1 microM, respectively) and for HOE-694 (4.0 and 10.0 microM, respectively) were also consistent with predominant activation of apical, rather than basolateral, NHE activity. Kinetic analysis revealed an increase in maximal transport velocity (Vmax, 15.50 +\/- 1.50 vs. 7.26 +\/- 3.07 mM\/min; n = 10, P &lt; 0.05), without a significant change in antiporter affinity for extracellular Na+. Incubation of PTC with 100 ng\/ml IGF-I produced an acute, reversible, and EIPA-inhibitable pHi increase of 0.05 +\/- 0.01 pH units (n = 5, P &lt; 0.05). The results suggest that IGF-I may contribute to the metachronous stimulation of apical NHE and PTC growth observed in many physiological and pathological conditions involving the human kidney. <\/jats:p>","DOI":"10.1152\/ajprenal.1997.272.4.f484","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T08:11:57Z","timestamp":1514016717000},"page":"F484-F490","source":"Crossref","is-referenced-by-count":5,"title":["Insulin-like growth factor I stimulates apical sodium\/hydrogen exchange in human proximal tubule cells"],"prefix":"10.1152","volume":"272","author":[{"given":"D. W.","family":"Johnson","sequence":"first","affiliation":[{"name":"Department of Medicine, University of Sydney, Australia."}]},{"given":"B. K.","family":"Brew","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Sydney, Australia."}]},{"given":"P.","family":"Poronnik","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Sydney, Australia."}]},{"given":"D. I.","family":"Cook","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Sydney, Australia."}]},{"given":"M. J.","family":"Field","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Sydney, Australia."}]},{"given":"A. Z.","family":"Gyory","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Sydney, Australia."}]},{"given":"C. A.","family":"Pollock","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Sydney, Australia."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1997.272.4.F484","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:15:26Z","timestamp":1567973726000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1997.272.4.F484"}},"issued":{"date-parts":[[1997,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1997,4,1]]}},"alternative-id":["10.1152\/ajprenal.1997.272.4.F484"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1997.272.4.f484","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1997,4,1]]}},{"indexed":{"date-parts":[[2024,6,17]],"date-time":"2024-06-17T20:28:52Z","timestamp":1718656132247},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1983,6,1]]},"abstract":"<jats:p> The transport of various organic anions via the pathway that mediates the exchange of urate or p-aminohippurate (PAH) for OH- or Cl- in dog renal microvillus membrane vesicles was investigated. The pH gradient-stimulated uptakes of tracer urate and PAH were significantly inhibited by 5 mM PAH, n-valerate, lactate, beta-hydroxybutyrate, pyruvate, acetoacetate, maleate, succinate, alpha-ketoglutarate, oxaloacetate, and cis-aconitate but not by 5 mM acetate, malate, oxalate, or citrate. the pH dependence of inhibition suggested that it was in their monovalent forms that these acid anions interacted with the urate exchange pathway. Outwardly directed gradients of succinate, lactate, and PAH stimulated uphill urate accumulation. Imposition of an inside-alkaline pH gradient stimulated the uphill accumulation of lactate and succinate. Na+ cotransport pathways for lactate and succinate were also present. In the presence of an inwardly directed Na+ gradient, lactate stimulated the uphill accumulation of urate, indicating that the pathways mediating Na+-lactate cotransport and lactate-urate exchange coexisted in at least some membrane vesicles. We conclude that the anion exchange pathway for urate in dog renal microvillus membrane vesicles has affinity for additional organic anions and can function in multiple exchange modes. Exchange of luminal urate or Cl- for intracellular organic anions or OH- is a possible mechanism for effecting uphill anion reabsorption in the proximal tubule. <\/jats:p>","DOI":"10.1152\/ajprenal.1983.244.6.f612","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T10:47:42Z","timestamp":1513939662000},"page":"F612-F621","source":"Crossref","is-referenced-by-count":13,"title":["Specificity and modes of the anion exchanger in dog renal microvillus membranes"],"prefix":"10.1152","volume":"244","author":[{"given":"S. E.","family":"Guggino","sequence":"first","affiliation":[]},{"given":"G. J.","family":"Martin","sequence":"additional","affiliation":[]},{"given":"P. S.","family":"Aronson","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1983.244.6.F612","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T14:27:17Z","timestamp":1567952837000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1983.244.6.F612"}},"issued":{"date-parts":[[1983,6,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1983,6,1]]}},"alternative-id":["10.1152\/ajprenal.1983.244.6.F612"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1983.244.6.f612","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1983,6,1]]}},{"indexed":{"date-parts":[[2024,6,17]],"date-time":"2024-06-17T20:31:01Z","timestamp":1718656261788},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1991,9,1]]},"abstract":"<jats:p> The present study utilized [15N]glutamine labeled at amide (5-N) and amino (2-N) groups to analyze the metabolic fate of glutamine nitrogen in basal and in acute pH regulation of ammoniagenesis. One-hour incubation of LLC-PK1 cultures in a media of pH 7.4, 7.0, or 7.6 containing either [5\u201315N]glutamine or [2\u201315N]glutamine resulted in parallel alterations in glutamine consumption in response to acute acid-base maneuvers. Incubation with [5\u201315N]glutamine resulted in substantial enrichment and production of ammonia at pH 7.4, which was unaffected by the changes in media pH, and in no significant enrichment of alanine, aspartate, and glutamate. In contrast, significant enrichment and production of 15N-labeled ammonia, alanine, aspartate, and glutamate were detected from cultures incubated with [2\u201315N]glutamine. Ammonia formation, from incubation with [2\u201315N]glutamine, was stimulated significantly by a low pH and inhibited by high pH. Alanine production was altered in a fashion similar to ammonia formation, whereas aspartate production was unaltered and glutamate formation significantly decreased by a low pH. Furthermore, a low pH significantly increased the production of alpha-ketoglutaramate in a fashion qualitatively similar to alanine production. In contrast to our prior conclusions based on total metabolite production, these studies indicate that although ammonia formation at pH 7.4 is predominantly generated from the mitochondrial phosphate-dependent glutaminase pathway, the increased ammonia formation in acute acidosis is a result of increased flux through glutamate dehydrogenase.(ABSTRACT TRUNCATED AT 250 WORDS) <\/jats:p>","DOI":"10.1152\/ajprenal.1991.261.3.f481","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T23:30:01Z","timestamp":1513985401000},"page":"F481-F487","source":"Crossref","is-referenced-by-count":2,"title":["Pathways of acute pH regulation of ammoniagenesis in LLC-PK1 cells: study with [15N]glutamine"],"prefix":"10.1152","volume":"261","author":[{"given":"A.","family":"Sahai","sequence":"first","affiliation":[{"name":"Department of Medicine, University of Southern California School of Medicine, Los Angeles 90033."}]},{"given":"I.","family":"Nissim","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Southern California School of Medicine, Los Angeles 90033."}]},{"given":"R. L.","family":"Tannen","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Southern California School of Medicine, Los Angeles 90033."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1991.261.3.F481","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:22:56Z","timestamp":1567970576000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1991.261.3.F481"}},"issued":{"date-parts":[[1991,9,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1991,9,1]]}},"alternative-id":["10.1152\/ajprenal.1991.261.3.F481"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1991.261.3.f481","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1991,9,1]]}},{"indexed":{"date-parts":[[2024,6,17]],"date-time":"2024-06-17T20:31:22Z","timestamp":1718656282295},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1994,10,1]]},"abstract":"<jats:p> The rabbit papillary epithelial cell line GRB-PAP1 was used to determine the ion transport characteristics of a model of the distal nephron and terminal collecting duct. When grown on permeable supports, monolayers developed a significant electrical resistance and a benzamil-sensitive short-circuit current, indicating that they had the property of electrogenic Na+ transport. Using the whole cell patch-clamp technique, we found that the dominant current in these cells was a slowly inactivating, time- and voltage-dependent K+ current. This current was activated by voltages more positive than -30 mV. At +30 mV, the peak outward currents were &gt; 300 pA. The magnitude of the outward currents and their reversal potentials depended strongly on the extracellular concentration of K+ and not on the extracellular concentration of Cl-. These currents were inhibited by either tetraethylammonium, 4-aminopyridine, charybdotoxin, or dendrotoxin. These characteristics, together with the kinetics of activation and inactivation, are the general characteristics of delayed rectifier channels seen in many muscle and neuronal cells. Because many of these types of channels share sequence homology with the Shaker family of channels cloned from Drosophila, we sought to identify a molecular correlate. Using reverse transcription followed by polymerase chain reaction to amplify Shaker-like sequences, we cloned and sequenced a single 881-bp fragment. The sequence shared identity with a recently reported rabbit Shaker channel that belongs to the subclass Kv 1.2. These data show that this renal papillary epithelial cell line, which has the capability of electrogenic Na+ transport, expresses functional delayed rectifier channels. <\/jats:p>","DOI":"10.1152\/ajprenal.1994.267.4.f671","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T23:37:30Z","timestamp":1513985850000},"page":"F671-F678","source":"Crossref","is-referenced-by-count":5,"title":["Functional and molecular evidence for Shaker-like K+ channels in rabbit renal papillary epithelial cell line"],"prefix":"10.1152","volume":"267","author":[{"given":"K. A.","family":"Volk","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, University of Iowa College ofMedicine, Iowa City."}]},{"given":"R. F.","family":"Husted","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Iowa College ofMedicine, Iowa City."}]},{"given":"C. J.","family":"Pruchno","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Iowa College ofMedicine, Iowa City."}]},{"given":"J. B.","family":"Stokes","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Iowa College ofMedicine, Iowa City."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1994.267.4.F671","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:55:36Z","timestamp":1567958136000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1994.267.4.F671"}},"issued":{"date-parts":[[1994,10,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1994,10,1]]}},"alternative-id":["10.1152\/ajprenal.1994.267.4.F671"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1994.267.4.f671","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1994,10,1]]}},{"indexed":{"date-parts":[[2024,9,15]],"date-time":"2024-09-15T22:44:23Z","timestamp":1726440263255},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1990,1,1]]},"abstract":"<jats:p> An epifluorometric method was used to quantify the bidirectional fluxes of fluorescein across the basolateral surfaces of nonperfused rabbit tubule segments in vitro. Proximal S2 segments, but not cortical collecting tubules or cortical thick ascending limbs, accumulated fluorescein to levels in cytoplasm over 100-fold greater than in the external medium. The rate of intracellular fluorescein accumulation was dependent on the concentration of the ligand in the external bath. The apparent Km was 10 microM and the Vmax was 623 x 10(-6) mol.min-1.l-1. Probenecid and ouabain inhibited fluorescein accumulation. We conclude that fluorescein is transported into the cytoplasm of proximal tubules by basolateral mechanisms that share features in common with the classical organic anion system. This fluorescent compound offers some unique advantages for the study of the organic anion transport system in intact cells. <\/jats:p>","DOI":"10.1152\/ajprenal.1990.258.1.f46","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T16:46:30Z","timestamp":1513961190000},"page":"F46-F51","source":"Crossref","is-referenced-by-count":4,"title":["Fluorescein transport in isolated proximal tubules in vitro: epifluorometric analysis"],"prefix":"10.1152","volume":"258","author":[{"given":"L. P.","family":"Sullivan","sequence":"first","affiliation":[{"name":"Department of Physiology, University of Kansas School of Medicine, Kansas City 66103."}]},{"given":"J. A.","family":"Grantham","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Kansas School of Medicine, Kansas City 66103."}]},{"given":"L.","family":"Rome","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Kansas School of Medicine, Kansas City 66103."}]},{"given":"D.","family":"Wallace","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Kansas School of Medicine, Kansas City 66103."}]},{"given":"J. J.","family":"Grantham","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Kansas School of Medicine, Kansas City 66103."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1990.258.1.F46","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:12:50Z","timestamp":1567955570000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1990.258.1.F46"}},"issued":{"date-parts":[[1990,1,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1990,1,1]]}},"alternative-id":["10.1152\/ajprenal.1990.258.1.F46"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1990.258.1.f46","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[1990,1,1]]}},{"indexed":{"date-parts":[[2024,6,17]],"date-time":"2024-06-17T20:00:49Z","timestamp":1718654449490},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1995,7,1]]},"abstract":"<jats:p> Adenosine 3',5'-cyclic monophosphate (cAMP), accumulated in the presence of adenosine, was measured in medullary portions of mouse thick ascending limbs of Henle's loop, suspended either in classic extracellular buffer or in the presence of added NaCl. Under control conditions (140 mmol\/l NaCl), adenosine (&lt; 10(-5) mol\/l) and N6-cyclohexyladenosine, an A1 adenosine receptor agonist, inhibit the cAMP accumulation induced by arginine vasopressin (AVP). On the other hand, high concentrations of adenosine and CGS-21680, an A2 adenosine receptor agonist, stimulate cAMP formation. Addition of NaCl (+300 mmol\/l) to extracellular buffer stimulates the release of endogenous adenosine. It also enhances A2 receptor-induced cAMP accumulation but suppresses A1 receptor-mediated inhibition of adenylyl cyclase. This hypertonic NaCl medium also potentiates the stimulatory action of AVP on adenylyl cyclase. The modifications of tubular responses to both AVP and A1 and A2 agonists, brought about by hypertonic NaCl, were all inhibited by adenosine deaminase, thereby demonstrating the involvement of endogenous adenosine. Adenosine, the release and the effects of which are modulated by hypertonic NaCl, thus appears to act as an endogenous physiological modulator of kidney medulla function. <\/jats:p>","DOI":"10.1152\/ajprenal.1995.269.1.f103","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T05:51:55Z","timestamp":1514008315000},"page":"F103-F109","source":"Crossref","is-referenced-by-count":8,"title":["Hypertonic NaCl enhances adenosine release and hormonal cAMP production in mouse thick ascending limb"],"prefix":"10.1152","volume":"269","author":[{"given":"M.","family":"Baudouin-Legros","sequence":"first","affiliation":[{"name":"Institut National de la Sante et de la Recherche Medicale Unite 323,Faculte de Medecine Necker-Enfants Malades, Paris, France."}]},{"given":"A.","family":"Badou","sequence":"additional","affiliation":[{"name":"Institut National de la Sante et de la Recherche Medicale Unite 323,Faculte de Medecine Necker-Enfants Malades, Paris, France."}]},{"given":"M.","family":"Paulais","sequence":"additional","affiliation":[{"name":"Institut National de la Sante et de la Recherche Medicale Unite 323,Faculte de Medecine Necker-Enfants Malades, Paris, France."}]},{"given":"M.","family":"Hammet","sequence":"additional","affiliation":[{"name":"Institut National de la Sante et de la Recherche Medicale Unite 323,Faculte de Medecine Necker-Enfants Malades, Paris, France."}]},{"given":"J.","family":"Teulon","sequence":"additional","affiliation":[{"name":"Institut National de la Sante et de la Recherche Medicale Unite 323,Faculte de Medecine Necker-Enfants Malades, Paris, France."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1995.269.1.F103","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:01:25Z","timestamp":1567972885000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1995.269.1.F103"}},"issued":{"date-parts":[[1995,7,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1995,7,1]]}},"alternative-id":["10.1152\/ajprenal.1995.269.1.F103"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1995.269.1.f103","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1995,7,1]]}},{"indexed":{"date-parts":[[2024,6,17]],"date-time":"2024-06-17T19:59:35Z","timestamp":1718654375979},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1997,2,1]]},"abstract":"<jats:p> A murine leukemia retroviral vector was engineered to contain the DNA encoding either the wild-type, rat aorta 20-kDa myosin light chain (MLC20) or a mutant form of MLC20 in which Thr18 and Ser19 were mutated into alanines. These mutations result in a MLC20 that cannot be phosphorylated by myosin light chain kinase. An 11-amino acid epitope from c-myc was added to both MLC20 sequences to facilitate identification of these proteins. Madin-Darby canine kidney cells were stably transduced, and MLC20 expression was demonstrated by Western blot analysis using a myc-specific antibody. MLC20 exchange was demonstrated by purifying myosin from the transduced cells and repeating the Western blot analysis. Actin-activated adenosinetriphosphatase assays on the purified myosins demonstrated approximately 50% decrease in the rate of ATP hydrolysis by the myosin containing the mutant MLC20. Transepithelial electrical resistance was decreased and mannitol flux was increased across monolayers of cells expressing mutant MLC20. These data demonstrate that MLC20 phosphorylation is involved in regulating paracellular permeability and epithelial barrier function. <\/jats:p>","DOI":"10.1152\/ajprenal.1997.272.2.f214","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T03:43:57Z","timestamp":1514000637000},"page":"F214-F221","source":"Crossref","is-referenced-by-count":4,"title":["Expression of a mutant myosin light chain that cannot be phosphorylated increases paracellular permeability"],"prefix":"10.1152","volume":"272","author":[{"given":"S.","family":"Gandhi","sequence":"first","affiliation":[{"name":"Department of Physiology and Biophysics, University of Illinois atChicago, 60612, USA."}]},{"given":"D. D.","family":"Lorimer","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, University of Illinois atChicago, 60612, USA."}]},{"given":"P.","family":"de Lanerolle","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, University of Illinois atChicago, 60612, USA."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1997.272.2.F214","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:16:27Z","timestamp":1567959387000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1997.272.2.F214"}},"issued":{"date-parts":[[1997,2,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1997,2,1]]}},"alternative-id":["10.1152\/ajprenal.1997.272.2.F214"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1997.272.2.f214","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1997,2,1]]}},{"indexed":{"date-parts":[[2024,6,17]],"date-time":"2024-06-17T18:04:31Z","timestamp":1718647471117},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1995,6,1]]},"abstract":"<jats:p> The association of hepatocyte growth factor (HGF) with its high-affinity receptor, c-met, has been shown to induce mitogenesis, motogenesis, and morphogenesis in renal epithelial cells (L. G. Cantley, E. J. G. Barros, M. Gandhi, M. Rauchman, and S. K. Nigam. Am. J. Physiol. 267 (Renal Fluid Electrolyte Physiol. 36): F271-F280, 1994), suggesting that HGF may be critical to the orchestration of both renal development and regeneration following injury. Although signal transduction pathways activated by c-met include the phosphatidylinositol 3-kinase (PI-3-kinase), phospholipase C gamma, ras, and others, the activation of PI-3-kinase has been the most striking in vivo. We therefore investigated whether the pathways that mediate phenotypic changes in inner medullary collecting duct cells are altered by inhibition of PI-3-kinase with the fungal metabolite, wortmannin. In these cells, the mean inhibitory concentration for in vitro wortmannin inhibition of PI-3-kinase was approximately 0.2 nM. At this low concentration, motogenesis (quantified by chemotaxis) and morphogenesis (by branching-process formation within collagen matrix) were inhibited in a striking and parallel fashion, while mitogenesis was inhibited to a lesser degree. These experiments suggest that activation of PI-3-kinase is critical for c-met-mediated chemotaxis and tubulogenesis. <\/jats:p>","DOI":"10.1152\/ajprenal.1995.268.6.f1211","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T00:34:24Z","timestamp":1513989264000},"page":"F1211-F1217","source":"Crossref","is-referenced-by-count":8,"title":["HGF-mediated chemotaxis and tubulogenesis require activation of the phosphatidylinositol 3-kinase"],"prefix":"10.1152","volume":"268","author":[{"given":"M. P.","family":"Derman","sequence":"first","affiliation":[{"name":"Division of Nephrology, Beth Israel Hospital, Harvard Medical School, Boston, Massachusetts 02215, USA."}]},{"given":"M. J.","family":"Cunha","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Beth Israel Hospital, Harvard Medical School, Boston, Massachusetts 02215, USA."}]},{"given":"E. J.","family":"Barros","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Beth Israel Hospital, Harvard Medical School, Boston, Massachusetts 02215, USA."}]},{"given":"S. K.","family":"Nigam","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Beth Israel Hospital, Harvard Medical School, Boston, Massachusetts 02215, USA."}]},{"given":"L. G.","family":"Cantley","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Beth Israel Hospital, Harvard Medical School, Boston, Massachusetts 02215, USA."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1995.268.6.F1211","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:01:05Z","timestamp":1567958465000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1995.268.6.F1211"}},"issued":{"date-parts":[[1995,6,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1995,6,1]]}},"alternative-id":["10.1152\/ajprenal.1995.268.6.F1211"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1995.268.6.f1211","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1995,6,1]]}},{"indexed":{"date-parts":[[2024,6,17]],"date-time":"2024-06-17T18:01:37Z","timestamp":1718647297356},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1985,12,1]]},"abstract":"<jats:p> We studied renal sodium handling, extracellular fluid volume (ECFV), plasma renin activity, aldosterone and norepinephrine, and blood pressure in eight healthy volunteers after equilibration on intakes of 20, 200, and 1,128 +\/- 141 meq sodium, respectively. Renal sodium handling was assessed by means of clearance studies during maximal water diuresis and lithium clearance. Urinary sodium excretions were 22 +\/- 4, 202 +\/- 19, and 1,052 +\/- 86 meq\/day. From the lower to the upper sodium intake level, 24-h creatinine clearance rose from 111 +\/- 7 to 136 +\/- 11 ml\/min and inulin clearance from 103 +\/- 9 to 129 +\/- 9 ml\/min, whereas proximal and distal fractional sodium reabsorption (FSRprox and FSRdist, respectively) fell from 86.8 +\/- 1.3 to 79.0 +\/- 2.7% and from 96.5 +\/- 0.5 to 76.0 +\/- 1.9%, respectively. During the normal sodium intake (200 meq), intermediate values were recorded. The changes in fractional lithium clearance were less consistent but correlated with FSRprox (r = 0.78, P less than 0.001) and not with FSRdist. Major changes in plasma renin activity, aldosterone, and, to a lesser extent, norepinephrine accompanied these changes in kidney function, displaying inverse and exponential correlations with daily sodium excretion and ECFV. No consistent rise in blood pressure was detected. These observations indicate that in healthy humans renal adaptation to vast variations in sodium intake includes resetting of glomerular filtration rate, FSRprox, and, in particular, FSRdist. Alterations in neurohumoral factors may play a dominant role in this adaptation. <\/jats:p>","DOI":"10.1152\/ajprenal.1985.249.6.f941","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T00:01:37Z","timestamp":1513987297000},"page":"F941-F947","source":"Crossref","is-referenced-by-count":18,"title":["Renal sodium handling in normal humans subjected to low, normal, and extremely high sodium supplies"],"prefix":"10.1152","volume":"249","author":[{"given":"J. C.","family":"Roos","sequence":"first","affiliation":[]},{"given":"H. A.","family":"Koomans","sequence":"additional","affiliation":[]},{"given":"E. J.","family":"Dorhout Mees","sequence":"additional","affiliation":[]},{"given":"I. M.","family":"Delawi","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1985.249.6.F941","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:30:02Z","timestamp":1567971002000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1985.249.6.F941"}},"issued":{"date-parts":[[1985,12,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1985,12,1]]}},"alternative-id":["10.1152\/ajprenal.1985.249.6.F941"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1985.249.6.f941","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1985,12,1]]}},{"indexed":{"date-parts":[[2024,6,17]],"date-time":"2024-06-17T19:58:40Z","timestamp":1718654320136},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1987,1,1]]},"abstract":"<jats:p> Studies performed in several animal species have demonstrated that glomerulotubular balance is maintained throughout development despite the many changes that occur in the factors known to control it. In an attempt to understand the nature of this phenomenon we quantified the magnitude and described the profile of these changes in guinea pigs. The changes in physical forces were assessed from measurements of hydrostatic and oncotic pressures, whereas those in the permeability characteristics of the proximal tubule epithelium were estimated from permeance to macromolecules of graded radii, histologic measurements of the intercellular channels, and measurements of end-proximal ratio of tubular fluid-to-plasma osmolality (TF\/Posm). Between 1 and 50 days of age the net pressure for reabsorption increased from 15.0 to 30.9 mmHg (P less than 0.01, n = 15) with the major change occurring during the first 2-3 wk of postnatal life. The urinary recovery of inulin, sucrose, and creatinine, injected in the early segment of proximal tubules did not vary with age. The urinary recovery of mannitol (MW 180 daltons, Stokes-Einstein radius 4.0 X 10(-10) m) increased from 92% at birth to 100% at 49 days of age (P less than 0.001, n = 24), consistent with a decrease of approximately 0.5 X 10(-10) m in the luminal openings of the paracellular channels. The length of the zonulae occludens and the width of the intercellular channels did not change during this period; however, the length of the channels increased from 5.0 +\/- 0.17 to 8.9 +\/- 0.48 micron (P less than 0.01, n = 16). These changes should result in an increase in resistance across the intercellular channels. Consistent with this assertion is the observation that the mean TF\/Posm of the fluid collected toward the end of the proximal convoluted tubule decreased as a function of age from 1.05 at day 2 to 0.98 at day 80 (P less than 0.001, n = 24). The findings support the hypothesis that during early postnatal life glomerulotubular balance is made possible by a high permeability of the proximal tubule, which compensates for the low net reabsorptive pressure. As the animal matures and the proximal tubule epithelium becomes tighter, for glomerulotubular balance to be maintained, an increase in the number of intercellular channels and in the active transport of sodium need to be postulated. <\/jats:p>","DOI":"10.1152\/ajprenal.1987.252.1.f188","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T21:52:49Z","timestamp":1513979569000},"page":"F188-F197","source":"Crossref","is-referenced-by-count":4,"title":["Factors affecting proximal tubular reabsorption during development"],"prefix":"10.1152","volume":"252","author":[{"given":"F. J.","family":"Kaskel","sequence":"first","affiliation":[]},{"given":"A. M.","family":"Kumar","sequence":"additional","affiliation":[]},{"given":"E. A.","family":"Lockhart","sequence":"additional","affiliation":[]},{"given":"A.","family":"Evan","sequence":"additional","affiliation":[]},{"given":"A.","family":"Spitzer","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1987.252.1.F188","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:45:52Z","timestamp":1567957552000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1987.252.1.F188"}},"issued":{"date-parts":[[1987,1,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1987,1,1]]}},"alternative-id":["10.1152\/ajprenal.1987.252.1.F188"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1987.252.1.f188","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1987,1,1]]}},{"indexed":{"date-parts":[[2024,6,17]],"date-time":"2024-06-17T20:00:12Z","timestamp":1718654412031},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1989,8,1]]},"abstract":"<jats:p> Changes in cytosolic calcium concentration (Cai2+) have been implicated in the regulation of intracellular pH (pHi) in several cell types. In the present study we investigated the mechanism by which an increase in Cai2+ stimulates H+ secretion and a rise in pHi in cultured rat inner medullary collecting duct (IMCD) cells. Confluent monolayers were made quiescent by incubation for 24 h in 0.1% serum before study. Changes in pHi and Cai2+ were measured with the fluorescent probes, 2,7-biscarboxyethyl-5(6)-carboxyfluorescein (BCECF) and fura-2. In nominally bicarbonate-free media containing 110 mM Na+ and 1 mM Ca2+, addition of the Ca2+ inophore, ionomycin (10 microM), produced a biphasic response in pHi, a transient acidification from 7.29 +\/- 0.07 to 7.12 +\/- 0.05 at 2 min followed by a sustained alkalinization to a steady-state value of 7.51 +\/- 0.10 at 10 min. The rate of alkalinization was dose dependent. The alkalinization was not affected by 1 mM amiloride, removal of extracellular Na+, or by the proton pump inhibitor, N-ethyl maleimide (NEM). Metabolic energy was not required, but removal of extracellular Ca2+ prevented the alkalinization. By use of the fluorescent probe bisoxonol to assess membrane potential, ionomycin was shown to cause depolarization under the same experimental conditions as those for alkalinization. The Ca2+-induced alkalinization was mimicked by cell depolarization (induced by raising extracellular K+ in the presence of valinomycin 1 microM). We conclude that changes in Cai2+ are important in the regulation of pHi in the IMCD. Ca2+-induced cell alkalinization may be mediated by changes in membrane ionic conductance. <\/jats:p>","DOI":"10.1152\/ajprenal.1989.257.2.f210","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T17:08:36Z","timestamp":1513962516000},"page":"F210-F217","source":"Crossref","is-referenced-by-count":2,"title":["Effect of increases in cytosolic Ca2+ on inner medullary collecting duct cell pH"],"prefix":"10.1152","volume":"257","author":[{"given":"I. N.","family":"Slotki","sequence":"first","affiliation":[{"name":"Thorndike Memorial Laboratory, Boston City Hospital,Massachusetts."}]},{"given":"J. H.","family":"Schwartz","sequence":"additional","affiliation":[{"name":"Thorndike Memorial Laboratory, Boston City Hospital,Massachusetts."}]},{"given":"E. A.","family":"Alexander","sequence":"additional","affiliation":[{"name":"Thorndike Memorial Laboratory, Boston City Hospital,Massachusetts."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1989.257.2.F210","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:15:15Z","timestamp":1567955715000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1989.257.2.F210"}},"issued":{"date-parts":[[1989,8,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1989,8,1]]}},"alternative-id":["10.1152\/ajprenal.1989.257.2.F210"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1989.257.2.f210","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1989,8,1]]}},{"indexed":{"date-parts":[[2024,8,23]],"date-time":"2024-08-23T00:41:08Z","timestamp":1724373668254},"reference-count":49,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,3,15]]},"abstract":"<jats:p> Our recent studies showed that contents of necrotic renal proximal tubular cells (RPTC) from 2 \u00d7 10<jats:sup>6<\/jats:sup> cells\/ml directly induced death of cultured renal interstitial fibroblasts. However, it remains unknown whether nonlethal number of necrotic RPTC would also alter the fate of renal interstitial fibroblasts. To address this issue, renal interstitial fibroblasts (NRK-49F) were exposed to necrotic RPTC supernatant (RPTC-Sup) obtained from 2 \u00d7 10<jats:sup>4<\/jats:sup> to 5 \u00d7 10<jats:sup>5<\/jats:sup> cells\/ml. These concentrations of RPTC did not induce cell death, but led to inactivation of renal fibroblasts as indicated by reduced expression of \u03b1-smooth muscle actin and fibronectin, two hallmarks of activated fibroblasts. Concurrently, the same doses of necrotic RPTC-Sup suppressed phosphorylation of epidermal growth factor receptor (EGFR) and signal transducers and activators of transcription-3 (STAT3) in a time- and dose-dependent manner, but did not affect phosphorylation of platelet-derived growth factor receptor-\u03b2, AKT, and extracellular signal-regulated kinase 1\/2. The presence of sodium orthovanadate, a general protein tyrosine phosphatase (PTP) inhibitor or TCS-401 (a selective PTP1B inhibitor), abrogated those effects of RPTC-Sup, whereas coincubation with the EGFR inhibitor (Gefitinib) or silencing of EGFR with siRNA preserved the ability of RPTC-Sup in suppressing renal fibroblast activation and STAT3 phosphorylation. Moreover, RPTC-Sup treatment induced PTP1B phosphorylation and its interaction with EGFR. Collectively, these results indicate that nonlethal necrotic RPTC-Sup can induce inactivation of renal interstitial fibroblasts, which occurs through a mechanism involved in PTP1B-mediated inhibition of EGFR signaling. <\/jats:p>","DOI":"10.1152\/ajprenal.00564.2012","type":"journal-article","created":{"date-parts":[[2013,1,3]],"date-time":"2013-01-03T07:22:31Z","timestamp":1357197751000},"page":"F698-F709","source":"Crossref","is-referenced-by-count":6,"title":["Necrotic renal epithelial cell inhibits renal interstitial fibroblast activation: role of protein tyrosine phosphatase 1B"],"prefix":"10.1152","volume":"304","author":[{"given":"Murugavel","family":"Ponnusamy","sequence":"first","affiliation":[{"name":"Department of Medicine, Rhode Island Hospital and Alpert Medical School of Brown University, Providence, Rhode Island; and"}]},{"given":"Li","family":"Ma","sequence":"additional","affiliation":[{"name":"Department of Medicine, Rhode Island Hospital and Alpert Medical School of Brown University, Providence, Rhode Island; and"}]},{"given":"Shougang","family":"Zhuang","sequence":"additional","affiliation":[{"name":"Department of Medicine, Rhode Island Hospital and Alpert Medical School of Brown University, Providence, Rhode Island; and"},{"name":"Department of Nephrology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI57301"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1177\/41.3.8429197"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/j.cytogfr.2004.03.006"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/j.ceb.2005.02.001"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1161\/01.ATV.0000201070.71787.b8"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/j.trsl.2011.06.002"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00406.2005"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/ncb2026"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.91"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.3109\/01902148.2010.524722"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007050532"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1038\/cddis.2011.26"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1007\/s00428-004-1155-5"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1038\/sj.cdd.4400851"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.23.11.3753-3762.2003"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M210194200"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/j.regpep.2011.11.010"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1007\/s00418-008-0452-5"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1038\/nm1275"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2011.300"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1042\/bj3270139"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2011050493"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1158\/0008-5472.CAN-07-0575"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1007\/s004410050009"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.387"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.2001.281.2.C563"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.108.113860"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.2011.01206.x"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2613.2011.00764.x"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.2337\/db07-1062"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.2337\/db06-0989"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00282.2009"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2010.154"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00215.2011"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00027.2012"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00473.2010"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1002\/path.4050"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00184.2001"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1172\/JCI8315"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1016\/j.clim.2006.09.008"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1080\/15216540210811"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200101000-00009"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1159\/000020622"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.2174\/1568026033452302"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1124\/mol.63.3.706"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1038\/nm.2144"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1038\/35052073"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M800061200"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1016\/S0079-6603(03)01006-7"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00564.2012","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T23:40:21Z","timestamp":1567986021000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00564.2012"}},"issued":{"date-parts":[[2013,3,15]]},"references-count":49,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2013,3,15]]}},"alternative-id":["10.1152\/ajprenal.00564.2012"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00564.2012","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2013,3,15]]}},{"indexed":{"date-parts":[[2024,7,25]],"date-time":"2024-07-25T05:52:42Z","timestamp":1721886762916},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1989,2,1]]},"abstract":"<jats:p> The efflux of the organic cation, tetraethylammonium (TEA), across proximal cell luminal membranes was studied using intact, perfused rabbit proximal tubules and isolated rabbit cortical brush-border membrane vesicles (BBMV). Increases of either the extravesicular H+ concentration (from pH 7.5 to pH 6.5) or the extravesicular concentration of unlabeled TEA (from 0.1 to 0.5 mM) increased the rate of efflux of radioactively labeled TEA from BBMV. Similarly, when proximal tubules were preloaded with labeled TEA and then submerged in a mineral oil bath, a rapid increase in either the H+ concentration (from pH 7.5 to pH 5.8) or the TEA concentration (from 0 to 1 mM) of the tubular perfusate produced an acute increase in efflux of the labeled TEA across the luminal brush-border membrane. These results with intact tubules and isolated membranes are consistent with previous suggestions that TEA transport across the brush border of proximal tubule cells involves a carrier-mediated countertransport process and represent the first demonstration with intact proximal tubules that the secretory flux of TEA occurs by an exchange with H+. <\/jats:p>","DOI":"10.1152\/ajprenal.1989.256.2.f290","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T21:05:13Z","timestamp":1513976713000},"page":"F290-F297","source":"Crossref","is-referenced-by-count":8,"title":["Brush-border TEA transport in intact proximal tubules and isolated membrane vesicles"],"prefix":"10.1152","volume":"256","author":[{"given":"W. H.","family":"Dantzler","sequence":"first","affiliation":[{"name":"Department of Physiology, College of Medicine, University of Arizona,Tucson 85724."}]},{"given":"O. H.","family":"Brokl","sequence":"additional","affiliation":[{"name":"Department of Physiology, College of Medicine, University of Arizona,Tucson 85724."}]},{"given":"S. H.","family":"Wright","sequence":"additional","affiliation":[{"name":"Department of Physiology, College of Medicine, University of Arizona,Tucson 85724."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1989.256.2.F290","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:07:55Z","timestamp":1567969675000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1989.256.2.F290"}},"issued":{"date-parts":[[1989,2,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1989,2,1]]}},"alternative-id":["10.1152\/ajprenal.1989.256.2.F290"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1989.256.2.f290","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1989,2,1]]}},{"indexed":{"date-parts":[[2024,6,17]],"date-time":"2024-06-17T16:32:18Z","timestamp":1718641938259},"reference-count":24,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1998,1,1]]},"abstract":"<jats:p> Although most cell membranes permit rapid flux of water, small nonelectrolytes, and ammonia, the apical membranes of bladder epithelial umbrella cells, which form the bladder permeability barrier, exhibit strikingly low permeabilities to these substances. In cystitis, disruption of the bladder permeability barrier may irritate the bladder wall layers underlying the epithelium, causing or exacerbating inflammation, and increasing urinary frequency, urgency, and bladder pain. To determine the effects of inflammation on the integrity of the permeability barrier, guinea pigs were sensitized with ovalbumin, and the bladders were exposed subsequently to antigen by instillation on the urinary side. Inflammation of the bladder wall markedly reduced transepithelial resistance of dissected epithelium mounted in Ussing chambers and increased water and urea permeabilities modestly at 2 h and more strikingly at 24 h after induction of the inflammation. Transmission and scanning electron microscopy of bladders at 30 min and 24 h after antigen exposure revealed disruption of tight junctions, denuding of patches of epithelium, and occasional loss of apical membrane architecture. These permeability and structural effects did not occur in nonsensitized animals in which the bladders were exposed to antigen and in sensitized animals exposed to saline vehicle rather than antigen. These results demonstrate that inflammation of the underlying muscle and lamina propria can disrupt the bladder permeability barrier by damaging tight junctions and apical membranes and causing sloughing of epithelial cells. Leakage of urinary constituents through the damaged epithelium may then exacerbate the inflammation in the underlying muscle layers. <\/jats:p>","DOI":"10.1152\/ajprenal.1998.274.1.f205","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T14:24:43Z","timestamp":1514039083000},"page":"F205-F214","source":"Crossref","is-referenced-by-count":22,"title":["Disruption of guinea pig urinary bladder  permeability barrier in noninfectious cystitis"],"prefix":"10.1152","volume":"274","author":[{"given":"John P.","family":"Lavelle","sequence":"first","affiliation":[{"name":"Division of Urology, Department of Surgery, and"}]},{"given":"Gerard","family":"Apodaca","sequence":"additional","affiliation":[{"name":"Laboratory of Epithelial Cell Biology, Renal-Electrolyte Division, Department of Medicine and Department of Cell Biology and Physiology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania 15213"}]},{"given":"Susan A.","family":"Meyers","sequence":"additional","affiliation":[{"name":"Laboratory of Epithelial Cell Biology, Renal-Electrolyte Division, Department of Medicine and Department of Cell Biology and Physiology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania 15213"}]},{"given":"Wily G.","family":"Ruiz","sequence":"additional","affiliation":[{"name":"Laboratory of Epithelial Cell Biology, Renal-Electrolyte Division, Department of Medicine and Department of Cell Biology and Physiology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania 15213"}]},{"given":"Mark L.","family":"Zeidel","sequence":"additional","affiliation":[{"name":"Laboratory of Epithelial Cell Biology, Renal-Electrolyte Division, Department of Medicine and Department of Cell Biology and Physiology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania 15213"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(17)38622-6"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1993.163"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1996.76.1.245"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1994.267.5.C1483"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(17)39722-7"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1038\/339478a0"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.99.3.435"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(17)37211-7"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(17)37823-0"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1159\/000139273"},{"key":"B11","first-page":"4286","volume":"52","author":"Lattime E. C.","year":"1992","journal-title":"Cancer Res."},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(01)67034-4"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1995.75.3.561"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1038\/297685a0"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1016\/0076-6879(90)92100-R"},{"issue":"29","key":"B16","first-page":"F769","volume":"260","author":"Molitoris B. A.","year":"1991","journal-title":"Am. J. Physiol."},{"issue":"40","key":"B17","first-page":"F886","volume":"271","author":"Negrete H. O.","year":"1996","journal-title":"Am. J. Physiol."},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)80106-3"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(17)32790-8"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1007\/BF00219006"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1007\/BF00239460"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1172\/JCI112250"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1002\/nau.1930120106"},{"issue":"40","key":"B26","first-page":"F243","volume":"271","author":"Zeidel M. L.","year":"1996","journal-title":"Am. J. Physiol."}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1998.274.1.F205","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T21:03:16Z","timestamp":1567976596000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1998.274.1.F205"}},"issued":{"date-parts":[[1998,1,1]]},"references-count":24,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1998,1,1]]}},"alternative-id":["10.1152\/ajprenal.1998.274.1.F205"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1998.274.1.f205","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1998,1,1]]}},{"indexed":{"date-parts":[[2024,6,17]],"date-time":"2024-06-17T19:49:58Z","timestamp":1718653798916},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1992,4,1]]},"abstract":"<jats:p> We have previously reported that vasopressin activates chloride channels, leading to depolarization of glomerular mesangial cells via both calcium-dependent and calcium-independent pathways (S.G. Kremer, W.V. Breuer, and K. L. Skorecki, J. Cell. Physiol. 138: 97-105, 1989). However, the calcium-independent pathways were not defined. Using fluorescent probes, we now demonstrate that activation of protein kinase C (PKC) results in cellular depolarization in the absence of a calcium signal. This depolarization is also mediated by an enhanced conductance to chloride. Downregulation of PKC partially attenuated but did not abolish the depolarization response to vasopressin. Depolarization persisted when, in addition, calcium responses were also abolished and prostaglandin production was eliminated, suggesting an additional pathway for depolarization. G protein activation by aluminum fluoride also resulted in cellular depolarization mediated by an enhanced conductance to chloride, which persisted when calcium and PKC-signaling pathways were eliminated. This suggests the presence of a calcium- and PKC-independent pathway for G protein-mediated chloride-dependent depolarization. These findings point to the presence of at least three separate signaling pathways available for the activation of mesangial cell chloride channels, i.e., calcium, PKC, and a G protein. <\/jats:p>","DOI":"10.1152\/ajprenal.1992.262.4.f668","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T09:03:44Z","timestamp":1514019824000},"page":"F668-F678","source":"Crossref","is-referenced-by-count":5,"title":["Multiple signaling pathways for Cl(-)-dependent depolarization of mesangial cells: role of Ca2+, PKC, and G proteins"],"prefix":"10.1152","volume":"262","author":[{"given":"S. G.","family":"Kremer","sequence":"first","affiliation":[{"name":"Department of Medicine and Pediatrics, University of Toronto, Ontario,Canada."}]},{"given":"W.","family":"Zeng","sequence":"additional","affiliation":[{"name":"Department of Medicine and Pediatrics, University of Toronto, Ontario,Canada."}]},{"given":"S.","family":"Sridhara","sequence":"additional","affiliation":[{"name":"Department of Medicine and Pediatrics, University of Toronto, Ontario,Canada."}]},{"given":"K. L.","family":"Skorecki","sequence":"additional","affiliation":[{"name":"Department of Medicine and Pediatrics, University of Toronto, Ontario,Canada."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1992.262.4.F668","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:17:15Z","timestamp":1567973835000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1992.262.4.F668"}},"issued":{"date-parts":[[1992,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1992,4,1]]}},"alternative-id":["10.1152\/ajprenal.1992.262.4.F668"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1992.262.4.f668","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1992,4,1]]}},{"indexed":{"date-parts":[[2024,6,17]],"date-time":"2024-06-17T17:59:37Z","timestamp":1718647177715},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1994,8,1]]},"abstract":"<jats:p> Hepatocyte growth factor (HGF) has been implicated in branching tubulogenesis of the developing kidney and in response to renal injury. We therefore examined the effects of response to renal injury. We therefore examined the effects of HGF on a recently described murine inner medullary collecting duct epithelial cell line (mIMCD-3 cells) in comparison with Madin-Darby canine kidney (MDCK) cells. HGF induced mitosis, scattering, and tubulogenesis in both mIMCD-3 cells and MDCK cells. However, mIMCD-3 cells underwent branching tubulogenesis under matrix conditions that did not support these morphogenetic changes in MDCK cells, suggesting substantial differences in regulation of tubulogenesis in these two cell types. In quiescent mIMCD-3 cells, the high-affinity receptor for HGF, c-met, was expressed in a nonphosphorylated state. After stimulation with HGF, there was a &gt; 10-fold increase in receptor tyrosine phosphorylation and selective association with at least two intracellular proteins, including the phosphatidylinositol-3-kinase. Thus mIMCD-3 cells, which undergo HGF-dependent mitosis, scattering, and branching tubulogenesis, express the c-met receptor in a highly regulated state and therefore should make an excellent model for examining the mechanisms of HGF-dependent tubulogenesis in the renal collecting duct. <\/jats:p>","DOI":"10.1152\/ajprenal.1994.267.2.f271","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T05:02:00Z","timestamp":1514005320000},"page":"F271-F280","source":"Crossref","is-referenced-by-count":17,"title":["Regulation of mitogenesis, motogenesis, and tubulogenesis by hepatocyte growth factor in renal collecting duct cells"],"prefix":"10.1152","volume":"267","author":[{"given":"L. G.","family":"Cantley","sequence":"first","affiliation":[{"name":"Division of Nephrology, Beth Israel Hospital, Harvard Medical School,Boston, Massachusetts."}]},{"given":"E. J.","family":"Barros","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Beth Israel Hospital, Harvard Medical School,Boston, Massachusetts."}]},{"given":"M.","family":"Gandhi","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Beth Israel Hospital, Harvard Medical School,Boston, Massachusetts."}]},{"given":"M.","family":"Rauchman","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Beth Israel Hospital, Harvard Medical School,Boston, Massachusetts."}]},{"given":"S. K.","family":"Nigam","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Beth Israel Hospital, Harvard Medical School,Boston, Massachusetts."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1994.267.2.F271","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:56:22Z","timestamp":1567972582000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1994.267.2.F271"}},"issued":{"date-parts":[[1994,8,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1994,8,1]]}},"alternative-id":["10.1152\/ajprenal.1994.267.2.F271"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1994.267.2.f271","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1994,8,1]]}},{"indexed":{"date-parts":[[2024,6,17]],"date-time":"2024-06-17T17:25:22Z","timestamp":1718645122599},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1981,10,1]]},"abstract":"<jats:p> Sodium absorption and K secretion were measured in isolated perfused rabbit cortical collecting tubules. To increase the range of transport rates some tubules were dissected from rabbit pretreated with DOcA. K secretin was unaffected by varying axial volume flow from 4 to 15 nl\/min. K secretion was, however, correlated with transepithelial voltage and Na absorption. The Na:K transfer ratio was 1.35. In tubules dissected from normal rabbits, K secretion was almost eliminated by reducing Na concentration in the lumen to near 0 and was unaffected by varying luminal Na concentration from 30 to 145 mM. These data, together with other experimental results reported by several investigators, are consistent with a model for K secretion that places the rate-limiting step at the Na-K pump located on the basolateral membrane. The apical (luminal) membrane appears to be highly permeable to K. <\/jats:p>","DOI":"10.1152\/ajprenal.1981.241.4.f395","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T09:05:17Z","timestamp":1513933517000},"page":"F395-F402","source":"Crossref","is-referenced-by-count":21,"title":["Potassium secretion by cortical collecting tubule: relation to sodium absorption, luminal sodium concentration, and transepithelial voltage"],"prefix":"10.1152","volume":"241","author":[{"given":"J. B.","family":"Stokes","sequence":"first","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1981.241.4.F395","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T14:19:18Z","timestamp":1567952358000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1981.241.4.F395"}},"issued":{"date-parts":[[1981,10,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1981,10,1]]}},"alternative-id":["10.1152\/ajprenal.1981.241.4.F395"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1981.241.4.f395","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1981,10,1]]}},{"indexed":{"date-parts":[[2024,6,17]],"date-time":"2024-06-17T20:36:58Z","timestamp":1718656618430},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1981,7,1]]},"abstract":"<jats:p> Techniques are presented for the isolation and perfusion of renal proximal tubules from the neotenic salamander Ambystoma tigrinum. Methods are described for a determination of normal values for fluid transport and electrophysiological parameters. Stable cellular microelectrode recordings are reported that constitute the first intracellular measurements in an isolated perfused tubule preparation. With identical solutions in lumen and bath, fluid reabsorption averaged 0.28 nl.min-1.mm-1, transepithelial potential difference averaged -4.5 mV, transepithelial resistance was 52.1 omega.cm2, and the transepithelial chloride-to-sodium transference number ratio was 3.4. The basolateral cell membrane potential difference averaged -59.6 mV, and the ratio of apical-to-basolateral cell membrane resistance was between 3.9 and 5. Viability of the isolated perfused salamander proximal tubule preparation is demonstrated by a detailed comparison of the present data with results of in vivo micropuncture experiments on both Necturus and intact Ambystoma kidneys. In addition to being an advantageous preparation for long-term intracellular recordings, the Ambystoma kidney is unique in that proximal tubules can be studied both in isolation and by conventional micropuncture. <\/jats:p>","DOI":"10.1152\/ajprenal.1981.241.1.f39","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T14:28:20Z","timestamp":1513952900000},"page":"F39-F52","source":"Crossref","is-referenced-by-count":8,"title":["Isolated perfused salamander proximal tubule: methods, electrophysiology, and transport"],"prefix":"10.1152","volume":"241","author":[{"given":"H.","family":"Sackin","sequence":"first","affiliation":[]},{"given":"E. L.","family":"Boulpaep","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1981.241.1.F39","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:21:12Z","timestamp":1567966872000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1981.241.1.F39"}},"issued":{"date-parts":[[1981,7,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1981,7,1]]}},"alternative-id":["10.1152\/ajprenal.1981.241.1.F39"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1981.241.1.f39","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1981,7,1]]}},{"indexed":{"date-parts":[[2022,3,31]],"date-time":"2022-03-31T10:59:18Z","timestamp":1648724358327},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1986,8,1]]},"abstract":"<jats:p> Following the ingestion of a high-potassium-content diet for only a few days, the plasma potassium of rats rises only modestly in response to a previously lethal dose of potassium salts. This acquired tolerance, termed potassium adaptation, is principally the result of increased capacity to excrete potassium into the urine. However, a substantial portion of the acute potassium dose is not immediately excreted and is apparently translocated into cells. Previous studies have failed to show an increase in the content of potassium of a variety of tissues from such animals. Using 86Rb as a potassium analogue, we have shown that the skeletal muscle of potassium-adapted rats takes up significantly greater amounts of potassium in vivo in response to an acute challenge than does that of control animals. Furthermore, the same animals exhibit greater efflux of 86Rb following the termination of the acute infusion. We have also shown that the Na+-K+-ATPase activity and ouabain-binding capacity of skeletal muscle microsomes are increased by the process of potassium adaptation. We conclude that skeletal muscle is an important participant in potassium adaptation and acts to temporarily buffer acute increases in the extracellular concentration of potassium. <\/jats:p>","DOI":"10.1152\/ajprenal.1986.251.2.f313","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T01:22:44Z","timestamp":1513992164000},"page":"F313-F318","source":"Crossref","is-referenced-by-count":1,"title":["Extrarenal potassium adaptation: role of skeletal muscle"],"prefix":"10.1152","volume":"251","author":[{"given":"J. D.","family":"Blachley","sequence":"first","affiliation":[]},{"given":"B. P.","family":"Crider","sequence":"additional","affiliation":[]},{"given":"J. H.","family":"Johnson","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1986.251.2.F313","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:36:55Z","timestamp":1567971415000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1986.251.2.F313"}},"issued":{"date-parts":[[1986,8,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1986,8,1]]}},"alternative-id":["10.1152\/ajprenal.1986.251.2.F313"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1986.251.2.f313","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1986,8,1]]}},{"indexed":{"date-parts":[[2024,6,30]],"date-time":"2024-06-30T08:28:35Z","timestamp":1719736115319},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1994,4,1]]},"abstract":"<jats:p> The intracellular concentrations of calcium and chloride have been suggested to be involved in the control of renin secretion from juxtaglomerular (JG) cells. We have tested these propositions on permeabilized JG cells. Rat glomeruli with attached JG cells were isolated by the magnetic iron technique, superfused, and permeabilized by 20 microM digitonin for 12 min. The calcium concentration was varied with Ca ethylene glycol-bis (beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) buffers [0 (5 MM EGTA without calcium), 17, 73, 170, 440, or 700 nM and 1.5, 15 or 150 microM]. These maneuvers had no effect on renin release, while 1.5 mM calcium caused a stimulation, which was not inhibited by 50 mM sucrose. Isosmotic increases in the chloride concentration to 25, 60, and 132 mM resulted in prompt stimulations of renin release. Similarly, iodide and nitrate stimulated renin release. We conclude that renin release from permeabilized JG cells is unaffected by calcium concentrations in the nano- and micromolar range, while the release is stimulated by chloride or other permeant anions. We suggest that in intact JG cells an increase in calcium inhibits renin release through activation of chloride channels followed by a drop in the intracellular chloride concentration. The stimulation caused by the high calcium concentration may be a toxic effect or may be due to stimulation of the fusion between granules and cell membrane in a way analogous to other secretory cells. <\/jats:p>","DOI":"10.1152\/ajprenal.1994.266.4.f604","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T05:55:18Z","timestamp":1514008518000},"page":"F604-F611","source":"Crossref","is-referenced-by-count":6,"title":["Renin release from permeabilized juxtaglomerular cells is stimulated by chloride but not by low calcium"],"prefix":"10.1152","volume":"266","author":[{"given":"B. L.","family":"Jensen","sequence":"first","affiliation":[{"name":"Division of Pathophysiology, Panum Institute, Copenhagen,Denmark."}]},{"given":"O.","family":"Skott","sequence":"additional","affiliation":[{"name":"Division of Pathophysiology, Panum Institute, Copenhagen,Denmark."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1994.266.4.F604","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:31:05Z","timestamp":1567960265000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1994.266.4.F604"}},"issued":{"date-parts":[[1994,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1994,4,1]]}},"alternative-id":["10.1152\/ajprenal.1994.266.4.F604"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1994.266.4.f604","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1994,4,1]]}},{"indexed":{"date-parts":[[2024,7,2]],"date-time":"2024-07-02T04:37:36Z","timestamp":1719895056851},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1984,2,1]]},"abstract":"<jats:p> Fluid (sodium) reabsorption, total glucose efflux, and reabsorption of angiotensin II and insulin from the proximal convoluted tubule were studied in rats by in vivo microperfusion. After 35 min of total renal artery occlusion, function was assessed at two intervals, 0-1 h (early recovery, ER) and 2-4 h (late recovery, LR). Light and electron microscopic evaluation showed 60-75% loss of proximal convoluted tubule brush border membrane in ER and nearly complete restoration of brush border in LR. No other structural abnormalities were evident. Renal blood flow was unchanged from control during both ER and LR. During ER, fluid reabsorption was reduced to 29.8 +\/- 5.2%, and total glucose efflux, at normal tubule loads, to 73.9 +\/- 5.5% of control. However, angiotensin II and insulin reabsorption were unchanged. In LR, fluid reabsorption remained significantly reduced at 54.3 +\/- 8.1% of control. Total glucose efflux from the proximal tubule was normal in LR at glucose loads of up to 400 pmol X min-1, but was significantly reduced at higher loads. Passive glucose efflux, measured in the presence of 10(-4)M phloridzin, was not altered by ischemia. Brief ischemia results in significant alterations in proximal tubular reabsorption of sodium and glucose, which correlate with a substantial loss of brush border during ER. However, despite restoration of cell morphology to normal in LR, transport defects for both sodium and glucose persist. <\/jats:p>","DOI":"10.1152\/ajprenal.1984.246.2.f159","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T17:14:42Z","timestamp":1513962882000},"page":"F159-F166","source":"Crossref","is-referenced-by-count":5,"title":["Recovery of proximal tubular function from ischemic injury"],"prefix":"10.1152","volume":"246","author":[{"given":"P. A.","family":"Johnston","sequence":"first","affiliation":[]},{"given":"H.","family":"Rennke","sequence":"additional","affiliation":[]},{"given":"N. G.","family":"Levinsky","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1984.246.2.F159","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:36:10Z","timestamp":1567967770000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1984.246.2.F159"}},"issued":{"date-parts":[[1984,2,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1984,2,1]]}},"alternative-id":["10.1152\/ajprenal.1984.246.2.F159"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1984.246.2.f159","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1984,2,1]]}},{"indexed":{"date-parts":[[2024,7,1]],"date-time":"2024-07-01T11:59:16Z","timestamp":1719835156294},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1992,5,1]]},"abstract":"<jats:p> Glyceraldehyde-3-phosphate dehydrogenase (EC 1.2.2.12) (GAPDH) is a multifunctional protein that associates with the cytoplasmic face of intact human erythrocyte membranes. This association has been postulated to be critically dependent on the interaction of GAPDH with the highly acidic NH2-terminal domain of the principal integral membrane protein of the erythrocyte plasma membrane, the band 3 anion exchanger (AE1). This domain is not conserved in murine erythrocyte AE1 and is fully deleted in the alternatively spliced AE1 isoform that is expressed in the kidney. The lack of conservation of this domain has been proposed to explain the reported absence of GAPDH association with rodent erythrocyte membranes. To determine whether GAPDH could be associated with AE1 proteins in rodent cell membranes, specific rabbit antibodies to peptide sequences of rat GAPDH and mouse AE1 were used to immunolocalize these proteins in sequential semithin sections of rat erythrocytes and kidney medulla. In rat erythrocytes, GAPDH immunoreactivity was predominantly membrane associated and colocalized with AE1. In the kidney medulla, GAPDH was concentrated in the basolateral membrane of type A intercalated cells, where it colocalized with the alternatively spliced kidney form of AE1. GAPDH immunoreactivity was not detected in the plasma membrane of any other cell type in the kidney, indicating its predominant association with AE1-rich membranes. If this membrane interaction occurs via AE1 binding, then GAPDH must have binding sites in addition to those previously described for such binding in human AE1. <\/jats:p>","DOI":"10.1152\/ajprenal.1992.262.5.f892","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T08:53:48Z","timestamp":1514019228000},"page":"F892-F896","source":"Crossref","is-referenced-by-count":6,"title":["Colocalization of GAPDH and band 3 (AE1) proteins in rat erythrocytes and kidney intercalated cell membranes"],"prefix":"10.1152","volume":"262","author":[{"given":"L.","family":"Ercolani","sequence":"first","affiliation":[{"name":"Renal Unit, Massachusetts General Hospital, Boston 02114."}]},{"given":"D.","family":"Brown","sequence":"additional","affiliation":[{"name":"Renal Unit, Massachusetts General Hospital, Boston 02114."}]},{"given":"A.","family":"Stuart-Tilley","sequence":"additional","affiliation":[{"name":"Renal Unit, Massachusetts General Hospital, Boston 02114."}]},{"given":"S. L.","family":"Alper","sequence":"additional","affiliation":[{"name":"Renal Unit, Massachusetts General Hospital, Boston 02114."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1992.262.5.F892","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:16:54Z","timestamp":1567973814000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1992.262.5.F892"}},"issued":{"date-parts":[[1992,5,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1992,5,1]]}},"alternative-id":["10.1152\/ajprenal.1992.262.5.F892"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1992.262.5.f892","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1992,5,1]]}},{"indexed":{"date-parts":[[2025,7,4]],"date-time":"2025-07-04T12:26:27Z","timestamp":1751631987607},"reference-count":7,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2015,7,1]]},"DOI":"10.1152\/ajprenal.00193.2015","type":"journal-article","created":{"date-parts":[[2015,5,14]],"date-time":"2015-05-14T01:02:41Z","timestamp":1431565361000},"page":"F33-F34","source":"Crossref","is-referenced-by-count":1,"title":["Continence and micturition: physiological mechanisms under behavioral control"],"prefix":"10.1152","volume":"309","author":[{"given":"Toby C.","family":"Chai","sequence":"first","affiliation":[{"name":"Department of Urology, Yale University School of Medicine, New Haven, Connecticut"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00072.2015"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90749.2008"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1126\/science.182.4115.939"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/S0031-9384(99)00131-6"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1038\/ncomms1812"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(05)67204-7"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/j.urology.2011.06.041"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00193.2015","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T01:15:02Z","timestamp":1567991702000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00193.2015"}},"issued":{"date-parts":[[2015,7,1]]},"references-count":7,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2015,7,1]]}},"alternative-id":["10.1152\/ajprenal.00193.2015"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00193.2015","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2015,7,1]]}},{"indexed":{"date-parts":[[2025,7,2]],"date-time":"2025-07-02T16:21:18Z","timestamp":1751473278579},"reference-count":41,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2002,2,1]]},"abstract":"<jats:p>The renin-angiotensin system plays an important role in the development of diabetic nephropathy. However, the mechanism of ANG II receptor regulation in the renal proximal tubule in the diabetic condition has not been elucidated. Thus we investigated the signal pathways involved in high-glucose-induced downregulation of ANG II binding in primary cultured renal proximal tubule cells. Twenty-five millimolar glucose, but not mannitol andl-glucose, induced downregulation of the AT<jats:sub>1<\/jats:sub>receptor (AT<jats:sub>1<\/jats:sub>R) because of a significant decline in maximal binding with no significant change in the affinity constant. Twenty-five millimolar glucose also decreased AT<jats:sub>1<\/jats:sub>R mRNA and protein levels. The 25 mM glucose-induced increase in the formation of lipid peroxides was prevented by antioxidants, protein kinase C (PKC) inhibitors, or L-type calcium channel blockers. These agents also blocked 25 mM glucose-induced downregulation of<jats:sup>125<\/jats:sup>I-ANG II binding. In addition, 25 mM glucose increased transforming growth factor (TGF)-\u03b21 secretion, and anti-TGF-\u03b2 antibody significantly blocked 25 mM glucose-induced downregulation of<jats:sup>125<\/jats:sup>I-ANG II binding. Furthermore, the 25 mM glucose-induced increase in TGF-\u03b21 secretion was inhibited by PKC inhibitors, L-type calcium channel blockers, or antioxidants. In conclusion, high glucose may induce downregulation of<jats:sup>125<\/jats:sup>I-ANG II binding via a PKC-oxidative stress-TGF-\u03b2 signal cascade in primary cultured rabbit renal proximal tubule cells.<\/jats:p>","DOI":"10.1152\/ajprenal.00080.2001","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:33:46Z","timestamp":1425414826000},"page":"F228-F237","source":"Crossref","is-referenced-by-count":23,"title":["The mechanism of angiotensin II binding downregulation by high glucose in primary renal proximal tubule cells"],"prefix":"10.1152","volume":"282","author":[{"given":"Soo Hyun","family":"Park","sequence":"first","affiliation":[{"name":"Hormone Research Center, Department of Veterinary Physiology, College of Veterinary Medicine, Chonnam National University, Kwangju 500-757, Korea"}]},{"given":"Ho Jae","family":"Han","sequence":"additional","affiliation":[{"name":"Hormone Research Center, Department of Veterinary Physiology, College of Veterinary Medicine, Chonnam National University, Kwangju 500-757, Korea"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.4.F603"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.47.4.668"},{"key":"B3","first-page":"S66","volume":"50","author":"Becker BN","year":"1996","journal-title":"Kidney Int"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.307"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/0003-2697(76)90527-3"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1677\/joe.0.1540355"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.264.4.F645"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.458"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.95.1.118"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.2337\/diab.39.6.667"},{"key":"B11","doi-asserted-by":"crossref","first-page":"1405","DOI":"10.1681\/ASN.V891405","volume":"8","author":"Craven PA","year":"1997","journal-title":"J Am Soc Nephrol"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.267.5.F776"},{"key":"B13","doi-asserted-by":"crossref","first-page":"B65","DOI":"10.2337\/diacare.22.1.65","volume":"22","author":"Friedman EA.","year":"1999","journal-title":"Diabetes Care"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.2337\/diacare.19.3.257"},{"key":"B15","doi-asserted-by":"crossref","first-page":"14555","DOI":"10.1016\/S0021-9258(18)47832-5","volume":"262","author":"Griendling KK","year":"1987","journal-title":"J Biol Chem"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/S0168-8227(99)00044-3"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/S0891-5849(98)00276-7"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.4.F628"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.4491414"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00104.x"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00119.x"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00048.x"},{"key":"B23","doi-asserted-by":"crossref","first-page":"1337","DOI":"10.1681\/ASN.V461337","volume":"4","author":"Kalinyak JE","year":"1993","journal-title":"J Am Soc Nephrol"},{"key":"B24","first-page":"S77","volume":"60","author":"King GL","year":"1997","journal-title":"Kidney Int"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119503"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.47.6.859"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1159\/000045855"},{"key":"B28","first-page":"1033","volume":"79","author":"Lebrethon MC","year":"1994","journal-title":"J Clin Endocrinol Metab"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1210\/endo.140.11.7089"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.266"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1016\/0003-2697(79)90738-3"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.0590051695.x"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1159\/000054200"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1210\/endo.142.2.7934"},{"key":"B35","first-page":"362","volume":"147","author":"Phillips AO","year":"1995","journal-title":"Am J Pathol"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1992.14"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.2337\/diab.45.4.522"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1007\/BF00410275"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1172\/JCI116079"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.1041350316"},{"key":"B41","first-page":"601","volume":"87","author":"Yaqoob M","year":"1994","journal-title":"QJM"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00080.2001","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,5,1]],"date-time":"2022-05-01T09:33:58Z","timestamp":1651397638000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00080.2001"}},"issued":{"date-parts":[[2002,2,1]]},"references-count":41,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2002,2,1]]}},"alternative-id":["10.1152\/ajprenal.00080.2001"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00080.2001","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2002,2,1]]}},{"indexed":{"date-parts":[[2025,7,2]],"date-time":"2025-07-02T16:37:03Z","timestamp":1751474223674},"reference-count":22,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2009,7]]},"abstract":"<jats:p> Animal models suggest that decreased renal endothelial nitric oxide synthase (eNOS) activity in old males promotes renal injury, whereas females are protected. We aimed to explore whether aging alters glomerular arginine uptake by CAT-1, the selective arginine supplier to eNOS in rats. Arginine uptake by glomeruli from young males (3 mo) was significantly higher than in young females. Old males (19 mo) exhibited a significant decrease in arginine transport compared with young males, whereas no differences were observed between old and young females. CAT-1 abundance remained unchanged in all experimental groups. The abundance of PKC\u03b1 (CAT-1 inhibitor) was significantly augmented in young females vs. young males, old vs. young males, and in old females vs. old males. No differences in PKC\u03b1 content were detected between old and young females. Phosphorylated PKC\u03b1 was significantly increased in old rats from both genders. \u03b1Tocopherol, a PKC inhibitor, produced a significant increase in arginine transport and restored NO generation in old males only. Ex vivo incubation of glomeruli from old males with PMA (PKC stimulant) significantly attenuated the effect of tocopherol on arginine uptake. In conclusion, attenuated glomerular arginine transport by CAT-1 contributes to the age-dependent, NO-deficient state in old male rats through upregulation of PKC\u03b1. In old females glomerular arginine transport is protected from the effects of PKC\u03b1 by an unknown mechanism. <\/jats:p>","DOI":"10.1152\/ajprenal.00020.2009","type":"journal-article","created":{"date-parts":[[2009,5,7]],"date-time":"2009-05-07T00:45:37Z","timestamp":1241657137000},"page":"F80-F84","source":"Crossref","is-referenced-by-count":11,"title":["Sexual dimorphism in glomerular arginine transport affects nitric oxide generation in old male rats"],"prefix":"10.1152","volume":"297","author":[{"given":"Idit F.","family":"Schwartz","sequence":"first","affiliation":[]},{"given":"Tamara","family":"Chernichovski","sequence":"additional","affiliation":[]},{"given":"Natalia","family":"Krishtol","sequence":"additional","affiliation":[]},{"given":"Avishai","family":"Grupper","sequence":"additional","affiliation":[]},{"given":"Ido","family":"Laron","sequence":"additional","affiliation":[]},{"given":"Doron","family":"Schwartz","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.00110107"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(89)90134-7"},{"key":"R3","unstructured":"Baylis C, Corman B. The aging kidney: insights from experimental studies. J Am Soc Nephrol 9: 699\u2013709, 1998."},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00830.x"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000048197.78764.D6"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1007\/BF00400651"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1111\/j.1432-1033.1996.0747h.x"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00619.2007"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/11.8.1542"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000060496.23144.A7"},{"key":"R11","unstructured":"Levi M, Rowe JW. Renal function and dysfunction in aging. In: The Kidney: Physiology and Pathophysiology (chapter 101), edited by Seldin DW and Giebisch G. New York: Raven, 1992, p. 3433\u20133456."},{"key":"R12","unstructured":"Macias-Nunez JF, Stewart CJ. Renal function in the elderly. In: Oxford Textbook of Clinical Nephrology, edited by Grunfeld JP, Ponticelli C, van Ypersal C, Davidson A, Camerun S. Oxford: Oxford Univ. Press, 1992, p. 56\u201370."},{"key":"R13","doi-asserted-by":"crossref","unstructured":"Mineo C, Ying YS, Chapline C, Jaken S, Anderson RG. Targeting of protein kinase C alpha to caveola. J Biol Chem 141: 601\u2013610, 1998.","DOI":"10.1083\/jcb.141.3.601"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1016\/S0047-6374(02)00003-9"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.01051.2007"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.97.11.5930"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.00522.2001"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000067"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1016\/j.atherosclerosis.2006.10.039"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.89.24.12043"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejphar.2003.12.036"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1046\/j.1440-1681.2001.03533.x"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00020.2009","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T22:55:50Z","timestamp":1567983350000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00020.2009"}},"issued":{"date-parts":[[2009,7]]},"references-count":22,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2009,7]]}},"alternative-id":["10.1152\/ajprenal.00020.2009"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00020.2009","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2009,7]]}},{"indexed":{"date-parts":[[2025,10,27]],"date-time":"2025-10-27T10:29:04Z","timestamp":1761560944274},"reference-count":49,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2005,6]]},"abstract":"<jats:p>We studied the signal pathway through which troglitazone (TRO) acts in inducing cellular acidosis in LLC-PK<jats:sub>1<\/jats:sub>-F<jats:sup>+<\/jats:sup>cells in relation to ammoniagenesis and DNA synthesis. Cells were grown to confluent monolayers in 30-mm chambers and monitored for intracellular pH (pH<jats:sub>i<\/jats:sub>) by the BCECF assay and activated ERK by phospo-ERK1\/2 antibodies. TRO induces a severe cellular acidosis (pH<jats:sub>i<\/jats:sub>6.68 \u00b1 0.10 vs. 7.28 \u00b1 0.07 time control at 4 min, P &lt; 0.01), whereas phospho-ERK1\/2 to total ERK1\/2 ratio increases 3.4-fold ( P &lt; 0.01). To determine whether ERK1\/2 was activated by cellular acidosis or TRO was acting via MEK1\/2 to activate ERK1\/2, cells were pretreated with specific inhibitors of MEK1\/2 activity, PD-098059 and U-0126, followed by the addition of TRO or vehicle. With MEK1\/2 activity inhibited, TRO treatment failed to activate ERK1\/2. Preventing ERK1\/2 activation abrogated the TRO-induced cellular acidosis and maintained the pH<jats:sub>i<\/jats:sub>within the low normal range (7.06 \u00b1 0.11). To determine whether blocking ERK activation prevents TRO's inhibitory effect on NHE activity, cells were acid-loaded and the recovery response was monitored as \u0394pH<jats:sub>i<\/jats:sub>\/ t over a 4-min recovery period. TRO inhibited NHE activity by 85% ( P &lt; 0.01), whereas blocking ERK activation restored the response. We measured activated ERK levels and pH<jats:sub>i<\/jats:sub>after 3- and 18-h exposure to TRO or extracellular acidosis (pHe = 6.95) to determine whether ERK activation was sustained. Whereas both TRO and extracellular acidosis increased activated ERK and decreased pH<jats:sub>i<\/jats:sub>after 3 h, only TRO sustained this response at 18 h. Furthermore, both enhanced ammoniagenesis and decreased DNA synthesis reflected the effect of TRO to induce and sustain a cellular acidosis.<\/jats:p>","DOI":"10.1152\/ajprenal.00205.2004","type":"journal-article","created":{"date-parts":[[2005,2,2]],"date-time":"2005-02-02T03:34:26Z","timestamp":1107315266000},"page":"F1257-F1266","source":"Crossref","is-referenced-by-count":10,"title":["Troglitazone's rapid and sustained activation of ERK1\/2 induces cellular acidosis in LLC-PK<sub>1<\/sub>-F<sup>+<\/sup>cells: physiological responses"],"prefix":"10.1152","volume":"288","author":[{"suffix":"III","given":"Robert","family":"Oliver","sequence":"first","affiliation":[]},{"given":"Ellen","family":"Friday","sequence":"additional","affiliation":[]},{"given":"Francesco","family":"Turturro","sequence":"additional","affiliation":[]},{"given":"Ashley","family":"Lacy","sequence":"additional","affiliation":[]},{"given":"Tomas","family":"Welbourne","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.46.27489"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.171"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.1.271"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2736(96)00050-8"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.49.4.539"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.00485.2001"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.281.3.F381"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1042\/bj3510095"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1016\/S1056-8727(01)00141-6"},{"key":"R10","unstructured":"Ecelbarger CAand Welbourne T.Rosiglitazone increases renal sodium\/hydrogen exchanger 3 protein and ammonium excretion in young rats.FASEB J16: 1169A, 2002."},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00054.x"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1007\/s002100000352"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1996.270.3.C825"},{"key":"R14","doi-asserted-by":"crossref","unstructured":"Gstraunthaler Gand Handler JS.Isolation, growth, and characterization of a gluconeogenic strain of renal cells.Am J Physiol Cell Physiol252: C232\u2013C238, 1987.","DOI":"10.1152\/ajpcell.1987.252.2.C232"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.2.F227"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2004.01.007"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M304400200"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.263.1.F83"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.49.6.1022"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1206885"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M201517200"},{"key":"R22","doi-asserted-by":"crossref","unstructured":"Lotspeich WD.Renal hypertrophy in metabolic acidosis and its relation to ammonia excretion.Am J Physiol208: 1135\u20131142, 1965.","DOI":"10.1152\/ajplegacy.1965.208.6.1135"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(95)90401-8"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00418.x"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1023\/A:1018446104071"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1996.270.3.C920"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M304907200"},{"key":"R28","doi-asserted-by":"crossref","unstructured":"Noel J, Roux D, and Pouyssegur J.Differential localization of Na+\/H+exchanger isoforms (NHE1 and NHE3) in polarized epithelial cell lines.J Cell Sci109: 929\u2013939, 1996.","DOI":"10.1242\/jcs.109.5.929"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.90.18.8319"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjc.6690617"},{"key":"R31","doi-asserted-by":"crossref","unstructured":"Pirkebner D, Fuetsch M, Wittmann W, Weiss H, Haller T, Schramek H, Margreiter R, and Amberger A.Reduction of intracellular pH inhibits constitutive expression of cyclooxygenase-2 in human colon cancer cells.J Cell Physiol198: 295\u2013301, 2003.","DOI":"10.1002\/jcp.10408"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M308099200"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1002\/1521-1878(200009)22:9<818::AID-BIES7>3.0.CO;2-6"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.2002.282.1.E231"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2443.2004.00793.x"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0705973"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1983.244.3.F223"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.00144.2004"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M108722200"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00418.x"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1158\/1078-0432.CCR-04-0879"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.48.2.254"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.12.7841"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00133.2001"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00182.2003"},{"key":"R47","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00506.2001"},{"key":"R48","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.1041640305"},{"key":"R49","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00314.2002"},{"key":"R50","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.2000.279.2.C410"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00205.2004","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,7,4]],"date-time":"2021-07-04T14:59:04Z","timestamp":1625410744000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00205.2004"}},"issued":{"date-parts":[[2005,6]]},"references-count":49,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2005,6]]}},"alternative-id":["10.1152\/ajprenal.00205.2004"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00205.2004","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2005,6]]}},{"indexed":{"date-parts":[[2025,10,28]],"date-time":"2025-10-28T05:49:17Z","timestamp":1761630557629},"reference-count":62,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2010,12]]},"abstract":"<jats:p>The voltage-gated potassium channel Kv1.3 has been recently identified as a molecular target that allows the selective pharmacological suppression of effector memory T cells (T<jats:sub>EM<\/jats:sub>) without affecting the function of na\u00efve T cells (T<jats:sub>N<\/jats:sub>) and central memory T cells (T<jats:sub>CM<\/jats:sub>). We found that Kv1.3 was expressed on glomeruli and some tubules in rats with anti-glomerular basement membrane glomerulonephritis (anti-GBM GN). A flow cytometry analysis using kidney cells revealed that most of the CD4<jats:sup>+<\/jats:sup>T cells and some of the CD8<jats:sup>+<\/jats:sup>T cells had the T<jats:sub>EM<\/jats:sub>phenotype (CD45RC<jats:sup>\u2212<\/jats:sup>CD62L<jats:sup>\u2212<\/jats:sup>). Double immunofluorescence staining using mononuclear cell suspensions isolated from anti-GBM GN kidney showed that Kv1.3 was expressed on T cells and some macrophages. We therefore investigated whether the Kv1.3 blocker Psora-4 can be used to treat anti-GBM GN. Rats that had been given an injection of rabbit anti-rat GBM antibody were also injected with Psora-4 or the vehicle intraperitoneally. Rats given Psora-4 showed less proteinuria and fewer crescentic glomeruli than rats given the vehicle. These results suggest that T<jats:sub>EM<\/jats:sub>and some macrophages expressing Kv1.3 channels play a critical role in the pathogenesis of crescentic GN and that Psora-4 will be useful for the treatment of rapidly progressive glomerulonephritis.<\/jats:p>","DOI":"10.1152\/ajprenal.00374.2010","type":"journal-article","created":{"date-parts":[[2010,9,2]],"date-time":"2010-09-02T02:05:48Z","timestamp":1283393148000},"page":"F1258-F1269","source":"Crossref","is-referenced-by-count":32,"title":["Voltage-gated potassium channel Kv1.3 blocker as a potential treatment for rat anti-glomerular basement membrane glomerulonephritis"],"prefix":"10.1152","volume":"299","author":[{"given":"Toshitake","family":"Hyodo","sequence":"first","affiliation":[{"name":"Department of Nephrology,"}]},{"given":"Takashi","family":"Oda","sequence":"additional","affiliation":[{"name":"Department of Nephrology,"}]},{"given":"Yuichi","family":"Kikuchi","sequence":"additional","affiliation":[{"name":"Department of Nephrology,"}]},{"given":"Keishi","family":"Higashi","sequence":"additional","affiliation":[{"name":"Department of Nephrology,"}]},{"given":"Taketoshi","family":"Kushiyama","sequence":"additional","affiliation":[{"name":"Department of Nephrology,"}]},{"given":"Kojiro","family":"Yamamoto","sequence":"additional","affiliation":[{"name":"Department of Nephrology,"}]},{"given":"Muneharu","family":"Yamada","sequence":"additional","affiliation":[{"name":"Department of Nephrology,"}]},{"given":"Shigenobu","family":"Suzuki","sequence":"additional","affiliation":[{"name":"Department of Nephrology,"}]},{"given":"Ryota","family":"Hokari","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, and"}]},{"given":"Manabu","family":"Kinoshita","sequence":"additional","affiliation":[{"name":"Department of Immunology and Microbiology, National Defense Medical College, Tokorozawa, Saitama, Japan; and"}]},{"given":"Shuhji","family":"Seki","sequence":"additional","affiliation":[{"name":"Department of Immunology and Microbiology, National Defense Medical College, Tokorozawa, Saitama, Japan; and"}]},{"given":"Hidehiko","family":"Fujinaka","sequence":"additional","affiliation":[{"name":"Department of Structural Pathology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan"}]},{"given":"Tadashi","family":"Yamamoto","sequence":"additional","affiliation":[{"name":"Department of Structural Pathology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan"}]},{"given":"Soichiro","family":"Miura","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, and"}]},{"given":"Hiroo","family":"Kumagai","sequence":"additional","affiliation":[{"name":"Department of Nephrology,"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1002\/art.24747"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1196\/annals.1381.003"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.167.7.3740"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.2332\/allergolint.R-07-159"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.602"},{"key":"B6","doi-asserted-by":"crossref","first-page":"2271","DOI":"10.1681\/ASN.V7112271","volume":"7","author":"Atkins RC","year":"1996","journal-title":"J Am Soc Nephrol"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1038\/sj.jid.5700717"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1124\/mol.104.008193"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.241497298"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0605136103"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.166.2.1009"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/S0958-1669(97)80130-9"},{"key":"B13","doi-asserted-by":"crossref","first-page":"499","DOI":"10.1681\/ASN.V103499","volume":"10","author":"Cunningham MA","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1124\/mol.106.026203"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1136\/ard.2009.124636"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.394"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1007\/s004030000167"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.00496.2005"},{"key":"B19","doi-asserted-by":"crossref","first-page":"4978","DOI":"10.4049\/jimmunol.158.10.4978","volume":"158","author":"Fujinaka H","year":"1997","journal-title":"J Immunol"},{"key":"B20","doi-asserted-by":"crossref","first-page":"1174","DOI":"10.1681\/ASN.V871174","volume":"8","author":"Fujinaka H","year":"1997","journal-title":"J Am Soc Nephrol"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1159\/000065019"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/j.tips.2004.03.010"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1016\/j.transproceed.2009.06.025"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-60761-500-2_26"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1124\/pr.55.4.9"},{"key":"B26","doi-asserted-by":"crossref","first-page":"5484","DOI":"10.4049\/jimmunol.158.11.5484","volume":"158","author":"Haas C","year":"1997","journal-title":"J Immunol"},{"key":"B27","doi-asserted-by":"crossref","first-page":"3713","DOI":"10.4049\/jimmunol.160.8.3713","volume":"160","author":"Haas C","year":"1998","journal-title":"J Immunol"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.10430"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1172\/JCI110304"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2249.1997.4091307.x"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000056604.13964.62"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.472"},{"key":"B33","doi-asserted-by":"crossref","first-page":"752","DOI":"10.1681\/ASN.V104752","volume":"10","author":"Kitching AR","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00091.2005"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.180.12.7948"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1016\/j.immuni.2008.07.015"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.166.11.6578"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/16.suppl_5.3"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008050556"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.3181\/0705-RM-148"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2009.07.020"},{"key":"B42","doi-asserted-by":"crossref","first-page":"2243","DOI":"10.4049\/jimmunol.163.4.2243","volume":"163","author":"Ring GH","year":"1999","journal-title":"J Immunol"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0501770102"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/18.3.607"},{"key":"B45","doi-asserted-by":"crossref","first-page":"2636","DOI":"10.1681\/ASN.V12122636","volume":"12","author":"Sakatsume M","year":"2001","journal-title":"J Am Soc Nephrol"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1016\/S0065-2776(07)96002-2"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1084\/jem.147.2.369"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1038\/ni969"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1186\/ar2477"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1172\/JCI116956"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005091013"},{"key":"B52","doi-asserted-by":"crossref","first-page":"3083","DOI":"10.4049\/jimmunol.142.9.3083","volume":"142","author":"Tomosugi NI","year":"1989","journal-title":"J Immunol"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1053\/gast.2003.50050"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.51.6.1745"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1124\/mol.65.6.1364"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M304388200"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M605617200"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2006.11.120"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1172\/JCI16921"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1517\/13543784.15.10.1167"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118700"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2010.04.088"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00374.2010","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,6,3]],"date-time":"2023-06-03T03:52:25Z","timestamp":1685764345000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00374.2010"}},"issued":{"date-parts":[[2010,12]]},"references-count":62,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2010,12]]}},"alternative-id":["10.1152\/ajprenal.00374.2010"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00374.2010","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2010,12]]}},{"indexed":{"date-parts":[[2025,10,28]],"date-time":"2025-10-28T18:26:52Z","timestamp":1761676012494},"reference-count":46,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,2,1]]},"abstract":"<jats:p> Tubuloglomerular feedback (TGF)-mediated constriction of the afferent arteriole is modulated by a balance between release of superoxide (O<jats:sub>2<\/jats:sub><jats:sup>\u2212<\/jats:sup>) and nitric oxide (NO) in macula densa (MD) cells. Aldosterone activates mineralocorticoid receptors that are expressed in the MD and induces both NO and O<jats:sub>2<\/jats:sub><jats:sup>\u2212<\/jats:sup> generation. We hypothesize that aldosterone enhances O<jats:sub>2<\/jats:sub><jats:sup>\u2212<\/jats:sup> production in the MD mediated by protein kinase C (PKC), which buffers the effect of NO in control of TGF response. Studies were performed in microdissected and perfused MD and in a MD cell line, MMDD1 cells. Aldosterone significantly enhanced O<jats:sub>2<\/jats:sub><jats:sup>\u2212<\/jats:sup> generation both in perfused MD and in MMDD1 cells. When aldosterone (10<jats:sup>\u22127<\/jats:sup> mol\/l) was added in the tubular perfusate, TGF response was reduced from 2.4 \u00b1 0.3 \u03bcm to 1.4 \u00b1 0.2 \u03bcm in isolated perfused MD. In the presence of tempol, a O<jats:sub>2<\/jats:sub><jats:sup>\u2212<\/jats:sup> scavenger, TGF response was 1.5 \u00b1 0.2 \u03bcm. In the presence of both tempol and aldosterone in the tubular perfusate, TGF response was further reduced to 0.4 \u00b1 0.2 \u03bcm. To determine if PKC is involved in aldosterone-induced O<jats:sub>2<\/jats:sub><jats:sup>\u2212<\/jats:sup> production, we exposed the O<jats:sub>2<\/jats:sub><jats:sup>\u2212<\/jats:sup> cells to a nonselective PKC inhibitor chelerythrine chloride, a specific PKC\u03b1 inhibitor Go6976, or a PKC\u03b1 siRNA, and the aldosterone-induced increase in O<jats:sub>2<\/jats:sub><jats:sup>\u2212<\/jats:sup> production was blocked. These data indicate that aldosterone-stimulated O<jats:sub>2<\/jats:sub><jats:sup>\u2212<\/jats:sup> production in the MD buffers the effect of NO in control of TGF response, an effect that was mediated by PKC\u03b1. <\/jats:p>","DOI":"10.1152\/ajprenal.00501.2012","type":"journal-article","created":{"date-parts":[[2012,12,6]],"date-time":"2012-12-06T05:50:05Z","timestamp":1354773005000},"page":"F326-F332","source":"Crossref","is-referenced-by-count":15,"title":["Interaction between nitric oxide and superoxide in the macula densa in aldosterone-induced alterations of tubuloglomerular feedback"],"prefix":"10.1152","volume":"304","author":[{"given":"Qian","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi; and"},{"name":"Department of Cardiac Surgery, Provincial Hospital Affiliated to Shandong University, Jinan, China"}]},{"given":"Lin","family":"Lin","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi; and"}]},{"given":"Yan","family":"Lu","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi; and"}]},{"given":"Haifeng","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi; and"}]},{"given":"Yanhua","family":"Duan","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi; and"}]},{"given":"Xiaolong","family":"Zhu","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi; and"}]},{"given":"Chengwei","family":"Zou","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi; and"},{"name":"Department of Cardiac Surgery, Provincial Hospital Affiliated to Shandong University, Jinan, China"}]},{"suffix":"Jr.","given":"R. Davis","family":"Manning","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi; and"}]},{"given":"Ruisheng","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi; and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1210\/jcem-46-1-105"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1210\/me.2006-0559"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90446.2008"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000083982.74108.54"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.ph.49.030187.001423"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1978.114"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1161\/hy1101.093423"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2010.30"},{"key":"B9","first-page":"193","volume":"9","author":"Briggs JP","year":"1986","journal-title":"Renal Physiol (Basel)"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.66033.x"},{"key":"B11","first-page":"1863","volume":"85","author":"Fardella CE","year":"2000","journal-title":"J Clin Endocrinol Metab"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.111.173195"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00762.2009"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.109.149062"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1016\/j.mce.2003.10.054"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.93.19.10500"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000259797.48382.b2"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118867"},{"key":"B19","first-page":"924","volume-title":"Textbook of Medical Physiology","author":"Hall JE","year":"2011"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00981.x"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.252.5.F825"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1210\/en.2007-0864"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1038\/onc.2010.415"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1986.250.5.C676"},{"key":"B25","first-page":"1145","volume":"15","author":"Le MC","year":"2004","journal-title":"J Am Soc Nephrol"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(05)74868-6"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00282.x"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90204.2008"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00515.2006"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000033275.17169.67"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00727.x"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1016\/j.mce.2003.10.018"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00650.2009"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.86.1.37"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000118519.66430.22"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00911.x"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1016\/j.mce.2003.10.047"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-201X.1997.d01-1962.x"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000201443.63240.a7"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.171317998"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1042\/BST0351049"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.5.F706"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000106135.02935.E1"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.258.3.F457"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.108.124594"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00596.2010"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00501.2012","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T23:40:30Z","timestamp":1567986030000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00501.2012"}},"issued":{"date-parts":[[2013,2,1]]},"references-count":46,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2013,2,1]]}},"alternative-id":["10.1152\/ajprenal.00501.2012"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00501.2012","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2013,2,1]]}},{"indexed":{"date-parts":[[2025,10,26]],"date-time":"2025-10-26T22:50:43Z","timestamp":1761519043652},"reference-count":33,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,2,1]]},"abstract":"<jats:p>This study aimed to estimate the relationship between pharmacokinetics and the antidiuretic effect of desmopressin. In the investigator-blind, randomized, parallel group study, 5 dose groups and 1 placebo group, each consisting of 12 healthy, overhydrated, nonsmoking male subjects 18\u201355 yr of age were infused intravenously over 2 h with placebo or 30, 60, 125, 250, and 500 ng desmopressin in 50 ml of normal saline. Plasma desmopressin and urine osmolality rose by variable amounts during the infusions of 60, 125, 250, and 500 ng desmopressin. Plotting mean urine osmolality against the concurrent mean plasma desmopressin yielded a temporal delay between pharmacokinetic (PK) and -dynamic (PD) responses in all dose groups. Using simulation from the indirect-response model, assuming a constant (4 ng\/ml) desmopressin concentration, this delay between PK and PD was estimated at 4 h (10th-90th percentile: 1.8\u20138.1). Within each group, however, there were large individual variations (2- to 10-fold) in the magnitude and duration of the antidiuretic effect. The antidiuretic effect of intravenous desmopressin in water-loaded healthy adults varies considerably due largely to factors other than individual differences in pharmacokinetics. The antidiuretic effect is time as well as dose dependent and may be self-amplifying. The most likely explanation for these findings is that the time required for a given level of plasma desmopressin to exert its maximum antidiuretic effect varies markedly from person to person due to individual differences in the kinetics of one or more of the intracellular mechanisms that promote the reabsorption of solute-free water by principal cells in renal collecting tubules.<\/jats:p>","DOI":"10.1152\/ajprenal.00502.2012","type":"journal-article","created":{"date-parts":[[2012,11,8]],"date-time":"2012-11-08T07:08:10Z","timestamp":1352358490000},"page":"F268-F278","source":"Crossref","is-referenced-by-count":20,"title":["Temporal delays and individual variation in antidiuretic response to desmopressin"],"prefix":"10.1152","volume":"304","author":[{"given":"Kristian Vinter","family":"Juul","sequence":"first","affiliation":[{"name":"Ferring International Pharmascience Center, Copenhagen, Denmark; and"}]},{"given":"Lars","family":"Erichsen","sequence":"additional","affiliation":[{"name":"Ferring International Pharmascience Center, Copenhagen, Denmark; and"}]},{"given":"Gary L.","family":"Robertson","sequence":"additional","affiliation":[{"name":"Clinical Research Center at Northwestern Memorial Hospital, Feinberg Medical School of Northwestern University, Chicago, Illinois"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1038\/nrendo.2011.100"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/S0008-6363(01)00328-5"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004121079"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1007\/s00439-011-1011-z"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/S1043-2760(00)00304-0"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0b013e3283094eb1"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1023\/A:1023238514015"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/nature03479"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1007\/s00285-003-0252-4"},{"key":"B10","doi-asserted-by":"crossref","first-page":"980","DOI":"10.1681\/ASN.V115980","volume":"11","author":"De Wardener HE","year":"2000","journal-title":"J Am Soc Nephrol"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0b013e3283050969"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00723.2009"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1586\/epr.11.14"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00119.2008"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1007\/s12020-011-9492-z"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00741.2010"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00199.2010"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0910683107"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(06)00305-3"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.90.24.11663"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.254"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00024.2001"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1211\/0022357044535"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0910646107"},{"key":"B25","first-page":"351","volume":"101","author":"Robertson GL","year":"1983","journal-title":"J Lab Clin Med"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.me.39.020188.002233"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/S0889-8529(18)30031-8"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.65.092101.142638"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0b013e32818b27bf"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.2174\/157488607781668891"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1046\/j.1464-410X.90.s3.3.x"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM198112243052601"},{"key":"B33","first-page":"51","volume":"117","author":"Zerbe RL","year":"1991","journal-title":"J Lab Clin Med"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00502.2012","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,1,31]],"date-time":"2022-01-31T01:08:49Z","timestamp":1643591329000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00502.2012"}},"issued":{"date-parts":[[2013,2,1]]},"references-count":33,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2013,2,1]]}},"alternative-id":["10.1152\/ajprenal.00502.2012"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00502.2012","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2013,2,1]]}},{"indexed":{"date-parts":[[2025,10,26]],"date-time":"2025-10-26T14:29:19Z","timestamp":1761488959455},"reference-count":53,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2012,9,15]]},"abstract":"<jats:p>Connexins in renal arterioles affect autoregulation of arteriolar tonus and renal blood flow and are believed to be involved in the transmission of the tubuloglomerular feedback (TGF) response across the cells of the juxtaglomerular apparatus. Connexin40 (Cx40) also plays a significant role in the regulation of renin secretion. We investigated the effect of deleting the Cx40 gene on autoregulation of afferent arteriolar diameter in response to acute changes in renal perfusion pressure. The experiments were performed using the isolated blood perfused juxtamedullary nephron preparation in kidneys obtained from wild-type or Cx40 knockout mice. Renal perfusion pressure was increased in steps from 75 to 155 mmHg, and the response in afferent arteriolar diameter was measured. Hereafter, a papillectomy was performed to inhibit TGF, and the pressure steps were repeated. Conduction of intercellular Ca<jats:sup>2+<\/jats:sup>changes in response to local electrical stimulation was examined in isolated interlobular arteries and afferent arterioles from wild-type or Cx40 knockout mice. Cx40 knockout mice had an impaired autoregulatory response to acute changes in renal perfusion pressure compared with wild-type mice. Inhibition of TGF by papillectomy significantly reduced autoregulation of afferent arteriolar diameter in wild-type mice. In Cx40 knockout mice, papillectomy did not affect the autoregulatory response, indicating that these mice have no functional TGF. Also, Cx40 knockout mice showed no conduction of intercellular Ca<jats:sup>2+<\/jats:sup>changes in response to local electrical stimulation of interlobular arteries, whereas the Ca<jats:sup>2+<\/jats:sup>response to norepinephrine was unaffected. These results suggest that Cx40 plays a significant role in the renal autoregulatory response of preglomerular resistance vessels.<\/jats:p>","DOI":"10.1152\/ajprenal.00026.2012","type":"journal-article","created":{"date-parts":[[2012,7,19]],"date-time":"2012-07-19T11:41:03Z","timestamp":1342698063000},"page":"F855-F863","source":"Crossref","is-referenced-by-count":23,"title":["Role of connexin40 in the autoregulatory response of the afferent arteriole"],"prefix":"10.1152","volume":"303","author":[{"given":"Charlotte Mehlin","family":"Sorensen","sequence":"first","affiliation":[{"name":"Institute of Biomedical Sciences, Division of Renal and Vascular Physiology, University of Copenhagen, Copenhagen, Denmark; and"}]},{"given":"Isaiah","family":"Giese","sequence":"additional","affiliation":[]},{"given":"Thomas Hartig","family":"Braunstein","sequence":"additional","affiliation":[{"name":"Danish National Research Foundation Center for Cardiac Arrhythmia, University of Copenhagen, Copenhagen, Denmark"}]},{"given":"Jens Christian","family":"Brasen","sequence":"additional","affiliation":[{"name":"Institute of Biomedical Sciences, Division of Renal and Vascular Physiology, University of Copenhagen, Copenhagen, Denmark; and"}]},{"given":"Max","family":"Salomonsson","sequence":"additional","affiliation":[{"name":"Institute of Biomedical Sciences, Division of Renal and Vascular Physiology, University of Copenhagen, Copenhagen, Denmark; and"}]},{"given":"Niels-Henrik","family":"Holstein-Rathlou","sequence":"additional","affiliation":[{"name":"Danish National Research Foundation Center for Cardiac Arrhythmia, University of Copenhagen, Copenhagen, Denmark"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"crossref","first-page":"479","DOI":"10.1007\/s004180100275","volume":"115","author":"Arensbak B","year":"2001","journal-title":"Histochem Cell Biol"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1902.sp000911"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1159\/000151767"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1984.246.3.F349"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.264.1.F166"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.2.F198"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1093\/cvr\/cvp340"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.86.6.649"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/physiolgenomics.00169.2002"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00016.2004"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00251.2003"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1089\/ars.2008.2117"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.506"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/0306-3623(94)90063-9"},{"key":"B15","doi-asserted-by":"crossref","first-page":"3440","DOI":"10.1016\/S0021-9258(19)83641-4","volume":"260","author":"Grynkiewicz G","year":"1985","journal-title":"J Biol Chem"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/S0008-6363(99)00174-1"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-201x.1999.00582.x"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00786.x"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/j.cardiores.2003.11.015"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00468.2007"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00340.2002"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1006\/mvre.1999.2216"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1172\/JCI18499"},{"key":"B24","doi-asserted-by":"crossref","first-page":"973","DOI":"10.1096\/fasebj.24.1_supplement.973.7","volume":"24","author":"Jobs A","year":"2010","journal-title":"FASEB J"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00766.2002"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008090943"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002423"},{"key":"B28","doi-asserted-by":"crossref","first-page":"4179","DOI":"10.1242\/dev.127.19.4179","volume":"127","author":"Kruger O","year":"2000","journal-title":"Development"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008030252"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90669.2008"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1988.255.3.F383"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.258.3.F537"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1990.129"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00242.2005"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00425.2005"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1055\/s-0028-1083813"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.5.F700"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00247.2001"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.64.4.790"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.65.050102.085738"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.258.3.F553"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.637"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1080\/10739680590895028"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00491.2007"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.1997.493bb.x"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.171317998"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.267.5.F879"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002673"},{"key":"B49","first-page":"I-132","author":"Thurau KWC","year":"1964","journal-title":"Circ Res Suppl 14\u201315"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.272.3.F372"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000258856.19922.45"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2010.257"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00509.x"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00026.2012","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,1,22]],"date-time":"2022-01-22T04:51:23Z","timestamp":1642827083000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00026.2012"}},"issued":{"date-parts":[[2012,9,15]]},"references-count":53,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2012,9,15]]}},"alternative-id":["10.1152\/ajprenal.00026.2012"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00026.2012","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2012,9,15]]}},{"indexed":{"date-parts":[[2025,10,27]],"date-time":"2025-10-27T10:52:00Z","timestamp":1761562320968},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1990,10,1]]},"abstract":"<jats:p> We assessed the effects of the peptide agonist, bradykinin (BK), and phorbol myristate acetate (PMA) on prostaglandin E2 (PGE2) production, cyclooxygenase (COX) activity and mass, and arachidonic acid (AA) release in Madin Darby canine kidney (MDCK) cells. PMA stimulated PGE2 production by increasing both AA release and the activity of COX. Using [35S]methionine labeling and immunoprecipitation, we demonstrated that the increased COX activity is due to new COX synthesis. Actinomycin D and cycloheximide blocked the PMA-stimulated COX activity but not AA release. Both PMA-stimulated AA release and COX activity were reduced by the protein kinase C inhibitor staurosporine (STP). Glucocorticoids failed to alter PMA- or BK-stimulated PGE2 production was reduced by STP, indicating BK acts in part through protein kinase C activation. BK increased PGE2 production in PMA-treated cells, suggesting a protein kinase C-independent mechanism of action as well. BK did not stimulate any change in COX activity. We conclude that in MDCK cells PMA, but not BK, can stimulate both AA release and COX synthesis. Stimulation of COX synthesis requires either prolonged activation of protein kinase C and\/or an additional nonprotein kinase C-mediated effect of PMA. <\/jats:p>","DOI":"10.1152\/ajprenal.1990.259.4.f698","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T17:24:25Z","timestamp":1513963465000},"page":"F698-F703","source":"Crossref","is-referenced-by-count":4,"title":["Regulation of eicosanoid biosynthesis by phorbol ester in Madin Darby canine kidney cells"],"prefix":"10.1152","volume":"259","author":[{"given":"D. W.","family":"Coyne","sequence":"first","affiliation":[{"name":"Department of Medicine and Pharmacology, Washington University Medical School, St. Louis, Missouri 63110."}]},{"given":"M.","family":"Mordhorst","sequence":"additional","affiliation":[{"name":"Department of Medicine and Pharmacology, Washington University Medical School, St. Louis, Missouri 63110."}]},{"given":"A. R.","family":"Morrison","sequence":"additional","affiliation":[{"name":"Department of Medicine and Pharmacology, Washington University Medical School, St. Louis, Missouri 63110."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1990.259.4.F698","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:17:19Z","timestamp":1567955839000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1990.259.4.F698"}},"issued":{"date-parts":[[1990,10,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1990,10,1]]}},"alternative-id":["10.1152\/ajprenal.1990.259.4.F698"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1990.259.4.f698","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1990,10,1]]}},{"indexed":{"date-parts":[[2025,10,28]],"date-time":"2025-10-28T00:28:47Z","timestamp":1761611327391},"reference-count":48,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,8,15]]},"abstract":"<jats:p> Angiotensin-converting enzyme-2 (ACE2) enhances the degradation of ANG II and its expression is altered in diabetic kidneys, but the regulation of this enzyme in the urine is unknown. Urinary ACE2 was studied in the db\/db model of type 2 diabetes and stretozotocin (STZ)-induced type 1 diabetes during several physiological and pharmacological interventions. ACE2 activity in db\/db mice was increased in the serum and to a much greater extent in the urine compared with db\/m controls. Neither a specific ANG II blocker, telmisartan, nor an ACE inhibitor, captopril, altered the levels of urinary ACE2 in db\/db or db\/m control mice. High-salt diet (8%) increased whereas low-salt diet (0.1%) decreased urinary ACE2 activity in the urine of db\/db mice. In STZ mice, urinary ACE2 was also increased, and insulin decreased it partly but significantly after several weeks of administration. The increase in urinary ACE2 activity in db\/db mice reflected an increase in enzymatically active protein with two bands identified of molecular size at 110 and 75 kDa and was associated with an increase in kidney cortex ACE2 protein at 110 kDa but not at 75 kDa. ACE2 activity was increased in isolated tubular preparations but not in glomeruli from db\/db mice. Administration of soluble recombinant ACE2 to db\/m and db\/db mice resulted in a marked increase in serum ACE2 activity, but no gain in ACE2 activity was detectable in the urine, further demonstrating that urinary ACE2 is of kidney origin. Increased urinary ACE2 was associated with more efficient degradation of exogenous ANG II (10<jats:sup>\u22129<\/jats:sup> M) in urine from db\/db compared with that from db\/m mice. Urinary ACE2 could be a potential biomarker of increased metabolism of ANG II in diabetic kidney disease. <\/jats:p>","DOI":"10.1152\/ajprenal.00600.2012","type":"journal-article","created":{"date-parts":[[2013,6,13]],"date-time":"2013-06-13T03:14:41Z","timestamp":1371093281000},"page":"F600-F611","source":"Crossref","is-referenced-by-count":63,"title":["Regulation of urinary ACE2 in diabetic mice"],"prefix":"10.1152","volume":"305","author":[{"given":"Jan","family":"Wysocki","sequence":"first","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Medicine, The Feinberg School of Medicine, Northwestern University, Chicago, Illinois; and"}]},{"given":"Laura","family":"Garcia-Halpin","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Medicine, The Feinberg School of Medicine, Northwestern University, Chicago, Illinois; and"}]},{"given":"Minghao","family":"Ye","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Medicine, The Feinberg School of Medicine, Northwestern University, Chicago, Illinois; and"}]},{"given":"Christoph","family":"Maier","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Medicine, The Feinberg School of Medicine, Northwestern University, Chicago, Illinois; and"}]},{"given":"Kurt","family":"Sowers","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Medicine, The Feinberg School of Medicine, Northwestern University, Chicago, Illinois; and"}]},{"given":"Kevin D.","family":"Burns","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Kidney Research Centre, Ottawa Hospital Research Institute, University of Ottawa, Ottawa, Ontario, Canada"}]},{"given":"Daniel","family":"Batlle","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Medicine, The Feinberg School of Medicine, Northwestern University, Chicago, Illinois; and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2011.381"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0062833"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/S1054-3589(10)59007-0"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.30.3.535"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00579.x"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1172\/JCI16980"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/advan.00049.2009"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00234.2012"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.231476798"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00036.2009"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajplung.00071.2009"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1172\/JCI114526"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M505111200"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1038\/nm1275"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1007\/s10989-006-9031-6"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90610.2008"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1797.2011.01467.x"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2007.11.022"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2012.83"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.110.163519"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.2337\/db09-1218"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00519.2009"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007050582"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00339.2011"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2009.61"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1210\/en.2008-0677"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.497"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1042\/BJ20040634"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.108.124339"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00139.2006"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00315.2002"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002373"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90488.2008"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)64239-3"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.2337\/db07-1212"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000060689.38912.CB"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M002615200"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M200581200"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-1759(99)00097-6"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2007.060977"},{"key":"B41","volume":"21","author":"Wysocki J","year":"2010","journal-title":"J Am Soc Nephrol"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.109.138420"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.2337\/db06-0033"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0037649"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00656.2011"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.112.198622"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000126192.27644.76"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006050423"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00600.2012","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T23:47:54Z","timestamp":1567986474000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00600.2012"}},"issued":{"date-parts":[[2013,8,15]]},"references-count":48,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2013,8,15]]}},"alternative-id":["10.1152\/ajprenal.00600.2012"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00600.2012","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2013,8,15]]}},{"indexed":{"date-parts":[[2025,10,29]],"date-time":"2025-10-29T13:31:31Z","timestamp":1761744691259},"reference-count":41,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2001,7,1]]},"abstract":"<jats:p>The effects of obstruction [urinary tract obstruction (UTO)] and relief on renal development were examined in an experimental model in the fetal lamb. Bladder outlet obstruction was performed at 60 days of gestation; relief was performed by vesicoamniotic shunting at 90 days of gestation. Studies were carried out in obstructed (OF60; n = 11), shunted (SF; n = 5), and control fetuses (CF; n= 11) at 120 days of gestation. Fetal UTO produced either hydronephrosis (64%) or dysplasia (36%); dysplasia was always associated with a reduction in the number of glomeruli [950 \u00b1 99 (dysplasia) vs. 1,852 \u00b1 249 (CF) glomeruli\/section]. Obstructed fetuses had lower creatinine clearance [0.76 \u00b1 0.41 (OF60) vs. 0.96 \u00b1 0.21 (CF) ml \u00b7 min<jats:sup>\u22121<\/jats:sup>\u00b7 kg<jats:sup>\u22121<\/jats:sup>], higher sodium fractional excretion [17.2 \u00b1 20.3 (OF60) vs. 2.4 \u00b1 3.7% (CF)], and higher urinary concentration [80 \u00b1 30 (OF60) vs. 43 \u00b1 22 (CF) \u03bcmol\/l] than controls. In SF, the number of glomeruli was increased at 120 days of gestation (1,643 \u00b1 106 glomeruli\/section) compared with nondiverted fetuses (1,379 \u00b1 502 glomeruli\/section), and the temporal pattern of PAX2, disrupted after obstruction, was restored. In conclusion, early fetal UTO leads to either renal hydronephrosis with normal glomerular development or dysplasia with a decreased number of glomeruli; in utero urine diversion performed before the end of nephrogenesis may allow a reversal of the glomerulogenesis arrest observed.<\/jats:p>","DOI":"10.1152\/ajprenal.2001.281.1.f26","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T14:16:05Z","timestamp":1514038565000},"page":"F26-F37","source":"Crossref","is-referenced-by-count":32,"title":["Recovery after relief of fetal urinary obstruction: morphological, functional and molecular aspects"],"prefix":"10.1152","volume":"281","author":[{"given":"Didier","family":"Edouga","sequence":"first","affiliation":[{"name":"Department of Physiology, Necker-Enfants Malades Hospital, Institut National de la Sant\u00e9 et la Recherche M\u00e9dicale Unit\u00e9356, Institut F\u00e9d\u00e9ratif de Recherche 58, Paris, France"}]},{"given":"Brigitte","family":"Hugueny","sequence":"additional","affiliation":[{"name":"Department of Physiology, Necker-Enfants Malades Hospital, Institut National de la Sant\u00e9 et la Recherche M\u00e9dicale Unit\u00e9356, Institut F\u00e9d\u00e9ratif de Recherche 58, Paris, France"}]},{"given":"Bernard","family":"Gasser","sequence":"additional","affiliation":[{"name":"Department of Physiology, Necker-Enfants Malades Hospital, Institut National de la Sant\u00e9 et la Recherche M\u00e9dicale Unit\u00e9356, Institut F\u00e9d\u00e9ratif de Recherche 58, Paris, France"}]},{"given":"Laurence","family":"Bussi\u00e8res","sequence":"additional","affiliation":[{"name":"Department of Physiology, Necker-Enfants Malades Hospital, Institut National de la Sant\u00e9 et la Recherche M\u00e9dicale Unit\u00e9356, Institut F\u00e9d\u00e9ratif de Recherche 58, Paris, France"}]},{"given":"Kathleen","family":"Laborde","sequence":"additional","affiliation":[{"name":"Department of Physiology, Necker-Enfants Malades Hospital, Institut National de la Sant\u00e9 et la Recherche M\u00e9dicale Unit\u00e9356, Institut F\u00e9d\u00e9ratif de Recherche 58, Paris, France"}]}],"member":"24","reference":[{"key":"B1","first-page":"1225","volume":"152","author":"Attar R","year":"1998","journal-title":"Am J Pathol"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(17)53351-0"},{"key":"B3","first-page":"213","volume":"3","author":"Bernstein J.","year":"1968","journal-title":"Ann Pathol"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1055\/s-2008-1063534"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.055003793.x"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/0002-9378(90)90026-4"},{"key":"B7","doi-asserted-by":"crossref","first-page":"787","DOI":"10.1242\/dev.109.4.787","volume":"109","author":"Dressler GR","year":"1990","journal-title":"Development"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.89.4.1179"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1038\/362065a0"},{"key":"B10","first-page":"279","volume":"3","author":"Eccles MR","year":"1992","journal-title":"Cell Growth Diff"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(01)65795-1"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1159\/000263855"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-3468(84)80348-6"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-3468(83)80003-7"},{"key":"B15","first-page":"4092","volume":"55","author":"Gnarra JR","year":"1995","journal-title":"Cancer Res"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM198203113061006"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(17)44860-9"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9378(12)91847-5"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1159\/000264315"},{"key":"B20","doi-asserted-by":"crossref","first-page":"265","DOI":"10.1016\/S0021-9258(19)52451-6","volume":"193","author":"Lowry OH","year":"1951","journal-title":"J Biol Chem"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM198607313150532"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1007\/BF01213331"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(17)38843-2"},{"key":"B24","first-page":"396","volume":"6","author":"Minoja M","year":"1995","journal-title":"J Am Soc Nephrol"},{"key":"B25","doi-asserted-by":"crossref","first-page":"1855","DOI":"10.1093\/clinchem\/42.11.1855","volume":"42","author":"Muller F","year":"1996","journal-title":"Clin Chem"},{"key":"B26","first-page":"813","volume":"82","author":"Muller F","year":"1993","journal-title":"Obstet Gynecol"},{"key":"B27","first-page":"459","volume":"77","author":"Osathanondh V","year":"1964","journal-title":"Arch Pathol"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1006\/dbio.2000.9618"},{"key":"B29","doi-asserted-by":"crossref","first-page":"653","DOI":"10.1681\/ASN.V84653","volume":"8","author":"Peters CA.","year":"1997","journal-title":"J Am Soc Nephrol"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(17)36640-5"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/9.1.1"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1159\/000264329"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(17)39528-9"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1016\/0002-9378(75)90057-5"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1203\/00006450-198109000-00005"},{"key":"B36","doi-asserted-by":"crossref","first-page":"867","DOI":"10.1242\/dev.121.3.867","volume":"121","author":"Ryan G","year":"1995","journal-title":"Development"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1038\/ng0495-358"},{"key":"B38","first-page":"586","volume":"73","author":"Sibony M","year":"1995","journal-title":"Lab Invest"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(17)38844-4"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118811"},{"key":"B41","first-page":"445A","volume":"10","author":"Yang SP","year":"1999","journal-title":"J Am Soc Nephrol"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.2001.281.1.F26","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:45:04Z","timestamp":1660189504000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.2001.281.1.F26"}},"issued":{"date-parts":[[2001,7,1]]},"references-count":41,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2001,7,1]]}},"alternative-id":["10.1152\/ajprenal.2001.281.1.F26"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.2001.281.1.f26","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2001,7,1]]}},{"indexed":{"date-parts":[[2025,11,2]],"date-time":"2025-11-02T07:07:27Z","timestamp":1762067247365},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1982,11,1]]},"abstract":"<jats:p> Brush border membrane vesicles were purified from rabbit renal cortex using a calcium-precipitation procedure, and the uptake of carboxylic acids was determined by a rapid-filtration method. L-Lactate, pyruvate (monocarboxylic acids), and succinate (dicarboxylic acid) demonstrated features of Na+ cotransport: enhanced initial rate (1 s) of uptake with an inward Na+ gradient compared with the Na+ -free control condition and transient accumulation of substrate within the vesicles. Kinetic parameters derived for L-lactate and succinate show that each substrate is transported via single pathway and that the two substrates exhibit marginal cross-inhibition. A range of monocarboxylic acids including pyruvate and ketone bodies appear to interact with the monocarboxylic acid carrier. The kinetics of Nat-dependent pyruvate uptake suggest at least two transport pathways-namely, that this monocarboxylate shares both the mono- and dicarboxylic acid carriers. We conclude that isolated rabbit renal microvillus membranes possess independent transport systems for mono- and polycarboxylic acids. <\/jats:p>","DOI":"10.1152\/ajprenal.1982.243.5.f456","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T15:39:20Z","timestamp":1513957160000},"page":"F456-F462","source":"Crossref","is-referenced-by-count":3,"title":["Pathways for carboxylic acid transport by rabbit renal brush border membrane vesicles"],"prefix":"10.1152","volume":"243","author":[{"given":"E.","family":"Nord","sequence":"first","affiliation":[]},{"given":"S. H.","family":"Wright","sequence":"additional","affiliation":[]},{"given":"I.","family":"Kippen","sequence":"additional","affiliation":[]},{"given":"E. M.","family":"Wright","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1982.243.5.F456","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:28:16Z","timestamp":1567967296000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1982.243.5.F456"}},"issued":{"date-parts":[[1982,11,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1982,11,1]]}},"alternative-id":["10.1152\/ajprenal.1982.243.5.F456"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1982.243.5.f456","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1982,11,1]]}},{"indexed":{"date-parts":[[2025,11,2]],"date-time":"2025-11-02T16:33:49Z","timestamp":1762101229516},"reference-count":45,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2012,2,1]]},"abstract":"<jats:p>Autophagy is a process of cellular degradation, and its dysfunction elicits many pathological symptoms. However, the contribution of autophagy to kidney glomerular function has not been fully clarified. We previously reported that LC3, a promising executor of autophagy, played an important role in recovery from podocyte damage in an experimental nephrosis model (Asanuma K, Tanida I, Shirato I, Ueno T, Takahara H, Nishitani T, Kominami E, Tomino Y. FASEB J 17: 1165\u20131167, 2003). \u03b3-Aminobutyric acid A receptor-associated protein (GABARAP), has recently been characterized as another homolog of LC3, although its precise role in autophagy remains unclear. We recently generated green fluorescent protein (GFP)-GABARAP transgenic mice, in which GFP-GABARAP is abundantly expressed in glomerular podocytes. We found that the transgenic mice showed no obvious phenotype, and podocytes isolated from these mice manifested autophagic activity almost equivalent to that of wild-type mice when measured in vitro. Surprisingly, a single injection of doxorubicin caused a greater increase in proteinuria and sclerotic glomeruli in transgenic mice compared with wild-type mice. Under these conditions, neither GFP-GABARAP nor endogenous GABARAP appeared to be recruited to autophagosomes, and both remained in the cytosol. Moreover, the cytosolic GFP-GABARAP was significantly colocalized with p62 to form aggregates. These results indicate that the GFP-GABARAP\/p62 complex is responsible for impairment of glomerular function and that it retards recovery from the effects of doxorubicin.<\/jats:p>","DOI":"10.1152\/ajprenal.00502.2010","type":"journal-article","created":{"date-parts":[[2011,11,3]],"date-time":"2011-11-03T01:20:11Z","timestamp":1320283211000},"page":"F380-F389","source":"Crossref","is-referenced-by-count":11,"title":["Doxorubicin-induced glomerulosclerosis with proteinuria in GFP-GABARAP transgenic mice"],"prefix":"10.1152","volume":"302","author":[{"given":"Miyuki","family":"Takagi-Akiba","sequence":"first","affiliation":[{"name":"Division of Nephrology, Department of Internal Medicine,"}]},{"given":"Katsuhiko","family":"Asanuma","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Internal Medicine,"}]},{"given":"Isei","family":"Tanida","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Cell Biology, National Institute of Infectious Diseases, Tokyo, Japan"}]},{"given":"Norihiro","family":"Tada","sequence":"additional","affiliation":[{"name":"Division of Genome Research, Research Institute for Diseases of Old Age, and"}]},{"given":"Juan Alejandro Oliva","family":"Trejo","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Internal Medicine,"},{"name":"Department of Biochemistry, Juntendo University Faculty of Medicine, and"}]},{"given":"Kanae","family":"Nonaka","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Internal Medicine,"}]},{"given":"Etsuko","family":"Asanuma","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Internal Medicine,"}]},{"given":"Eiki","family":"Kominami","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, Juntendo University Faculty of Medicine, and"}]},{"given":"Takashi","family":"Ueno","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, Juntendo University Faculty of Medicine, and"}]},{"given":"Yasuhiko","family":"Tomino","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Internal Medicine,"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0700917104"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI200523371"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1007\/s10157-003-0259-6"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1096\/fj.02-0580fje"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000130167.30769.55"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200507002"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00055.2009"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M605024200"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1007\/s11248-007-9107-x"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1172\/JCI39492"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M802182200"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.01370"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/19.21.5720"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.01131"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1038\/73456"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000037401.02391.76"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2007.10.035"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004121084"},{"key":"B19","doi-asserted-by":"crossref","first-page":"S64","DOI":"10.1038\/ki.1994.47","volume":"45","author":"Kriz W","year":"1994","journal-title":"Kidney Int Suppl"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.67097.x"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1097\/00001756-200107200-00009"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00308.x"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1159\/000101793"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1038\/nature06639"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.e03-09-0704"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2009.05.023"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1007\/BF00240371"},{"key":"B28","doi-asserted-by":"crossref","first-page":"697","DOI":"10.1681\/ASN.V85697","volume":"8","author":"Mundel P","year":"1997","journal-title":"J Am Soc Nephrol"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000039661.06947.FD"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-4159.2004.02692.x"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1016\/0378-1119(91)90434-D"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00033.2009"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)64357-X"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000410"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.2000.2333"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M200385200"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.4161\/auto.2871"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1016\/j.metabol.2006.08.026"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1007\/s00280-009-1164-9"},{"key":"B40","doi-asserted-by":"crossref","first-page":"2440","DOI":"10.1681\/ASN.V10112440","volume":"10","author":"Tryggvason K","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.19"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.4161\/auto.6085"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00342.x"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1038\/emboj.2010.74"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)64369-6"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00502.2010","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,12,14]],"date-time":"2021-12-14T05:47:21Z","timestamp":1639460841000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00502.2010"}},"issued":{"date-parts":[[2012,2,1]]},"references-count":45,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2012,2,1]]}},"alternative-id":["10.1152\/ajprenal.00502.2010"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00502.2010","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2012,2,1]]}},{"indexed":{"date-parts":[[2025,11,2]],"date-time":"2025-11-02T16:21:08Z","timestamp":1762100468026},"reference-count":46,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2006,9]]},"abstract":"<jats:p>Renal prostaglandins modulate the activity of a number of the transport systems in the kidney, including the Na-K-ATPase. Not only do prostaglandins have acute affects on renal Na-K-ATPase, but in addition prostaglandins have chronic affects, which include regulation at the transcriptional level. Previously, we have presented evidence that one such prostaglandin, PGE<jats:sub>1<\/jats:sub>, stimulates the transcription of the human Na-K-ATPase \u03b2<jats:sub>1<\/jats:sub>-subunit gene in Madin-Darby canine kidney cells via cAMP- and Ca<jats:sup>2+<\/jats:sup>-mediated pathways (Taub M, Borsick M, Geisel J, Matlhagela K, Rajkhowa T, and Allen C. Exp Cell Res 299: 1\u201314, 2004; Matlhagela K, Borsick M, Rajkhowa T, and Taub M. J Biol Chem 280: 334\u2013346, 2005). Evidence was presented indicating that PGE<jats:sub>1<\/jats:sub>stimulation was mediated through the binding of cAMP-regulatory element binding protein (CREB) to a prostaglandin-responsive element (PGRE) as well as Sp1 binding to an adjacent Sp1 site. In this report, we present evidence from EMSAs and DNA affinity precipitation studies that another PGRE present in the Na-K-ATPase \u03b2<jats:sub>1<\/jats:sub>-subunit promoter similarly binds CREB and Sp1. The evidence that indicates a requirement for CREB as well as Sp1 for gene activation through both PGREs (PGRE1 and PGRE3) includes studies with a dominant negative CREB (KCREB), Drosophila SL2 cells, and PGRE mutants. The results of these studies are indicative of a synergism between Sp1 and CREB in mediating regulation by PGRE3; while regulation occurring through PGRE1 also involves Sp1 and CREB, the mechanism appears to be distinct.<\/jats:p>","DOI":"10.1152\/ajprenal.00452.2005","type":"journal-article","created":{"date-parts":[[2006,2,15]],"date-time":"2006-02-15T03:03:36Z","timestamp":1139972616000},"page":"F635-F646","source":"Crossref","is-referenced-by-count":9,"title":["Regulation of the Na-K-ATPase \u03b2<sub>1<\/sub>-subunit promoter by multiple prostaglandin-responsive elements"],"prefix":"10.1152","volume":"291","author":[{"given":"Keikantse","family":"Matlhagela","sequence":"first","affiliation":[{"name":"Biochemistry Department, School of Medicine and Biomedical Sciences, State University of New York at Buffalo, Buffalo, New York"}]},{"given":"Mary","family":"Taub","sequence":"additional","affiliation":[{"name":"Biochemistry Department, School of Medicine and Biomedical Sciences, State University of New York at Buffalo, Buffalo, New York"}]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/19.9.2499"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1992.262.4.C845"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1016\/0003-2697(76)90527-3"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1152\/ajplung.1997.272.3.L542"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1210\/mend-1-1-83"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.98.3.992"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.14.8225"},{"key":"R8","unstructured":"Coleman RA, Smith WL, and Narumiya S.International Union of Pharmacology classification of prostanoid receptors: properties, distribution, and structure of the receptors and their subtypes.Pharmacol Rev46: 205\u2013229, 1994."},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(88)90144-4"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.33.20702"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/11.5.1475"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.R100023200"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1078\/0171-9335-00079"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/21.11.2619"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(91)80801-9"},{"key":"R16","unstructured":"Gick GG, Ismail-Beigi F, and Edelman IS.Hormonal regulation of Na,K-ATPase.Prog Clin Biol Res268: 277\u2013295, 1988."},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2002-10-3174"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1152\/physiol.00013.2004"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.biochem.71.102201.141218"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.272.4.F460"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1997.7781"},{"key":"R22","doi-asserted-by":"crossref","unstructured":"Lescale-Matys L, Hensley CB, Crnkovic-Markovic R, Putnam DS, and McDonough AA.Low K+increases Na,K-ATPase abundance in LLC-PK1\/Cl4 cells by differentially increasing \u03b2, and not \u03b1, subunit mRNA.J Biol Chem265: 17935\u201317940, 1990.","DOI":"10.1016\/S0021-9258(18)38253-X"},{"key":"R23","doi-asserted-by":"crossref","unstructured":"Lingrel JBand Kuntzweiler T.Na-ATPase.J Biol Chem269: 19659\u201319662, 1994.","DOI":"10.1016\/S0021-9258(17)32067-7"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1016\/S0079-6603(08)60708-4"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M411415200"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.130.5.1105"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/cdg295"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1981.240.3.F159"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.94.13.6764"},{"key":"R31","doi-asserted-by":"crossref","unstructured":"Nillni EAand Sevarino KA.The biology of pro-thyrotropin-releasing hormone-derived peptides.Endocr Rev20: 599\u2013648, 1999.","DOI":"10.1210\/edrv.20.5.0379"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.90.12.5479"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.16.2.694"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.14.8225"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.84.8.2198"},{"key":"R36","doi-asserted-by":"crossref","unstructured":"Taormino JPand Fambrough DM.Pre-translational regulation of the (Na++ K+)-ATPase in response to demand for ion transport in cultured chicken skeletal muscle.J Biol Chem265: 4116\u20134123, 1990.","DOI":"10.1016\/S0021-9258(19)39710-8"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1016\/j.yexcr.2004.04.046"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.76.7.3338"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.1041510215"},{"key":"R41","doi-asserted-by":"crossref","unstructured":"Walton KM, Rehfuss RP, Chrivia JC, Lochner JE, and Goodman RH.A dominant repressor of cyclic adenosine 3\u2032,5\u2032-monophosphate (cAMP)-regulated enhancer-binding protein activity inhibits the cAMP-mediated induction of the somatostatin promoter in vivo.Mol Endocrinol6: 647\u2013655, 1992.","DOI":"10.1210\/mend.6.4.1350057"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M004759200"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1998.274.2.C356"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1089\/thy.1998.8.897"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.2001.281.1.C147"},{"key":"R46","doi-asserted-by":"publisher","DOI":"10.1042\/bj3301469"},{"key":"R47","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00200.2002"},{"key":"R48","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0501076102"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00452.2005","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,7,23]],"date-time":"2021-07-23T23:43:42Z","timestamp":1627083822000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00452.2005"}},"issued":{"date-parts":[[2006,9]]},"references-count":46,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2006,9]]}},"alternative-id":["10.1152\/ajprenal.00452.2005"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00452.2005","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2006,9]]}},{"indexed":{"date-parts":[[2025,10,30]],"date-time":"2025-10-30T07:09:40Z","timestamp":1761808180695},"reference-count":81,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1999,6,1]]},"abstract":"<jats:p>The Na-K\/H-K-ATPase gene family is divided in three subgroups including the Na-K-ATPases, mainly involved in whole body and cellular ion homeostasis, the gastric H-K-ATPase involved in gastric fluid acidification, and the newly described nongastric H-K-ATPases for which the identification of physiological roles is still in its infancy. The first member of this last subfamily was first identified in 1992, rapidly followed by the molecular cloning of several other members. The relationship between each member remains unclear. The functional properties of these H-K-ATPases have been studied after their ex vivo expression in various functional expression systems, including the Xenopus laevisoocyte, the insect Sf9 cell line, and the human HEK 293 cells. All these H-K-ATPase \u03b1-subunits appear to encode H-K-ATPases when exogenously expressed in such expression systems. Recent data suggest that these H-K-ATPases could also transport Na<jats:sup>+<\/jats:sup>in exchange for K<jats:sup>+<\/jats:sup>, revealing a complex cation transport selectivity. Moreover, they display a unique pharmacological profile compared with the canonical Na-K-ATPases or the gastric H-K-ATPase. In addition to their molecular and functional characterizations, a major goal is to correlate the molecular expression of these cloned H-K-ATPases with the native K-ATPases activities described in vivo. This appears to be more complex than anticipated. The discrepancies between the functional data obtained by exogenous expression of the nongastric H-K-ATPases and the physiological data obtained in native organs could have several explanations as discussed in the present review. Extensive studies will be required in the future to better understand the physiological role of these H-K-ATPases, especially in disease processes including ionic or acid-base disorders.<\/jats:p>","DOI":"10.1152\/ajprenal.1999.276.6.f812","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T18:00:01Z","timestamp":1514052001000},"page":"F812-F824","source":"Crossref","is-referenced-by-count":24,"title":["The nongastric H<sup>+<\/sup>-K<sup>+<\/sup>-ATPases: molecular and functional properties"],"prefix":"10.1152","volume":"276","author":[{"given":"Frederic","family":"Jaisser","sequence":"first","affiliation":[{"name":"Institut National de la Sant\u00e9 et de la Recherche M\u00e9dicale, Unit\u00e9 478, Institut F\u00e9d\u00e9ratif de Recherche Cellules \u00c9pith\u00e9liales, Facult\u00e9 de M\u00e9decine Xavier Bichat, Universit\u00e9 Paris VII, F-75870 Paris Cedex 18, France"}]},{"given":"Ahmed T.","family":"Beggah","sequence":"additional","affiliation":[{"name":"Institut National de la Sant\u00e9 et de la Recherche M\u00e9dicale, Unit\u00e9 478, Institut F\u00e9d\u00e9ratif de Recherche Cellules \u00c9pith\u00e9liales, Facult\u00e9 de M\u00e9decine Xavier Bichat, Universit\u00e9 Paris VII, F-75870 Paris Cedex 18, France"}]}],"member":"24","reference":[{"key":"B1","first-page":"7","volume":"9","author":"Amlal H.","year":"1998","journal-title":"J. Am. Soc. Nephrol."},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.39.22764"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.28.17668"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1998.275.3.C669"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.13.6092"},{"key":"B6","doi-asserted-by":"crossref","first-page":"24437","DOI":"10.1016\/S0021-9258(19)51103-6","volume":"269","author":"Beguin P.","year":"1994","journal-title":"J. Biol. Chem."},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/16.14.4250"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.32.20179"},{"issue":"34","key":"B9","first-page":"F743","volume":"265","author":"Bertorello A. M.","year":"1993","journal-title":"Am. J. Physiol."},{"key":"B10","doi-asserted-by":"crossref","first-page":"23420","DOI":"10.1016\/S0021-9258(17)31532-6","volume":"269","author":"Blanco G.","year":"1994","journal-title":"J. Biol. Chem."},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.91.18.8542"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1021\/bi00001a039"},{"issue":"41","key":"B13","first-page":"F124","volume":"272","author":"Buffin-Meyer B.","year":"1997","journal-title":"Am. J. Physiol."},{"key":"B14","doi-asserted-by":"crossref","first-page":"25632","DOI":"10.1016\/S0021-9258(19)74436-6","volume":"268","author":"Burns E. L.","year":"1993","journal-title":"J. Biol. Chem."},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1002\/j.1460-2075.1992.tb05218.x"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1996.271.3.C753"},{"key":"B17","doi-asserted-by":"crossref","first-page":"1","DOI":"10.1242\/jeb.198.1.1","volume":"198","author":"Chow D. C.","year":"1995","journal-title":"J. Exp. Biol."},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.14.7894"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.47.29759"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.1997.tb52308.x"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.11.6516"},{"key":"B22","first-page":"19","volume":"9","author":"Cougnon M.","year":"1998","journal-title":"J. Am. Soc. Nephrol."},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.13.7277"},{"key":"B24","doi-asserted-by":"crossref","first-page":"13740","DOI":"10.1016\/S0021-9258(18)42276-4","volume":"267","author":"Crowson M. S.","year":"1992","journal-title":"J. Biol. Chem."},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.39.23683"},{"issue":"24","key":"B26","first-page":"G1005","volume":"261","author":"Del Castillo J. R.","year":"1991","journal-title":"Am. J. Physiol."},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/12.1Part1.387"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.1997.tb52309.x"},{"key":"B29","doi-asserted-by":"crossref","first-page":"6550","DOI":"10.1016\/S0021-9258(17)37407-0","volume":"269","author":"Eakle K. A.","year":"1994","journal-title":"J. Biol. Chem."},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.23.13937"},{"issue":"38","key":"B31","first-page":"F551","volume":"269","author":"Fejes-Toth G.","year":"1995","journal-title":"Am. J. Physiol."},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.23.14072"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-199709000-00005"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.121.2.283"},{"issue":"40","key":"B35","first-page":"F539","volume":"271","author":"Grishin A. V.","year":"1996","journal-title":"Am. J. Physiol."},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.43.27772"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1993.265.4.C1080"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.123.6.1421"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1007\/BF00374871"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.103.4.605"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1996.270.2.C679"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.123.6.1751"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1021\/bi00212a018"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.139.6.1545"},{"key":"B46","first-page":"349","volume":"22","author":"Kone B. C.","year":"1996","journal-title":"Miner. Electrolyte Metab."},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.5.2543"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.1998.00841.x"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.47.29682"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118247"},{"key":"B51","doi-asserted-by":"crossref","first-page":"8255","DOI":"10.1016\/S0021-9258(17)37187-9","volume":"269","author":"Lemas M. V.","year":"1994","journal-title":"J. Biol. Chem."},{"key":"B52","doi-asserted-by":"crossref","first-page":"19659","DOI":"10.1016\/S0021-9258(17)32067-7","volume":"269","author":"Lingrel J. B.","year":"1994","journal-title":"J. Biol. Chem."},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1016\/S0079-6603(08)60708-4"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.93.17.9132"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1997.272.5.C1717"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.37.22754"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.109.3.1057"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1995.268.5.C1207"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.18.11075"},{"key":"B60","first-page":"209","volume":"9","author":"Mense M.","year":"1998","journal-title":"J. Am. Soc. Nephrol."},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.11.6521"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1995.269.4.C992"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.8.4068"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1016\/0016-5085(92)90304-H"},{"key":"B65","doi-asserted-by":"crossref","first-page":"16757","DOI":"10.1016\/S0021-9258(18)37456-8","volume":"263","author":"Polvani C.","year":"1988","journal-title":"J. Biol. Chem."},{"key":"B66","doi-asserted-by":"crossref","first-page":"17854","DOI":"10.1016\/S0021-9258(19)84651-3","volume":"264","author":"Polvani C.","year":"1989","journal-title":"J. Biol. Chem."},{"issue":"37","key":"B67","first-page":"G424","volume":"274","author":"Rajendran V. M.","year":"1998","journal-title":"Am. J. Physiol."},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.1992.tb43797.x"},{"key":"B69","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1999.276.2.C350"},{"key":"B71","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.4.1904"},{"key":"B72","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.84.12.4039"},{"key":"B73","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.87.3.1178"},{"issue":"45","key":"B73a","first-page":"F799","volume":"276","author":"Silver R. B.","year":"1999","journal-title":"Am. J. Physiol."},{"key":"B74","doi-asserted-by":"publisher","DOI":"10.1006\/geno.1996.0125"},{"key":"B75","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(87)80677-4"},{"key":"B76","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/17.11.3029"},{"key":"B77","doi-asserted-by":"publisher","DOI":"10.2170\/jjphysiol.42.577"},{"key":"B78","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(95)00313-X"},{"key":"B79","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.1997.tb52260.x"},{"key":"B80","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1996.sp021241"},{"issue":"38","key":"B81","first-page":"F1","volume":"269","author":"Wingo C. S.","year":"1995","journal-title":"Am. J. Physiol."},{"issue":"37","key":"B82","first-page":"F1141","volume":"268","author":"Younes-Ibrahim M.","year":"1995","journal-title":"Am. J. Physiol."}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1999.276.6.F812","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:54:34Z","timestamp":1660190074000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1999.276.6.F812"}},"issued":{"date-parts":[[1999,6,1]]},"references-count":81,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1999,6,1]]}},"alternative-id":["10.1152\/ajprenal.1999.276.6.F812"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1999.276.6.f812","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1999,6,1]]}},{"indexed":{"date-parts":[[2025,10,31]],"date-time":"2025-10-31T07:44:25Z","timestamp":1761896665195},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1992,5,1]]},"abstract":"<jats:p> The transport of ketone bodies across the luminal membrane of the nephron was studied by means of micropuncture techniques in rats in normal acid-base state. The concentration of beta-hydroxybutyrate (beta-HB) and acetoacetate (AcAc) in plasma, tubular fluid and urine was measured by an ultramicromethod using enzymatic cycling. At endogenous plasma ketone body concentration, approximately 80% of the filtered load of beta-HB and AcAc was reabsorbed in the proximal convoluted tubule, the remaining fraction being almost completely reabsorbed between the late proximal convoluted and the distal tubule; under these conditions, the urinary excretion of ketone bodies was less than 1% of the filtered load. A progressive elevation to steady-state levels of plasma beta-HB resulted in a progressive reduction of the fractional reabsorption of beta-HB and AcAc in the proximal convoluted tubule, which means that reabsorption of ketone bodies in this nephron segment is saturable. No net secretion of ketone bodies could be demonstrated along the nephron even at the highest plasma ketone body concentrations reached. In clearance experiments, the capacity of the rat kidney for reabsorbing both beta-HB and AcAc was found to be limited by a maximal tubular capacity (Tm). The data suggest that, in the young Wistar rat nephron, most of the reabsorption of ketone bodies is carrier mediated. <\/jats:p>","DOI":"10.1152\/ajprenal.1992.262.5.f762","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T03:53:48Z","timestamp":1514001228000},"page":"F762-F769","source":"Crossref","is-referenced-by-count":6,"title":["Transport of beta-hydroxybutyrate and acetoacetate along rat nephrons: a micropuncture study"],"prefix":"10.1152","volume":"262","author":[{"given":"B.","family":"Ferrier","sequence":"first","affiliation":[{"name":"Centre National de la Recherche Scientifique, Unite de RechercheAssociee 1177, Institut National de la Sante et de la Recherche Medicale,Unite 80, Faculte de Medecine Alexis Carrel, Lyon, France."}]},{"given":"M.","family":"Martin","sequence":"additional","affiliation":[{"name":"Centre National de la Recherche Scientifique, Unite de RechercheAssociee 1177, Institut National de la Sante et de la Recherche Medicale,Unite 80, Faculte de Medecine Alexis Carrel, Lyon, France."}]},{"given":"B.","family":"Janbon","sequence":"additional","affiliation":[{"name":"Centre National de la Recherche Scientifique, Unite de RechercheAssociee 1177, Institut National de la Sante et de la Recherche Medicale,Unite 80, Faculte de Medecine Alexis Carrel, Lyon, France."}]},{"given":"G.","family":"Baverel","sequence":"additional","affiliation":[{"name":"Centre National de la Recherche Scientifique, Unite de RechercheAssociee 1177, Institut National de la Sante et de la Recherche Medicale,Unite 80, Faculte de Medecine Alexis Carrel, Lyon, France."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1992.262.5.F762","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:16:38Z","timestamp":1567959398000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1992.262.5.F762"}},"issued":{"date-parts":[[1992,5,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1992,5,1]]}},"alternative-id":["10.1152\/ajprenal.1992.262.5.F762"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1992.262.5.f762","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1992,5,1]]}},{"indexed":{"date-parts":[[2025,11,1]],"date-time":"2025-11-01T13:41:22Z","timestamp":1762004482294},"reference-count":43,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,3,1]]},"abstract":"<jats:p>Sensory neurons with afferent axons from the kidney are extraordinary in their response to electrical stimulation. More than 50% exhibit a tonic firing pattern, i.e., sustained action potential firing throughout depolarizing, pointing to an increased excitability, whereas nonrenal neurons show mainly a phasic response, i.e., less than five action potentials. Here we investigated whether these peculiar firing characteristics of renal afferent neurons are due to differences in the expression of voltage-gated sodium channels (Na<jats:sub>v<\/jats:sub>s). Dorsal root ganglion (DRG) neurons from rats (Th<jats:sub>11<\/jats:sub>-L<jats:sub>2<\/jats:sub>) were recorded by the current-clamp technique and distinguished as \u201ctonic\u201d or \u201cphasic.\u201d In voltage-clamp recordings, Na<jats:sub>v<\/jats:sub>s were characterized by their tetrodotoxoxin (TTX) sensitivity, and their molecular identity was revealed by RT-PCR. The firing pattern of 66 DRG neurons (41 renal and 25 nonrenal) was investigated. Renal neurons exhibited more often a tonic firing pattern (56.1 vs. 12%). Tonic neurons showed a more positive threshold (\u221221.75 \u00b1 1.43 vs.\u221229.33 \u00b1 1.63 mV; P &lt; 0.05), a higher overshoot (56.74 [53.6\u201360.96] vs. 46.79 mV [38.63\u201354.75]; P &lt; 0.05) and longer action potential duration (4.61 [4.15\u20135.85] vs. 3.35 ms [2.12\u20135.67]; P &lt; 0.05). These findings point to an increased presence of the TTX-resistant Na<jats:sub>v<\/jats:sub>s 1.8 and 1.9. Furthermore, tonic neurons exhibited a relatively higher portion of TTX-resistant sodium currents. Interestingly, mRNA expression of TTX-resistant sodium channels was significantly increased in renal, predominantly tonic, DRG neurons. Hence, under physiological conditions, renal sensory neurons exhibit predominantly a firing pattern associated with higher excitability. Our findings support that this is due to an increased expression and activation of TTX-resistant Na<jats:sub>v<\/jats:sub>s.<\/jats:p>","DOI":"10.1152\/ajprenal.00011.2012","type":"journal-article","created":{"date-parts":[[2013,1,3]],"date-time":"2013-01-03T07:22:31Z","timestamp":1357197751000},"page":"F491-F497","source":"Crossref","is-referenced-by-count":11,"title":["Sensory renal innervation: a kidney-specific firing activity due to a unique expression pattern of voltage-gated sodium channels?"],"prefix":"10.1152","volume":"304","author":[{"given":"Wolfgang","family":"Freisinger","sequence":"first","affiliation":[{"name":"Department of Internal Medicine 4\/Nephrology and Hypertension, University of Erlangen-N\u00fcrnberg, Erlangen, Germany; and"}]},{"given":"Johannes","family":"Schatz","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine 4\/Nephrology and Hypertension, University of Erlangen-N\u00fcrnberg, Erlangen, Germany; and"}]},{"given":"Tilmann","family":"Ditting","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine 4\/Nephrology and Hypertension, University of Erlangen-N\u00fcrnberg, Erlangen, Germany; and"}]},{"given":"Angelika","family":"Lampert","sequence":"additional","affiliation":[{"name":"Department of Physiology and Pathophysiology, University of Erlangen-N\u00fcrnberg, Erlangen, Germany"}]},{"given":"Sonja","family":"Heinlein","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine 4\/Nephrology and Hypertension, University of Erlangen-N\u00fcrnberg, Erlangen, Germany; and"}]},{"given":"Nena","family":"Lale","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine 4\/Nephrology and Hypertension, University of Erlangen-N\u00fcrnberg, Erlangen, Germany; and"}]},{"given":"Roland","family":"Schmieder","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine 4\/Nephrology and Hypertension, University of Erlangen-N\u00fcrnberg, Erlangen, Germany; and"}]},{"given":"Roland","family":"Veelken","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine 4\/Nephrology and Hypertension, University of Erlangen-N\u00fcrnberg, Erlangen, Germany; and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1038\/379257a0"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2003.039131"},{"key":"B3","doi-asserted-by":"crossref","first-page":"S12","DOI":"10.1681\/ASN.V55s12","volume":"5","author":"Batlle D","year":"1994","journal-title":"J Am Soc Nephrol"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1172\/JCI116444"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.22-23-10277.2002"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/0272-6386(95)90456-5"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1124\/pr.57.4.4"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/jn.01033.2006"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/jn.00100.2011"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.19-24-j0001.1999"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.18-23-09607.1998"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1038\/nprot.2009.91"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/jn.1995.73.5.2094"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1038\/labinvest.3700208"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1016\/j.jpain.2005.09.006"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1111\/j.1526-4637.2009.00719.x"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1093\/brain\/awh514"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00647.2009"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90599.2008"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.108.116129"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1993.sp019583"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1216080109"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.91054.2008"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/jn.2001.86.3.1351"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2006.113597"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000097549.70134.D8"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(09)60566-3"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000199984.78039.36"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1042\/cs0750029"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/jn.2001.86.2.629"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/jn.1997.78.6.3198"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1007\/s11906-009-0078-6"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMc0904179"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1111\/j.1460-9568.2008.06267.x"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1016\/j.expneurol.2007.01.038"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.22.6.884"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1016\/j.pain.2012.04.022"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.107.092643"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1016\/0896-6273(89)90113-X"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1186\/1744-8069-4-38"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2012.228460"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1159\/000316528"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.103"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00011.2012","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,2,5]],"date-time":"2022-02-05T03:36:25Z","timestamp":1644032185000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00011.2012"}},"issued":{"date-parts":[[2013,3,1]]},"references-count":43,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2013,3,1]]}},"alternative-id":["10.1152\/ajprenal.00011.2012"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00011.2012","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2013,3,1]]}},{"indexed":{"date-parts":[[2025,11,1]],"date-time":"2025-11-01T09:06:48Z","timestamp":1761988008245},"reference-count":16,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2004,12]]},"DOI":"10.1152\/ajprenal.00090.2004","type":"journal-article","created":{"date-parts":[[2004,11,2]],"date-time":"2004-11-02T21:18:22Z","timestamp":1099430302000},"page":"F1294-F1295","source":"Crossref","is-referenced-by-count":5,"title":["Plasma S-nitrosothiols and chronic renal failure"],"prefix":"10.1152","volume":"287","author":[{"given":"Daniela","family":"Giustarini","sequence":"first","affiliation":[{"name":"Department of Neurosciences, Pharmacology Unit \u2028 University of Siena\u2028 Via A.Moro, 4 53100 Siena, Italy"}]},{"given":"Ranieri","family":"Rossi","sequence":"additional","affiliation":[{"name":"Department of Neurosciences, Pharmacology Unit \u2028 University of Siena\u2028 Via A.Moro, 4 53100 Siena, Italy"}]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1016\/j.tips.2004.04.009"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/18.1.153"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000106716.22153.BB"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1038\/nm0503-481"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1016\/j.freeradbiomed.2003.11.011"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1161\/hh1301.092678"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1016\/S1089-8603(03)00044-2"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfg243"},{"key":"R9","unstructured":"Tsikas D and Frolich JC. S-nitrosoalbumin plasma levels in health and disease: facts or artifacts? Value of analytical chemistry in nitric oxide clinical research (Abstract). Circ Res 90: e39, 2002."},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1016\/j.cccn.2003.09.014"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1016\/S0009-8981(02)00339-X"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfg243"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1016\/S0009-8981(03)00046-9"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1016\/j.tips.2004.04.009"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1161\/hh1301.092678"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000122071.55721.BC"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00090.2004","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T21:50:25Z","timestamp":1567979425000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00090.2004"}},"issued":{"date-parts":[[2004,12]]},"references-count":16,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2004,12]]}},"alternative-id":["10.1152\/ajprenal.00090.2004"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00090.2004","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2004,12]]}},{"indexed":{"date-parts":[[2025,11,2]],"date-time":"2025-11-02T16:20:11Z","timestamp":1762100411467},"reference-count":37,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2006,4]]},"abstract":"<jats:p>The arachidonate signaling pathways comprise prostanoids formed by cyclooxygenases, EETs, and HETEs formed by cytochrome P-450 (CYP) enzymes and HETEs and leukotrienes generated by lipoxygenases. Whereas the intrarenal localization of cyclooxygenases and of some CYP enzymes along the nephron has already been determined, the localization of lipoxygenases and leukotriene-forming enzymes together with leukotriene receptors in the kidney is less clear. This study therefore aimed to determine the expression of 5-, 12-, and 15-lipoxygenases as well as the leukotriene receptors along the rat nephron. The kidneys were dissected into cortex and outer and inner medulla, and the microdissected nephron segments were collected after a collagenase digestion. mRNA abundance was determined by RT-PCR and real-time PCR. 15-LOX mRNA showed a characteristic expression pattern along the distal nephron. 12-LOX mRNA was only found in the glomerulus. Similarly, 5-LOX mRNAs together with 5-LOX-activating protein mRNAs were expressed in the glomerulus and also in the vasa recta. The leukotriene A4 hydrolase was found in all nephron segments, whereas leukotriene C4 synthase mRNA could not be found in any nephron segment. The leukotriene receptor B4 and the cysteinyl leukotriene receptor type 1 were selectively expressed in the glomerulus, whereas cysteinyl receptor type 2 was not found in any nephron segment. Our data suggest that the glomerulus is a major source and target for 5- and 12-HETE and for leukotrienes. The collecting duct system, on the other hand, appears to be a major source of 15-HETE.<\/jats:p>","DOI":"10.1152\/ajprenal.00169.2005","type":"journal-article","created":{"date-parts":[[2005,10,12]],"date-time":"2005-10-12T03:23:56Z","timestamp":1129087436000},"page":"F864-F872","source":"Crossref","is-referenced-by-count":19,"title":["Gene expression of 5-, 12-, and 15-lipoxygenases and leukotriene receptors along the rat nephron"],"prefix":"10.1152","volume":"290","author":[{"given":"Stephan W.","family":"Reinhold","sequence":"first","affiliation":[]},{"given":"Helga","family":"Vitzthum","sequence":"additional","affiliation":[]},{"given":"Thomas","family":"Filbeck","sequence":"additional","affiliation":[]},{"given":"Konrad","family":"Wolf","sequence":"additional","affiliation":[]},{"given":"Christos","family":"Lattas","sequence":"additional","affiliation":[]},{"given":"G\u00fcnter A. J.","family":"Riegger","sequence":"additional","affiliation":[]},{"given":"Armin","family":"Kurtz","sequence":"additional","affiliation":[]},{"given":"Bernhard K.","family":"Kr\u00e4mer","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.10.1.61"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(12)80692-5"},{"key":"R3","doi-asserted-by":"crossref","unstructured":"Badr KF.Five-lipoxygenase products in glomerular immune injury.J Am Soc Nephrol3: 907\u2013915, 1992.","DOI":"10.1681\/ASN.V34907"},{"key":"R4","doi-asserted-by":"crossref","unstructured":"Chomczynski Pand Sacchi N.Single step method of RNA isolation by acid guadinium thiocyanate-phenol-chloroform extraction.Anal Biochem162: 156\u2013159, 1987.","DOI":"10.1016\/0003-2697(87)90021-2"},{"key":"R5","unstructured":"Claesson HE, Jakobsson PH, Steinhilber D, Odlander B, and Samuelsson B.Expression of 5-lipoxygenase and biosynthesis of leukotriene B4 in human monomorphonuclear leukocytes.J Lipid Mediat6: 15\u201322, 1993."},{"key":"R6","doi-asserted-by":"crossref","unstructured":"Evans JF.Cysteinyl leukotriene receptors.Prostaglandins Other Lipid Mediat68: 587\u2013597, 2002.","DOI":"10.1016\/S0090-6980(02)00057-6"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.89.9.3962"},{"key":"R8","doi-asserted-by":"crossref","unstructured":"Hedi Hand Norbert G.5-Lipoxygenase pathway, dendritic cells, and adaptive immunity.J Biomed Biotechnol2: 99\u2013105, 2004.","DOI":"10.1155\/S1110724304310041"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1038\/22572"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.2.F395"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.89.8.3521"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1006\/pupt.1997.0075"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000099702.16315.DE"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1161\/01.ATV.15.7.942"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00286.x"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1159\/000075811"},{"key":"R17","unstructured":"Labat C, Ortiz JL, Norel X, Gorenne I, Verley J, Abram TS, Cuthbert NJ, Tudhope SR, Norman P, Gardiner P and Brink C.A second cysteinyl receptor in human lung.J Pharmacol Exp Ther263: 800\u2013805, 1992."},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-291X(03)01456-6"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1096\/fj.02-0416fje"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2249.1999.00858.x"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.23.13375"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115110"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00257.x"},{"key":"R24","unstructured":"Nie D, Tang K, Diglio C, and Honn KV.Eicosanoid regulation of angiogenesis: role of endothelial arachidonate 12-lipoxygenase.Blood95: 2304\u20132311, 2000."},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1997.273.1.R293"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00181.2002"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.2001.4865"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1126\/science.2820055"},{"key":"R29","doi-asserted-by":"crossref","unstructured":"Sasaki M, Hori MT, Hino T, Golub MS, and Tuck ML.Elevated 12-lipoxygenase activity in the spontaneously hypertensive rat.Am J Hypertens10: 371\u2013378, 1997.","DOI":"10.1016\/S0895-7061(96)00488-8"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1291\/hypres.27.417"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.273.4.F650"},{"key":"R32","doi-asserted-by":"crossref","unstructured":"Scoggan KA, Jakobsson PH, and Ford-Hutchinson AW.Production of leukotriene C4 in different human tissues is attributable to distinct membrane bound biosynthetic enzymes.J Biol Chem11: 10182\u201310187, 1997.","DOI":"10.1074\/jbc.272.15.10182"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.2000.3140"},{"key":"R34","unstructured":"Valdivielso JM, Montero A, Badr KF, and Munger A.Inhibition of 5-lipoxygenase activating protein decreases proteinuria in diabetic rats.J Nephrol16: 85\u201394, 2003."},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00615.x"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1084\/jem.178.6.1935"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1993.180"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00169.2005","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,7,18]],"date-time":"2021-07-18T14:11:35Z","timestamp":1626617495000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00169.2005"}},"issued":{"date-parts":[[2006,4]]},"references-count":37,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2006,4]]}},"alternative-id":["10.1152\/ajprenal.00169.2005"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00169.2005","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2006,4]]}},{"indexed":{"date-parts":[[2025,11,2]],"date-time":"2025-11-02T16:41:18Z","timestamp":1762101678050},"reference-count":48,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2003,7]]},"abstract":"<jats:p>High-protein diets exacerbate glomerular hyperfiltration and the progression of diabetic nephropathy. The purpose of this study was to determine whether amino acids also produce nonhemodynamic injury in the glomerulus. When rat mesangial cells were cultured with an amino acid mixture designed to replicate the composition in plasma after protein feeding, production of mRNA (Northern blot analysis) and\/or protein (ELISA or Western blot analysis) for transforming growth factor-\u03b2<jats:sub>1<\/jats:sub>(TGF-\u03b2<jats:sub>1<\/jats:sub>), fibronectin, thrombospondin-1 (TSP-1), and collagen IV were enhanced in a manner comparable to a culture with high glucose (30.5 mM). The bioactive portion of total TGF-\u03b2 (NRK assay) increased in response to amino acids. The TSP-1 antagonist LSKL peptide reduced bioactive TGF-\u03b2 and fibronectin, indicating the dependence of TGF-\u03b2<jats:sub>1<\/jats:sub>activation on TSP-1. DNA synthesis ([<jats:sup>3<\/jats:sup>H]thymidine incorporation), an index of cellular proliferation, increased in response to amino acids and was further enhanced by culture with increased levels of both amino acids and glucose. TGF-\u03b2<jats:sub>1<\/jats:sub>and matrix proteins increased when mesangial cells were cultured with excess l-arginine (2.08 mM) alone. Although l-arginine is the precursor of nitric oxide (NO), such responses to amino acids do not appear to be mediated through increased NO production. NO metabolites decreased in the media, and these responses to mixed amino acids or l-arginine were not prevented by NO synthase inhibition. In conclusion, amino acids induce indicators of response to injury in mesangial cells, even when hemodynamic stress is absent. In conditions associated with increased circulating amino acids, such as diabetes and\/or a high-protein diet, direct cellular effects could contribute to glomerular injury.<\/jats:p>","DOI":"10.1152\/ajprenal.00419.2002","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:38:32Z","timestamp":1425415112000},"page":"F79-F86","source":"Crossref","is-referenced-by-count":16,"title":["Amino acids induce indicators of response to injury in glomerular mesangial cells"],"prefix":"10.1152","volume":"285","author":[{"given":"Rick L.","family":"Meek","sequence":"first","affiliation":[]},{"given":"Sheryl K.","family":"Cooney","sequence":"additional","affiliation":[]},{"given":"Stephanie D.","family":"Flynn","sequence":"additional","affiliation":[]},{"given":"Robert F.","family":"Chouinard","sequence":"additional","affiliation":[]},{"given":"Maria H.","family":"Poczatek","sequence":"additional","affiliation":[]},{"given":"Joanne E.","family":"Murphy-Ullrich","sequence":"additional","affiliation":[]},{"given":"Katherine R.","family":"Tuttle","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"REF1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI3042"},{"key":"REF2","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.372"},{"key":"REF3","doi-asserted-by":"publisher","DOI":"10.1093\/ajcn\/29.4.340"},{"key":"REF4","doi-asserted-by":"publisher","DOI":"10.1159\/000020505"},{"key":"REF5","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM198209093071104"},{"key":"REF6","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115014"},{"key":"REF7","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.059002673.x"},{"key":"REF8","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.0610s1106.x"},{"key":"REF9","doi-asserted-by":"publisher","DOI":"10.2337\/diab.46.4.671"},{"key":"REF10","doi-asserted-by":"publisher","DOI":"10.1001\/archinte.1977.03630160069014"},{"key":"REF11","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/10.4.497"},{"key":"REF12","doi-asserted-by":"crossref","unstructured":"Ha Hand Lee HB.Reactive oxygen species as glucose signaling molecules in mesangial cells cultured under high glucose.Kidney Int77: S19-S25, 2000.","DOI":"10.1046\/j.1523-1755.2000.07704.x"},{"key":"REF13","doi-asserted-by":"publisher","DOI":"10.2337\/diab.46.5.847"},{"key":"REF14","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00421.x"},{"key":"REF15","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.483"},{"key":"REF16","doi-asserted-by":"crossref","unstructured":"Ishii N, Patel KP, Lane PH, Taylor T, Bian K, Murad F, Pollock JS, and Carmines PK.Nitric oxide synthesis and oxidative stress in the renal cortex of rats with diabetes mellitus.J Am Soc Nephrol12: 1630-1639, 2001.","DOI":"10.1681\/ASN.V1281630"},{"key":"REF17","doi-asserted-by":"crossref","unstructured":"Isono M, Cruz MC, Chen S, Hong SW, and Ziyadeh FN.Extracellular signal-regulated kinase mediates stimulation of TGF-\u03b21and matrix by high glucose in mesangial cells.J Am Soc Nephrol11: 2222-2230, 2000.","DOI":"10.1681\/ASN.V11122222"},{"key":"REF18","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117251"},{"key":"REF19","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.9.5830"},{"key":"REF20","doi-asserted-by":"publisher","DOI":"10.1016\/S1359-6101(99)00029-5"},{"key":"REF21","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.10.4552"},{"key":"REF22","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.07705.x"},{"key":"REF23","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1990.110"},{"key":"REF24","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-124-7-199604010-00002"},{"key":"REF25","doi-asserted-by":"crossref","unstructured":"Perrella MA, Yoshizumi M, Fen Z, Tsai JC, Hsieh CM, Kourembanas S, and Lee ME.Transforming growth factor-\u03b21, but not dexamethasone, down-regulates nitric oxide synthase mRNA after its induction by interleukin-1\u03b2 in rat smooth muscle cells.J Biol Chem269: 14595-14600, 1994.","DOI":"10.1016\/S0021-9258(17)36665-6"},{"key":"REF26","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00994.x"},{"key":"REF27","doi-asserted-by":"publisher","DOI":"10.1042\/cs1030403"},{"key":"REF28","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)64649-4"},{"key":"REF29","doi-asserted-by":"crossref","unstructured":"Ray PE, Bruggeman LA, Horikoshi S, Aguilera G, and Klotman PE.Angiotensin II stimulates human fetal mesangial cell proliferation and fibronectin biosynthesis by binding to AT1receptors.Kidney Int43: 177-184, 1994.","DOI":"10.1038\/ki.1994.21"},{"key":"REF30","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.19.13586"},{"key":"REF31","unstructured":"Riser BL, Cortes P, Heilig C, Grondin J, Ladson-Wofford S, Patterson D, and Narins RG.Cyclic stretching force selectively up-regulates transforming growth factor-\u03b2 isoforms in cultured rat mesangial cells.Am J Pathol148: 1915-1923, 1996."},{"key":"REF32","doi-asserted-by":"crossref","unstructured":"Ruilope LM, Casal MC, Praga M, Alcazar JM, Decap G, Lahera V, and Rodicio JL.Additive antiproteinuric effect of converting enzyme inhibition and a low protein intake.JAmSoc Nephrol3: 1307-1311, 1992.","DOI":"10.1681\/ASN.V361307"},{"key":"REF33","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.122.4.923"},{"key":"REF34","doi-asserted-by":"crossref","unstructured":"Scivitaro V, Ganz MB, and Weiss M.AGEs induce oxidative stress and activate protein kinase C-\u03b2IIin neonatal mesangial cells.Am J Physiol Renal Physiol278: F676-F683, 2000.","DOI":"10.1152\/ajprenal.2000.278.4.F676"},{"key":"REF35","unstructured":"Sellitti DF, Pithon-Curi TC, Hirszel P, and Doi SQ.Glutamine synergistically increases mesangial cell proliferation induced by high glucose levels (Abstract).J Am Soc Nephrol13: 297A, 2002."},{"key":"REF36","doi-asserted-by":"publisher","DOI":"10.2337\/diab.44.10.1139"},{"key":"REF37","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00273.x"},{"key":"REF38","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.48.10.2066"},{"key":"REF39","doi-asserted-by":"publisher","DOI":"10.1159\/000044989"},{"key":"REF40","doi-asserted-by":"crossref","unstructured":"Trachtman H, Futterweit S, and Crimmins DL.High glucose inhibits nitric oxide production in cultured rat mesangial cells.J Am Soc Nephrol8: 1276-1282, 1997.","DOI":"10.1681\/ASN.V881276"},{"key":"REF41","doi-asserted-by":"crossref","unstructured":"Tuttle KRand Bruton JL.Effect of insulin therapy on renal hemodynamic response amino acids and renal hypertrophy in non-insulin-dependent diabetes.Kidney Int43: 167-173, 1992.","DOI":"10.1038\/ki.1992.274"},{"key":"REF42","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199106063242304"},{"key":"REF43","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00155.2001"},{"key":"REF44","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M108360200"},{"key":"REF45","doi-asserted-by":"crossref","unstructured":"Wolf G.Cell cycle regulation in diabetic nephropathy.Kidney Int77: S59-S66, 2000.","DOI":"10.1046\/j.1523-1755.2000.07710.x"},{"key":"REF46","doi-asserted-by":"crossref","unstructured":"Yevdokimova N, Wahab NA, and Mason RM.Thrombospondin-1 is the key activator of TGF-\u03b21in human mesangial cells exposed to high glucose.J Am Soc Nephrol12: 703-712, 2001.","DOI":"10.1681\/ASN.V124703"},{"key":"REF47","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.82.17.5963"},{"key":"REF48","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117004"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00419.2002","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,5,1]],"date-time":"2022-05-01T09:37:33Z","timestamp":1651397853000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00419.2002"}},"issued":{"date-parts":[[2003,7]]},"references-count":48,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2003,7]]}},"alternative-id":["10.1152\/ajprenal.00419.2002"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00419.2002","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2003,7]]}},{"indexed":{"date-parts":[[2025,11,7]],"date-time":"2025-11-07T19:03:50Z","timestamp":1762542230510},"reference-count":40,"publisher":"American Physiological Society","issue":"11","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,12,1]]},"abstract":"<jats:p>p53, a pivotal protein in the apoptotic pathway, has been identified as a mediator of transcriptional responses to ischemia-reperfusion (IR) injury. The characteristics and functional significance of the p53 response in vivo are largely unknown in IR-induced kidney injury. Therapeutic opportunities of delivering small interfering RNA (siRNA) via venous injection have gained recognition; however, systemic adverse effects of siRNA therapy should be considered. To prevent IR-induced kidney injury, we tested the efficacy of transarterial administration of siRNA targeting p53 (p53 siRNA). Female C57BL\/6 mice underwent unilateral renal artery ischemia for 30 min, followed by reperfusion. siRNA experiments utilized short hairpin (sh) RNA plasmid-based approaches. Transfection of shRNA was performed using cationic polymer transfection reagent. Injection of synthetic p53 shRNA into the left renal artery just after ischemia improved tubular injury, apoptosis, and the swelling of mitochondria in cells of the thick ascending limb of Henle (mTALH) at the outer medullary regions. Staining of upregulated p53 was colocalized with the inducible expression of glycogen synthase kinase-3\u03b2 (GSK-3\u03b2) at mTALH after IR injury. p53 shRNA inhibited GSK-3\u03b2 expression and restored \u03b2-catenin expression at mTALH. For IR-induced kidney injury, transarterial delivery of p53 siRNA is an effective pharmacological intervention. Targeting siRNA to p53 leads to an attenuation of apoptosis and mitochondrial damage through the downregulation of GSK-3\u03b2 expression and upregulation of \u03b2-catenin. Local delivery of vectors such as p53 siRNA through a transaortic catheter is clinically useful in reducing the adverse effect of siRNA-related therapy.<\/jats:p>","DOI":"10.1152\/ajprenal.00279.2013","type":"journal-article","created":{"date-parts":[[2013,10,10]],"date-time":"2013-10-10T16:01:17Z","timestamp":1381420877000},"page":"F1617-F1627","source":"Crossref","is-referenced-by-count":18,"title":["Silencing of p53 RNA through transarterial delivery ameliorates renal tubular injury and downregulates GSK-3\u03b2 expression after ischemia-reperfusion injury"],"prefix":"10.1152","volume":"305","author":[{"given":"Takayuki","family":"Fujino","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, Cardiovascular Respiratory and Neurology Division, Asahikawa Medical University, Asahikawa, Japan"}]},{"given":"Sharifi","family":"Muhib","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Cardiovascular Respiratory and Neurology Division, Asahikawa Medical University, Asahikawa, Japan"}]},{"given":"Nobuyuki","family":"Sato","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Cardiovascular Respiratory and Neurology Division, Asahikawa Medical University, Asahikawa, Japan"}]},{"given":"Naoyuki","family":"Hasebe","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Cardiovascular Respiratory and Neurology Division, Asahikawa Medical University, Asahikawa, Japan"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/S0955-0674(98)80031-8"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/382638a0"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/S0955-0674(98)80039-2"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M105725200"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1002\/biot.201100054"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.00176.2006"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1093\/carcin\/bgi120"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1007\/s10637-011-9695-4"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M109.049411"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1038\/nm.2507"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1126\/science.1099320"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1038\/nrc3318"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2009.347"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/0925-4773(96)00597-7"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1172\/JCI19906"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000040596.23073.01"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118498"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)81333-1"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/j.neulet.2006.09.026"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M206402200"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/20.1.27"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000088027.54400.C6"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M110.101147"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008111204"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-148-11-200806030-00003"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.49.2.263"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1007\/s000180050449"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002731"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.32.19929"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1038\/nm.2290"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1186\/1750-1326-5-7"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000395"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.21.20.6768-6781.2001"},{"key":"B34","doi-asserted-by":"crossref","first-page":"2297","DOI":"10.1681\/ASN.V10112297","volume":"10","author":"Schwartz JH","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1002\/bies.1045"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007101101"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0707659"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1016\/j.addr.2009.04.006"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000012567.95445.55"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.122062299"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00279.2013","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,3,8]],"date-time":"2022-03-08T18:17:16Z","timestamp":1646763436000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00279.2013"}},"issued":{"date-parts":[[2013,12,1]]},"references-count":40,"journal-issue":{"issue":"11","published-print":{"date-parts":[[2013,12,1]]}},"alternative-id":["10.1152\/ajprenal.00279.2013"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00279.2013","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2013,12,1]]}},{"indexed":{"date-parts":[[2025,11,8]],"date-time":"2025-11-08T22:35:39Z","timestamp":1762641339042},"reference-count":43,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2010,5]]},"abstract":"<jats:p> We examined the mechanisms that maintain stable renal tissue Po<jats:sub>2<\/jats:sub> during moderate renal ischemia, when changes in renal oxygen delivery (\u1e0ao<jats:sub>2<\/jats:sub>) and consumption (V\u0307o<jats:sub>2<\/jats:sub>) are mismatched. When renal artery pressure (RAP) was reduced progressively from 80 to 40 mmHg, V\u0307o<jats:sub>2<\/jats:sub> (\u221238 \u00b1 7%) was reduced more than \u1e0ao<jats:sub>2<\/jats:sub> (\u221226 \u00b1 4%). Electrical stimulation of the renal nerves (RNS) reduced \u1e0ao<jats:sub>2<\/jats:sub> (\u221249 \u00b1 4% at 2 Hz) more than V\u0307o<jats:sub>2<\/jats:sub> (\u221230 \u00b1 7% at 2 Hz). Renal arterial infusion of angiotensin II reduced \u1e0ao<jats:sub>2<\/jats:sub> (\u221238 \u00b1 3%) but not V\u0307o<jats:sub>2<\/jats:sub> (+10 \u00b1 10%). Despite mismatched changes in \u1e0ao<jats:sub>2<\/jats:sub> and V\u0307o<jats:sub>2<\/jats:sub>, renal tissue Po<jats:sub>2<\/jats:sub> remained remarkably stable at \u226540 mmHg RAP, during RNS at \u22642 Hz, and during angiotensin II infusion. The ratio of sodium reabsorption to V\u0307o<jats:sub>2<\/jats:sub> was reduced by all three ischemic stimuli. None of the stimuli significantly altered the gradients in Pco<jats:sub>2<\/jats:sub> or pH across the kidney. Fractional oxygen extraction increased and renal venous Po<jats:sub>2<\/jats:sub> fell during 2-Hz RNS and angiotensin II infusion, but not when RAP was reduced to 40 mmHg. Thus reduced renal V\u0307o<jats:sub>2<\/jats:sub> can help prevent tissue hypoxia during mild renal ischemia, but when renal V\u0307o<jats:sub>2<\/jats:sub> is reduced less than \u1e0ao<jats:sub>2<\/jats:sub>, other mechanisms prevent a fall in renal Po<jats:sub>2<\/jats:sub>. These mechanisms do not include increased efficiency of renal oxygen utilization for sodium reabsorption or reduced washout of carbon dioxide from the kidney, leading to increased oxygen extraction. However, increased oxygen extraction could be driven by altered countercurrent exchange of carbon dioxide and\/or oxygen between renal arteries and veins. <\/jats:p>","DOI":"10.1152\/ajprenal.00647.2009","type":"journal-article","created":{"date-parts":[[2010,3,4]],"date-time":"2010-03-04T01:51:05Z","timestamp":1267667465000},"page":"F1235-F1243","source":"Crossref","is-referenced-by-count":38,"title":["Multiple mechanisms act to maintain kidney oxygenation during renal ischemia in anesthetized rabbits"],"prefix":"10.1152","volume":"298","author":[{"given":"Roger G.","family":"Evans","sequence":"first","affiliation":[{"name":"Department of Physiology, Monash University,"}]},{"given":"Gabriela A.","family":"Eppel","sequence":"additional","affiliation":[{"name":"Department of Physiology, Monash University,"}]},{"given":"Sylvia","family":"Michaels","sequence":"additional","affiliation":[{"name":"Department of Physiology, Monash University,"}]},{"given":"Sandra L.","family":"Burke","sequence":"additional","affiliation":[{"name":"Baker IDI Heart and Diabetes Institute, Melbourne, Australia;"}]},{"given":"Mehdi","family":"Nematbakhsh","sequence":"additional","affiliation":[{"name":"Department of Physiology, Monash University,"},{"name":"Isfahan Kidney Research Center\/Applied Physiology Research Center, Department of Physiology, Isfahan University of Medical Sciences, Isfahan, Iran;"}]},{"given":"Geoffrey A.","family":"Head","sequence":"additional","affiliation":[{"name":"Baker IDI Heart and Diabetes Institute, Melbourne, Australia;"}]},{"given":"Joan F.","family":"Carroll","sequence":"additional","affiliation":[{"name":"University of North Texas Health Science Center, Fort Worth, Texas; and"}]},{"given":"Paul M.","family":"O'Connor","sequence":"additional","affiliation":[{"name":"Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1984.247.1.F61"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1988.255.2.F349"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1988.255.2.F361"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200401000-00010"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000079785.13922.F6"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1097\/00003246-199602000-00003"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2001.013280"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1999.277.1.R112"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.259.2.F357"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.2000.279.2.R629"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1007\/s00395-006-0621-4"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.ph.50.030188.003253"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1984.246.5.F592"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.2001.00927.x"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00061.2002"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200501000-00003"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90230.2008"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1982.242.1.F78"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00151.2002"},{"key":"B20","first-page":"211","volume-title":"Brenner and Rector's The Kidney","author":"Gullans SR","year":"1996","edition":"5"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1977.232.3.F215"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.108.786913"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1973.53.4.836"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.51.6.711"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1016\/0034-5687(89)90069-8"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1996.270.4.H1453"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1983.245.5.F545"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1961.tb02147.x"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00436.2006"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1159\/000114203"},{"key":"B31","doi-asserted-by":"crossref","first-page":"13","DOI":"10.1152\/ajplegacy.1960.199.1.13","volume":"199","author":"Levy MN","year":"1960","journal-title":"Am J Physiol"},{"key":"B32","doi-asserted-by":"crossref","first-page":"937","DOI":"10.1152\/ajplegacy.1959.196.4.937","volume":"196","author":"Levy MN","year":"1959","journal-title":"Am J Physiol"},{"key":"B33","doi-asserted-by":"crossref","first-page":"1111","DOI":"10.1152\/ajplegacy.1959.197.5.1111","volume":"197","author":"Levy MN","year":"1959","journal-title":"Am J Physiol"},{"key":"B34","doi-asserted-by":"crossref","first-page":"38","DOI":"10.1152\/ajplegacy.1938.122.1.38","volume":"122","author":"Levy SE","year":"1938","journal-title":"Am J Physiol"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1093\/cvr\/28.3.303"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1159\/000142938"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.2006.04475.x"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.2006.04391.x"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00275.2005"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.107.097832"},{"key":"B41","doi-asserted-by":"crossref","first-page":"576","DOI":"10.1152\/ajplegacy.1966.211.3.576","volume":"211","author":"Torelli G","year":"1966","journal-title":"Am J Physiol"},{"key":"B42","doi-asserted-by":"crossref","first-page":"336","DOI":"10.1152\/ajplegacy.1934.109.2.336","volume":"109","author":"Van Slyke DD","year":"1934","journal-title":"Am J Physiol"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.90677.2008"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00647.2009","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T00:06:56Z","timestamp":1567987616000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00647.2009"}},"issued":{"date-parts":[[2010,5]]},"references-count":43,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2010,5]]}},"alternative-id":["10.1152\/ajprenal.00647.2009"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00647.2009","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2010,5]]}},{"indexed":{"date-parts":[[2025,11,20]],"date-time":"2025-11-20T12:20:28Z","timestamp":1763641228370},"reference-count":52,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2008,7]]},"abstract":"<jats:p> We carried out a yeast two-hybrid screen to identify proteins that interact with large-conductance Ca<jats:sup>2+<\/jats:sup>-activated K<jats:sup>+<\/jats:sup> (BK<jats:sub>Ca<\/jats:sub>) channels encoded by the Slo1 gene. Nephrin, an essential adhesion and scaffolding molecule expressed in podocytes, emerged in this screen. The Slo1-nephrin interaction was confirmed by coimmunoprecipitation from the brain and kidney, from HEK-293T cells expressing both proteins, and by glutathione S-transferase pull-down assays. We detected nephrin binding to the Slo1<jats:sub>VEDEC<\/jats:sub> splice variant, which is typically retained in intracellular stores, and to the \u03b24-subunit. However, we did not detect significant binding of nephrin to the Slo1<jats:sub>QEERL<\/jats:sub> or Slo1<jats:sub>EMVYR<\/jats:sub> splice variants. Coexpression of nephrin with Slo1<jats:sub>VEDEC<\/jats:sub> increased expression of functional BK<jats:sub>Ca<\/jats:sub> channels on the surface of HEK-293T cells but did not affect steady-state surface expression of the other COOH-terminal Slo1 variants. Nephrin did not affect the kinetics or voltage dependence of channel activation in HEK-293T cells expressing Slo1. Stimulation of Slo1<jats:sub>VEDEC<\/jats:sub> surface expression in HEK-293T cells was also observed by coexpressing a small construct encoding only the distal COOH-terminal domains of nephrin that interact with Slo1. Reduction of endogenous nephrin expression by application of small interfering RNA to differentiated cells of an immortalized podocyte cell line markedly reduced the steady-state surface expression of Slo1 as assessed by electrophysiology and cell-surface biotinylation assays. Nephrin therefore plays a role in organizing the surface expression of ion channel proteins in podocytes and may play a role in outside-in signaling to allow podocytes to adapt to mechanical or neurohumoral stimuli originating in neighboring cells. <\/jats:p>","DOI":"10.1152\/ajprenal.00140.2008","type":"journal-article","created":{"date-parts":[[2008,5,15]],"date-time":"2008-05-15T00:58:23Z","timestamp":1210813103000},"page":"F235-F246","source":"Crossref","is-referenced-by-count":51,"title":["Nephrin binds to the COOH terminus of a large-conductance Ca<sup>2+<\/sup>-activated K<sup>+<\/sup> channel isoform and regulates its expression on the cell surface"],"prefix":"10.1152","volume":"295","author":[{"given":"Eun Young","family":"Kim","sequence":"first","affiliation":[]},{"given":"Kyoung-Jae","family":"Choi","sequence":"additional","affiliation":[]},{"given":"Stuart E.","family":"Dryer","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.275.9.6453"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1152\/jn.2000.84.6.2767"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1152\/jn.00796.2004"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.2337\/db06-0693"},{"key":"R5","unstructured":"Drenckhahn D, Franke RP. Ultrastructural organization of contractile and cytoskeletal proteins in glomerular podocytes of chicken, rat, and man. Lab Invest 59: 673\u2013682, 1988."},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2005.103143"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.00948-07"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2007.061116"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.C100452200"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.23.14.4917-4928.2003"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004080679"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.3109\/07853890108995962"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1038\/nature04662"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1016\/S1097-2765(00)80057-X"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1152\/jn.00009.2007"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuroscience.2007.03.038"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1124\/mol.107.038026"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1159\/000174083"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-005-2116-1"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)63354-8"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1086\/302182"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1152\/jn.2002.88.2.954"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1172\/JCI200318242"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000253095.44186.72"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.immunol.25.022106.141618"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1016\/j.febslet.2007.01.077"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006091010"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuroscience.2007.10.013"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000145046.24268.0D"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0506870102"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1007\/BF00240371"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1006\/excr.1997.3739"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1080\/07853890600978149"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1016\/j.molmed.2007.06.006"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00020.2002"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/10.1.1"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1038\/ng1592"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.60.2.423"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.14.7962"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)64829-8"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0402660101"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0401702101"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1172\/JCI200112849"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)63080-5"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1096\/fj.06-6152fje"},{"key":"R46","doi-asserted-by":"publisher","DOI":"10.1172\/JCI27414"},{"key":"R47","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.200509436"},{"key":"R48","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M208411200"},{"key":"R49","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.20-10-03563.2000"},{"key":"R50","doi-asserted-by":"publisher","DOI":"10.1126\/science.1106215"},{"key":"R51","doi-asserted-by":"publisher","DOI":"10.1159\/000101797"},{"key":"R52","doi-asserted-by":"publisher","DOI":"10.1124\/mol.107.039743"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00140.2008","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T22:53:54Z","timestamp":1567983234000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00140.2008"}},"issued":{"date-parts":[[2008,7]]},"references-count":52,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2008,7]]}},"alternative-id":["10.1152\/ajprenal.00140.2008"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00140.2008","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2008,7]]}},{"indexed":{"date-parts":[[2025,11,18]],"date-time":"2025-11-18T20:52:37Z","timestamp":1763499157386},"reference-count":41,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2002,10,1]]},"abstract":"<jats:p>ROMK channels are present in the cortical collecting ducts of kidney and are responsible for K<jats:sup>+<\/jats:sup>secretion in this nephron segment. Recent studies suggest that endocytosis of ROMK channels is important for regulation of K<jats:sup>+<\/jats:sup>secretion in cortical collecting ducts. We investigated the molecular mechanisms for endocytosis of ROMK channels expressed in Xenopus laevis oocytes and cultured Madin-Darby canine kidney cells. When plasma membrane insertion of newly synthesized channel proteins was blocked by incubation with brefeldin A, ROMK currents decreased with a half-time of \u223c6 h. Coexpression with the Lys44\u2192Ala dominant-negative mutant dynamin, but not wild-type dynamin, reduced the rate of reduction of ROMK in the presence of brefeldin A. Mutation of Asn371 to Ile in the putative NPXY internalization motif of ROMK1 abolished the effect of the Lys44\u2192Ala dynamin mutant on endocytosis of the channel. Coimmunoprecipitation study and confocal fluorescent imaging revealed that ROMK channels associated with clathrin coat proteins in Madin-Darby canine kidney cells. These results provide compelling evidence for endocytosis of ROMK channels via clathrin-coated vesicles.<\/jats:p>","DOI":"10.1152\/ajprenal.00378.2001","type":"journal-article","created":{"date-parts":[[2013,8,19]],"date-time":"2013-08-19T19:58:09Z","timestamp":1376942289000},"page":"F630-F639","source":"Crossref","is-referenced-by-count":60,"title":["Evidence for endocytosis of ROMK potassium channel via clathrin-coated vesicles"],"prefix":"10.1152","volume":"283","author":[{"given":"Wei-Zhong","family":"Zeng","sequence":"first","affiliation":[{"name":"Departments of Medicine and"}]},{"given":"Victor","family":"Babich","sequence":"additional","affiliation":[{"name":"Departments of Medicine and"}]},{"given":"Bernardo","family":"Ortega","sequence":"additional","affiliation":[{"name":"Department of Biomedical Science, University of Sheffield, Sheffield S102TN, United Kingdom; and"}]},{"given":"Raymond","family":"Quigley","sequence":"additional","affiliation":[{"name":"Pediatrics, University of Texas Southwestern Medical Center, Dallas, Texas 75390-8856;"}]},{"given":"Stanley J.","family":"White","sequence":"additional","affiliation":[{"name":"Department of Biomedical Science, University of Sheffield, Sheffield S102TN, United Kingdom; and"}]},{"given":"Paul A.","family":"Welling","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland 21201"}]},{"given":"Chou-Long","family":"Huang","sequence":"additional","affiliation":[{"name":"Departments of Medicine and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.143.7.1871"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.6.3791"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1038\/378623a0"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.268.6.F1132"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajplung.1999.276.4.L659"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1999.1016"},{"key":"B7","doi-asserted-by":"crossref","first-page":"3116","DOI":"10.1016\/S0021-9258(19)39742-X","volume":"265","author":"Chen WJ","year":"1990","journal-title":"J Biol Chem"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.127.4.915"},{"key":"B9","doi-asserted-by":"crossref","first-page":"29363","DOI":"10.1016\/S0021-9258(18)43884-7","volume":"269","author":"Dascher C","year":"1994","journal-title":"J Biol Chem"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.3.F525"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.382"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.383"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.141.1.85"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.122.3.565"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1038\/362031a0"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1038\/35882"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/0955-0674(95)80015-8"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/S0955-0674(98)80065-3"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.275.14.10182"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.10.5820"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.7.12.2007"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.273.5.F718"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.cellbio.12.1.575"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1997.77.3.759"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1006\/dbio.1995.1209"},{"key":"B27","doi-asserted-by":"crossref","first-page":"303","DOI":"10.1038\/36882","volume":"390","author":"Naren AP","year":"1997","journal-title":"Nature"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.2000.00005.x"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.104.4.693"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.5.F805"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1999.277.1.C174"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.10.11.3891"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)81128-9"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1016\/0955-0674(94)90074-4"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1126\/science.279.5351.696"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.30.20812"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.biochem.66.1.511"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.41.25537"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1038\/375645a0"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M000783200"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(91)90533-5"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1994.266.3.C809"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00378.2001","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,3,4]],"date-time":"2022-03-04T03:44:59Z","timestamp":1646365499000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00378.2001"}},"issued":{"date-parts":[[2002,10,1]]},"references-count":41,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2002,10,1]]}},"alternative-id":["10.1152\/ajprenal.00378.2001"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00378.2001","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2002,10,1]]}},{"indexed":{"date-parts":[[2025,11,18]],"date-time":"2025-11-18T20:51:17Z","timestamp":1763499077885},"reference-count":29,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2012,8,1]]},"abstract":"<jats:p> Ectonucleoside triphosphate diphosphohydrolase-1 hydrolyzes extracellular ATP and ADP to AMP. Previously, we showed that CD39 is expressed at several sites within the kidney and thus may impact the availability of type 2 purinergic receptor (P2-R) ligands. Because P2-Rs appear to regulate urinary concentrating ability, we have evaluated renal water handling in transgenic mice (TG) globally overexpressing hCD39. Under basal conditions, TG mice exhibited significantly impaired urinary concentration and decreased protein abundance of AQP2 in the kidney compared with wild-type (WT) mice. Urinary excretion of total nitrates\/nitrites was significantly higher in TG mice, but the excretion of AVP or PGE<jats:sub>2<\/jats:sub> was equivalent to control WT mice. There were no significant differences in electrolyte-free water clearance or fractional excretion of sodium. Under stable hydrated conditions (gelled diet feeding), the differences between the WT and TG mice were negated, but the decrease in urine osmolality persisted. When water deprived, TG mice failed to adequately concentrate urine and exhibited impaired AVP responses. However, the increases in urinary osmolalities in response to subacute dDAVP or chronic AVP treatment were similar in TG and WT mice. These observations suggest that TG mice have impaired urinary concentrating ability despite normal AVP levels. We also note impaired AVP release in response to water deprivation but that TG kidneys are responsive to exogenous dDAVP or AVP. We infer that heightened nucleotide scavenging by increased levels of CD39 altered the release of endogenous AVP in response to dehydration. We propose that ectonucleotidases and modulated purinergic signaling impact urinary concentration and indicate potential utility of targeted therapy for the treatment of water balance disorders. <\/jats:p>","DOI":"10.1152\/ajprenal.00060.2012","type":"journal-article","created":{"date-parts":[[2012,5,24]],"date-time":"2012-05-24T03:17:24Z","timestamp":1337829444000},"page":"F420-F430","source":"Crossref","is-referenced-by-count":10,"title":["Defective renal water handling in transgenic mice over-expressing human CD39\/NTPDase1"],"prefix":"10.1152","volume":"303","author":[{"given":"Yue","family":"Zhang","sequence":"first","affiliation":[{"name":"Nephrology Research, Department of Veterans Administration Salt Lake City Health Care System, Salt Lake City, Utah;"},{"name":"Department of Medicine, University of Utah Health Sciences Center, Salt Lake City, Utah;"}]},{"given":"Kaiya L.","family":"Morris","sequence":"additional","affiliation":[{"name":"Nephrology Research, Department of Veterans Administration Salt Lake City Health Care System, Salt Lake City, Utah;"},{"name":"Department of Medicine, University of Utah Health Sciences Center, Salt Lake City, Utah;"}]},{"given":"Shannon K.","family":"Sparrow","sequence":"additional","affiliation":[{"name":"Nephrology Research, Department of Veterans Administration Salt Lake City Health Care System, Salt Lake City, Utah;"},{"name":"Department of Medicine, University of Utah Health Sciences Center, Salt Lake City, Utah;"}]},{"given":"Karen M.","family":"Dwyer","sequence":"additional","affiliation":[{"name":"Immunology Research Centre, Department of Medicine, University of Melbourne, St. Vincent's Hospital, Fitzroy, Victoria, Australia"}]},{"given":"Keiichi","family":"Enjyoji","sequence":"additional","affiliation":[{"name":"Transplant Institute and Gastroenterology Division, Beth Israel Deaconess Medical Center\/Harvard Medical School, Harvard University, Boston, Massachusetts; and"}]},{"given":"Simon C.","family":"Robson","sequence":"additional","affiliation":[{"name":"Transplant Institute and Gastroenterology Division, Beth Israel Deaconess Medical Center\/Harvard Medical School, Harvard University, Boston, Massachusetts; and"}]},{"given":"Bellamkonda K.","family":"Kishore","sequence":"additional","affiliation":[{"name":"Nephrology Research, Department of Veterans Administration Salt Lake City Health Care System, Salt Lake City, Utah;"},{"name":"Department of Medicine, University of Utah Health Sciences Center, Salt Lake City, Utah;"},{"name":"Department of Physiology, University of Utah Health Sciences Center, Salt Lake City, Utah;"},{"name":"Center on Aging, University of Utah Health Sciences Center, Salt Lake City, Utah;"}]}],"member":"24","reference":[{"key":"B1","first-page":"16","volume-title":"Renal and Electrolyte Disorders","author":"Berl T","year":"2010"},{"key":"B1a","doi-asserted-by":"publisher","DOI":"10.1152\/ajplung.00298.2005"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-6143.2010.03257.x"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/B978-0-12-385526-8.00010-2"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1172\/JCI19560"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00053.2006"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000251306.40546.08"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.3346\/jkms.2006.21.1.1"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00108.2004"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1007\/s11302-009-9151-5"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/B978-0-12-385526-8.00009-6"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-2952(03)00158-8"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/B978-0-12-385526-8.00008-4"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1146\/annurev-physiol-021909-135825"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.109.143404"},{"key":"B16","volume-title":"Extracellular Nucleotides and Nucleosides: Release, Receptors and Physiological and Pathophysiological Effects. Current Topics in Membranes (Vol. 54)","author":"Schwiebert EM","year":"2003"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.6.F945"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2826.2011.02268.x"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00163.2009"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00495.2006"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00432.2007"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007040443"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1007\/s11302-009-9150-6"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbamcr.2008.01.024"},{"key":"B25","doi-asserted-by":"crossref","first-page":"598a","DOI":"10.1681\/ASN.2009050552","volume":"21","author":"Zhang Y","year":"2010","journal-title":"J Am Soc Nephrol"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00549.2010"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00382.2009"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90774.2008"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90311.2008"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00060.2012","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T00:29:38Z","timestamp":1567988978000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00060.2012"}},"issued":{"date-parts":[[2012,8,1]]},"references-count":29,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2012,8,1]]}},"alternative-id":["10.1152\/ajprenal.00060.2012"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00060.2012","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2012,8,1]]}},{"indexed":{"date-parts":[[2025,11,19]],"date-time":"2025-11-19T06:59:42Z","timestamp":1763535582174,"version":"3.37.3"},"reference-count":44,"publisher":"American Physiological Society","issue":"3","funder":[{"DOI":"10.13039\/501100001353","name":"National Kidney Foundation (NKF)","doi-asserted-by":"publisher","award":["NKF-Mini"],"award-info":[{"award-number":["NKF-Mini"]}],"id":[{"id":"10.13039\/501100001353","id-type":"DOI","asserted-by":"publisher"}]},{"name":"US-NIH","award":["R56DK116828"],"award-info":[{"award-number":["R56DK116828"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2019,3,1]]},"abstract":"<jats:p> G protein-coupled receptors (GPCRs) in the kidney regulate the reabsorption of essential nutrients, ions, and water from the glomerular filtrate. Abnormalities in renal epithelial ion transport play important roles in the pathogenesis of essential hypertension. The orphan G protein-coupled receptor 37L1 (GPR37L1), also known as endothelin receptor type B-like protein (ETBR-LP2), is expressed in several regions in the brain, but its expression profile and function in peripheral tissues are poorly understood. We found that GPR37L1 mRNA expression is highest in the brain, followed by the stomach, heart, testis, and ovary, with moderate expression in the kidney, pancreas, skeletal muscle, liver, lung, and spleen. Immunofluorescence analyses revealed the expression of GPR37L1 in specific regions within some organs. In the kidney, GPR37L1 is expressed in the apical membrane of renal proximal tubule cells. In human renal proximal tubule cells, the transient expression of GPR37LI increased intracellular sodium, whereas the silencing of GPR37LI decreased intracellular sodium. Inhibition of Na<jats:sup>+<\/jats:sup>\/H<jats:sup>+<\/jats:sup> exchanger isoform 3 (NHE3) activity abrogated the GPR37L1-mediated increase in intracellular sodium. Renal-selective silencing of Gpr37l1 in mice increased urine output and sodium excretion and decreased systolic and diastolic blood pressures. The renal-selective silencing of GPR37L1 decreased the protein expression of NHE3 but not the expression of Na<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-ATPase or sodium-glucose cotransporter 2. Our findings show that in the kidney, GPR37L1 participates in renal proximal tubule luminal sodium transport and regulation of blood pressure by increasing the renal expression and function of NHE3 by decreasing cAMP production. The role of GPR37L1, expressed in specific cell types in organs other than the kidney, remains to be determined. <\/jats:p>","DOI":"10.1152\/ajprenal.00289.2018","type":"journal-article","created":{"date-parts":[[2018,12,19]],"date-time":"2018-12-19T11:21:57Z","timestamp":1545218517000},"page":"F506-F516","source":"Crossref","is-referenced-by-count":18,"title":["G protein-coupled receptor 37L1 regulates renal sodium transport and blood pressure"],"prefix":"10.1152","volume":"316","author":[{"given":"Xiaoxu","family":"Zheng","sequence":"first","affiliation":[{"name":"Department of Medicine, The George Washington University, Washington, District of Columbia"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4144-1887","authenticated-orcid":false,"given":"Laureano D.","family":"Asico","sequence":"additional","affiliation":[{"name":"Department of Medicine, The George Washington University, Washington, District of Columbia"}]},{"given":"Xiaobo","family":"Ma","sequence":"additional","affiliation":[{"name":"Department of Medicine, The George Washington University, Washington, District of Columbia"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5359-4848","authenticated-orcid":false,"given":"Prasad R.","family":"Konkalmatt","sequence":"additional","affiliation":[{"name":"Department of Medicine, The George Washington University, Washington, District of Columbia"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1097\/01.mnh.0000174146.52915.5d"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-008-0595-1"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1126\/scisignal.aad1089"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.111.185744"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.108.117366"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00119.2014"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1124\/mol.63.6.1256"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-62703-125-7_20"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1007\/BF00270578"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1002\/cphy.c110058"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1155\/2010\/238080"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1007\/s00441-009-0859-x"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M200835200"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0707516"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00060.2009"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1172\/jci.insight.85888"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.00902"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.45.28672"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1038\/nrd2518"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00017.2003"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1126\/science.1109237"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/S0169-328X(99)00092-3"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1002\/glia.23480"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1006\/meth.2001.1262"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1219004110"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2010.01.076"},{"key":"B27","first-page":"156","volume-title":"Brenner and Rector\u2019s The Kidney","author":"Mount DB","year":"2007","edition":"8"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1111\/bph.13509"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1038\/nchembio.2266"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1038\/sj.gt.3301279"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0111053"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2008.08.040"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1016\/S0166-6851(01)00411-X"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.e08-01-0019"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000112421.18551.1e"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.3389\/fphar.2015.00275"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1177\/1087057113475480"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1016\/S0378-4347(00)00628-9"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-5793(98)00170-7"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0230374100"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M112.428458"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1997.6408"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0038745"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.67.031103.153004"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00289.2018","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,24]],"date-time":"2019-09-24T04:41:10Z","timestamp":1569300070000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00289.2018"}},"issued":{"date-parts":[[2019,3,1]]},"references-count":44,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2019,3,1]]}},"alternative-id":["10.1152\/ajprenal.00289.2018"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00289.2018","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2019,3,1]]}},{"indexed":{"date-parts":[[2025,12,11]],"date-time":"2025-12-11T20:42:40Z","timestamp":1765485760963},"reference-count":51,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2014,3,15]]},"abstract":"<jats:p> Blood oxygen level-dependent (BOLD) MRI data of kidney, while indicative of tissue oxygenation level (Po<jats:sub>2<\/jats:sub>), is in fact influenced by multiple confounding factors, such as R<jats:sub>2<\/jats:sub>, perfusion, oxygen permeability, and hematocrit. We aim to explore the feasibility of extracting tissue Po<jats:sub>2<\/jats:sub> from renal BOLD data. A method of two steps was proposed: first, a Monte Carlo simulation to estimate blood oxygen saturation (SHb) from BOLD signals, and second, an oxygen transit model to convert SHb to tissue Po<jats:sub>2<\/jats:sub>. The proposed method was calibrated and validated with 20 pigs (12 before and after furosemide injection) in which BOLD-derived tissue Po<jats:sub>2<\/jats:sub> was compared with microprobe-measured values. The method was then applied to nine healthy human subjects (age: 25.7 \u00b1 3.0 yr) in whom BOLD was performed before and after furosemide. For the 12 pigs before furosemide injection, the proposed model estimated renal tissue Po<jats:sub>2<\/jats:sub> with errors of 2.3 \u00b1 5.2 mmHg (5.8 \u00b1 13.4%) in cortex and \u22120.1 \u00b1 4.5 mmHg (1.7 \u00b1 18.1%) in medulla, compared with microprobe measurements. After injection of furosemide, the estimation errors were 6.9 \u00b1 3.9 mmHg (14.2 \u00b1 8.4%) for cortex and 2.6 \u00b1 4.0 mmHg (7.7 \u00b1 11.5%) for medulla. In the human subjects, BOLD-derived medullary Po<jats:sub>2<\/jats:sub> increased from 16.0 \u00b1 4.9 mmHg (SHb: 31 \u00b1 11%) at baseline to 26.2 \u00b1 3.1 mmHg (SHb: 53 \u00b1 6%) at 5 min after furosemide injection, while cortical Po<jats:sub>2<\/jats:sub> did not change significantly at \u223c58 mmHg (SHb: 92 \u00b1 1%). Our proposed method, validated with a porcine model, appears promising for estimating tissue Po<jats:sub>2<\/jats:sub> from renal BOLD MRI data in human subjects. <\/jats:p>","DOI":"10.1152\/ajprenal.00575.2013","type":"journal-article","created":{"date-parts":[[2014,1,23]],"date-time":"2014-01-23T03:29:26Z","timestamp":1390447766000},"page":"F579-F587","source":"Crossref","is-referenced-by-count":52,"title":["Measurement of renal tissue oxygenation with blood oxygen level-dependent MRI and oxygen transit modeling"],"prefix":"10.1152","volume":"306","author":[{"given":"Jeff L.","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Radiology, University of Utah, Salt Lake City, Utah;"}]},{"given":"Glen","family":"Morrell","sequence":"additional","affiliation":[{"name":"Department of Radiology, University of Utah, Salt Lake City, Utah;"}]},{"given":"Henry","family":"Rusinek","sequence":"additional","affiliation":[{"name":"Department of Radiology, New York University, New York, New York;"}]},{"given":"Lizette","family":"Warner","sequence":"additional","affiliation":[{"name":"Philips Healthcare, Cleveland, Ohio;"}]},{"given":"Pierre-Hugues","family":"Vivier","sequence":"additional","affiliation":[{"name":"Department of Radiology, Rouen University Hospital, Rouen, France;"}]},{"given":"Alfred K.","family":"Cheung","sequence":"additional","affiliation":[{"name":"Division of Nephrology, University of Utah, Salt Lake City, Utah; and"}]},{"given":"Lilach O.","family":"Lerman","sequence":"additional","affiliation":[{"name":"Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota"}]},{"given":"Vivian S.","family":"Lee","sequence":"additional","affiliation":[{"name":"Department of Radiology, University of Utah, Salt Lake City, Utah;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1002\/jmri.22552"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuroimage.2009.08.010"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1093\/jac\/6.3.381"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1055\/s-2007-993100"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1002\/mrm.1910340103"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.267.6.F1063"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199503093321006"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1148\/radiol.11110518"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1002\/mrm.1910130207"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1148\/radiol.2432060655"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00222.2006"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.57.s75.12.x"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.350"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfn064"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1002\/mrm.21108"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000418"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1522-2594(199903)41:3<499::AID-MRM12>3.0.CO;2-O"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1109\/TBME.2002.807657"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuroimage.2005.09.032"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1007\/BF01955753"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1919.sp001839"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/jcbfm.1987.88"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00347.2006"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/advan.00012.2007"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1002\/jmri.20176"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1007\/s004240050455"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1002\/mrm.21512"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.87.24.9868"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-3495(93)81441-3"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1984.247.2.F303"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1159\/000090610"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.94.12.3271"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1016\/S0008-6363(96)00065-X"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.3109\/08860229209106636"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-4615-5865-1_23"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1097\/RLI.0b013e31815597c5"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1002\/mrm.1072"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1097\/00004647-199812000-00012"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007040420"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1148\/radiol.2473070877"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1002\/jmri.1880070113"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1148\/radiol.10091735"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1002\/jmri.22501"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1097\/RLI.0b013e3181f0213f"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1002\/mrm.1910320610"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejrad.2011.03.045"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1002\/mrm.21489"},{"key":"B48","volume-title":"ISMRM","author":"Zhang JL","year":"2012"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1148\/radiol.09090891"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00074.2002"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1985.249.6.F898"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00575.2013","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T00:05:11Z","timestamp":1567987511000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00575.2013"}},"issued":{"date-parts":[[2014,3,15]]},"references-count":51,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2014,3,15]]}},"alternative-id":["10.1152\/ajprenal.00575.2013"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00575.2013","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2014,3,15]]}},{"indexed":{"date-parts":[[2025,12,11]],"date-time":"2025-12-11T20:37:49Z","timestamp":1765485469242},"reference-count":85,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2010,7]]},"abstract":"<jats:p>The fine regulation of Na<jats:sup>+<\/jats:sup>and K<jats:sup>+<\/jats:sup>transport takes place in the cortical distal nephron. It is well established that K<jats:sup>+<\/jats:sup>secretion occurs through apical K<jats:sup>+<\/jats:sup>channels: the ROMK and the Ca<jats:sup>2+<\/jats:sup>- and voltage-dependent maxi-K. Previously, we identified the voltage-gated Kv1.3 channel in the inner medulla of the rat kidney (Escobar LI, Mart\u00ednez-T\u00e9llez JC, Salas M, Castilla SA, Carrisoza R, Tapia D, V\u00e1zquez M, Bargas J, Bol\u00edvar JJ. Am J Physiol Cell Physiol 286: C965\u2013C974, 2004). To examine the role of Kv1.3 in the renal regulation of K<jats:sup>+<\/jats:sup>homeostasis, we characterized the effect of dietary K<jats:sup>+<\/jats:sup>on the molecular and functional expression of this channel. We performed real-time-PCR and immunoblot assays in kidneys from rats fed a control (CK; 1.2% wt\/wt) or high-K<jats:sup>+<\/jats:sup>(HK; 10% wt\/wt) diet for 5\u201315 days. Kv1.3 mRNA and protein expression did not change with HK in the whole kidney. However, dietary K<jats:sup>+<\/jats:sup>loading provoked a change in the cellular distribution of Kv1.3 from the cytoplasm to apical membranes. Immunolocalization of Kv1.3 detected the channel exclusively in the intercalated cells. We investigated whether Kv1.3 mediated K<jats:sup>+<\/jats:sup>transport in microperfused cortical collecting ducts (CCDs). The HK diet led to an increase in net K<jats:sup>+<\/jats:sup>transport from 7.4 \u00b1 1.1 (CK) to 11.4 \u00b1 1.0 (HK) pmol\u00b7min<jats:sup>\u22121\u00b7<\/jats:sup>mm<jats:sup>\u22121<\/jats:sup>. Luminal margatoxin, a specific blocker of Kv1.3, decreased net K<jats:sup>+<\/jats:sup>secretion in HK CCDs to 6.0 \u00b1 1.6 pmol\u00b7min<jats:sup>\u22121\u00b7<\/jats:sup>mm<jats:sup>\u22121<\/jats:sup>. Our data provide the first evidence that Kv1.3 channels participate in K<jats:sup>+<\/jats:sup>secretion and that apical membrane localization of Kv1.3 is enhanced in the intercalated cells by dietary K<jats:sup>+<\/jats:sup>loading.<\/jats:p>","DOI":"10.1152\/ajprenal.00697.2009","type":"journal-article","created":{"date-parts":[[2010,4,29]],"date-time":"2010-04-29T02:14:22Z","timestamp":1272507262000},"page":"F255-F264","source":"Crossref","is-referenced-by-count":19,"title":["Potassium secretion by voltage-gated potassium channel Kv1.3 in the rat kidney"],"prefix":"10.1152","volume":"299","author":[{"given":"Rolando","family":"Carrisoza-Gayt\u00e1n","sequence":"first","affiliation":[{"name":"Departamento de Fisiolog\u00eda, Facultad de Medicina, Universidad Nacional Aut\u00f3noma de M\u00e9xico, Mexico City;"}]},{"given":"Carolina","family":"Salvador","sequence":"additional","affiliation":[{"name":"Departamento de Fisiolog\u00eda, Facultad de Medicina, Universidad Nacional Aut\u00f3noma de M\u00e9xico, Mexico City;"}]},{"given":"Lisa M.","family":"Satlin","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Mount Sinai School of Medicine, New York, New York; and"}]},{"given":"Wen","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Mount Sinai School of Medicine, New York, New York; and"}]},{"given":"Beth","family":"Zavilowitz","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Mount Sinai School of Medicine, New York, New York; and"}]},{"given":"Norma A.","family":"Bobadilla","sequence":"additional","affiliation":[{"name":"Unidad de Fisiolog\u00eda Molecular, Instituto de Investigaciones Biom\u00e9dicas, Universidad Nacional Aut\u00f3noma de M\u00e9xico e Instituto Nacional de Ciencias M\u00e9dicas y Nutrici\u00f3n, Mexico City, M\u00e9xico"}]},{"given":"Joyce","family":"Trujillo","sequence":"additional","affiliation":[{"name":"Unidad de Fisiolog\u00eda Molecular, Instituto de Investigaciones Biom\u00e9dicas, Universidad Nacional Aut\u00f3noma de M\u00e9xico e Instituto Nacional de Ciencias M\u00e9dicas y Nutrici\u00f3n, Mexico City, M\u00e9xico"}]},{"given":"Laura I.","family":"Escobar","sequence":"additional","affiliation":[{"name":"Departamento de Fisiolog\u00eda, Facultad de Medicina, Universidad Nacional Aut\u00f3noma de M\u00e9xico, Mexico City;"}]}],"member":"24","reference":[{"key":"B1","first-page":"455","volume-title":"The Kidney","author":"Alpern RJ","year":"2000"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00800.x"},{"key":"B3","first-page":"281","volume":"2","author":"Arkett SA","year":"1994","journal-title":"3 Receptors Channels"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000388"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1988.47"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1007\/s00418-009-0658-1"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/j.tips.2004.03.010"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1007\/s002329900189"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.90.21.10036"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.253.5.F896"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00074.2003"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00002.2008"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.18-16-06126.1998"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/jn.2000.83.4.2332"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.252.3.F458"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.3.F525"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-002-0873-2"},{"key":"B18","doi-asserted-by":"crossref","first-page":"18866","DOI":"10.1016\/S0021-9258(17)46707-X","volume":"268","author":"Garcia-Calvo M","year":"1993","journal-title":"J Biol Chem"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.5.F817"},{"key":"B20","doi-asserted-by":"crossref","first-page":"2533","DOI":"10.1681\/ASN.V7122533","volume":"7","author":"Ginns SM","year":"1996","journal-title":"J Am Soc Nephrol"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1172\/JCI106399"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00018.2007"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00191.2009"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-3495(03)74585-8"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1016\/B978-012088488-9.50057-7"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00051.2003"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.10430"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000120368.59693.A8"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1093\/molehr\/6.4.303"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1982.243.3.F211"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00037.2002"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.5.2639"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0609555104"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1979.79"},{"key":"B35","first-page":"127A","volume":"20","author":"Liu W","year":"2009","journal-title":"J Am Soc Nephrol"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1006\/meth.2001.1262"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M205627200"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M206644200"},{"key":"B39","first-page":"1301","volume-title":"The Kidney: Physiology and Pathophysiology","author":"Malnic G","year":"2008"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00083.2002"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.2001.81.1.85"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00057.2005"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/physiolgenomics.00160.2007"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.261.4.F696"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.104.4.693"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.273.3.F404"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.5.F805"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00970.x"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00191.2006"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1016\/j.imlet.2003.11.020"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00340.2004"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1111\/j.1460-9568.2005.04384.x"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.071516798"},{"key":"B54","doi-asserted-by":"crossref","first-page":"913","DOI":"10.1681\/ASN.V105913","volume":"10","author":"Sabolic I","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1007\/s00018-008-8393-7"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.266.1.F57"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.270.3.F391"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.ph.55.030193.001411"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1038\/ng1096-152"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.056689"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1982.243.5.F487"},{"key":"B62","first-page":"202","volume":"13","author":"Stokes JB","year":"1993","journal-title":"Semin Nephrol"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1002\/j.1460-2075.1989.tb08483.x"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0804236105"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.268.3.F490"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00458.2005"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M708223200"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.5.F913"},{"key":"B69","doi-asserted-by":"crossref","first-page":"827","DOI":"10.1681\/ASN.V134827","volume":"13","author":"Wall SM","year":"2002","journal-title":"J Am Soc Nephrol"},{"key":"B70","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00309.2005"},{"key":"B71","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.259.3.F494"},{"key":"B72","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.1.F165"},{"key":"B73","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.66.032102.112025"},{"key":"B74","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00093.2005"},{"key":"B75","doi-asserted-by":"publisher","DOI":"10.1016\/B978-012088488-9.50047-4"},{"key":"B76","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-008-0593-3"},{"key":"B77","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-001-0737-1"},{"key":"B78","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.281.2.F206"},{"key":"B79","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.5.F786"},{"key":"B80","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00191.2003"},{"key":"B81","doi-asserted-by":"crossref","first-page":"437","DOI":"10.1152\/ajplegacy.1971.221.2.437","volume":"221","author":"Wright FS","year":"1971","journal-title":"Am J Physiol"},{"key":"B82","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/ddg049"},{"key":"B83","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0308450100"},{"key":"B84","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118700"},{"key":"B85","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M212301200"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00697.2009","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,10,26]],"date-time":"2021-10-26T21:13:17Z","timestamp":1635282797000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00697.2009"}},"issued":{"date-parts":[[2010,7]]},"references-count":85,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2010,7]]}},"alternative-id":["10.1152\/ajprenal.00697.2009"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00697.2009","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2010,7]]}},{"indexed":{"date-parts":[[2025,12,11]],"date-time":"2025-12-11T20:28:51Z","timestamp":1765484931688},"reference-count":42,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2006,5]]},"abstract":"<jats:p>The renal-specific Na<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-2Cl<jats:sup>\u2212<\/jats:sup>cotransporter NKCC2 belongs to the SLC12 gene family; it is the target for loop diuretics and the cause of type I Bartter's syndrome. Because the NKCC2 sequence contains two putative N-linked glycosylation sites, one of which is conserved with the renal Na<jats:sup>+<\/jats:sup>-Cl<jats:sup>\u2212<\/jats:sup>cotransporter in which glycosylation affects thiazide affinity, we assessed the role of glycosylation on NKCC2 functional properties. One (N442Q or N452Q) or both (N442,452Q) N-glycosylation sites were eliminated by site-directed mutagenesis. Wild-type NKCC2 and mutant clones were expressed in Xenopus laevis oocytes and analyzed by<jats:sup>86<\/jats:sup>Rb<jats:sup>+<\/jats:sup>influx, Western blotting, and confocal microscopy. Inhibition of glycosylation with tunicamycin in wild-type NKCC2-injected oocytes resulted in an 80% reduction of NKCC2 activity. Immunoblot of injected oocytes revealed that glycosylation of NKCC2 was completely prevented in N442,452Q-injected oocytes. Functional activity was reduced by 50% in N442Q- and N452Q-injected oocytes and by 80% in oocytes injected with N442,452Q, whereas confocal microscopy of oocytes injected with wild-type or mutant enhanced green fluorescent protein-tagged NKCC2 clones revealed that surface fluorescence intensity was reduced \u223c20% in single mutants and 50% in the double mutant. Ion transport kinetic analyses revealed no changes in cation affinity and a small increase in Cl<jats:sup>\u2212<\/jats:sup>affinity by N442Q and N442,452Q. However, a slight decrease in bumetanide affinity was observed. Our data demonstrate that NKCC2 is glycosylated and suggest that prevention of glycosylation reduces its functional expression by affecting insertion into the plasma membrane and the intrinsic activity of the cotransporter.<\/jats:p>","DOI":"10.1152\/ajprenal.00071.2005","type":"journal-article","created":{"date-parts":[[2005,11,16]],"date-time":"2005-11-16T02:58:48Z","timestamp":1132109928000},"page":"F1094-F1102","source":"Crossref","is-referenced-by-count":60,"title":["Activity of the renal Na<sup>+<\/sup>-K<sup>+<\/sup>-2Cl<sup>\u2212<\/sup>cotransporter is reduced by mutagenesis of<i>N<\/i>-glycosylation sites: role for protein surface charge in Cl<sup>\u2212<\/sup>transport"],"prefix":"10.1152","volume":"290","author":[{"given":"Anah\u00ed","family":"Paredes","sequence":"first","affiliation":[]},{"given":"Consuelo","family":"Plata","sequence":"additional","affiliation":[]},{"given":"Manuel","family":"Rivera","sequence":"additional","affiliation":[]},{"given":"Erika","family":"Moreno","sequence":"additional","affiliation":[]},{"given":"Norma","family":"V\u00e1zquez","sequence":"additional","affiliation":[]},{"given":"Rosario","family":"Mu\u00f1oz-Clares","sequence":"additional","affiliation":[]},{"given":"Steven C.","family":"Hebert","sequence":"additional","affiliation":[]},{"given":"Gerardo","family":"Gamba","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00110.x"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(93)80129-I"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1006\/exnr.1996.0019"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1021\/bi048741q"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1002\/jmor.1051360203"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.3.F619"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.bi.56.070187.002433"},{"key":"R8","unstructured":"Gagnon E, Bergeron MJ, Brunet GM, Daigle ND, Simard CF, and Isenring P.Molecular mechanisms of Cl transport by the renal Na-K-Cl cotransporter: identification of an intracellular locus that may form part of a high affinity Cl-binding site.J Biol Chem279: 5648\u20135654, 2003."},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00107.2002"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00712.x"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200009000-00013"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00011.2004"},{"key":"R13","doi-asserted-by":"crossref","unstructured":"Gamba G, Miyanoshita A, Lombardi M, Lytton J, Lee WS, Hediger MA, and Hebert SC.Molecular cloning, primary structure and characterization of two members of the mammalian electroneutral sodium-(potassium)-chloride cotransporter family expressed in kidney.J Biol Chem269: 17713\u201317722, 1994.","DOI":"10.1016\/S0021-9258(17)32499-7"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.90.7.2749"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M007751200"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.C200021200"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1983.245.3.C235"},{"key":"R18","doi-asserted-by":"crossref","unstructured":"Hayes G, Busch A, Lotscher M, Waldegger S, Lang F, Verrey F, Biber J, and Murer H.Role ofN-linked glycosylation in rat renal Na\/Pi-cotransport.J Biol Chem269: 24143\u201324149, 1994.","DOI":"10.1016\/S0021-9258(19)51060-2"},{"key":"R19","doi-asserted-by":"crossref","unstructured":"Hebert SC.Nephron heterogeneity. In:Handbook of Physiology. Renal Physiology. Bethesda, MD: Am. Physiol. Soc. 1992, sect. 8, vol.I, chapt. 20, p. 875\u2013925.","DOI":"10.1002\/cphy.cp080120"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000043903.93452.D0"},{"key":"R21","doi-asserted-by":"crossref","unstructured":"Igarashi P, Vanden Heuver GB, Payne JA, and Forbush B III.Cloning, embryonic expression, and alternative splicing of a murine kidney-specific Na-K-Cl cotransporter.Am J Physiol Renal Fluid Electrolyte Physiol269: F406\u2013F418, 1995.","DOI":"10.1152\/ajprenal.1995.269.3.F405"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1016\/S1095-6433(01)00420-2"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.6"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.1.F96"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1042\/bj3020253"},{"key":"R26","doi-asserted-by":"crossref","unstructured":"Li Hand Pajor AM.Mutagenesis of theN-glycosylation site of hNaSi-1 reduces transport activity.Am J Physiol Cell Physiol285: C1188\u2013C1196, 2003.","DOI":"10.1152\/ajpcell.00162.2003"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00421.2002"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1021\/bi992301v"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M400602200"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0504332102"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.16.9437"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.91.10.4544"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1999.276.2.H359"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M110442200"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00044.2004"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1038\/ng0696-183"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000064948.39199.A0"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000097370.29737.5B"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.090091297"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00124.2004"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.258.4.F908"},{"key":"R42","doi-asserted-by":"crossref","unstructured":"Yusufi ANK, Szczepanska-Konkel MX, and Dousa TP.Role ofN-linked oligosaccharides in the transport activity of the Na+\/H+antiporter in rat renal brush-border membrane.J Biol Chem263: 13683\u201313691, 1988.","DOI":"10.1016\/S0021-9258(18)68295-X"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00071.2005","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,7,19]],"date-time":"2021-07-19T22:17:00Z","timestamp":1626733020000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00071.2005"}},"issued":{"date-parts":[[2006,5]]},"references-count":42,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2006,5]]}},"alternative-id":["10.1152\/ajprenal.00071.2005"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00071.2005","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2006,5]]}},{"indexed":{"date-parts":[[2025,12,12]],"date-time":"2025-12-12T13:15:54Z","timestamp":1765545354630},"reference-count":80,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2005,11]]},"abstract":"<jats:p>This review article summarizes current knowledge about the locations and possible functions of annexin family members in the kidney. Beginning with an introduction on common structural and biochemical features as well as general functional characteristics of annexins, the paper focuses on individual members with documented and\/or proposed physiological relevance for renal development, structure, and functions. Three main aspects of annexin function in kidney epithelia emerge from the available experimental data. First, annexins are required for membrane organization and membrane transport events required for the establishment\/maintenance of epithelial polarity. Second, there is accumulating evidence of an association of annexins with ion channels, as membrane-guiding auxiliary proteins or modulators of channel activity. Last but not least, some annexins seem to work as extracellular autocrine modulators of receptor function under different physiological conditions.<\/jats:p>","DOI":"10.1152\/ajprenal.00089.2005","type":"journal-article","created":{"date-parts":[[2005,10,6]],"date-time":"2005-10-06T17:48:06Z","timestamp":1128620886000},"page":"F949-F956","source":"Crossref","is-referenced-by-count":38,"title":["Expression and functions of annexins in the kidney"],"prefix":"10.1152","volume":"289","author":[{"given":"Arseni","family":"Markoff","sequence":"first","affiliation":[]},{"given":"Volker","family":"Gerke","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1016\/S0005-2736(00)00262-5"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1096\/fj.02-0070com"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200307098"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1259\/bjr\/30385847"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1159\/000066788"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1016\/0022-2836(91)90002-N"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.cellbio.14.1.111"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1002\/cbf.1076"},{"key":"R9","doi-asserted-by":"crossref","unstructured":"Chan HC, Kaetzel MA, Gotter AL, Dedman JR, and Nelson DJ.Annexin IV inhibits calmodulin-dependent protein kinase II-activated chloride conductance. A novel mechanism for ion channel regulation.J Biol Chem269: 32464\u201332468, 1994.","DOI":"10.1016\/S0021-9258(18)31658-2"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1042\/bj3320681"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1007\/s004180050275"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(80)90446-8"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.128.6.1043"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.120.1.77"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1016\/S0167-4889(97)00038-4"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00030.2001"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1002\/j.1460-2075.1985.tb04023.x"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1016\/S1050-1738(99)00020-1"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1096\/fj.02-0239fje"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M207747200"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1016\/0167-4889(94)90098-1"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M313025200"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-0854.2004.00210.x"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.200308803"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1096\/fj.01-0855com"},{"key":"R26","unstructured":"Huber R, Berendes R, Burger A, Luecke H, and Karshikov A.Annexin V: crystal structure and its implication on function. In:The Annexins, edited by Moss SE. London: Portland, 1992, p. 105\u2013124."},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1093\/oxfordjournals.molbev.a004120"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1002\/j.1460-2075.1988.tb03089.x"},{"key":"R29","doi-asserted-by":"crossref","unstructured":"Kaetzel MA, Chan HC, Dubinsky WP, Dedman JR, and Nelson DJ.A role for annexin IV in epithelial cell function. Inhibition of calcium-activated chloride conductance.J Biol Chem269: 5297\u20135302, 1994.","DOI":"10.1016\/S0021-9258(17)37687-1"},{"key":"R30","doi-asserted-by":"crossref","unstructured":"Kaetzel MA, Hazarika P, and Dedman JR.Differential distribution of three 35-kDa annexin calcium-dependent phospholipid-binding proteins.J Biol Chem264: 14463\u201314470, 1989.","DOI":"10.1016\/S0021-9258(18)71701-8"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1007\/s002590100578"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M409009200"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1159\/000189279"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(94)80523-7"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.142.6.1413"},{"key":"R36","doi-asserted-by":"crossref","unstructured":"Lahorte CM, van de Wiele C, Bacher K, van den Bossche B, Thierens H, van Belle S, Slegers G, and Dierckx RA.Biodistribution and dosimetry study of 123I-rh-annexin V in mice and humans.Nucl Med Commun24: 871\u2013880, 2003.","DOI":"10.1097\/01.mnm.0000084585.29433.58"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1006\/jmbi.1997.1183"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1006\/cbir.2000.0629"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M306361200"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1016\/S0969-2126(01)00152-6"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1172\/JCI19684"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.2.719"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.1041650212"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1016\/S0009-8981(00)00218-7"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1007\/BF03220017"},{"key":"R46","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/cdg321"},{"key":"R47","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.1041530305"},{"key":"R48","doi-asserted-by":"publisher","DOI":"10.1016\/S0960-9822(01)00321-9"},{"key":"R49","doi-asserted-by":"publisher","DOI":"10.1186\/gb-2004-5-4-219"},{"key":"R50","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200108042"},{"key":"R51","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.146.4.843"},{"key":"R52","doi-asserted-by":"crossref","unstructured":"Pepinsky RB, Tizard R, Mattaliano RJ, Sinclair LK, Miller GT, Browning JL, Chow EP, Burne C, Huang KS, Pratt D, Wachter L, Hession C, Frey AZ, and Wallner BP.Five distinct calcium and phospholipid binding proteins share homology with lipocortin I.J Biol Chem263: 10799\u201310811, 1988.","DOI":"10.1016\/S0021-9258(18)38041-4"},{"key":"R53","doi-asserted-by":"publisher","DOI":"10.1189\/jlb.1103552"},{"key":"R54","unstructured":"Perretti Mand Gavins FN.Annexin 1: an endogenous anti-inflammatory protein.News Physiol Sci18: 60\u201364, 2003."},{"key":"R55","doi-asserted-by":"publisher","DOI":"10.1006\/jmbi.1994.1129"},{"key":"R56","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.76.10.5212"},{"key":"R57","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199904013401310"},{"key":"R58","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)63479-7"},{"key":"R59","unstructured":"Ravassa S, Bennaghmouch A, Kenis H, Lindhout T, Hackeng T, Narula J, Hofstra L, and Reutelingsperger C.Annexin A5 downregulates surface expression of tissue factor: a novel mechanism of regulating the membrane receptor repertoire.J Biol Chem280: 6028\u20136035, 2004."},{"key":"R60","doi-asserted-by":"publisher","DOI":"10.1016\/0304-4157(94)90019-1"},{"key":"R61","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.01245"},{"key":"R62","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.01208"},{"key":"R63","doi-asserted-by":"publisher","DOI":"10.1038\/4965"},{"key":"R64","doi-asserted-by":"publisher","DOI":"10.1006\/jsbi.1998.4003"},{"key":"R65","doi-asserted-by":"publisher","DOI":"10.1006\/jsbi.2000.4286"},{"key":"R66","doi-asserted-by":"publisher","DOI":"10.1006\/jmbi.2000.4423"},{"key":"R67","doi-asserted-by":"publisher","DOI":"10.1007\/s000180050066"},{"key":"R68","doi-asserted-by":"publisher","DOI":"10.1023\/A:1009205925714"},{"key":"R69","doi-asserted-by":"publisher","DOI":"10.1042\/bj3190123"},{"key":"R70","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.7.9.1359"},{"key":"R71","doi-asserted-by":"crossref","unstructured":"Seville RA, Nijjar S, Barnett MW, Masse K, and Jones EA.Annexin IV (Xanx-4) has a functional role in the formation of pronephric tubules.Development129: 1693\u20131704, 2002.","DOI":"10.1242\/dev.129.7.1693"},{"key":"R72","doi-asserted-by":"crossref","unstructured":"Simons Kand Toomre D.Lipid rafts and signal transduction.Nat Rev1: 31\u201339, 2000.","DOI":"10.1038\/35036052"},{"key":"R73","unstructured":"Solito E, de Coupade C, Parente L, Flower RJ, and Russo-Marie F.Human annexin 1 is highly expressed during the differentiation of the epithelial cell line A 549: involvement of nuclear factor interleukin 6 in phorbol ester induction of annexin 1.Cell Growth Differ9: 327\u2013336, 1998."},{"key":"R74","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.bb.23.060194.001205"},{"key":"R75","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/cdg162"},{"key":"R76","unstructured":"Waisman DM.Annexin II tetramer: structure and function.Mol Cell Biochem149: 301\u2013322, 1995."},{"key":"R77","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.116.2.405"},{"key":"R78","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1991.56"},{"key":"R79","doi-asserted-by":"crossref","unstructured":"Yamada A, Irie K, Hirota T, Ooshio T, Fukuhara A, and Takai Y.Involvement of the annexin II-S100A10 complex in the formation of E-cadherin-based adherens junctions in Madin-Darby canine kidney cells.J Biol Chem280: 6016\u20136027, 2004.","DOI":"10.1074\/jbc.M408215200"},{"key":"R80","doi-asserted-by":"crossref","unstructured":"Zobiack N, Rescher U, Laarmann S, Michgehl S, Schmidt MA, and Gerke V.Cell surface attachment of pedestal forming enteropathogenicE. coliinduces a clustering of raft components and a recruitment of annexin 2.J Cell Sci115: 91\u201398, 2002.","DOI":"10.1242\/jcs.115.1.91"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00089.2005","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,7,18]],"date-time":"2021-07-18T11:03:52Z","timestamp":1626606232000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00089.2005"}},"issued":{"date-parts":[[2005,11]]},"references-count":80,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2005,11]]}},"alternative-id":["10.1152\/ajprenal.00089.2005"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00089.2005","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2005,11]]}},{"indexed":{"date-parts":[[2025,12,11]],"date-time":"2025-12-11T07:34:17Z","timestamp":1765438457958,"version":"3.37.3"},"reference-count":43,"publisher":"American Physiological Society","issue":"2","funder":[{"DOI":"10.13039\/501100003554","name":"Lundbeckfonden (Lundbeck Foundation)","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100003554","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001732","name":"Danish National Research Foundation (Danmarks Grundforskningsfond)","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100001732","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Danish Genetically Modified Animal Resource"},{"DOI":"10.13039\/100008392","name":"Danish Medical Research Council","doi-asserted-by":"crossref","id":[{"id":"10.13039\/100008392","id-type":"DOI","asserted-by":"crossref"}]},{"name":"The Water and Salt Center"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2017,2,1]]},"abstract":"<jats:p>Aquaporin 11 (AQP11) is a channel protein with unknown biological function that is expressed in multiple tissues, including the kidney proximal tubule (PT) epithelium. Constitutive deletion of Aqp11 in mice ( Aqp11<jats:sup>\u2212\/\u2212<\/jats:sup>) results in early postnatal vacuolization in the PT and development of apparent cysts at 2 wk of age. Electron microscopy of adult Aqp11<jats:sup>\u2212\/\u2212<\/jats:sup>mouse PT cells revealed a dilated rough endoplasmic reticulum. These changes may cause renal failure and premature death. This study examined 1) whether postnatal deletion of Aqp11 affects PT injury and cyst formation, 2) the temporal role of Aqp11 deletion on cyst development, and 3) the nature of apparent cysts. Tamoxifen-inducible Aqp11<jats:sup>\u2212\/\u2212<\/jats:sup>mice were generated (Ti- Aqp11<jats:sup>\u2212\/\u2212<\/jats:sup>). Deletion of Aqp11 at postnatal days (P) P2, P4, P6, P8, and P12 was investigated. Deranged renal development, especially in kidney cortex, PT cell vacuolization, and apparent tubular cysts developed only in mice where Aqp11 gene disruption was induced until P8. Aqp11 gene deletion from P12 onward did not result in a clear deficiency in renal development, PT injury, or cyst formation. Intraperitoneal injection of biotinylated-dextran (10 kDa) into adult mice resulted in extensive endocytic dextran uptake in both cystic Aqp11<jats:sup>\u2212\/\u2212<\/jats:sup>and control PT epithelium, respectively. This suggests that apparent cysts are not membrane-enclosed structures but represent PT dilations. We conclude that Aqp11<jats:sup>\u2212\/\u2212<\/jats:sup>mice develop cyst-like dilated proximal tubules without documented cysts at time of death.<\/jats:p>","DOI":"10.1152\/ajprenal.00065.2016","type":"journal-article","created":{"date-parts":[[2016,9,1]],"date-time":"2016-09-01T02:48:57Z","timestamp":1472698137000},"page":"F343-F351","source":"Crossref","is-referenced-by-count":15,"title":["Temporal deletion of<i>Aqp11<\/i>in mice is linked to the severity of cyst-like disease"],"prefix":"10.1152","volume":"312","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5597-8880","authenticated-orcid":false,"given":"Michael","family":"R\u00fctzler","sequence":"first","affiliation":[{"name":"Department of Health Science and Technology, Aalborg University, Aalborg, Denmark; and"}]},{"given":"Aleksandra","family":"Rojek","sequence":"additional","affiliation":[{"name":"Department of Health Science and Technology, Aalborg University, Aalborg, Denmark; and"},{"name":"Department of Biomedicine, Aarhus University, Aarhus, Denmark"}]},{"given":"Mads Vammen","family":"Damgaard","sequence":"additional","affiliation":[{"name":"Department of Health Science and Technology, Aalborg University, Aalborg, Denmark; and"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2160-591X","authenticated-orcid":false,"given":"Arne","family":"Andreasen","sequence":"additional","affiliation":[{"name":"Department of Biomedicine, Aarhus University, Aarhus, Denmark"}]},{"given":"Robert A.","family":"Fenton","sequence":"additional","affiliation":[{"name":"Department of Biomedicine, Aarhus University, Aarhus, Denmark"}]},{"given":"S\u00f8ren","family":"Nielsen","sequence":"additional","affiliation":[{"name":"Department of Health Science and Technology, Aalborg University, Aalborg, Denmark; and"}]}],"member":"24","reference":[{"doi-asserted-by":"publisher","key":"B1","DOI":"10.1111\/febs.12653"},{"doi-asserted-by":"publisher","key":"B2","DOI":"10.1369\/jhc.2008.952044"},{"doi-asserted-by":"publisher","key":"B3","DOI":"10.1152\/ajprenal.00383.2005"},{"doi-asserted-by":"publisher","key":"B4","DOI":"10.1073\/pnas.1432873100"},{"key":"B5","doi-asserted-by":"crossref","first-page":"15634","DOI":"10.1016\/S0021-9258(19)37635-5","volume":"263","author":"Denker BM","year":"1988","journal-title":"J Biol Chem"},{"doi-asserted-by":"publisher","key":"B6","DOI":"10.1016\/S0140-6736(14)60763-7"},{"doi-asserted-by":"publisher","key":"B7","DOI":"10.1038\/sj.ki.5002794"},{"doi-asserted-by":"publisher","key":"B8","DOI":"10.1186\/1471-2091-7-14"},{"doi-asserted-by":"publisher","key":"B9","DOI":"10.1016\/j.ydbio.2007.08.021"},{"doi-asserted-by":"publisher","key":"B10","DOI":"10.3109\/02713683.2011.593108"},{"doi-asserted-by":"publisher","key":"B11","DOI":"10.1016\/j.stem.2008.01.014"},{"key":"B12","first-page":"341","volume":"75","author":"Hyde-Dunn J","year":"1997","journal-title":"Methods Mol Biol"},{"doi-asserted-by":"publisher","key":"B13","DOI":"10.1074\/jbc.M110.180968"},{"doi-asserted-by":"publisher","key":"B14","DOI":"10.1681\/ASN.2013060614"},{"doi-asserted-by":"publisher","key":"B15","DOI":"10.1038\/ng.400"},{"doi-asserted-by":"publisher","key":"B16","DOI":"10.1007\/BF00233959"},{"doi-asserted-by":"publisher","key":"B17","DOI":"10.1093\/hmg\/ddm299"},{"doi-asserted-by":"publisher","key":"B18","DOI":"10.1111\/j.1600-0722.2009.00695.x"},{"doi-asserted-by":"publisher","key":"B19","DOI":"10.1111\/j.1600-0722.2009.00708.x"},{"key":"B20","first-page":"309","volume":"36","author":"Le Poole IC","year":"2000","journal-title":"Animal"},{"doi-asserted-by":"publisher","key":"B21","DOI":"10.1016\/j.ymeth.2004.10.010"},{"doi-asserted-by":"publisher","key":"B22","DOI":"10.1016\/S0070-2153(10)90005-7"},{"doi-asserted-by":"publisher","key":"B23","DOI":"10.1002\/oby.20792"},{"doi-asserted-by":"publisher","key":"B24","DOI":"10.1016\/j.febslet.2008.11.012"},{"key":"B25","doi-asserted-by":"crossref","first-page":"16564","DOI":"10.1016\/S0021-9258(19)85456-X","volume":"268","author":"Moestrup SK","year":"1993","journal-title":"J Biol Chem"},{"doi-asserted-by":"publisher","key":"B26","DOI":"10.1128\/MCB.25.17.7770-7779.2005"},{"doi-asserted-by":"publisher","key":"B27","DOI":"10.1083\/jcb.120.2.371"},{"doi-asserted-by":"publisher","key":"B28","DOI":"10.1096\/fj.08-111872"},{"doi-asserted-by":"publisher","key":"B29","DOI":"10.1038\/nm1675"},{"doi-asserted-by":"publisher","key":"B30","DOI":"10.1038\/jid.2015.335"},{"doi-asserted-by":"publisher","key":"B31","DOI":"10.1152\/ajpgi.00208.2012"},{"doi-asserted-by":"publisher","key":"B32","DOI":"10.1152\/ajprenal.00305.2004"},{"doi-asserted-by":"publisher","key":"B33","DOI":"10.1016\/j.stem.2007.03.002"},{"doi-asserted-by":"publisher","key":"B34","DOI":"10.1016\/j.yexcr.2014.11.003"},{"key":"B35","doi-asserted-by":"crossref","first-page":"6407","DOI":"10.1016\/S0021-9258(18)38133-X","volume":"266","author":"Smith BL","year":"1991","journal-title":"J Biol Chem"},{"doi-asserted-by":"publisher","key":"B36","DOI":"10.1681\/ASN.2008030296"},{"doi-asserted-by":"publisher","key":"B37","DOI":"10.1089\/ars.2013.5236"},{"doi-asserted-by":"publisher","key":"B38","DOI":"10.1007\/s00467-010-1731-7"},{"doi-asserted-by":"publisher","key":"B39","DOI":"10.1016\/j.bbadis.2011.04.012"},{"doi-asserted-by":"publisher","key":"B40","DOI":"10.1016\/j.bbamem.2006.11.005"},{"doi-asserted-by":"publisher","key":"B41","DOI":"10.1016\/j.jsb.2011.01.003"},{"doi-asserted-by":"publisher","key":"B42","DOI":"10.1681\/ASN.2007010056"},{"doi-asserted-by":"publisher","key":"B43","DOI":"10.1016\/j.micron.2014.10.002"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00065.2016","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,7,7]],"date-time":"2022-07-07T14:17:29Z","timestamp":1657203449000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00065.2016"}},"issued":{"date-parts":[[2017,2,1]]},"references-count":43,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2017,2,1]]}},"alternative-id":["10.1152\/ajprenal.00065.2016"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00065.2016","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2017,2,1]]}},{"indexed":{"date-parts":[[2025,9,12]],"date-time":"2025-09-12T17:44:24Z","timestamp":1757699064554},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1986,1,1]]},"abstract":"<jats:p> The effects of a hypertonic extracellular medium on furosemide-sensitive Na and K fluxes were studied in isolated cells from the rabbit medullary thick ascending limb of Henle's loop (mTALH). In the control incubation medium, the furosemide-sensitive 22Na uptake was 379.1 +\/- 24.4 pmol . mg protein-1 . min-1 and the furosemide-sensitive 86Rb uptake was 30.5 +\/- 16.9. The furosemide-sensitive 22Na flux was not stimulated by K gradients directed into the cells, and, conversely, the furosemide-sensitive 86Rb flux was not stimulated by Na gradients directed into the cells. These findings are consistent with a Na-Cl cotransport system. In the presence of 200 mM mannitol, the furosemide-sensitive 22Na and 86Rb fluxes were increased dramatically to 919.4 +\/- 76.6 and 106.1 +\/- 29.2 pmol . mg protein-1 . min-1, respectively. When the osmolarity of the incubation medium was increased, not only were the furosemide-sensitive fluxes increased but these fluxes became inter-dependent, i.e., removing Na or K prevented the increase in the furosemide-sensitive flux of the other cation. This finding is consistent with a Na-K-2Cl cotransport system in the mTALH cells. The data suggest that the Na-Cl and the Na-K-2Cl cotransport systems may be distinct functions of the same furosemide-sensitive cotransport system and that their expression may be regulated by changes in cell volume. <\/jats:p>","DOI":"10.1152\/ajprenal.1986.250.1.f176","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T01:37:17Z","timestamp":1513993037000},"page":"F176-F180","source":"Crossref","is-referenced-by-count":16,"title":["Effect of osmolarity on cation fluxes in medullary thick ascending limb cells"],"prefix":"10.1152","volume":"250","author":[{"given":"J. L.","family":"Eveloff","sequence":"first","affiliation":[]},{"given":"J.","family":"Calamia","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1986.250.1.F176","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:38:00Z","timestamp":1567971480000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1986.250.1.F176"}},"issued":{"date-parts":[[1986,1,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1986,1,1]]}},"alternative-id":["10.1152\/ajprenal.1986.250.1.F176"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1986.250.1.f176","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1986,1,1]]}},{"indexed":{"date-parts":[[2025,9,13]],"date-time":"2025-09-13T16:18:06Z","timestamp":1757780286717,"version":"3.40.3"},"reference-count":28,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2025,2,1]]},"abstract":"<jats:p> Podocyte cytoskeletal proteins are crucial for podocyte integrity and maintenance of slit diaphragms as urinary filtration barriers. In this study, we focused on a novel protein, FAM114A1, that was the top classifier gene in MN in the gene expression study. We show that FAM114A1 is a podocyte-specific protein in the kidney and is upregulated in glomerular injury. FAM114A1 is associated with the podocyte cytoskeleton and silencing FAM114A1 affected podocyte cell morphology and functions. <\/jats:p>","DOI":"10.1152\/ajprenal.00203.2024","type":"journal-article","created":{"date-parts":[[2025,1,17]],"date-time":"2025-01-17T07:50:50Z","timestamp":1737100250000},"page":"F289-F299","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["Characterization of FAM114A1: a novel podocyte cytoskeleton-associated protein upregulated in glomerular injury"],"prefix":"10.1152","volume":"328","author":[{"ORCID":"https:\/\/orcid.org\/0009-0002-8741-1090","authenticated-orcid":false,"given":"Norifumi","family":"Hayashi","sequence":"first","affiliation":[{"name":"Boston University","place":["United States"]},{"id":[{"id":"https:\/\/ror.org\/0535cbe18","id-type":"ROR","asserted-by":"publisher"}],"name":"Kanazawa Medical University","place":["Japan"]}]},{"given":"Sudhir","family":"Kumar","sequence":"additional","affiliation":[{"name":"Boston University","place":["United States"]}]},{"given":"Claire","family":"Trivin-Avillach","sequence":"additional","affiliation":[{"name":"Boston University","place":["United States"]}]},{"given":"Xueping","family":"Fan","sequence":"additional","affiliation":[{"name":"Boston University","place":["United States"]}]},{"given":"Shana V.","family":"Stoddard","sequence":"additional","affiliation":[{"name":"Rhodes College","place":["United States"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6822-8413","authenticated-orcid":false,"given":"Ryoko","family":"Akai","sequence":"additional","affiliation":[{"name":"Kanazawa Medical University","place":["Japan"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7392-8753","authenticated-orcid":false,"given":"Keiji","family":"Fujimoto","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/0535cbe18","id-type":"ROR","asserted-by":"publisher"}],"name":"Kanazawa Medical University","place":["Japan"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8753-1979","authenticated-orcid":false,"given":"Takao","family":"Iwawaki","sequence":"additional","affiliation":[{"name":"Kanazawa Medical University","place":["Japan"]}]},{"given":"Hitoshi","family":"Yokoyama","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/0535cbe18","id-type":"ROR","asserted-by":"publisher"}],"name":"Kanazawa Medical University","place":["Japan"]}]},{"given":"Kengo","family":"Furuichi","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/0535cbe18","id-type":"ROR","asserted-by":"publisher"}],"name":"Kanazawa Medical University","place":["Japan"]}]},{"suffix":"Jr.","given":"Laurence H.","family":"Beck","sequence":"additional","affiliation":[{"name":"Boston University","place":["United States"]}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfq665"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa0810457"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2020.06.020"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2020071082"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2017020143"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2021060784"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-4159.2006.04093.x"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.V134946"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/j.ajpath.2019.12.009"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1038\/nprot.2015.053"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1093\/bioinformatics\/19.1.163"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/gki370"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1002\/pro.3330"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1107\/S0907444909042073"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/gkm216"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1002\/jcc.20084"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1797.2012.01619.x"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-019-45217-9"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1002\/0471142301.ns0528s46"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1038\/73456"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1038\/ng.505"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1042\/BST20140272"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-0854.2006.00419.x"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.00073-19"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1172\/jci.insight.152783"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2012.426"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00328.x"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1172\/JCI20402"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00203.2024","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,4,2]],"date-time":"2025-04-02T14:11:27Z","timestamp":1743603087000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00203.2024"}},"issued":{"date-parts":[[2025,2,1]]},"references-count":28,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2025,2,1]]}},"alternative-id":["10.1152\/ajprenal.00203.2024"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00203.2024","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2025,2,1]]},"assertion":[{"value":"2024-07-16","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2024-08-12","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2025-01-07","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2025-02-03","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2025,9,12]],"date-time":"2025-09-12T18:25:15Z","timestamp":1757701515043},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1993,8,1]]},"abstract":"<jats:p> The present studies were performed to assess, in the isolated perfused juxtaglomerular apparatus of the rabbit kidney, the effect of exogenous adenosine on renin secretion stimulated by a low NaCl concentration at the macula densa. Addition of adenosine to the bath resulted in a change of renin secretion from 30.4 to 23.9 nGU\/min at an adenosine concentration of 10(-6) M (n = 7; P = NS), from 38.6 to 17.9 nGU\/min at a concentration of 10(-4) M (n = 7; P = 0.038), and from 18.4 to 5.8 nGU\/min at 10(-2) M (P = 0.0053). Addition of the A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine at 10(-5) M fully reversed the effect of adenosine at 10(-4) M, but not at 10(-2) M. Inhibition of adenosine breakdown by the adenosine deaminase inhibitor pentostatin (10(-6) M) enhanced the inhibitory effect of adenosine with renin secretion falling from 61.7 to 19.5 nGU\/min at 10(-6) M adenosine (P = 0.035) and from 44.7 to 13.5 nGU\/min at 10(-4) M adenosine (n = 0.027). A marked inhibition of NaCl-dependent renin secretion was caused by both angiotensin II (P = 0.011) and angiotensin III (P = 0.006), both at 10(-8) M. These results show that adenosine is capable of reducing macula densa-mediated renin secretion, but that this effect, even at very high concentrations or during adenosine deaminase blockade, does not fully mimic the inhibitory potency of increasing luminal NaCl concentration. Because the marked effect caused by angiotensins establishes the potential of this preparation to demonstrate inhibitory hormonal influences, it is concluded that adenosine does not appear to be the sole paracrine factor responsible for the NaCl-induced reduction of renin secretion. <\/jats:p>","DOI":"10.1152\/ajprenal.1993.265.2.f187","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T05:16:32Z","timestamp":1514006192000},"page":"F187-F194","source":"Crossref","is-referenced-by-count":9,"title":["Effects of adenosine and angiotensin on macula densa-stimulated renin secretion"],"prefix":"10.1152","volume":"265","author":[{"given":"J. N.","family":"Lorenz","sequence":"first","affiliation":[{"name":"Department of Physiology, University of Michigan, Ann Arbor48104."}]},{"given":"H.","family":"Weihprecht","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Michigan, Ann Arbor48104."}]},{"given":"X. R.","family":"He","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Michigan, Ann Arbor48104."}]},{"given":"O.","family":"Skott","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Michigan, Ann Arbor48104."}]},{"given":"J. P.","family":"Briggs","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Michigan, Ann Arbor48104."}]},{"given":"J.","family":"Schnermann","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Michigan, Ann Arbor48104."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1993.265.2.F187","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:27:05Z","timestamp":1567960025000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1993.265.2.F187"}},"issued":{"date-parts":[[1993,8,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1993,8,1]]}},"alternative-id":["10.1152\/ajprenal.1993.265.2.F187"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1993.265.2.f187","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1993,8,1]]}},{"indexed":{"date-parts":[[2025,9,13]],"date-time":"2025-09-13T16:22:26Z","timestamp":1757780546246},"reference-count":35,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2014,1,1]]},"abstract":"<jats:p> The aim of the study is to explore the role of miR-194 in mediating the effect of high-K (HK) intake on ROMK channel. Northern blot analysis showed that miR-194 was expressed in kidney and that HK intake increased while low-K intake decreased the expression of miR-194. Real-time PCR analysis further demonstrated that HK intake increased the miR-194 expression in the cortical collecting duct. HK intake decreased the expression of intersectin 1 (ITSN1) which enhanced With-No-Lysine Kinase (WNK)-induced endocytosis of ROMK. Expression of miR-194 mimic decreased luciferase reporter gene activity in HEK293 T cells transfected with ITSN-1\u20133\u2032UTR containing the complementary seed sequence for miR-194. In contrast, transfection of miR-194 inhibitor increased the luciferase activity. This effect was absent in the cells transfected with mutated 3\u2032UTR of ITSN1 in which the complimentary seed sequence was deleted. Moreover, the inhibition of miR-194 expression increased the protein level of endogenous ITSN1 in HEK293T cells. Expression of miR-194 mimic also decreased the translation of exogenous ITSN1 in the cells transfected with the ITSN1 containing 3\u2032UTR but not with 3\u2032UTR-free ITSN1. Expression of pre-miR-194 increased K currents and ROMK expression in the plasma membrane in ROMK-transfected cells. Coexpression of ITSN1 reversed the stimulatory effect of miR-194 on ROMK channels. This effect was reversed by coexpression of ITSN1. We conclude that miR-194 regulates ROMK channel activity by modulating ITSN1 expression thereby enhancing ITSN1\/WNK-dependent endocytosis. It is possible that miR-194 is involved in mediating the effect of a HK intake on ROMK channel activity. <\/jats:p>","DOI":"10.1152\/ajprenal.00349.2013","type":"journal-article","created":{"date-parts":[[2013,11,7]],"date-time":"2013-11-07T02:36:04Z","timestamp":1383791764000},"page":"F53-F60","source":"Crossref","is-referenced-by-count":20,"title":["MicroRNA-194 (miR-194) regulates ROMK channel activity by targeting intersectin 1"],"prefix":"10.1152","volume":"306","author":[{"given":"Dao-Hong","family":"Lin","sequence":"first","affiliation":[{"name":"Department of Pharmacology, New York Medical College, Valhalla, New York"}]},{"given":"Peng","family":"Yue","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, New York Medical College, Valhalla, New York"}]},{"given":"Chengbiao","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, New York Medical College, Valhalla, New York"}]},{"given":"Wen-Hui","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, New York Medical College, Valhalla, New York"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M414610200"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00150.2003"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010020134"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009111186"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1038\/nrg2455"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90527.2008"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0912701107"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1172\/JCI30087"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00051.2003"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1038\/ng1271"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.70.113006.100651"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009050530"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0510609103"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1172\/JCI34922"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00160.2002"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/physiol.00044.2004"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00301.2003"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M109.041582"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010090927"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M705574200"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.109.144428"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M806551200"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2011121144"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/gks1228"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0504332102"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/S0167-4781(01)00276-7"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0611728104"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M109739200"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1101\/gr.6587008"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0603109103"},{"key":"B32","first-page":"547","volume":"66","author":"Wang W","year":"2004","journal-title":"Annu Rev Med"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009070718"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.281.2.F206"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M212301200"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0907855106"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00349.2013","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T23:55:03Z","timestamp":1567986903000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00349.2013"}},"issued":{"date-parts":[[2014,1,1]]},"references-count":35,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2014,1,1]]}},"alternative-id":["10.1152\/ajprenal.00349.2013"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00349.2013","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2014,1,1]]}},{"indexed":{"date-parts":[[2025,9,12]],"date-time":"2025-09-12T18:38:11Z","timestamp":1757702291354},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1995,8,1]]},"abstract":"<jats:p> The mechanism by which the renal medulla establishes and maintains a gradient of osmolarity along the corticomedullary axis, especially in the inner medulla, where there is no active transmural flux out of the ascending limbs of Henle, remains a source of controversy. We show here that, if realistic values of urea permeability in the inner medullary descending limbs and water permeability in the upper inner medullary section of the collecting ducts are taken into account, even a model including the three-dimensional vascular bundle structures [A. S. Wexler, R. E. Kalaba, and D. J. Marsh. Am. J. Physiol. 260 (Renal Fluid Electrolyte Physiol. 29): F368-F383, 1991] fails to explain the experimentally observed inner medullary osmolality gradient. We show here that this failure can be overcome by application of an external osmotic driving force, an idea recently revived by J. F. Jen and J. L. Stephenson (Bull. Math. Biol. 56: 491-514, 1994) in the context of a single-solute, single-loop central core model. We show that inclusion of such an external driving force with a value equivalent to at least 100 mosM of inner medullary interstitial osmolytes in the three-dimensional model of Wexler et al. accounts for a physiological osmolality gradient, even in the face of realistic permeability values. Furthermore, inclusion of the external driving force makes the model less dependent on the positions of descending and ascending limbs of Henle with respect to the collecting ducts. In an effort to assess whether there is any experimental basis for osmolytes, we show that a significant amount of extra inner medullary interstitial osmolytes is plausible, based on extrapolation from existing experimental data. <\/jats:p>","DOI":"10.1152\/ajprenal.1995.269.2.f159","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T01:13:31Z","timestamp":1513991611000},"page":"F159-F171","source":"Crossref","is-referenced-by-count":21,"title":["Inner medullary external osmotic driving force in a 3-D model of the renal concentrating mechanism"],"prefix":"10.1152","volume":"269","author":[{"given":"S. R.","family":"Thomas","sequence":"first","affiliation":[{"name":"Institut National de la Sante et de la Recherche Medicale Unite 323,Necker Faculty of Medicine, Paris, France."}]},{"given":"A. S.","family":"Wexler","sequence":"additional","affiliation":[{"name":"Institut National de la Sante et de la Recherche Medicale Unite 323,Necker Faculty of Medicine, Paris, France."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1995.269.2.F159","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:02:56Z","timestamp":1567958576000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1995.269.2.F159"}},"issued":{"date-parts":[[1995,8,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1995,8,1]]}},"alternative-id":["10.1152\/ajprenal.1995.269.2.F159"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1995.269.2.f159","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1995,8,1]]}},{"indexed":{"date-parts":[[2025,9,12]],"date-time":"2025-09-12T17:54:37Z","timestamp":1757699677260},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1991,10,1]]},"abstract":"<jats:p> To evaluate the contribution of paracellular shunt pathway in ascending thin limb (ATL) of hamsters, we examined the effect of protamine, a selective blocker of paracellular conductance, on salt-diffusion voltage (dVT) and transmural resistance (RT) during in vitro microperfusion. Lumen-negative dVT generated on reduction of lumen NaCl concentration was increased further from -7.3 +\/- 0.5 to -10.3 +\/- 0.7 mV when 300 micrograms\/ml protamine was added to the lumen, and calculated Na+\/Cl- permeability ratio was decreased from 0.46 +\/- 0.03 to 0.31 +\/- 0.03. Although the effect of protamine persisted after removal of the agent from the lumen, addition of 30 U\/ml heparin returned the dVT toward the control level. The effect of protamine was dose dependent from 30 to 300 micrograms\/ml. Protamine also exerted its effect from the bath, and the effect was inhibited by heparin either from the lumen or from the bath. The inhibitory effect was almost the same when the orientation of imposed NaCl gradient was reversed. Inhibition of transcellular Cl- transport with 0.1 mM 5-nitro-2-(3-phenylpropylamino)-benzoate (NPPB) in the bath caused lumen-positive dVT. This voltage was decreased significantly by protamine. Protamine markedly decreased the apparent transference number for Na+ but slightly increased the value for Cl-. Transmural cable analysis showed that 300 micrograms\/ml protamine added to the lumen increased RT from 0.59 +\/- 0.10 to 1.20 +\/- 0.20 omega.cm2, with the effect being reversed by 30 U\/ml heparin.(ABSTRACT TRUNCATED AT 250 WORDS) <\/jats:p>","DOI":"10.1152\/ajprenal.1991.261.4.f593","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T23:30:54Z","timestamp":1513985454000},"page":"F593-F599","source":"Crossref","is-referenced-by-count":6,"title":["Effect of protamine on ion conductance of ascending thin limb of Henle's loop from hamsters"],"prefix":"10.1152","volume":"261","author":[{"given":"S.","family":"Koyama","sequence":"first","affiliation":[{"name":"Department of Pharmacology, Jichi Medical School, Tochigi,Japan."}]},{"given":"K.","family":"Yoshitomi","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Jichi Medical School, Tochigi,Japan."}]},{"given":"M.","family":"Imai","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Jichi Medical School, Tochigi,Japan."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1991.261.4.F593","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:22:56Z","timestamp":1567970576000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1991.261.4.F593"}},"issued":{"date-parts":[[1991,10,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1991,10,1]]}},"alternative-id":["10.1152\/ajprenal.1991.261.4.F593"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1991.261.4.f593","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1991,10,1]]}},{"indexed":{"date-parts":[[2025,4,18]],"date-time":"2025-04-18T06:25:55Z","timestamp":1744957555507,"version":"3.37.3"},"reference-count":73,"publisher":"American Physiological Society","issue":"6","funder":[{"DOI":"10.13039\/100000050","name":"HHS | NIH | National Heart, Lung, and Blood Institute (NHBLI)","doi-asserted-by":"publisher","award":["HL128355"],"award-info":[{"award-number":["HL128355"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Veterans Health Administration, ORD, BLRD","award":["BX000893"],"award-info":[{"award-number":["BX000893"]}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)","doi-asserted-by":"publisher","award":["P30DK096493","DK087893"],"award-info":[{"award-number":["P30DK096493","DK087893"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2016,12,1]]},"abstract":"<jats:p>Activated immune cell populations contribute to hypertension in part through inciting damage to the kidney and by provoking inappropriate sodium reabsorption in the nephron. Inflammatory mediators called cytokines produced by T lymphocytes and macrophages act on specific sodium transporters in the kidney, augmenting their activity or expression, with consequent expansion of intravascular fluid volume and cardiac output. The overlapping functions of these cytokines, each of which may activate multiple receptors, present challenges in precisely targeting inflammatory signaling cascades in hypertension. Moreover, broad immune suppression could expose the hypertensive patient to disproportional risks of infection or malignancy. Nevertheless, the possibility that incisive immunomodulatory therapies could provide cardiovascular and renal protection through both blood pressure-dependent and -independent mechanisms justifies comprehensive investigation into the relevant signaling pathways and tissue sites in which inflammatory cytokines function to exaggerate blood pressure elevation and target organ damage in hypertension.<\/jats:p>","DOI":"10.1152\/ajprenal.00273.2016","type":"journal-article","created":{"date-parts":[[2016,8,25]],"date-time":"2016-08-25T01:58:44Z","timestamp":1472090324000},"page":"F1153-F1158","source":"Crossref","is-referenced-by-count":9,"title":["Targeting cytokine signaling in salt-sensitive hypertension"],"prefix":"10.1152","volume":"311","author":[{"given":"Steven D.","family":"Crowley","sequence":"first","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Duke University and Durham Veterans Affairs Medical Centers, Durham, North Carolina"}]},{"given":"Alexander D.","family":"Jeffs","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Duke University and Durham Veterans Affairs Medical Centers, Durham, North Carolina"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/j.amjcard.2009.12.059"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/sj.jhh.1001785"},{"key":"B3","first-page":"419","volume":"134","author":"Bertani T","year":"1989","journal-title":"Am J Pathol"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.110.158071"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00426.2011"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.115.05779"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00344.2010"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000077913.60364.D2"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1038\/nm.2541"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0605545103"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00373.2009"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-2143(97)90178-5"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00298.2009"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00454.2010"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.34.1.113"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/j.vph.2007.05.007"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1001\/jama.2010.650"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000198545.01860.90"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.00518-15"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/S1473-3099(03)00545-0"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM198808183190703"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1126\/science.2063193"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20070657"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006080918"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00633.2014"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.114.04975"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1161\/ATVBAHA.114.304108"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1172\/JCI74084"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.256.5.F810"},{"key":"B30","doi-asserted-by":"crossref","first-page":"A11888","DOI":"10.1161\/circ.130.suppl_2.11888","volume":"130","author":"Kossmann S","year":"2014","journal-title":"Circulation"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.113.02620"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1111\/bph.13230"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00289.2015"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(08)60655-8"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009060615"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00207.2009"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1038\/nm.3221"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1038\/nm.1960"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.109.145094"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000124490.27666.B2"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.112.199265"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)64445-8"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.116.07493"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1016\/0024-3205(90)90309-F"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00557.2012"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.111.189761"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.112.122556"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1016\/j.ahj.2011.06.012"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1172\/JCI76327"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1016\/S0169-409X(01)00141-7"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1161\/ATVBAHA.107.153080"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.258.4.F761"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90297.2008"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.110.150409"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1210\/en.2015-1408"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.115.06011"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00525.2012"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.107.102152"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1093\/ajh\/5.4.224"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.114.04147"},{"key":"B61","first-page":"293","volume":"172","author":"van Lanschot JJ","year":"1991","journal-title":"Surg Gynecol Obstet"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.110.157685"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.109.930446"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1165\/ajrcmb.11.6.7946395"},{"key":"B65","first-page":"cm1","volume":"3","author":"Weber A","year":"2010","journal-title":"Sci Signal"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.111.034470"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1172\/JCI60113"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.1016\/j.tibtech.2015.06.009"},{"key":"B69","doi-asserted-by":"publisher","DOI":"10.1038\/jhh.2013.80"},{"key":"B70","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.114.03863"},{"key":"B71","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2015.11.013"},{"key":"B72","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.111.261768"},{"key":"B73","doi-asserted-by":"publisher","DOI":"10.1172\/JCI81550"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00273.2016","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,7,7]],"date-time":"2022-07-07T00:38:04Z","timestamp":1657154284000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00273.2016"}},"issued":{"date-parts":[[2016,12,1]]},"references-count":73,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2016,12,1]]}},"alternative-id":["10.1152\/ajprenal.00273.2016"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00273.2016","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2016,12,1]]}},{"indexed":{"date-parts":[[2025,4,11]],"date-time":"2025-04-11T23:43:59Z","timestamp":1744415039837},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1984,3,1]]},"abstract":"<jats:p> To determine whether preexistent glomerular injury and the nephrotic syndrome increase renal susceptibility to ischemic renal injury, normal rats and rats with either experimental minimal-change disease (Adriamycin nephropathy) (AN) or membranous nephropathy (passive Heymann nephritis) (PHN) underwent renal functional and histologic studies under either basal conditions or 18 h after bilateral renal artery occlusion (over 30 min). Prior to renal ischemia AN and PHN rats had minimally depressed glomerular filtration rate (GFR), normal (AN) or increased (PHN) renal blood flow (RBF), heavy proteinuria, hypoalbuminemia, decreased urine sodium excretion, extensive glomerular foot process fusion, and intratubular hyalin cast formation. Losses of GFR in response to ischemia were comparable among the three groups of rats (controls, 0.29; AN, 0.28; PHN, 0.25 ml X min-1 X 100 g body wt-1) despite prevailing differences in postischemic hemodynamics. Neither light nor transmission electron microscopy showed any differences in the degree of ischemic renal injury. These results suggest that 1) glomerulopathy and the nephrotic syndrome do not significantly increase renal susceptibility to ischemic renal injury; 2) the syndrome of acute renal failure that occurs in patients with minimal-change glomerulopathy is not due to a marked susceptibility of these kidneys to clinically occult ischemic events; and 3) foot process fusion is probably not a pathophysiologically significant lesion in ischemic acute renal failure, as previously suggested. <\/jats:p>","DOI":"10.1152\/ajprenal.1984.246.3.f272","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T17:13:23Z","timestamp":1513962803000},"page":"F272-F281","source":"Crossref","is-referenced-by-count":1,"title":["Glomerulopathy does not increase renal susceptibility to acute ischemic injury"],"prefix":"10.1152","volume":"246","author":[{"given":"R. A.","family":"Zager","sequence":"first","affiliation":[]},{"given":"L. A.","family":"Baltes","sequence":"additional","affiliation":[]},{"given":"H. M.","family":"Sharma","sequence":"additional","affiliation":[]},{"given":"W. G.","family":"Couser","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1984.246.3.F272","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:36:09Z","timestamp":1567967769000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1984.246.3.F272"}},"issued":{"date-parts":[[1984,3,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1984,3,1]]}},"alternative-id":["10.1152\/ajprenal.1984.246.3.F272"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1984.246.3.f272","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1984,3,1]]}},{"indexed":{"date-parts":[[2025,6,20]],"date-time":"2025-06-20T12:26:46Z","timestamp":1750422406702,"version":"3.37.3"},"reference-count":59,"publisher":"American Physiological Society","issue":"1","funder":[{"DOI":"10.13039\/501100000024","name":"Gouvernement du Canada | Canadian Institutes of Health Research (Instituts de recherche en sant\u00e9 du Canada)","doi-asserted-by":"publisher","award":["MOP-125988","MOP-133492"],"award-info":[{"award-number":["MOP-125988","MOP-133492"]}],"id":[{"id":"10.13039\/501100000024","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2018,7,1]]},"abstract":"<jats:p>SLK is essential for embryonic development and may play a key role in wound healing, tumor growth, and metastasis. Expression and activation of SLK are increased in kidney development and during recovery from ischemic acute kidney injury. Overexpression of SLK in glomerular epithelial cells\/podocytes in vivo induces injury and proteinuria. Conversely, reduced SLK expression leads to abnormalities in cell adhesion, spreading, and motility. Tight regulation of SLK expression thus may be critical for normal renal structure and function. We produced podocyte-specific SLK-knockout mice to address the functional role of SLK in podocytes. Mice with podocyte-specific deletion of SLK showed reduced glomerular SLK expression and activity compared with control. Podocyte-specific deletion of SLK resulted in albuminuria at 4\u20135 mo of age in male mice and 8\u20139 mo in female mice, which persisted for up to 13 mo. At 11\u201312 mo, knockout mice showed ultrastructural changes, including focal foot process effacement and microvillous transformation of podocyte plasma membranes. Mean foot process width was approximately twofold greater in knockout mice compared with control. Podocyte number was reduced by 35% in knockout mice compared with control, and expression of nephrin, synaptopodin, and podocalyxin was reduced in knockout mice by 20\u201330%. In summary, podocyte-specific deletion of SLK leads to albuminuria, loss of podocytes, and morphological evidence of podocyte injury. Thus, SLK is essential to the maintenance of podocyte integrity as mice age.<\/jats:p>","DOI":"10.1152\/ajprenal.00238.2017","type":"journal-article","created":{"date-parts":[[2017,11,29]],"date-time":"2017-11-29T15:20:28Z","timestamp":1511968828000},"page":"F186-F198","source":"Crossref","is-referenced-by-count":10,"title":["Ste20-like kinase, SLK, a novel mediator of podocyte integrity"],"prefix":"10.1152","volume":"315","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4348-2348","authenticated-orcid":false,"given":"Andrey V.","family":"Cybulsky","sequence":"first","affiliation":[{"name":"Department of Medicine, McGill University Health Centre Research Institute, McGill University, Montreal, Quebec, Canada"}]},{"given":"Joan","family":"Papillon","sequence":"additional","affiliation":[{"name":"Department of Medicine, McGill University Health Centre Research Institute, McGill University, Montreal, Quebec, Canada"}]},{"given":"Julie","family":"Guillemette","sequence":"additional","affiliation":[{"name":"Department of Medicine, McGill University Health Centre Research Institute, McGill University, Montreal, Quebec, Canada"}]},{"given":"Natalya","family":"Belkina","sequence":"additional","affiliation":[{"name":"Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland"}]},{"given":"Genaro","family":"Patino-Lopez","sequence":"additional","affiliation":[{"name":"Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland"}]},{"given":"Elena","family":"Torban","sequence":"additional","affiliation":[{"name":"Department of Medicine, McGill University Health Centre Research Institute, McGill University, Montreal, Quebec, Canada"}]}],"member":"24","reference":[{"doi-asserted-by":"publisher","key":"B1","DOI":"10.4161\/cam.22495"},{"doi-asserted-by":"publisher","key":"B2","DOI":"10.1002\/dvdy.24106"},{"doi-asserted-by":"publisher","key":"B3","DOI":"10.1038\/nrneph.2013.78"},{"doi-asserted-by":"publisher","key":"B4","DOI":"10.1038\/nrneph.2010.103"},{"doi-asserted-by":"publisher","key":"B5","DOI":"10.1159\/000313948"},{"doi-asserted-by":"publisher","key":"B6","DOI":"10.1371\/journal.pone.0177226"},{"doi-asserted-by":"publisher","key":"B7","DOI":"10.1155\/2011\/563128"},{"doi-asserted-by":"publisher","key":"B8","DOI":"10.2353\/ajpath.2010.100263"},{"doi-asserted-by":"publisher","key":"B9","DOI":"10.1152\/ajprenal.00234.2006"},{"doi-asserted-by":"publisher","key":"B10","DOI":"10.1152\/ajprenal.00144.2003"},{"doi-asserted-by":"publisher","key":"B11","DOI":"10.1016\/S0962-8924(01)01980-8"},{"doi-asserted-by":"publisher","key":"B12","DOI":"10.1152\/ajprenal.00062.2011"},{"doi-asserted-by":"publisher","key":"B13","DOI":"10.1007\/s00424-009-0674-y"},{"doi-asserted-by":"publisher","key":"B14","DOI":"10.1002\/phy2.86"},{"doi-asserted-by":"publisher","key":"B15","DOI":"10.1002\/gene.20011"},{"doi-asserted-by":"publisher","key":"B16","DOI":"10.1038\/ki.2010.238"},{"doi-asserted-by":"publisher","key":"B17","DOI":"10.1074\/jbc.M115.696781"},{"doi-asserted-by":"publisher","key":"B18","DOI":"10.1046\/j.1365-2443.2000.00337.x"},{"doi-asserted-by":"publisher","key":"B19","DOI":"10.1002\/cm.21276"},{"doi-asserted-by":"publisher","key":"B20","DOI":"10.1146\/annurev-physiol-020911-153238"},{"doi-asserted-by":"publisher","key":"B21","DOI":"10.1161\/CIRCRESAHA.107.164764"},{"doi-asserted-by":"publisher","key":"B22","DOI":"10.1074\/jbc.M511744200"},{"doi-asserted-by":"publisher","key":"B23","DOI":"10.4161\/auto.19821"},{"doi-asserted-by":"publisher","key":"B24","DOI":"10.1172\/JCI118697"},{"doi-asserted-by":"publisher","key":"B25","DOI":"10.1016\/j.bbamcr.2015.06.005"},{"doi-asserted-by":"publisher","key":"B26","DOI":"10.1091\/mbc.E16-12-0828"},{"doi-asserted-by":"publisher","key":"B27","DOI":"10.1152\/ajprenal.00478.2012"},{"doi-asserted-by":"publisher","key":"B28","DOI":"10.1371\/journal.pone.0011545"},{"doi-asserted-by":"publisher","key":"B29","DOI":"10.1016\/j.kint.2017.04.022"},{"doi-asserted-by":"publisher","key":"B30","DOI":"10.1074\/jbc.M111.302018"},{"doi-asserted-by":"publisher","key":"B31","DOI":"10.1083\/jcb.201401049"},{"doi-asserted-by":"publisher","key":"B32","DOI":"10.1002\/gene.10164"},{"doi-asserted-by":"publisher","key":"B33","DOI":"10.1074\/jbc.M510763200"},{"key":"B34","doi-asserted-by":"crossref","first-page":"1589","DOI":"10.1681\/ASN.V1281589","volume":"12","author":"Orlando RA","year":"2001","journal-title":"J Am Soc Nephrol"},{"doi-asserted-by":"publisher","key":"B35","DOI":"10.1152\/physrev.00020.2002"},{"doi-asserted-by":"publisher","key":"B36","DOI":"10.1038\/emboj.2008.8"},{"doi-asserted-by":"publisher","key":"B37","DOI":"10.1152\/ajprenal.90421.2008"},{"doi-asserted-by":"publisher","key":"B38","DOI":"10.1186\/s13395-016-0119-1"},{"doi-asserted-by":"publisher","key":"B39","DOI":"10.1038\/onc.2012.488"},{"doi-asserted-by":"publisher","key":"B40","DOI":"10.1152\/ajpcell.00121.2016"},{"doi-asserted-by":"publisher","key":"B41","DOI":"10.1038\/sj.onc.1203119"},{"doi-asserted-by":"publisher","key":"B42","DOI":"10.1128\/MCB.20.2.684-696.2000"},{"doi-asserted-by":"publisher","key":"B43","DOI":"10.1186\/1471-2164-15-725"},{"doi-asserted-by":"publisher","key":"B44","DOI":"10.1186\/2044-5040-3-16"},{"doi-asserted-by":"publisher","key":"B45","DOI":"10.1002\/mus.20000"},{"doi-asserted-by":"publisher","key":"B46","DOI":"10.1091\/mbc.E08-07-0707"},{"doi-asserted-by":"publisher","key":"B47","DOI":"10.1016\/j.semnephrol.2013.08.009"},{"doi-asserted-by":"publisher","key":"B48","DOI":"10.1172\/JCI12539"},{"doi-asserted-by":"publisher","key":"B49","DOI":"10.1111\/j.1523-1755.2004.00964.x"},{"doi-asserted-by":"publisher","key":"B50","DOI":"10.1681\/ASN.2013080859"},{"doi-asserted-by":"publisher","key":"B51","DOI":"10.1083\/jcb.201207047"},{"doi-asserted-by":"publisher","key":"B52","DOI":"10.1074\/jbc.M205899200"},{"doi-asserted-by":"publisher","key":"B53","DOI":"10.1152\/ajprenal.00030.2010"},{"doi-asserted-by":"publisher","key":"B54","DOI":"10.1038\/nrneph.2011.151"},{"doi-asserted-by":"publisher","key":"B55","DOI":"10.1681\/ASN.2005010055"},{"doi-asserted-by":"publisher","key":"B56","DOI":"10.14814\/phy2.12636"},{"doi-asserted-by":"publisher","key":"B57","DOI":"10.1016\/S0167-4889(99)00164-0"},{"doi-asserted-by":"publisher","key":"B58","DOI":"10.1371\/journal.pone.0082818"},{"doi-asserted-by":"publisher","key":"B59","DOI":"10.1091\/mbc.E13-03-0137"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00238.2017","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,9]],"date-time":"2022-08-09T16:50:41Z","timestamp":1660063841000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00238.2017"}},"issued":{"date-parts":[[2018,7,1]]},"references-count":59,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2018,7,1]]}},"alternative-id":["10.1152\/ajprenal.00238.2017"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00238.2017","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2018,7,1]]}},{"indexed":{"date-parts":[[2025,4,4]],"date-time":"2025-04-04T21:24:28Z","timestamp":1743801868304},"reference-count":65,"publisher":"American Physiological Society","issue":"10","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,11,15]]},"abstract":"<jats:p>CD44 family members are cell surface glycoproteins, which are expressed on tubular epithelial cells (TEC) solely upon kidney injury and are involved in renal fibrosis development. Renal interstitial fibrosis is the final manifestation of chronic kidney diseases and is regulated by a complex network of cytokines, including the profibrotic factor transforming growth factor-\u03b21 (TGF-\u03b21) and the two antifibrotic cytokines bone morphogenic protein-7 (BMP-7) and hepatocyte growth factor (HGF). The present study investigates the potential role of CD44 standard (CD44s) and CD44v3-v10 (CD44v3) isoforms as modulators of the balance between TGF-\u03b21 and HGF\/BMP-7. CD44s is the shortest and most common isoform. CD44v3-v10 (CD44v3) has heparan sulfate moieties, which enable the binding to HGF\/BMP-7, and hence, might exert renoprotective effects. Using transgenic mice overexpressing either CD44s or CD44v3 specifically on proximal TEC, we found that in vitro the overexpression of CD44v3 on primary TEC renders cells less susceptible to TGF-\u03b21 profibrotic actions and more sensitive to BMP-7 and HGF compared with TEC overexpressing CD44s. One day after unilateral ureteric obstruction, obstructed kidneys from CD44v3 transgenic mice showed less tubular damage and myofibroblasts accumulation, which was associated with decreased TGF-\u03b21 signaling and increased BMP-7 synthesis and signaling compared with kidneys from wild-type and CD44s transgenic mice. These data suggest that CD44v3 plays a renoprotective role in early stage of chronic obstructive nephropathy.<\/jats:p>","DOI":"10.1152\/ajprenal.00340.2013","type":"journal-article","created":{"date-parts":[[2013,9,12]],"date-time":"2013-09-12T01:03:09Z","timestamp":1378947789000},"page":"F1445-F1454","source":"Crossref","is-referenced-by-count":7,"title":["CD44v3-v10 reduces the profibrotic effects of TGF-\u03b21 and attenuates tubular injury in the early stage of chronic obstructive nephropathy"],"prefix":"10.1152","volume":"305","author":[{"given":"Elena","family":"Rampanelli","sequence":"first","affiliation":[{"name":"Department of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands;"}]},{"given":"Kasper","family":"Rouschop","sequence":"additional","affiliation":[{"name":"Maastricht Radiation Oncology (Maastro), GROW School for Oncology and Developmental Biology, University of Maastricht, Maastricht, The Netherlands; and"}]},{"given":"Gwendoline J. D.","family":"Teske","sequence":"additional","affiliation":[{"name":"Department of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands;"}]},{"given":"Nike","family":"Claessen","sequence":"additional","affiliation":[{"name":"Department of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands;"}]},{"given":"Jaklien C.","family":"Leemans","sequence":"additional","affiliation":[{"name":"Department of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands;"}]},{"given":"Sandrine","family":"Florquin","sequence":"additional","affiliation":[{"name":"Department of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands;"},{"name":"Department of Pathology, Radboud University Nijmegen Center, Nijmegen, The Netherlands"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00382.x"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200003000-00006"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.128.4.687"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.298"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M204320200"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1038\/sj.emboj.7601421"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1006\/excr.1999.4391"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/17.11.3091"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1097\/TP.0b013e3181bcccea"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00417.x"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.0021.2001"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1053\/ajkd.2002.30563"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.64.s86.4.x"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1038\/ncb0808-883"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00103.x"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1186\/1476-9255-7-19"},{"key":"B17","doi-asserted-by":"crossref","first-page":"9165","DOI":"10.1016\/S0021-9258(18)98327-4","volume":"268","author":"Graziani A","year":"1993","journal-title":"J Biol Chem"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.128.4.673"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1097\/00005176-199007000-00018"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00052.2009"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-291X(03)01500-6"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M210559200"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1172\/JCI0215518"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)64092-8"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1097\/TP.0b013e3181e86b42"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1165\/rcmb.2002-0243OC"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajplung.00410.2007"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1002\/path.2844"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2010.090459"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.E05-08-0767"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1042\/CS20120252"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.2741\/3035"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.2741\/3211"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1093\/carcin\/bgp183"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.167.8.4368"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.2174\/1566524054553478"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00580.x"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1101\/gad.242602"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfq518"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00767.x"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200402138"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1038\/nrm1004"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009070722"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00576.2007"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00479.x"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5001711"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000115703.30835.96"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.312"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1172\/JCI200319270"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.00141.2010"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.89.24.12160"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/12.7.1344"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.16.9490"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1995.2267"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.10.6499"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117866"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/14.11.2554"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1002\/path.2277"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1053\/ajkd.2001.27422"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2007.07.146"},{"key":"B61","doi-asserted-by":"crossref","first-page":"163","DOI":"10.1101\/gad.14.2.163","volume":"14","author":"Yu Q","year":"2000","journal-title":"Genes Dev"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1101\/gad.925702"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1038\/nm888"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfh060"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00480.2005"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00340.2013","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,3,6]],"date-time":"2022-03-06T02:23:44Z","timestamp":1646533424000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00340.2013"}},"issued":{"date-parts":[[2013,11,15]]},"references-count":65,"journal-issue":{"issue":"10","published-print":{"date-parts":[[2013,11,15]]}},"alternative-id":["10.1152\/ajprenal.00340.2013"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00340.2013","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2013,11,15]]}},{"indexed":{"date-parts":[[2025,9,17]],"date-time":"2025-09-17T14:55:02Z","timestamp":1758120902453},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1984,11,1]]},"abstract":"<jats:p> To examine the interactions among the renal nerves, prostaglandins, and renal arterial pressure in the regulation of renin secretion, experiments using low-frequency renal nerve stimulation (LFRNS; supramaximal voltage, 0.5 ms, 0.5 Hz) were performed in anesthetized dogs. LFRNS, which did not affect renal hemodynamics or urinary sodium excretion, increased renin secretion rate before (79 +\/- 16 ng\/min) but significantly less after renal arterial administration of indomethacin or meclofenamate (26 +\/- 7 ng\/min). In a separate group of dogs, LFRNS increased both renin secretion rate (266 +\/- 139 ng\/min) and renal prostaglandin E2 secretion rate (2,080 +\/- 635 ng\/min). LFRNS does not alter input stimuli to the renal vascular baroreceptor or tubular macula densa receptor mechanisms for renin secretion and represents a direct neural stimulus for renin secretion; this also increases renal prostaglandin E2 secretion rate, which contributes to the increase in renin secretion rate. The renin secretion rate response of innervated and denervated kidneys to reduction in renal arterial pressure to 50 mmHg was examined before and after indomethacin\/meclofenamate administration. The observation that indomethacin\/meclofenamate decreased but did not abolish the renin secretion rate response to aortic constriction in innervated kidneys suggests the presence of a prostaglandin-independent mechanism that is mediated by an interaction between the renal nerves and the tubular macula densa receptor, as indomethacin\/meclofenamate essentially abolished the renin secretion rate response to aortic constriction in denervated kidneys. <\/jats:p>","DOI":"10.1152\/ajprenal.1984.247.5.f706","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T15:59:48Z","timestamp":1513958388000},"page":"F706-F713","source":"Crossref","is-referenced-by-count":5,"title":["Interactions among renal nerves, prostaglandins, and renal arterial pressure in the regulation of renin release"],"prefix":"10.1152","volume":"247","author":[{"given":"J. L.","family":"Osborn","sequence":"first","affiliation":[]},{"given":"U. C.","family":"Kopp","sequence":"additional","affiliation":[]},{"given":"M. D.","family":"Thames","sequence":"additional","affiliation":[]},{"given":"G. F.","family":"DiBona","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1984.247.5.F706","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:29:29Z","timestamp":1567967369000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1984.247.5.F706"}},"issued":{"date-parts":[[1984,11,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1984,11,1]]}},"alternative-id":["10.1152\/ajprenal.1984.247.5.F706"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1984.247.5.f706","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1984,11,1]]}},{"indexed":{"date-parts":[[2025,5,23]],"date-time":"2025-05-23T12:49:00Z","timestamp":1748004540205},"reference-count":51,"publisher":"American Physiological Society","issue":"11","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,6,1]]},"abstract":"<jats:p>Renal ischemia-reperfusion injury (IRI) is a common cause of acute kidney injury (AKI), occurring with hypotension and cardiovascular surgery and inevitably during kidney transplantation. Mortality from AKI is high due to incomplete knowledge of the pathogenesis of IRI and the lack of an effective therapy. Inflammation accompanies IRI and increases the blood level of C-reactive protein (CRP), a biomarker of worsened outcomes in AKI. To test if CRP is causal in AKI we subjected wild-type mice (WT) and human CRP transgenic mice (CRPtg) to bilateral renal IRI (both pedicles clamped for 30 min at 37\u00b0C then reperfused for 24 h). Serum human CRP level was increased approximately sixfold after IRI in CRPtg (10.62 \u00b1 1.31 \u03bcg\/ml at baseline vs. 72.01 \u00b1 9.41 \u03bcg\/ml at 24 h) but was not elevated by sham surgery wherein kidneys were manipulated but not clamped. Compared with WT, serum creatinine, urine albumin, and histological evidence of kidney damage were increased after IRI in CRPtg mice. RT-PCR analysis of mRNA isolated from whole kidneys of CRPtg and WT subjected to IRI revealed that in CRPtg kidneys 1) upregulation of markers of macrophage classical activation (M1 markers) was blunted, 2) downregulation of markers of macrophage alternative activation (M2 markers) was more robust, and 3) expression of the activating receptor Fc\u03b3RI was increased. Our finding that CRP exacerbates IRI-induced AKI, perhaps by shifting the balance of macrophage activation and Fc\u03b3R expression towards a detrimental portfolio, might make CRP a promising therapeutic target for the treatment of AKI.<\/jats:p>","DOI":"10.1152\/ajprenal.00476.2012","type":"journal-article","created":{"date-parts":[[2013,3,28]],"date-time":"2013-03-28T02:40:33Z","timestamp":1364438433000},"page":"F1358-F1365","source":"Crossref","is-referenced-by-count":38,"title":["C-reactive protein exacerbates renal ischemia-reperfusion injury"],"prefix":"10.1152","volume":"304","author":[{"given":"Melissa A.","family":"Pegues","sequence":"first","affiliation":[{"name":"Department of Medicine, University of Alabama, Birmingham, Alabama"}]},{"given":"Mark A.","family":"McCrory","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Alabama, Birmingham, Alabama"}]},{"given":"Abolfazl","family":"Zarjou","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Alabama, Birmingham, Alabama"}]},{"given":"Alexander J.","family":"Szalai","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Alabama, Birmingham, Alabama"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1155\/2009\/137072"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2011.217"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfs256"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20072565"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1159\/000320595"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1002\/j.1460-2075.1987.tb02745.x"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1161\/ATVBAHA.111.225508"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199902113400607"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2011.241"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00431.x"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1084\/jem.123.2.365"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.182"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1002\/immu.200390018"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1159\/000319871"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1161\/01.ATV.0000013786.80104.D4"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/j.clim.2008.08.016"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1038\/mtna.2012.44"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfm694"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009060615"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.5414\/CN106921"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1038\/labinvest.2011.42"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.380"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1007\/s00125-011-2237-y"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1018369108"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1161\/01.ATV.0000147407.17137.02"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.02610607"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1006\/jaut.2002.0615"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1038\/nri2448"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2004-03-1109"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9343(00)00612-4"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1016\/j.transproceed.2007.02.023"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M407629200"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1172\/JCI36150"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.178.1.530"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2011.16"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000042700.48769.59"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00210.x"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1172\/JCI7817"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00762.x"},{"key":"B40","doi-asserted-by":"crossref","first-page":"5294","DOI":"10.4049\/jimmunol.160.11.5294","volume":"160","author":"Szalai AJ","year":"1998","journal-title":"J Immunol"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1002\/art.11026"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M110277200"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfl511"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1016\/S0161-5890(01)00042-6"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2008.070825"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1042\/bj2660283"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1002\/art.20672"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1186\/1471-2369-12-30"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(00)70200-9"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00072.2006"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00594.2010"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00476.2012","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,6,30]],"date-time":"2023-06-30T18:04:21Z","timestamp":1688148261000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00476.2012"}},"issued":{"date-parts":[[2013,6,1]]},"references-count":51,"journal-issue":{"issue":"11","published-print":{"date-parts":[[2013,6,1]]}},"alternative-id":["10.1152\/ajprenal.00476.2012"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00476.2012","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2013,6,1]]}},{"indexed":{"date-parts":[[2025,5,15]],"date-time":"2025-05-15T05:47:56Z","timestamp":1747288076532},"reference-count":45,"publisher":"American Physiological Society","issue":"7","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,4,1]]},"abstract":"<jats:p> This study tested the hypothesis that Rho kinase contributes to the enhanced pressor response to acute angiotensin II in intact male growth-restricted and gonadectomized female growth-restricted rats. Mean arterial pressure (MAP) and renal function were determined in conscious animals pretreated with enalapril (250 mg\/l in drinking water) for 1 wk to block the endogenous renin-angiotensin system and normalize blood pressure (baseline). Blood pressure and renal hemodynamics did not differ at baseline. Acute Ang II (100 ng\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7min<jats:sup>\u22121<\/jats:sup>) induced a greater increase in MAP and renal vascular resistance and enhanced reduction in glomerular filtration rate in intact male growth-restricted rats compared with intact male controls ( P &lt; 0.05). Cotreatment with the Rho kinase inhibitor fasudil (33 \u03bcg\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7min<jats:sup>\u22121<\/jats:sup>) significantly attenuated these hemodynamic changes ( P &lt; 0.05), but it did not abolish the differential increase in blood pressure above baseline, suggesting that the impact of intrauterine growth restriction on blood pressure in intact male growth-restricted rats is independent of Rho kinase. Gonadectomy in conjunction with fasudil returned blood pressure back to baseline in male growth-restricted rats, and yet glomerular filtration rate remained significantly reduced ( P &lt; 0.05). Thus, these data suggest a role for enhanced renal sensitivity to acute Ang II in the developmental programming of hypertension in male growth-restricted rats. However, inhibition of Rho kinase had no effect on the basal or enhanced increase in blood pressure induced by acute Ang II in the gonadectomized female growth-restricted rat. Therefore, these studies suggest that Rho kinase inhibition exerts a sex-specific effect on blood pressure sensitivity to acute Ang II in growth-restricted rats. <\/jats:p>","DOI":"10.1152\/ajprenal.00687.2012","type":"journal-article","created":{"date-parts":[[2013,1,24]],"date-time":"2013-01-24T05:25:23Z","timestamp":1359005123000},"page":"F900-F907","source":"Crossref","is-referenced-by-count":21,"title":["Sex differences in the enhanced responsiveness to acute angiotensin II in growth-restricted rats: role of fasudil, a Rho kinase inhibitor"],"prefix":"10.1152","volume":"304","author":[{"given":"Norma B.","family":"Ojeda","sequence":"first","affiliation":[{"name":"Department of Pediatrics, University of Mississippi Medical Center, Jackson, Mississippi;"},{"name":"Department of Physiology, University of Mississippi Medical Center, Jackson, Mississippi; and"},{"name":"Women's Health Research Center, University of Mississippi Medical Center, Jackson, Mississippi"}]},{"given":"Thomas P.","family":"Royals","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Mississippi Medical Center, Jackson, Mississippi; and"}]},{"given":"Barbara T.","family":"Alexander","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Mississippi Medical Center, Jackson, Mississippi; and"},{"name":"Women's Health Research Center, University of Mississippi Medical Center, Jackson, Mississippi"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00446.2003"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000053448.95913.3D"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000153319.20340.2a"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0b013e3283406f57"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1111\/j.1743-6109.2009.01282.x"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1097\/00005344-200210000-00002"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1161\/ATVBAHA.111.228304"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1016\/j.cardiores.2007.06.029"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00725.2006"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1038\/nm.2079"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1016\/0002-9343(72)90050-2"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.111.184986"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.110.166827"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000238125.21656.9e"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1161\/01.STR.0000039340.62995.F2"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.01232.2007"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.110.168674"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2010.187849"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00641.2009"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1007\/s11906-011-0187-x"},{"key":"B21","author":"Nuno DW","journal-title":"Exp Diabetes Res"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00045.2011"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.107.091785"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00311.2006"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.112.192955"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00219.2011"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00096.2010"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000111832.47667.13"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-201X.2004.01328.x"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.2012.02468.x"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1186\/2042-6410-3-7"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00638.2009"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00364.2005"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1016\/j.cardiores.2006.09.007"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00864.2007"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1089\/ars.2005.7.1302"},{"key":"B37","doi-asserted-by":"crossref","first-page":"1791","DOI":"10.1097\/01.hjh.0000420814.28280.42","volume":"30","author":"Viegas VU","year":"2012","journal-title":"J Hypertens"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1097\/01.hjh.0000234125.01638.3b"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00178.2004"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2005.084889"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200007000-00014"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1203\/00006450-200104000-00005"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00037.2003"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.2011.01437.x"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.107.106203"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00687.2012","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:38:09Z","timestamp":1567971489000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00687.2012"}},"issued":{"date-parts":[[2013,4,1]]},"references-count":45,"journal-issue":{"issue":"7","published-print":{"date-parts":[[2013,4,1]]}},"alternative-id":["10.1152\/ajprenal.00687.2012"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00687.2012","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2013,4,1]]}},{"indexed":{"date-parts":[[2025,7,15]],"date-time":"2025-07-15T03:45:50Z","timestamp":1752551150681,"version":"3.37.3"},"reference-count":54,"publisher":"American Physiological Society","issue":"3","funder":[{"DOI":"10.13039\/501100002347","name":"Bundesministerium f\u00fcr Bildung und Forschung","doi-asserted-by":"publisher","award":["01GM1518B"],"award-info":[{"award-number":["01GM1518B"]}],"id":[{"id":"10.13039\/501100002347","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100002347","name":"Bundesministerium f\u00fcr Bildung und Forschung","doi-asserted-by":"publisher","award":["01GM1901B"],"award-info":[{"award-number":["01GM1901B"]}],"id":[{"id":"10.13039\/501100002347","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100006360","name":"Bundesministerium f\u00fcr Wirtschaft und Energie","doi-asserted-by":"publisher","award":["16KN077229"],"award-info":[{"award-number":["16KN077229"]}],"id":[{"id":"10.13039\/501100006360","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2024,9,1]]},"abstract":"<jats:p> This research investigated the use of nifurpirinol in nanomolar amounts as a prodrug to reliably induce focal segmental glomerulosclerosis (FSGS)-like damage in transgenic zebrafish larvae. Through proteomic analysis of isolated zebrafish glomeruli, we were further able to identify proteins that are significantly regulated after the manifestation of FSGS. These results are expected to expand our knowledge of the pathomechanism of FSGS. <\/jats:p>","DOI":"10.1152\/ajprenal.00116.2024","type":"journal-article","created":{"date-parts":[[2024,7,11]],"date-time":"2024-07-11T18:01:11Z","timestamp":1720720871000},"page":"F463-F475","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["Investigating FSGS-like injury in zebrafish larvae by nifurpirinol: efficacy and molecular insight"],"prefix":"10.1152","volume":"327","author":[{"ORCID":"https:\/\/orcid.org\/0009-0005-9149-7335","authenticated-orcid":false,"given":"Marianne","family":"Klawitter","sequence":"first","affiliation":[{"name":"Department of Anatomy and Cell Biology, University Medicine Greifswald, Greifswald, Germany"}]},{"given":"Francescapaola","family":"Mattias","sequence":"additional","affiliation":[{"name":"Department of Anatomy and Cell Biology, University Medicine Greifswald, Greifswald, Germany"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8717-5927","authenticated-orcid":false,"given":"Felix","family":"Kliewe","sequence":"additional","affiliation":[{"name":"Department of Anatomy and Cell Biology, University Medicine Greifswald, Greifswald, Germany"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1507-0402","authenticated-orcid":false,"given":"Elke","family":"Hammer","sequence":"additional","affiliation":[{"name":"Interfaculty Institute for Genetics and Functional Genomics, University Medicine Greifswald, Greifswald, Germany"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5689-3448","authenticated-orcid":false,"given":"Uwe","family":"V\u00f6lker","sequence":"additional","affiliation":[{"name":"Interfaculty Institute for Genetics and Functional Genomics, University Medicine Greifswald, Greifswald, Germany"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9371-2709","authenticated-orcid":false,"given":"Stefan","family":"Simm","sequence":"additional","affiliation":[{"name":"Institute of Bioinformatics, University Medicine Greifswald, Greifswald, Germany"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1629-4982","authenticated-orcid":false,"given":"Florian","family":"Siegerist","sequence":"additional","affiliation":[{"name":"Department of Anatomy and Cell Biology, University Medicine Greifswald, Greifswald, Germany"}]},{"given":"Sophie","family":"Daniel","sequence":"additional","affiliation":[{"name":"Department of Anatomy and Cell Biology, University Medicine Greifswald, Greifswald, Germany"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8549-510X","authenticated-orcid":false,"given":"Maximilian","family":"Schindler","sequence":"additional","affiliation":[{"name":"Department of Anatomy and Cell Biology, University Medicine Greifswald, Greifswald, Germany"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6817-4099","authenticated-orcid":false,"given":"Nicole","family":"Endlich","sequence":"additional","affiliation":[{"name":"Department of Anatomy and Cell Biology, University Medicine Greifswald, Greifswald, Germany"}]}],"member":"24","reference":[{"doi-asserted-by":"publisher","key":"B1","DOI":"10.1016\/S0140-6736(20)30045-3"},{"doi-asserted-by":"publisher","key":"B2","DOI":"10.1016\/S0272-6386(97)90485-6"},{"doi-asserted-by":"publisher","key":"B3","DOI":"10.1056\/NEJMra1106556"},{"doi-asserted-by":"publisher","key":"B4","DOI":"10.1681\/ASN.2017090958"},{"doi-asserted-by":"publisher","key":"B5","DOI":"10.1046\/j.1523-1755.1998.00044.x"},{"doi-asserted-by":"publisher","key":"B6","DOI":"10.1152\/physrev.00020.2002"},{"doi-asserted-by":"publisher","key":"B7","DOI":"10.1038\/nm0502-522"},{"doi-asserted-by":"publisher","key":"B8","DOI":"10.1681\/ASN.V1261164"},{"doi-asserted-by":"publisher","key":"B9","DOI":"10.1681\/ASN.2012030302"},{"doi-asserted-by":"publisher","key":"B10","DOI":"10.1152\/ajprenal.00478.2012"},{"doi-asserted-by":"publisher","key":"B11","DOI":"10.1093\/ndt\/13.6.1368"},{"doi-asserted-by":"publisher","key":"B12","DOI":"10.1016\/S0272-6386(97)90005-6"},{"doi-asserted-by":"publisher","key":"B13","DOI":"10.1016\/j.kint.2021.05.015"},{"doi-asserted-by":"publisher","key":"B14","DOI":"10.1016\/j.xkme.2022.100501"},{"key":"B15","first-page":"213","volume":"10","author":"Cameron JS","year":"1978","journal-title":"Clin Nephrol"},{"doi-asserted-by":"publisher","key":"B16","DOI":"10.1681\/ASN.2014090859"},{"doi-asserted-by":"publisher","key":"B17","DOI":"10.1152\/ajprenal.00338.2017"},{"doi-asserted-by":"publisher","key":"B18","DOI":"10.1681\/ASN.0000000000000235"},{"doi-asserted-by":"publisher","key":"B19","DOI":"10.1111\/apha.12754"},{"doi-asserted-by":"publisher","key":"B20","DOI":"10.1038\/srep43655"},{"doi-asserted-by":"publisher","key":"B21","DOI":"10.1016\/j.ydbio.2007.06.022"},{"doi-asserted-by":"publisher","key":"B22","DOI":"10.1038\/ki.2011.256"},{"doi-asserted-by":"publisher","key":"B23","DOI":"10.1152\/ajprenal.00335.2023"},{"doi-asserted-by":"publisher","key":"B24","DOI":"10.1038\/nature12111"},{"doi-asserted-by":"publisher","key":"B25","DOI":"10.1242\/dev.125.23.4655"},{"doi-asserted-by":"publisher","key":"B26","DOI":"10.1096\/fj.202000724R"},{"doi-asserted-by":"publisher","key":"B27","DOI":"10.1681\/ASN.2011080776"},{"doi-asserted-by":"publisher","key":"B28","DOI":"10.1186\/1471-213X-10-76"},{"doi-asserted-by":"publisher","key":"B29","DOI":"10.1111\/wrr.12633"},{"doi-asserted-by":"publisher","key":"B30","DOI":"10.1371\/journal.pone.0242436"},{"doi-asserted-by":"publisher","key":"B32","DOI":"10.1038\/nmeth.2019"},{"doi-asserted-by":"publisher","key":"B33","DOI":"10.1002\/pmic.201900192"},{"doi-asserted-by":"publisher","key":"B34","DOI":"10.1038\/s41598-017-05949-y"},{"doi-asserted-by":"publisher","key":"B35","DOI":"10.1016\/j.xinn.2021.100141"},{"doi-asserted-by":"publisher","key":"B36","DOI":"10.1111\/jcmm.13816"},{"doi-asserted-by":"publisher","key":"B37","DOI":"10.1093\/ndt\/gfl113"},{"doi-asserted-by":"publisher","key":"B38","DOI":"10.1016\/j.pathol.2022.10.016"},{"doi-asserted-by":"publisher","key":"B39","DOI":"10.1007\/s00125-011-2178-5"},{"doi-asserted-by":"publisher","key":"B40","DOI":"10.1126\/science.1260419"},{"doi-asserted-by":"publisher","key":"B41","DOI":"10.1681\/ASN.2006060675"},{"doi-asserted-by":"publisher","key":"B42","DOI":"10.1681\/ASN.2021030294"},{"doi-asserted-by":"publisher","key":"B43","DOI":"10.1038\/ki.2015.197"},{"doi-asserted-by":"publisher","key":"B44","DOI":"10.1681\/ASN.2019101032"},{"doi-asserted-by":"publisher","key":"B45","DOI":"10.1038\/sj.ki.5000160"},{"doi-asserted-by":"publisher","key":"B46","DOI":"10.1016\/j.ajpath.2014.08.007"},{"doi-asserted-by":"publisher","key":"B47","DOI":"10.1093\/ndt\/gft511"},{"doi-asserted-by":"publisher","key":"B48","DOI":"10.1038\/ki.2009.386"},{"doi-asserted-by":"publisher","key":"B49","DOI":"10.1681\/ASN.2008070709"},{"doi-asserted-by":"publisher","key":"B50","DOI":"10.1016\/j.kint.2019.01.037"},{"doi-asserted-by":"publisher","key":"B51","DOI":"10.1111\/j.1523-1755.2005.00568.x"},{"doi-asserted-by":"publisher","key":"B52","DOI":"10.1016\/0002-9343(72)90017-4"},{"doi-asserted-by":"publisher","key":"B53","DOI":"10.1038\/ki.2010.21"},{"doi-asserted-by":"publisher","key":"B54","DOI":"10.3389\/fendo.2023.1083614"},{"doi-asserted-by":"publisher","key":"B55","DOI":"10.1371\/journal.pone.0017838"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00116.2024","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,8,20]],"date-time":"2024-08-20T18:52:46Z","timestamp":1724179966000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00116.2024"}},"issued":{"date-parts":[[2024,9,1]]},"references-count":54,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2024,9,1]]}},"alternative-id":["10.1152\/ajprenal.00116.2024"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00116.2024","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2024,9,1]]},"assertion":[{"value":"2024-04-12","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2024-06-14","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2024-06-28","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2024-08-20","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2025,7,31]],"date-time":"2025-07-31T00:38:02Z","timestamp":1753922282430,"version":"3.40.5"},"reference-count":46,"publisher":"American Physiological Society","issue":"6","funder":[{"name":"Swedish Heart and Lung Foundation","award":["20140416"],"award-info":[{"award-number":["20140416"]}]},{"name":"Medical Faculty ALF-grant"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2019,6,1]]},"abstract":"<jats:p> Emerging evidence indicates that endogenous production of endothelin (ET)-1, a 21-amino acid peptide vasoconstrictor, plays an important role in proteinuric kidney disease. Previous studies in rats have shown that chronic administration of ET-1 leads to increased glomerular albumin leakage. The underlying mechanisms are, however, currently not known. Here, we used size-exclusion chromatography to measure glomerular sieving coefficients for neutral FITC-Ficoll (molecular Stokes-Einstein radius: 15\u201380 \u00c5, molecular weight: 70 kDa\/400 kDa) in anesthetized male Sprague-Dawley rats ( n = 12) at baseline and at 5, 15, 30, and 60 min after intravenous administration of ET-1. In separate experiments, ET-1 was given together with the selective ET type A (ET<jats:sub>A<\/jats:sub>) or ET type B (ET<jats:sub>B<\/jats:sub>) receptor antagonists JKC-301 and BQ-788, respectively. At both 15 and 30 min postadministration, the glomerular sieving coefficient for macromolecular Ficoll (70 \u00c5) was significantly increased to 4.4 \u00d7 10<jats:sup>\u22125<\/jats:sup>\u2009\u00b1\u20090.7 \u00d7 10<jats:sup>\u22125<\/jats:sup> ( P = 0.024) and 4.5 \u00d7 10<jats:sup>\u22125<\/jats:sup>\u2009\u00b1\u20090.8 \u00d7 10<jats:sup>\u22125<\/jats:sup> ( P = 0.007), respectively, compared with baseline (2.2 \u00d7 10<jats:sup>\u22125<\/jats:sup>\u2009\u00b1\u20090.4 \u00d710<jats:sup>\u22125<\/jats:sup>). Decreased urine production after ET-1 prevented the use of higher doses of ET-1. Data analysis using the two-pore model indicated changes in large-pore permeability after ET-1, with no changes in the small-pore pathway. Administration of ET<jats:sub>A<\/jats:sub> blocker abrogated the permeability changes induced by ET-1 at 30 min, whereas blockade of ET<jats:sub>B<\/jats:sub> receptors was ineffective. Mean arterial pressure was only significantly increased at 60 min, being 123\u2009\u00b1\u20094 mmHg compared with 111\u2009\u00b1\u20092 mmHg at baseline ( P = 0.02). We conclude that ET-1 evoked small, delayed, and sustained increases in glomerular permeability, mediated via the ET<jats:sub>A<\/jats:sub> receptor. <\/jats:p>","DOI":"10.1152\/ajprenal.00040.2019","type":"journal-article","created":{"date-parts":[[2019,3,13]],"date-time":"2019-03-13T10:38:41Z","timestamp":1552473521000},"page":"F1173-F1179","source":"Crossref","is-referenced-by-count":8,"title":["Sustained, delayed, and small increments in glomerular permeability to macromolecules during systemic ET-1 infusion mediated via the ET<sub>A<\/sub> receptor"],"prefix":"10.1152","volume":"316","author":[{"given":"Julia","family":"Dolinina","sequence":"first","affiliation":[{"name":"Department of Nephrology, Sk\u00e5ne University Hospital, Clinical Sciences Lund, Lund University, Lund, Sweden"}]},{"given":"Anna","family":"Rippe","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Sk\u00e5ne University Hospital, Clinical Sciences Lund, Lund University, Lund, Sweden"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2471-6914","authenticated-orcid":false,"given":"Carl M.","family":"\u00d6berg","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Sk\u00e5ne University Hospital, Clinical Sciences Lund, Lund University, Lund, Sweden"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00488.2005"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00153.2012"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00710.2009"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00154.2013"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/j.memsci.2012.03.001"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1172\/JCI113880"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2013.58-c1"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0000000000000185"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1985.249.3.F374"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00610.2017"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2016.02.018"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/j.tcb.2007.06.006"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00312.2009"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00097.2007"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00498.2017"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00190.2006"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1002\/bdd.2510030408"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1042\/cs0900385"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.pharmtox.41.1.851"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1159\/000328687"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2014.143"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1172\/JCI114079"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00373.2015"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2011040369"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00220.2015"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009060593"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00016.x"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00066.2017"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00366.2013"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00621.2012"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1016\/j.cardfail.2004.05.006"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1016\/j.jchf.2017.02.021"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1096\/fasebj.9.12.7672512"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.273.5.F749"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1111\/sdi.12534"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.3747\/pdi.2014.00110"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2011020158"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1016\/j.lfs.2012.06.007"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1038\/nm.3843"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1038\/nature19319"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013010018"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1126\/scisignal.2001200"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.263.4.F601"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008050482"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2017.07.024"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1038\/332411a0"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00040.2019","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T14:12:13Z","timestamp":1567951933000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00040.2019"}},"issued":{"date-parts":[[2019,6,1]]},"references-count":46,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2019,6,1]]}},"alternative-id":["10.1152\/ajprenal.00040.2019"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00040.2019","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2019,6,1]]}},{"indexed":{"date-parts":[[2025,8,12]],"date-time":"2025-08-12T21:58:28Z","timestamp":1755035908424},"reference-count":12,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2016,12,1]]},"DOI":"10.1152\/ajprenal.00454.2016","type":"journal-article","created":{"date-parts":[[2016,12,12]],"date-time":"2016-12-12T20:50:32Z","timestamp":1481575832000},"page":"F1391-F1392","source":"Crossref","is-referenced-by-count":13,"title":["Inconsistent blood pressure phenotype in female Dahl salt-sensitive rats"],"prefix":"10.1152","volume":"311","author":[{"given":"Margaret A.","family":"Zimmerman","sequence":"first","affiliation":[{"name":"Department of Pharmacology, Tulane University, New Orleans, Louisiana"}]},{"given":"Sarah H.","family":"Lindsey","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Tulane University, New Orleans, Louisiana"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00061.2014"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/505612a"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00458.2015"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.114.04179"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00377.2014"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000142893.08655.96"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000153318.74544.cc"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.7.3.340"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1016\/j.steroids.2009.10.010"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.23.6.786"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.27.3.546"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.01322.2007"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00454.2016","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T17:23:33Z","timestamp":1567963413000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00454.2016"}},"issued":{"date-parts":[[2016,12,1]]},"references-count":12,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2016,12,1]]}},"alternative-id":["10.1152\/ajprenal.00454.2016"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00454.2016","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2016,12,1]]}},{"indexed":{"date-parts":[[2025,11,26]],"date-time":"2025-11-26T16:08:41Z","timestamp":1764173321389},"reference-count":27,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2006,11]]},"abstract":"<jats:p>A low nephron endowment may be associated with hypertension. Nephrogenesis is the process that leads to the formation of nephrons until week 36 of gestation in humans and may be inhibited by many factors like intrauterine growth restriction and premature birth. To study the consequences of a low glomerular number, animal models have been developed. We describe a model of postnatal food restriction in the rat in which litter size is increased to 20 pups, which leads to growth restriction. In the rat, active nephrogenesis continues until postnatal day 8, which coincides with the growth restriction in our model. Design-based stereological methods were used to estimate glomerular number and volume. Our results show an \u223c25% lower glomerular number in rats after postnatal food restriction (30,800 glomeruli\/kidney) compared with control rats (39,600 glomeruli\/kidney, P &lt; 0.001). Mean glomerular volume was increased by 35% in the growth-restricted rats ( P = 0.006). There was a significant negative correlation between glomerular volume and glomerular number ( r = \u22120.76, P &lt; 0.001). We conclude that postnatal food restriction in the rat leads to a low nephron endowment with compensatory enlargement. It is therefore a suitable model to study the effect of intrauterine growth restriction or prematurity on kidney development and the consequences of a reduced glomerular number in later life.<\/jats:p>","DOI":"10.1152\/ajprenal.00158.2006","type":"journal-article","created":{"date-parts":[[2006,6,15]],"date-time":"2006-06-15T00:28:33Z","timestamp":1150331313000},"page":"F1104-F1107","source":"Crossref","is-referenced-by-count":53,"title":["Postnatal food restriction in the rat as a model for a low nephron endowment"],"prefix":"10.1152","volume":"291","author":[{"given":"Michiel F.","family":"Schreuder","sequence":"first","affiliation":[]},{"given":"Jens R.","family":"Nyengaard","sequence":"additional","affiliation":[]},{"given":"Floor","family":"Remmers","sequence":"additional","affiliation":[]},{"given":"Joanna AE","family":"van Wijk","sequence":"additional","affiliation":[]},{"given":"Henriette A.","family":"Delemarre-van de Waal","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1093\/ajh\/1.4.335"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1651-2227.2004.tb00844.x"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1016\/j.ajog.2005.05.041"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1016\/j.bone.2003.04.001"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2818.1986.tb02764.x"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2818.1999.00457.x"},{"key":"R7","doi-asserted-by":"crossref","unstructured":"Guron G, Marcussen N, Nilsson A, Sundelin B, and Friberg P.Postnatal time frame for renal vulnerability to enalapril in rats.J Am Soc Nephrol10: 1550\u20131560, 1999.","DOI":"10.1681\/ASN.V1071550"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-0528.1992.tb13726.x"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1053\/anep.2003.50017"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1981.241.1.F85"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1177\/0148607103027004260"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00018.x"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000041"},{"key":"R14","doi-asserted-by":"crossref","unstructured":"Huizinga CT, Engelbregt MJ, Rekers-Mombarg LT, Vaessen SF, Delemarre-van de Waal HA, and Fodor M.Ligation of the uterine artery and early postnatal food restriction\u2014animal models for growth retardation.Horm Res62: 233\u2013240, 2004.","DOI":"10.1159\/000081467"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(02)09834-3"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.36.2.286"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa020549"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1007\/s004670050374"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-199212007-00010"},{"key":"R20","unstructured":"Nigam SK, Aperia AC, and Brenner BM.Development and maturation of the kidney. In:Brenner and Rector's The Kidney, edited by Brenner BM. Philadelphia, PA: Saunders, 1996, p. 72\u201398."},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1006\/mvre.1993.1022"},{"key":"R22","doi-asserted-by":"crossref","unstructured":"Nyengaard JR.Stereologic methods and their application in kidney research.J Am Soc Nephrol10: 1100\u20131123, 1999.","DOI":"10.1681\/ASN.V1051100"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.0590051663.x"},{"key":"R24","doi-asserted-by":"crossref","unstructured":"Pryde PG, Sedman AB, Nugent CE, and Barr M Jr.Angiotensin-converting enzyme inhibitor fetopathy.J Am Soc Nephrol3: 1575\u20131582, 1993.","DOI":"10.1681\/ASN.V391575"},{"key":"R25","doi-asserted-by":"crossref","unstructured":"Rodriguez MM, Gomez AH, Abitbol CL, Chandar JJ, Duara S, and Zilleruelo GE.Histomorphometric analysis of postnatal glomerulogenesis in extremely preterm infants.Pediatr Dev Pathol7: 17\u201325, 2004.","DOI":"10.1007\/s10024-003-3029-2"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004100875"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2818.1984.tb02501.x"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00158.2006","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,7,28]],"date-time":"2021-07-28T10:50:45Z","timestamp":1627469445000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00158.2006"}},"issued":{"date-parts":[[2006,11]]},"references-count":27,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2006,11]]}},"alternative-id":["10.1152\/ajprenal.00158.2006"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00158.2006","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2006,11]]}},{"indexed":{"date-parts":[[2025,11,27]],"date-time":"2025-11-27T10:43:09Z","timestamp":1764240189139,"version":"3.37.3"},"reference-count":44,"publisher":"American Physiological Society","issue":"1","funder":[{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)","doi-asserted-by":"publisher","award":["R01DK093462"],"award-info":[{"award-number":["R01DK093462"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2019,1,1]]},"abstract":"<jats:p> Aging is a risk factor for certain forms of kidney injury due to normal physiological changes, but the role of aging in cisplatin-induced kidney injury is not well defined in humans or animal models of the disease. To improve on current knowledge in this field, we treated 8- and 40-wk-old FVB\/n mice with one high dose of cisplatin as a model of acute kidney injury or with repeated low doses of cisplatin (7 mg\/kg cisplatin once a week for 4 wk) as a clinically relevant model of chronic kidney disease to determine if aging exacerbates cisplatin-induced kidney injury. Levels of acute kidney injury were comparable in 8- and 40-wk-old mice. In 40-wk-old mice, fibrotic markers were elevated basally, but treatment with cisplatin did not exacerbate fibrosis. We concluded that this may be the result of a decreased inflammatory response in 40-wk-old cisplatin-treated mice compared with 8-wk-old mice. Despite a decreased inflammatory response, the level of immune cell infiltration was greater in 40-wk-old cisplatin-treated mice than 8-wk-old mice. Our data highlight the importance of examining age as a risk factor for cisplatin-induced kidney injury. <\/jats:p>","DOI":"10.1152\/ajprenal.00463.2018","type":"journal-article","created":{"date-parts":[[2018,11,28]],"date-time":"2018-11-28T06:32:16Z","timestamp":1543386736000},"page":"F162-F172","source":"Crossref","is-referenced-by-count":15,"title":["Moderate aging does not exacerbate cisplatin-induced kidney injury or fibrosis despite altered inflammatory cytokine expression and immune cell infiltration"],"prefix":"10.1152","volume":"316","author":[{"given":"Cierra N.","family":"Sharp","sequence":"first","affiliation":[{"name":"Department of Pharmacology\/Toxicology, University of Louisville, Louisville, Kentucky"}]},{"given":"Mark","family":"Doll","sequence":"additional","affiliation":[{"name":"Department of Pharmacology\/Toxicology, University of Louisville, Louisville, Kentucky"}]},{"given":"Tess V.","family":"Dupre","sequence":"additional","affiliation":[{"name":"College of Pharmacology\/Toxicology, University of Arizona, Tucson, Arizona"}]},{"given":"Levi J.","family":"Beverly","sequence":"additional","affiliation":[{"name":"Department of Pharmacology\/Toxicology, University of Louisville, Louisville, Kentucky"},{"name":"Department of Medicine, University of Louisville, Louisville, Kentucky"},{"name":"James Graham Brown Cancer Center, Louisville, Kentucky"}]},{"given":"Leah J.","family":"Siskind","sequence":"additional","affiliation":[{"name":"Department of Pharmacology\/Toxicology, University of Louisville, Louisville, Kentucky"},{"name":"James Graham Brown Cancer Center, Louisville, Kentucky"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.3109\/1354750X.2015.1123354"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1111\/ped.12542"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1007\/s00134-009-1724-9"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/physiolgenomics.00071.2010"},{"key":"B5","first-page":"277","volume":"85","author":"Bolton WK","year":"1976","journal-title":"Am J Pathol"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1111\/j.0105-2896.2005.00276.x"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/j.jcgg.2013.04.002"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1097\/MD.0000000000001251"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00138.2007"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1001\/jama.298.17.2038"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1097\/00000421-200104000-00018"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2015.3"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1016\/0002-9343(84)90280-8"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.2174\/1389203717666160909152205"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00217.2015"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa1611391"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2015.327"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.2217\/cpr.14.46"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/S0074-7696(08)61527-2"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.3390\/toxins2112490"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2012080838"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.12811211"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1111\/j.1349-7006.1995.tb03315.x"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1186\/cc12540"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1155\/2014\/967826"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002786"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1111\/j.1532-5415.1990.tb01592.x"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.02780312"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2009.06.006"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1172\/JCI200215606"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1007\/s00109-015-1366-z"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1016\/j.amjsurg.2008.06.033"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pbio.0020427"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00543.2007"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00512.2015"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00285.2017"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejca.2009.06.032"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2016.183"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1200\/JCO.1994.12.10.2121"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2015010079"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.3390\/ijms150915358"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1007\/s11357-015-9844-3"},{"key":"B44","first-page":"755","volume":"109","author":"Wick G","year":"1997","journal-title":"Wien Klin Wochenschr"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1111\/j.1474-9726.2009.00478.x"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00463.2018","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,19]],"date-time":"2019-09-19T14:40:34Z","timestamp":1568904034000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00463.2018"}},"issued":{"date-parts":[[2019,1,1]]},"references-count":44,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2019,1,1]]}},"alternative-id":["10.1152\/ajprenal.00463.2018"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00463.2018","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2019,1,1]]}},{"indexed":{"date-parts":[[2025,10,17]],"date-time":"2025-10-17T19:46:58Z","timestamp":1760730418431},"reference-count":50,"publisher":"American Physiological Society","issue":"7","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,4,1]]},"abstract":"<jats:p>Tumor necrosis factor-alpha (TNF-\u03b1) has been implicated in salt-sensitive hypertension and renal injury (RI) induced by angiotensin II (ANG II). To determine the receptor type of TNF-\u03b1 involved in this mechanism, we evaluated the responses to chronic ANG II infusion (25 ng\/min by implanted minipump) given with high-salt diet (HS; 4% NaCl) for 2 wk in gene knockout mice for TNF-\u03b1 receptor type 1 (TNFR1KO; n = 6) and type 2 (TNFR2KO; n = 6) and compared the responses with those in wild-type (WT; C57BL\/6; n = 6) mice. Blood pressure in these mice was measured by implanted radiotelemetry as well as by tail-cuff plethysmography. RI responses were assessed by measuring macrophage cell infiltration (CD68<jats:sup>+<\/jats:sup>immunohistochemistry), glomerulosclerosis (PAS staining), and interstitial fibrosis (Gomori's trichrome staining) in renal tissues at the end of the treatment period. The increase in mean arterial pressure induced by ANG II + HS treatment was not different in these three groups of mice (TNFR1KO, 114 \u00b1 1 to 161 \u00b1 7 mmHg; TNFR2KO, 113 \u00b1 1 to 161 \u00b1 3 mmHg; WT, 110 \u00b1 3 to 154 \u00b1 3 mmHg). ANG II + HS-induced RI changes were similar in TNFR1KO mice but significantly less in TNFR2KO mice (macrophage infiltration, 0.02 \u00b1 0.01 vs. 1.65 \u00b1 0.45 cells\/mm<jats:sup>2<\/jats:sup>; glomerulosclerosis, 26.3 \u00b1 2.6 vs. 35.7 \u00b1 2.2% area; and interstitial fibrosis, 5.2 \u00b1 0.6 vs. 8.1 \u00b1 1.1% area) compared with the RI changes in WT mice. The results suggest that a direct activation of TNF-\u03b1 receptors may not be required in inducing hypertensive response to chronic ANG II administration with HS intake, but the induction of inflammatory responses leading to renal injury are mainly mediated by TNF-\u03b1 receptor type 2.<\/jats:p>","DOI":"10.1152\/ajprenal.00525.2012","type":"journal-article","created":{"date-parts":[[2013,2,7]],"date-time":"2013-02-07T06:58:13Z","timestamp":1360220293000},"page":"F991-F999","source":"Crossref","is-referenced-by-count":34,"title":["TNF-\u03b1 type 2 receptor mediates renal inflammatory response to chronic angiotensin II administration with high salt intake in mice"],"prefix":"10.1152","volume":"304","author":[{"given":"Purnima","family":"Singh","sequence":"first","affiliation":[{"name":"Department of Physiology, Hypertension &amp; Renal Center of Excellence, Tulane, University Health Sciences Center, New Orleans, Louisiana"}]},{"given":"Laleh","family":"Bahrami","sequence":"additional","affiliation":[{"name":"Department of Physiology, Hypertension &amp; Renal Center of Excellence, Tulane, University Health Sciences Center, New Orleans, Louisiana"}]},{"given":"Alexander","family":"Castillo","sequence":"additional","affiliation":[{"name":"Department of Physiology, Hypertension &amp; Renal Center of Excellence, Tulane, University Health Sciences Center, New Orleans, Louisiana"}]},{"given":"Dewan S. A.","family":"Majid","sequence":"additional","affiliation":[{"name":"Department of Physiology, Hypertension &amp; Renal Center of Excellence, Tulane, University Health Sciences Center, New Orleans, Louisiana"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1002\/j.1460-2075.1994.tb06327.x"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1989.98"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1007\/s001090000168"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1007\/BF03401714"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00426.2011"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1097\/HJH.0b013e3282fe6eaa"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00344.2010"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.0902514"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/j.lfs.2012.02.022"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1038\/hr.2009.91"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00466.2007"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000198545.01860.90"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1038\/372560a0"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-199715120-00016"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1093\/ajcp\/20.7_ts.661"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00153.2006"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20070657"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(92)91638-U"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.1998.tb02258.x"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1991.201"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00300.x"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004080676"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00047.2010"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000169152.59854.36"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00351.2011"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00708.2005"},{"key":"B27","doi-asserted-by":"crossref","first-page":"598","DOI":"10.4049\/jimmunol.158.2.598","volume":"158","author":"Lin RH","year":"1997","journal-title":"J Immunol"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1002\/jlb.61.5.551"},{"key":"B29","volume-title":"Histopathological Methods and Color Atlas of Special Stains and Tissue Artifacts","author":"Luna LG","year":"1992","edition":"1"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.35.2.587"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1053\/gast.2002.30347"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)64445-8"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.35.1.193"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.16.10784"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00101.2003"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.105.088062"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1038\/364798a0"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.62.s82.4.x"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1007\/BF01793854"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90297.2008"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1006\/taap.2001.9304"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.107.102152"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1006\/clim.2001.5027"},{"key":"B44","first-page":"281","volume":"38","author":"Thommesen L","year":"2005","journal-title":"J Biochem Mol Biol"},{"key":"B45","volume-title":"Theory and practice of histological techniques","author":"Totty Mucins BA","year":"2008"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1172\/JCI200523348"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1161\/hh0901.089987"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1152\/ajplung.00301.2011"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000085649.28268.DF"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1038\/377348a0"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00525.2012","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,6,29]],"date-time":"2023-06-29T09:02:39Z","timestamp":1688029359000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00525.2012"}},"issued":{"date-parts":[[2013,4,1]]},"references-count":50,"journal-issue":{"issue":"7","published-print":{"date-parts":[[2013,4,1]]}},"alternative-id":["10.1152\/ajprenal.00525.2012"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00525.2012","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2013,4,1]]}},{"indexed":{"date-parts":[[2025,10,12]],"date-time":"2025-10-12T20:08:54Z","timestamp":1760299734551,"version":"3.37.3"},"reference-count":30,"publisher":"American Physiological Society","issue":"3","funder":[{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)","doi-asserted-by":"publisher","award":["DK099276","DK098582"],"award-info":[{"award-number":["DK099276","DK098582"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2018,3,1]]},"abstract":"<jats:p> storage is the most prevalent method for graft preservation in kidney transplantation (KTX). The protective effects of various preservation solutions have been studied extensively in both clinical trials and experimental animal models. However, a paucity of studies have examined the effect of different preservation solutions on graft function in mouse KTX; in addition, the tolerance of the transplanted grafts to further insult has not been evaluated, which was the objective of the present study. We performed mouse KTX in three groups, with the donor kidneys preserved in different solutions for 60 min: saline, mouse serum, and University of Wisconsin (UW) solution. The graft functions were assessed by kidney injury markers and glomerular filtration rate (GFR). The grafts that were preserved in UW solution exhibited better functions, reflected by 50 and 70% lower plasma creatinine levels as well as 30 and 55% higher plasma creatinine levels in GFR than serum and saline groups, respectively, during the first week after transplants. To examine the graft function in response to additional insult, we induced ischemia-reperfusion injury (IRI) by clamping the renal pedicle for 18 min at 4 wk after KTX. We found that the grafts preserved in UW solution exhibited ~30 and 20% less injury assessed by kidney injury markers and histology than in other two preservation solutions. Taken together, our results demonstrated that UW solution exhibited a better protective effect in transplanted renal grafts in mice. UW solution is recommended for use in mouse KTX for reducing confounding factors such as IRI during surgery. <\/jats:p>","DOI":"10.1152\/ajprenal.00475.2017","type":"journal-article","created":{"date-parts":[[2017,11,15]],"date-time":"2017-11-15T11:00:20Z","timestamp":1510743620000},"page":"F381-F387","source":"Crossref","is-referenced-by-count":17,"title":["Effects of different storage solutions on renal ischemia tolerance after kidney transplantation in mice"],"prefix":"10.1152","volume":"314","author":[{"given":"Lei","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Molecular Pharmacology and Physiology, University of South Florida College of Medicine, Tampa, Florida"}]},{"given":"Jin","family":"Wei","sequence":"additional","affiliation":[{"name":"Department of Molecular Pharmacology and Physiology, University of South Florida College of Medicine, Tampa, Florida"}]},{"given":"Shan","family":"Jiang","sequence":"additional","affiliation":[{"name":"Department of Molecular Pharmacology and Physiology, University of South Florida College of Medicine, Tampa, Florida"}]},{"given":"Hui-Hua","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Molecular Pharmacology and Physiology, University of South Florida College of Medicine, Tampa, Florida"}]},{"given":"Liying","family":"Fu","sequence":"additional","affiliation":[{"name":"Tampa General Hospital, Tampa, Florida"}]},{"given":"Jie","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Molecular Pharmacology and Physiology, University of South Florida College of Medicine, Tampa, Florida"}]},{"given":"Ruisheng","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Molecular Pharmacology and Physiology, University of South Florida College of Medicine, Tampa, Florida"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1097\/00007890-198336060-00008"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.3389\/fendo.2015.00105"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1172\/JCI23378"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1034\/j.1600-6143.2003.00081.x"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/j.asjsur.2015.07.001"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007111267"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.181.2.1179"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1159\/000327033"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1053\/ajkd.1998.v31.pm9631835"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.05571008"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1016\/j.transproceed.2008.01.064"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/0011-2240(88)90038-7"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.02570310"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.4161\/org.5.3.9582"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1002\/lt.21372"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00423.x"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/j.cryobiol.2009.06.004"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2011.11.034"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1172\/JCI0215623"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1034\/j.1600-6143.2002.20502.x"},{"key":"B21","first-page":"676","volume":"103","author":"Ploeg RJ","year":"1988","journal-title":"Surgery"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1155\/2012\/127215"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.med.46.1.235"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1097\/00007890-199002000-00004"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/jappl.1998.84.6.2154"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.4103\/0975-7406.124301"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1001\/jama.2009.1322"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00347.2016"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00039.2017"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.115.07032"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00475.2017","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,20]],"date-time":"2019-09-20T00:37:49Z","timestamp":1568939869000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00475.2017"}},"issued":{"date-parts":[[2018,3,1]]},"references-count":30,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2018,3,1]]}},"alternative-id":["10.1152\/ajprenal.00475.2017"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00475.2017","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2018,3,1]]}},{"indexed":{"date-parts":[[2025,10,12]],"date-time":"2025-10-12T20:06:42Z","timestamp":1760299602841},"reference-count":41,"publisher":"American Physiological Society","issue":"4","funder":[{"name":"Nationa research foundation of Korea","award":["2015R1A5A2009124","2013R1A1A2009257"],"award-info":[{"award-number":["2015R1A5A2009124","2013R1A1A2009257"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2017,10,1]]},"abstract":"<jats:p>Regulation of lipogenesis by pathophysiological factors in the liver and skeletal muscle is well understood; however, regulation in the kidney is still unclear. To elucidate nutritional regulation of lipogenic factors in the kidney, we measured the renal expression of lipogenic transcriptional factors and enzymes during fasting and refeeding in chow-fed and high-fat-fed mice. We also examined the regulatory effect of the liver X receptor (LXR) on the expression of lipogenic factors. The renal gene expression of sterol regulatory element-binding protein (SREBP)-1c and fatty acid synthase (FAS) was reduced by fasting for 48 h and restored by refeeding, whereas the mRNA levels of forkhead box O (FOXO)1\/3 were increased by fasting and restored by refeeding. Accordingly, protein levels of SREBP-1, FAS, and phosphorylated FOXO1\/3 were reduced by fasting and restored by refeeding. The patterns of lipogenic factors expression in the kidney were similar to those in the liver and skeletal muscle. However, this phasic regulation of renal lipogenic gene expression was blunted in diet-induced obese mice. LXR agonist TO901317 increased the lipogenic gene expression and the protein levels of SREBP-1 precursor and FAS but not nuclear SREBP-1. Moreover, increases in insulin-induced gene mRNA and nuclear carbohydrate-responsive element binding protein (ChREBP) levels were observed in the TO901317-treated mice. These results suggest that the kidney shows flexible suppression and restoration of lipogenic factors following fasting and refeeding in lean mice, but this is blunted in obese mice. LXR is involved in the renal expression of lipogenic enzymes, and ChREBP may mediate the response.<\/jats:p>","DOI":"10.1152\/ajprenal.00594.2016","type":"journal-article","created":{"date-parts":[[2017,5,25]],"date-time":"2017-05-25T00:40:30Z","timestamp":1495672830000},"page":"F887-F898","source":"Crossref","is-referenced-by-count":5,"title":["Nutritional regulation of renal lipogenic factor expression in mice: comparison to regulation in the liver and skeletal muscle"],"prefix":"10.1152","volume":"313","author":[{"given":"Suk-Jeong","family":"Kim","sequence":"first","affiliation":[{"name":"Department of Physiology, College of Medicine, Yeungnam University, Daegu, Republic of Korea; and"},{"name":"Smart-Aging Convergence Research Center, College of Medicine, Yeungnam University, Daegu, Republic of Korea"}]},{"given":"Ji-Eun","family":"Kim","sequence":"additional","affiliation":[{"name":"Department of Physiology, College of Medicine, Yeungnam University, Daegu, Republic of Korea; and"},{"name":"Smart-Aging Convergence Research Center, College of Medicine, Yeungnam University, Daegu, Republic of Korea"}]},{"given":"Yong-Woon","family":"Kim","sequence":"additional","affiliation":[{"name":"Department of Physiology, College of Medicine, Yeungnam University, Daegu, Republic of Korea; and"}]},{"given":"Jong-Yeon","family":"Kim","sequence":"additional","affiliation":[{"name":"Department of Physiology, College of Medicine, Yeungnam University, Daegu, Republic of Korea; and"}]},{"given":"So-Young","family":"Park","sequence":"additional","affiliation":[{"name":"Department of Physiology, College of Medicine, Yeungnam University, Daegu, Republic of Korea; and"},{"name":"Smart-Aging Convergence Research Center, College of Medicine, Yeungnam University, Daegu, Republic of Korea"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"crossref","first-page":"1220","DOI":"10.1194\/jlr.M100417-JLR200","volume":"43","author":"Amemiya-Kudo M","year":"2002","journal-title":"J Lipid Res"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M406522200"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1042\/BJ20040162"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1042\/BJ20110702"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M605023200"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M507339200"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M112.347211"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2014.87"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1186\/s12986-016-0122-x"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2005.12.022"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1194\/jlr.M400261-JLR200"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M204887200"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1093\/humupd\/dmm009"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1038\/ncomms6190"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1002\/hep.26951"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0405067102"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1021\/jf3019084"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.54.6.1684"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00195.2009"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M500801200"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1210\/en.2007-1461"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2005.04.005"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2006.01.139"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M300553200"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbadis.2011.03.015"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1124\/mol.106.022608"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1101\/gad.844900"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.cellbio.16.1.459"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/j.exger.2015.05.009"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1210\/en.2009-0466"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119247"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.53.2007.S36"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M110650200"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0401715101"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1530\/JOE-16-0142"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1194\/jlr.M067181"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1038\/nrm2190"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1016\/j.cellsig.2016.11.004"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1002\/hep.26272"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M109.050914"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1194\/jlr.M053439"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00594.2016","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2020,10,8]],"date-time":"2020-10-08T12:34:48Z","timestamp":1602160488000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00594.2016"}},"issued":{"date-parts":[[2017,10,1]]},"references-count":41,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2017,10,1]]}},"alternative-id":["10.1152\/ajprenal.00594.2016"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00594.2016","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2017,10,1]]}},{"indexed":{"date-parts":[[2025,10,13]],"date-time":"2025-10-13T19:59:59Z","timestamp":1760385599050},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1991,2,1]]},"abstract":"<jats:p> Canine renal cells in culture (MDCK cells) accumulate organic osmolytes, including myo-inositol (MI), in response to hypertonic stress. When medium tonicity is increased, intracellular concentration of MI rises because hypertonicity elicits increased uptake of MI via Na-MI cotransporter(s). To study the mechanism for this increase in cotransporter activity, poly(A)+ RNA isolated from MDCK cells maintained in hypertonic or isotonic medium was injected into Xenopus oocytes, and Na-dependent MI uptake was measured 3\u20135 days later. Poly(A)+ RNA from hypertonic cells induced clear expression of the cotransporter. In contrast, oocytes injected with poly(A)+ RNA isolated from MDCK cells maintained in isotonic medium exhibited cotransporter activity like oocytes injected with water. Upon size fractionation of RNA, peak activity appeared in a fraction that contained poly(A)+ RNA with median size of approximately 4 kilobases. Na-dependent MI uptake by poly(A)+ RNA-injected oocytes was inhibited by both phlorizin and phloretin. We suggest that hypertonicity-induced upregulation of the Na-MI cotransporter involves an increase in mRNA and synthesis of cotransporter protein(s). <\/jats:p>","DOI":"10.1152\/ajprenal.1991.260.2.f258","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T23:40:01Z","timestamp":1513986001000},"page":"F258-F263","source":"Crossref","is-referenced-by-count":6,"title":["Renal Na-myo-inositol cotransporter mRNA expression in Xenopus oocytes: regulation by hypertonicity"],"prefix":"10.1152","volume":"260","author":[{"given":"H. M.","family":"Kwon","sequence":"first","affiliation":[{"name":"Department of Medicine, Johns Hopkins University School of Medicine, Baltimore 21205."}]},{"given":"A.","family":"Yamauchi","sequence":"additional","affiliation":[{"name":"Department of Medicine, Johns Hopkins University School of Medicine, Baltimore 21205."}]},{"given":"S.","family":"Uchida","sequence":"additional","affiliation":[{"name":"Department of Medicine, Johns Hopkins University School of Medicine, Baltimore 21205."}]},{"given":"R. B.","family":"Robey","sequence":"additional","affiliation":[{"name":"Department of Medicine, Johns Hopkins University School of Medicine, Baltimore 21205."}]},{"given":"A.","family":"Garcia-Perez","sequence":"additional","affiliation":[{"name":"Department of Medicine, Johns Hopkins University School of Medicine, Baltimore 21205."}]},{"given":"M. B.","family":"Burg","sequence":"additional","affiliation":[{"name":"Department of Medicine, Johns Hopkins University School of Medicine, Baltimore 21205."}]},{"given":"J. S.","family":"Handler","sequence":"additional","affiliation":[{"name":"Department of Medicine, Johns Hopkins University School of Medicine, Baltimore 21205."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1991.260.2.F258","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:26:07Z","timestamp":1567970767000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1991.260.2.F258"}},"issued":{"date-parts":[[1991,2,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1991,2,1]]}},"alternative-id":["10.1152\/ajprenal.1991.260.2.F258"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1991.260.2.f258","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1991,2,1]]}},{"indexed":{"date-parts":[[2025,10,13]],"date-time":"2025-10-13T20:00:07Z","timestamp":1760385607033,"version":"3.41.0"},"reference-count":58,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1998,6,1]]},"abstract":"<jats:p>P-glycoprotein (Mdr1p) is an ATP-dependent drug efflux pump that is overexpressed in multidrug-resistant cells and some cancers. Mdr1p is also expressed in normal tissues like the kidney, where it can mediate transepithelial drug transport. A human urinary compound that reverses multidrug resistance and blocks [<jats:sup>3<\/jats:sup>H]azidopine photolabeling of P-glycoprotein was purified to homogeneity and identified by<jats:sup>1<\/jats:sup>H-NMR and mass spectrometry as the synthetic surfactant nonylphenol ethoxylate (NPE). Multidrug-resistant Chinese hamster ovary (CHO) C5 cells accumulated less [<jats:sup>3<\/jats:sup>H]NPE than parental drug-sensitive Aux-B1 cells, and Mdr1p substrates, verapamil and cyclosporin A, increased this surfactant\u2019s accumulation in C5 cells. NPE blocked the net transepithelial transport (basolateral to apical) of [<jats:sup>3<\/jats:sup>H]cyclosporin A in epithelia formed by Madin-Darby canine kidney (MDCK) cells. Net transepithelial transport (basal to apical) of [<jats:sup>3<\/jats:sup>H]NPE was demonstrated in MDCK cells and was inhibited by cyclosporin A. These findings show NPE is a Mdr1p substrate excreted into urine by kidney P-glycoprotein. NPE is a widely used surfactant and a known hormone disrupter that is readily absorbed orally or topically. The current findings indicate the function of kidney Mdr1p may be to eliminate exogenous compounds from the body.<\/jats:p>","DOI":"10.1152\/ajprenal.1998.274.6.f1127","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T15:24:19Z","timestamp":1514042659000},"page":"F1127-F1139","source":"Crossref","is-referenced-by-count":3,"title":["Identification of the synthetic surfactant nonylphenol ethoxylate: a P-glycoprotein substrate in human urine"],"prefix":"10.1152","volume":"274","author":[{"given":"Jeffrey H. M.","family":"Charuk","sequence":"first","affiliation":[{"name":"Medical Research Council Group in Membrane Biology, Department of Medicine, University of Toronto; and"}]},{"given":"Arthur A.","family":"Grey","sequence":"additional","affiliation":[{"name":"Molecular Medicine Research Centre, Department of Medical Genetics and Microbiology, University of Toronto, Toronto, Ontario, Canada M5S 1A8"}]},{"given":"Reinhart A. F.","family":"Reithmeier","sequence":"additional","affiliation":[{"name":"Medical Research Council Group in Membrane Biology, Department of Medicine, University of Toronto; and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1994.267.5.C1351"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.1041450303"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/0006-2952(87)90139-0"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2736(76)90059-6"},{"key":"B5","first-page":"936","volume":"47","author":"Carmichael J.","year":"1987","journal-title":"Cancer Res."},{"issue":"35","key":"B6","first-page":"F66","volume":"266","author":"Charuk J. H. M.","year":"1994","journal-title":"Am. J. Physiol."},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/0006-291X(92)90816-4"},{"issue":"38","key":"B8","first-page":"F31","volume":"269","author":"Charuk J. H. M.","year":"1995","journal-title":"Am. J. Physiol."},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(86)90595-7"},{"key":"B10","first-page":"897","volume":"51","author":"Coon J. S.","year":"1991","journal-title":"Cancer Res."},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.86.2.695"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.2.1026"},{"issue":"32","key":"B16","first-page":"F613","volume":"263","author":"De Lannoy I. A. M.","year":"1992","journal-title":"Am. J. Physiol."},{"key":"B17","doi-asserted-by":"crossref","first-page":"388","DOI":"10.1016\/S0022-3565(25)38448-X","volume":"268","author":"De Lannoy I. A. M.","year":"1994","journal-title":"J. Pharmacol. Exp. Ther."},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2736(93)90339-2"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1111\/j.1432-1033.1995.tb20352.x"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/0041-008X(80)90245-8"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1996.270.3.C910"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.22.12897"},{"key":"B24","first-page":"16","volume":"20","author":"Finnegan J. K.","year":"1953","journal-title":"Proc. Sci. Sect. Toilet Goods Assoc."},{"key":"B25","doi-asserted-by":"crossref","first-page":"247","DOI":"10.1515\/tsd-1979-160503","volume":"16","author":"Gerhardt W.","year":"1979","journal-title":"Tenside Deterg."},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.2166\/wst.1987.0225"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1126\/science.6740328"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-291X(88)80073-1"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.bi.62.070193.002125"},{"key":"B30","first-page":"341","volume":"22","author":"Harris J. M.","year":"1984","journal-title":"J. Polym. Sci. Part D Macromol. Rev."},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1016\/0076-6879(79)56066-2"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.cb.08.110192.000435"},{"key":"B33","doi-asserted-by":"crossref","first-page":"14880","DOI":"10.1016\/S0021-9258(18)63784-6","volume":"264","author":"Horio M.","year":"1989","journal-title":"J. Biol. Chem."},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1016\/0016-5085(92)90173-V"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1016\/0006-291X(90)91913-D"},{"key":"B37","doi-asserted-by":"crossref","first-page":"903","DOI":"10.1016\/S0021-9258(17)35258-4","volume":"266","author":"Ichikawa M.","year":"1991","journal-title":"J. Biol. Chem."},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2736(93)90083-C"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1016\/0166-445X(93)90064-8"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1016\/0041-008X(66)90129-3"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1016\/0041-008X(63)90070-X"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1016\/0006-291X(89)91988-8"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1038\/bjc.1993.338"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1210\/endo-102-5-1429"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1007\/BF02635812"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1016\/0048-3575(80)90102-9"},{"key":"B49","first-page":"1195","volume":"32","author":"Riehm H.","year":"1972","journal-title":"Cancer Res."},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.6.3280"},{"key":"B51","doi-asserted-by":"crossref","first-page":"7884","DOI":"10.1016\/S0021-9258(18)47650-8","volume":"262","author":"Safa A. R.","year":"1987","journal-title":"J. Biol. Chem."},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.94.8.4028"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(94)90212-7"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118214"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1021\/bi00417a001"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(93)90380-9"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1289\/ehp.9192167"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1023\/A:1018920728800"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.84.21.7735"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1016\/0378-1119(88)90057-1"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)81370-7"},{"key":"B63","first-page":"4199","volume":"50","author":"Woodcock D. M.","year":"1990","journal-title":"Cancer Res."},{"key":"B64","doi-asserted-by":"crossref","first-page":"782","DOI":"10.1016\/S0021-9258(19)85010-X","volume":"264","author":"Yang C.-P. H.","year":"1989","journal-title":"J. Biol. Chem."},{"key":"B65","doi-asserted-by":"crossref","first-page":"15973","DOI":"10.1016\/S0021-9258(17)33958-3","volume":"269","author":"Zhang L.","year":"1994","journal-title":"J. Biol. Chem."},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.39.22859"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1998.274.6.F1127","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,6,29]],"date-time":"2025-06-29T04:39:13Z","timestamp":1751171953000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1998.274.6.F1127"}},"issued":{"date-parts":[[1998,6,1]]},"references-count":58,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1998,6,1]]}},"alternative-id":["10.1152\/ajprenal.1998.274.6.F1127"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1998.274.6.f1127","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[1998,6,1]]}},{"indexed":{"date-parts":[[2025,10,15]],"date-time":"2025-10-15T16:35:16Z","timestamp":1760546116440},"reference-count":40,"publisher":"American Physiological Society","issue":"10","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2012,5,15]]},"abstract":"<jats:p> Endothelial progenitor cells (EPCs) protect the kidney from acute ischemic injury. The aim of this study was to analyze whether pretreatment of murine \u201cearly outgrowth\u201d EPCs (eEPCs) with the hormone melatonin increases the cells' renoprotective effects in the setting of murine acute ischemic renal failure. Male (8\u201312 wk old) C57Bl\/6N mice were subjected to unilateral ischemia-reperfusion injury postuninephrectomy (40 min). Postischemic animals were injected with either 0.5\u00d710<jats:sup>6<\/jats:sup> untreated syngeneic murine eEPCs or with cells, pretreated with melatonin for 1 h. Injections were performed shortly after reperfusion of the kidney. While animals injected with untreated cells developed acute renal failure, eEPC pretreatment with melatonin dramatically improved renoprotective actions of the cells. These effects were completely reversed after cell pretreatment with melatonin and the MT-1\/-2 antagonist luzindole. In vitro analysis revealed that melatonin reduced the amount of tumor growth factor-\u03b2-induced eEPC apoptosis\/necrosis. Secretion of vascular endothelial growth factor by the cells was markedly stimulated by the hormone. In addition, migratory activity of eEPCs was enhanced by melatonin and supernatant from melatonin-treated eEPCs stimulated migration of cultured mature endothelial cells. In summary, melatonin was identified as a new agonist of eEPCs in acute ischemic kidney injury. <\/jats:p>","DOI":"10.1152\/ajprenal.00445.2011","type":"journal-article","created":{"date-parts":[[2012,2,23]],"date-time":"2012-02-23T02:02:32Z","timestamp":1329962552000},"page":"F1305-F1312","source":"Crossref","is-referenced-by-count":46,"title":["The hormone melatonin stimulates renoprotective effects of \u201cearly outgrowth\u201d endothelial progenitor cells in acute ischemic kidney injury"],"prefix":"10.1152","volume":"302","author":[{"given":"D.","family":"Patschan","sequence":"first","affiliation":[{"name":"Abteilung f\u00fcr Nephrologie und Rheumatologie, Universit\u00e4tsklinikum G\u00f6ttingen, G\u00f6ttingen, Germany;"}]},{"given":"A.","family":"Hildebrandt","sequence":"additional","affiliation":[{"name":"Abteilung f\u00fcr Nephrologie und Rheumatologie, Universit\u00e4tsklinikum G\u00f6ttingen, G\u00f6ttingen, Germany;"}]},{"given":"J.","family":"Rinneburger","sequence":"additional","affiliation":[{"name":"Abteilung f\u00fcr Nephrologie und Rheumatologie, Universit\u00e4tsklinikum G\u00f6ttingen, G\u00f6ttingen, Germany;"}]},{"given":"J. T.","family":"Wessels","sequence":"additional","affiliation":[{"name":"Abteilung f\u00fcr Nephrologie und Rheumatologie, Universit\u00e4tsklinikum G\u00f6ttingen, G\u00f6ttingen, Germany;"},{"name":"Molecular and Optical Live Cell Imaging (MOLCI), UMG, G\u00f6ttingen, Germany; and"}]},{"given":"S.","family":"Patschan","sequence":"additional","affiliation":[{"name":"Abteilung f\u00fcr Nephrologie und Rheumatologie, Universit\u00e4tsklinikum G\u00f6ttingen, G\u00f6ttingen, Germany;"}]},{"given":"J. U.","family":"Becker","sequence":"additional","affiliation":[{"name":"Institut f\u00fcr Pathologie, Medizinische Hochschule Hannover, Hannover, Germany"}]},{"given":"E.","family":"Henze","sequence":"additional","affiliation":[{"name":"Abteilung f\u00fcr Nephrologie und Rheumatologie, Universit\u00e4tsklinikum G\u00f6ttingen, G\u00f6ttingen, Germany;"}]},{"given":"A.","family":"Kr\u00fcger","sequence":"additional","affiliation":[{"name":"Abteilung f\u00fcr Nephrologie und Rheumatologie, Universit\u00e4tsklinikum G\u00f6ttingen, G\u00f6ttingen, Germany;"}]},{"given":"G. A.","family":"M\u00fcller","sequence":"additional","affiliation":[{"name":"Abteilung f\u00fcr Nephrologie und Rheumatologie, Universit\u00e4tsklinikum G\u00f6ttingen, G\u00f6ttingen, Germany;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.85.3.221"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1126\/science.275.5302.964"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2249.1994.tb06579.x"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/j.tibs.2006.10.002"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/j.exphem.2007.04.002"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2009.080606"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1164\/rccm.200303-372OC"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1081\/JDI-120015677"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0912701107"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009111119"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2003-01-0223"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2005-04-1509"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000121732.85572.6F"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/j.febslet.2005.07.080"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007111200"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-079X.2007.00459.x"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1634\/stemcells.2007-1000"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000128974.07460.34"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000027584.85865.B4"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.5.F910"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1155\/2010\/317068"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1034\/j.1600-079X.2003.00059.x"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1034\/j.1600-079X.2002.02910.x"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00454.2005"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006070759"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1002\/jca.20208"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00485.2009"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1016\/j.coph.2005.10.013"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1081\/CBI-120027984"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000058702.69484.A0"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1016\/S0079-6123(08)81008-4"},{"key":"B32","first-page":"3","volume":"66","author":"Richardson GS","year":"2005","journal-title":"J Clin Psychiatry"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1034\/j.1600-079X.2002.01858.x"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00386.2007"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00007.2005"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000137877.89448.78"},{"key":"B37","first-page":"657","volume":"30","author":"Winczyk K","year":"2009","journal-title":"Neuro Endocrinol Lett"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2008-12-195750"},{"key":"B39","first-page":"50","volume":"1796","author":"Yoder MC","year":"2009","journal-title":"Biochim Biophys Acta"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2006-08-043471"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00445.2011","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:24:10Z","timestamp":1567974250000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00445.2011"}},"issued":{"date-parts":[[2012,5,15]]},"references-count":40,"journal-issue":{"issue":"10","published-print":{"date-parts":[[2012,5,15]]}},"alternative-id":["10.1152\/ajprenal.00445.2011"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00445.2011","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2012,5,15]]}},{"indexed":{"date-parts":[[2025,10,21]],"date-time":"2025-10-21T15:28:05Z","timestamp":1761060485066},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1985,11,1]]},"abstract":"<jats:p> Early proximal convoluted tubules were perfused in vivo with equilibrium Ringer buffered at pH 7.65 and 6.5 to characterize phosphate absorption due to changes in extracellular and intracellular hydrogen ion concentration. Phosphate absorption is normally greater from intraluminal pH 7.65 compared with pH 6.5 in thyroparathyroidectomized rats with fractional phosphate excretion of 0.5%. Metabolic alkalosis produced by bicarbonate infusion in rats ingesting normal amounts of phosphate (45 mg\/day) resulted in an increase in overall renal phosphate reabsorption (fractional phosphate excretion 0.3%). The Jmax and Km values were: pH 7.65, 33.67 +\/- 13.49 pmol X min-1 X mm-1, and 1.74 +\/- 0.30 mM; pH 6.5, 24.87 +\/- 6.22 and 0.50 +\/- 0.25, respectively. By contrast, rats on a high dietary phosphate intake (180 mg\/day) demonstrated a large increase in urinary phosphate excretion (18%) following bicarbonate infusion, which was due to a decrease in tubular phosphate absorption from both alkaline and acidic luminal pH values. Acute metabolic acidosis did not significantly alter tubular transport at either intraluminal pH value. In contrast, rats maintained on an elevated dietary acid intake for 5 days had a phosphaturia (fractional excretion 7.1%) and diminished reabsorptive capacity. Dietary acidosis also decreased tubular phosphate transport in rats previously maintained on phosphate-restricted diets. These data suggest that acid-base balance may modulate tubular phosphate transport independent of intraluminal pH and phosphate concentration. Further, these changes depend on the chronicity of exposure and act independent but integral to the effects of parathyroid hormone and the intrinsic adaptation to dietary phosphate availability. <\/jats:p>","DOI":"10.1152\/ajprenal.1985.249.5.f769","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T00:00:57Z","timestamp":1513987257000},"page":"F769-F779","source":"Crossref","is-referenced-by-count":2,"title":["Effects of metabolic acidosis, alkalosis, and dietary hydrogen ion intake on phosphate transport in the proximal convoluted tubule"],"prefix":"10.1152","volume":"249","author":[{"given":"G. A.","family":"Quamme","sequence":"first","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1985.249.5.F769","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:29:43Z","timestamp":1567970983000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1985.249.5.F769"}},"issued":{"date-parts":[[1985,11,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1985,11,1]]}},"alternative-id":["10.1152\/ajprenal.1985.249.5.F769"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1985.249.5.f769","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1985,11,1]]}},{"indexed":{"date-parts":[[2025,10,21]],"date-time":"2025-10-21T15:28:06Z","timestamp":1761060486095},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1994,2,1]]},"abstract":"<jats:p> The present study investigates ATP effects on Ca2+ mobilization in bovine glomerular endothelial cells (GEC) and the receptors mediating ATP response. Extracellular ATP stimulated a rise in inositol 1,4,5-trisphosphate and cytosolic free Ca2+ concentration ([Ca2+]i) in a dose-dependent manner. Extracellular Ca2+ depletion did not prevent [Ca2+]i rise. ATP effects were not mediated by P1, P2x, and P2t purinoceptors, since the P1 receptor agonist adenosine and the P2x receptor agonist [alpha,beta-CH2]ATP had no effect on inositol 1-monophosphate (IP) formation and Ca2+ mobilization and ATP does not activate P2t receptors. The P2y receptor antagonist reactive blue (10(-3) M) had little inhibitory effect on ATP (10(-5) M)-stimulated IP formation (15.6 +\/- 4.2%) and Ca2+ rise (7.0 +\/- 3.0%). According to the classification of purinoceptors, ATP is less potent than 2-methylthioadenosine 5'-triphosphate (2-MeS-ATP) in stimulating P2y receptors. In GEC, however, the rank order of potency in stimulating IP and [Ca2+]i rise was ATP &gt; 2-MeS-ATP &gt; ADP. The pyrimidine nucleotide UTP (10(-3) M) induced maximal IP formation (653 +\/- 37%) and Ca2+ mobilization (591 +\/- 22 nM) similar to ATP (IP 647 +\/- 27%; [Ca2+]i 583 +\/- 15 nM). At submaximal (10(-5) M) but not at maximal (10(-3) M) doses ATP and UTP effects were additive. ATP and UTP induced specific cross-desensitization. It is concluded that the purinergic nucleotide ATP and pyrimidine nucleotide UTP mediate their effects by a common nucleotide receptor. This receptor differs from P2z and P2y1 receptors, since by definition UTP does not activate these receptors.(ABSTRACT TRUNCATED AT 250 WORDS) <\/jats:p>","DOI":"10.1152\/ajprenal.1994.266.2.f210","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T11:03:50Z","timestamp":1514027030000},"page":"F210-F217","source":"Crossref","is-referenced-by-count":5,"title":["ATP stimulates Ca2+ mobilization by a nucleotide receptor in glomerular endothelial cells"],"prefix":"10.1152","volume":"266","author":[{"given":"V. A.","family":"Briner","sequence":"first","affiliation":[{"name":"Department of Medicine, University Hospital, Bern, Switzerland."}]},{"given":"F.","family":"Kern","sequence":"additional","affiliation":[{"name":"Department of Medicine, University Hospital, Bern, Switzerland."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1994.266.2.F210","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:31:54Z","timestamp":1567974714000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1994.266.2.F210"}},"issued":{"date-parts":[[1994,2,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1994,2,1]]}},"alternative-id":["10.1152\/ajprenal.1994.266.2.F210"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1994.266.2.f210","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1994,2,1]]}},{"indexed":{"date-parts":[[2025,10,22]],"date-time":"2025-10-22T03:01:34Z","timestamp":1761102094584},"reference-count":29,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2014,1,1]]},"abstract":"<jats:p>The importance of membrane-bound PGE synthase 1 (mPGES1) in the regulation of renal function has been examined in mPGES1-deficient mice or by evaluating changes in its expression. However, it is unknown whether prolonged mPGES1 inhibition induces significant changes of renal function when Na<jats:sup>+<\/jats:sup>intake is normal or low. This study examined the renal effects elicited by a selective mPGES1 inhibitor (PF-458) during 7 days in conscious chronically instrumented dogs with normal Na<jats:sup>+<\/jats:sup>intake (NSI) or low Na<jats:sup>+<\/jats:sup>intake (LSI). Results obtained in both in vitro and in vivo studies have strongly suggested that PF-458 is a selective mPGES1 inhibitor. The administration of 2.4 mg\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7day<jats:sup>\u22121<\/jats:sup>PF-458 to dogs with LSI did not induce significant changes in renal blood flow (RBF) and glomerular filtration rate (GFR). A larger dose of PF-458 (9.6 mg\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7day<jats:sup>\u22121<\/jats:sup>) reduced RBF ( P &lt; 0.05) but not GFR in dogs with LSI and did not induce changes of renal hemodynamic in dogs with NSI. Both doses of PF-458 elicited a decrease ( P &lt; 0.05) in PGE<jats:sub>2<\/jats:sub>and an increase ( P &lt; 0.05) in 6-keto-PGF<jats:sub>1\u03b1<\/jats:sub>. The administration of PF-458 did not induce significant changes in renal excretory function, plasma renin activity, and plasma aldosterone and thromboxane B<jats:sub>2<\/jats:sub>concentrations in dogs with LSI or NSI. The results obtained suggest that mPGES1 is involved in the regulation of RBF when Na<jats:sup>+<\/jats:sup>intake is low and that the renal effects elicited by mPGES1 inhibition are modulated by a compensatory increment in PGI<jats:sub>2<\/jats:sub>. These results may have some therapeutical implications since it has been shown that prolonged mPGES1 inhibition has lower renal effects than those elicited by nonsteroidal anti-inflammatory drugs or selective cyclooxygenase-2 inhibitors.<\/jats:p>","DOI":"10.1152\/ajprenal.00492.2013","type":"journal-article","created":{"date-parts":[[2013,11,7]],"date-time":"2013-11-07T02:36:04Z","timestamp":1383791764000},"page":"F68-F74","source":"Crossref","is-referenced-by-count":12,"title":["Renal effects induced by prolonged mPGES1 inhibition"],"prefix":"10.1152","volume":"306","author":[{"given":"Francisco","family":"Salazar","sequence":"first","affiliation":[{"name":"Department of Physiology, School of Medicine, Campus Mare Nostrum of Excellence, University of Murcia, Murcia, Spain; and"}]},{"given":"Michael L.","family":"Vazquez","sequence":"additional","affiliation":[{"name":"Pfizer, Incorporated, St. Louis, Missouri"}]},{"given":"Jaime L.","family":"Masferrer","sequence":"additional","affiliation":[{"name":"Pfizer, Incorporated, St. Louis, Missouri"}]},{"given":"Gabriel","family":"Mbalaviele","sequence":"additional","affiliation":[{"name":"Pfizer, Incorporated, St. Louis, Missouri"}]},{"given":"Maria T.","family":"Llinas","sequence":"additional","affiliation":[{"name":"Department of Physiology, School of Medicine, Campus Mare Nostrum of Excellence, University of Murcia, Murcia, Spain; and"}]},{"given":"Fara","family":"Saez","sequence":"additional","affiliation":[{"name":"Department of Physiology, School of Medicine, Campus Mare Nostrum of Excellence, University of Murcia, Murcia, Spain; and"}]},{"given":"Grace","family":"Arhancet","sequence":"additional","affiliation":[{"name":"Pfizer, Incorporated, St. Louis, Missouri"}]},{"given":"F. Javier","family":"Salazar","sequence":"additional","affiliation":[{"name":"Department of Physiology, School of Medicine, Campus Mare Nostrum of Excellence, University of Murcia, Murcia, Spain; and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.111.180554"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/j.bmcl.2012.11.109"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.63.1.579"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1172\/JCI27540"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.109.145631"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006040343"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00433.2002"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.32.1.33"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1111\/j.1532-5415.1997.tb02964.x"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00591.2007"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00772.2010"},{"key":"B12","author":"Howe LR","journal-title":"Prostaglandins Other Lipid Mediat"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.109.144840"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00508.2011"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000251306.40546.08"},{"key":"B16","doi-asserted-by":"crossref","first-page":"219","DOI":"10.1242\/jeb.202.3.219","volume":"202","author":"Kurtz A","year":"1999","journal-title":"J Exp Biol"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/j.bcp.2010.01.003"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1172\/JCI200318018"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1155\/2007\/85091"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000036451.76323.29"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00493.x"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1097\/FJC.0b013e31828399ae"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1993.293"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.87.6.504"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1332766100"},{"key":"B26","doi-asserted-by":"crossref","first-page":"1570","DOI":"10.1046\/j.1523-1755.2002.00615.x","volume":"62","author":"Vizthum H","year":"2002","journal-title":"Kidney Int"},{"key":"B27","author":"Watanabe K","journal-title":"Prostaglandins Other Lipid Mediat 68\u201369: 401\u2013407, 2002"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1038\/aps.2010.99"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejphar.2008.01.021"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00492.2013","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,3,11]],"date-time":"2022-03-11T19:03:18Z","timestamp":1647025398000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00492.2013"}},"issued":{"date-parts":[[2014,1,1]]},"references-count":29,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2014,1,1]]}},"alternative-id":["10.1152\/ajprenal.00492.2013"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00492.2013","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2014,1,1]]}},{"indexed":{"date-parts":[[2025,9,25]],"date-time":"2025-09-25T15:43:56Z","timestamp":1758815036301,"version":"3.41.0"},"reference-count":47,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2001,1,1]]},"abstract":"<jats:p>The proposed feedback between angiotensin II AT<jats:sub>2<\/jats:sub>and AT<jats:sub>1<\/jats:sub>receptors prompted us to study AT<jats:sub>1<\/jats:sub>receptor expression in kidneys of male AT<jats:sub>2<\/jats:sub>receptor-gene disrupted mice ( agtr2 \u2212\/y). In wild-type ( agtr2 +\/y) mice, AT<jats:sub>1<\/jats:sub>receptor binding and mRNA is abundant in glomeruli, and AT<jats:sub>1<\/jats:sub>receptor binding is also high in the inner stripe of the outer medulla. AT<jats:sub>2<\/jats:sub>receptors are scarce, primarily associated to cortical vascular structures. In agtr2 \u2212\/y mice, AT<jats:sub>1<\/jats:sub>receptor binding and mRNA were increased in the kidney glomeruli, and AT<jats:sub>1<\/jats:sub>receptor binding was higher in the rest of the cortex and outer stripe of the outer medulla, but not in its inner stripe, indicating different cellular regulation. Although AT<jats:sub>2<\/jats:sub>receptor expression is very low in male agtr 2 +\/y mice, their gene disruption alters AT<jats:sub>1<\/jats:sub>receptor expression. AT<jats:sub>1<\/jats:sub>upregulation alone may explain the AT<jats:sub>2<\/jats:sub>gene-disrupted mice phenotype such as increased blood pressure, higher sensitivity to angiotensin II, and altered renal function. The indirect AT<jats:sub>1<\/jats:sub>\/AT<jats:sub>2<\/jats:sub>receptor feedback could have clinical significance because AT<jats:sub>1<\/jats:sub>antagonists are widely used in medical practice.<\/jats:p>","DOI":"10.1152\/ajprenal.2001.280.1.f71","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T13:34:15Z","timestamp":1514036055000},"page":"F71-F78","source":"Crossref","is-referenced-by-count":21,"title":["Increased AT<sub>1<\/sub>receptor expression and mRNA in kidney glomeruli of AT<sub>2<\/sub>receptor gene-disrupted mice"],"prefix":"10.1152","volume":"280","author":[{"given":"Juan M.","family":"Saavedra","sequence":"first","affiliation":[{"name":"Section on Pharmacology, National Institute of Mental Health, Bethesda, Maryland 20892; and"}]},{"given":"Walter","family":"H\u00e4user","sequence":"additional","affiliation":[{"name":"Section on Pharmacology, National Institute of Mental Health, Bethesda, Maryland 20892; and"}]},{"given":"Gladys","family":"Ciuffo","sequence":"additional","affiliation":[{"name":"Section on Pharmacology, National Institute of Mental Health, Bethesda, Maryland 20892; and"}]},{"given":"Giorgia","family":"Egidy","sequence":"additional","affiliation":[{"name":"Section on Pharmacology, National Institute of Mental Health, Bethesda, Maryland 20892; and"}]},{"given":"Kwang-Lae","family":"Hoe","sequence":"additional","affiliation":[{"name":"Section on Pharmacology, National Institute of Mental Health, Bethesda, Maryland 20892; and"}]},{"given":"Olaf","family":"J\u00f6hren","sequence":"additional","affiliation":[{"name":"Section on Pharmacology, National Institute of Mental Health, Bethesda, Maryland 20892; and"}]},{"given":"Takaaki","family":"Sembonmatsu","sequence":"additional","affiliation":[{"name":"Vanderbilt University, Department of Biochemistry, School of Medicine, Nashville, Tennessee 37232"}]},{"given":"Tadashi","family":"Inagami","sequence":"additional","affiliation":[{"name":"Vanderbilt University, Department of Biochemistry, School of Medicine, Nashville, Tennessee 37232"}]},{"given":"In\u00e9s","family":"Armando","sequence":"additional","affiliation":[{"name":"Section on Pharmacology, National Institute of Mental Health, Bethesda, Maryland 20892; and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"crossref","first-page":"S23","DOI":"10.1681\/ASN.V1081763","volume":"10","author":"Allen AM","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B2","first-page":"S30","volume":"10","author":"Ardaillou R.","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119829"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.265.2.F264"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/0196-9781(94)00150-5"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.426"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.24.5.531"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.261.3.F512"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(17)34918-2"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.262.2.F326"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.26.3.471"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00820.x"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-2999(98)00134-4"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(95)00092-5"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1038\/377744a0"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2736(94)90072-8"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1038\/377748a0"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.76.5.693"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/0006-291X(91)91982-I"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.28.4.663"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1097\/00001756-199512150-00024"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1993.174"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.16"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118807"},{"key":"B25","first-page":"502A","volume":"9","author":"Li WG","year":"1998","journal-title":"J Am Soc Nephrol"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117792"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.1998.00893.x"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1172\/JCI1885"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1159\/000045121"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.59.1.395"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1016\/0304-3940(91)90687-O"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0701906"},{"key":"B34","first-page":"1779","volume":"13","author":"Munoz-Garcia R","year":"1995","journal-title":"J Hypertens"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.27.3.760"},{"key":"B36","first-page":"S189","volume":"10","author":"Navar LG","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1016\/0165-0270(89)90135-0"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.30.5.1238"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-291X(05)80983-0"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.262.2.F236"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1006\/cbir.1996.0021"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118630"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119531"},{"key":"B44","first-page":"R1103","volume":"27","author":"Siragy HM","year":"1997","journal-title":"Am J Physiol"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.11.6506"},{"key":"B46","doi-asserted-by":"crossref","first-page":"205","DOI":"10.1016\/S0031-6997(25)00446-6","volume":"45","author":"Timmermans PB","year":"1993","journal-title":"Pharmacol Rev"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1992.429"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.1996.tb03077.x"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.2001.280.1.F71","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,6,29]],"date-time":"2025-06-29T04:37:47Z","timestamp":1751171867000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.2001.280.1.F71"}},"issued":{"date-parts":[[2001,1,1]]},"references-count":47,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2001,1,1]]}},"alternative-id":["10.1152\/ajprenal.2001.280.1.F71"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.2001.280.1.f71","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2001,1,1]]}},{"indexed":{"date-parts":[[2025,9,24]],"date-time":"2025-09-24T10:30:58Z","timestamp":1758709858157},"reference-count":46,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2002,1,1]]},"abstract":"<jats:p>The tubular localization of 1,25-dihydroxyvitamin D[1,25(OH)<jats:sub>2<\/jats:sub>D<jats:sub>3<\/jats:sub>]-stimulated calmodulin binding proteins (CaMBP-Ds) in the rat kidney and the specificity of their induction were characterized to better understand renal responses to protracted 1,25(OH)<jats:sub>2<\/jats:sub>D<jats:sub>3<\/jats:sub>treatment in vivo. None of the other hormones tested (parathyroid hormone, calcitonin, estradiol-17\u03b2, testosterone, progesterone, hydrocortisone, or dexamethasone) stimulated the CaMBP-Ds, whereas maximal 1,25(OH)<jats:sub>2<\/jats:sub>D<jats:sub>3<\/jats:sub>stimulation occurred after a 5- to 7-day treatment with 100 ng\/day 1,25(OH)<jats:sub>2<\/jats:sub>D<jats:sub>3<\/jats:sub>. With the exception of the more ubiquitously distributed CaMBP-D150, the CaMBP-Ds were localized in distal, but not proximal, tubule preparations. 1,25(OH)<jats:sub>2<\/jats:sub>D<jats:sub>3<\/jats:sub>induction of vitamin D receptors and the CaMBP-Ds was similar with respect to dose-response and time course. Finally, the CaMBP-Ds remained elevated for at least 4 wk after 1,25(OH)<jats:sub>2<\/jats:sub>D<jats:sub>3<\/jats:sub>withdrawal. Because the vitamin D-stimulated renal CaMBP-Ds are principally proteins of the distal tubule, they may be associated with renal regulation of Ca<jats:sup>2+<\/jats:sup>homeostasis. The sustained induction of CaMBP-Ds is important in addressing the question of whether their induction is a function of normal Ca<jats:sup>2+<\/jats:sup>homeostasis or a pathophysiological consequence of hypervitaminosis D and hypercalcemia.<\/jats:p>","DOI":"10.1152\/ajprenal.00286.2000","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:33:25Z","timestamp":1425414805000},"page":"F77-F84","source":"Crossref","is-referenced-by-count":12,"title":["1,25-Dihydroxyvitamin D-stimulated calmodulin binding proteins: a sustained effect on distal tubules"],"prefix":"10.1152","volume":"282","author":[{"given":"Emmanuel K. O.","family":"Siaw","sequence":"first","affiliation":[{"name":"Department of Physiology, Tulane University School of Medicine, New Orleans, Louisiana 70112"}]},{"given":"Marian R.","family":"Walters","sequence":"additional","affiliation":[{"name":"Department of Physiology, Tulane University School of Medicine, New Orleans, Louisiana 70112"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-291X(80)80222-1"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1210\/endo.136.4.7895661"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/0006-291X(92)91672-D"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2736(94)90016-7"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1172\/JCI112241"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1210\/endo-118-2-727"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.261.5.F799"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.257.5.F842"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1988.174"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1172\/JCI113196"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1210\/endo.132.1.8419116"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.90.4.1345"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1096\/fasebj.2.3.3280376"},{"key":"B14","first-page":"F146","volume":"242","author":"El-Dahr SS","year":"1982","journal-title":"Am J Physiol Renal Fluid Electrolyte Physiol"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.1992.262.1.E126"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1359\/jbmr.1998.13.3.454"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.253.2.F358"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/S0076-6879(83)02021-2"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1111\/j.1432-1033.1983.tb07706.x"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1993.1872"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2736(94)90091-4"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/0006-291X(88)90747-4"},{"key":"B23","doi-asserted-by":"crossref","first-page":"13428","DOI":"10.1016\/S0021-9258(18)33466-5","volume":"257","author":"Kawashima H","year":"1982","journal-title":"J Biol Chem"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.78.2.1199"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1016\/0076-6879(90)91029-6"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1002\/jbmr.5650060309"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.1991.260.3.E447"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1210\/endo.134.1.7506210"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1139\/o90-128"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1985.248.2.F296"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1982.232"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1210\/edrv-3-4-331"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1016\/0143-4160(85)90018-1"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1016\/0076-6879(67)10125-0"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1042\/bj2570259"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1210\/endo-109-3-981"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1979.237.5.F350"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1159\/000138248"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1007\/BF00225520"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1007\/BF00737226"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1982.95"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1981.241.4.F403"},{"key":"B44","first-page":"719","volume":"13","author":"Walters MR.","year":"1992","journal-title":"Endocr Rev"},{"key":"B45","first-page":"47","volume":"4","author":"Walters MR.","year":"1995","journal-title":"Endocr Rev Monogr"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1016\/0016-5085(92)90174-W"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1016\/0169-6009(91)90078-E"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00286.2000","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,5,1]],"date-time":"2022-05-01T09:33:37Z","timestamp":1651397617000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00286.2000"}},"issued":{"date-parts":[[2002,1,1]]},"references-count":46,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2002,1,1]]}},"alternative-id":["10.1152\/ajprenal.00286.2000"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00286.2000","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2002,1,1]]}},{"indexed":{"date-parts":[[2025,9,23]],"date-time":"2025-09-23T14:15:51Z","timestamp":1758636951578},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1992,9,1]]},"abstract":"<jats:p> beta 2-Microglobulin (beta 2M) polymerizes to form amyloid fibrils that deposit and cause destructive bone lesions in patients on chronic dialytic therapy. beta 2 M is mitogenic to osteoblasts; however, its effect on bone mineralization is unknown. To determine whether beta 2M causes bone demineralization, neonatal mouse calvariae were incubated with and without beta 2M, and net calcium flux was calculated. Following a 48-h but not 3- or 24-h incubation, beta 2M (10(-8)-10(-6) M) induced a net calcium efflux. The efflux was similar to that observed with 10(-10) M parathyroid hormone (PTH) but less than that observed with 10(-8 M PTH. Devitalizing the calvariae resulted in a net calcium influx that was unaffected by the addition of beta 2M, indicating a cell-mediated phenomenon. The release of beta-glucuronidase, an osteoclast enzyme, increased after a 48-h but not a 24-h incubation with beta 2M. Calcitonin, an osteoclast inhibitor, blocked the beta 2M-induced calcium efflux and beta-glucuronidase release, suggesting osteoclast involvement. Thus beta 2M induces a dose- and time-dependent, cell-mediated calcium efflux from neonatal mouse calvariae that involves osteoclast stimulation. <\/jats:p>","DOI":"10.1152\/ajprenal.1992.263.3.f540","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T04:57:08Z","timestamp":1514005028000},"page":"F540-F545","source":"Crossref","is-referenced-by-count":3,"title":["Beta 2-microglobulin induces calcium efflux from cultured neonatal mouse calvariae"],"prefix":"10.1152","volume":"263","author":[{"given":"S. M.","family":"Moe","sequence":"first","affiliation":[{"name":"Nephrology Program, Pritzker School of Medicine, University ofChicago, Illinois 60637."}]},{"given":"S. M.","family":"Sprague","sequence":"additional","affiliation":[{"name":"Nephrology Program, Pritzker School of Medicine, University ofChicago, Illinois 60637."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1992.263.3.F540","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:24:43Z","timestamp":1567959883000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1992.263.3.F540"}},"issued":{"date-parts":[[1992,9,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1992,9,1]]}},"alternative-id":["10.1152\/ajprenal.1992.263.3.F540"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1992.263.3.f540","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1992,9,1]]}},{"indexed":{"date-parts":[[2025,8,31]],"date-time":"2025-08-31T23:10:35Z","timestamp":1756681835480},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1990,10,1]]},"abstract":"<jats:p> To investigate the direct epithelial effects of corticosteroids on renal ion transport, we studied the influence of the pure glucocorticoid agonist RU 28362 and aldosterone on Na+ and K+ transport in primary cultures of immunodissected rabbit cortical collecting duct (CCD) cells. When grown on permeable supports in a steroid-free medium, CCD monolayers exhibited a lumen-negative transepithelial potential difference (PD) of 5.2 +\/- 1.07 mV and a short-circuit current (SCC) of 8.54 +\/- 2.2 microA\/cm2. Transepithelial resistance averaged 660 +\/- 49 omega\/cm2. The cultures actively reabsorbed Na+ and secreted K+. Both aldosterone and RU 28362 significantly increased PD and SCC; the effects were time and dose dependent. The effect of RU 28362 was completely prevented by the glucocorticoid receptor antagonist RU 486, whereas ZK 91587, a specific mineralocorticoid receptor antagonist, did not block its effect. Both aldosterone and RU 28362 increased the bath-to-lumen concentration ratio of Na+ while lowering that of K+, indicating an increased Na+ reabsorption and K+ secretion. The number of Na(+)-K(+)-ATPase units was significantly enhanced (approximately 2-fold) by both RU 28362 and aldosterone. These results demonstrate that, in cultured CCD cells, not only aldosterone but also a pure glucocorticoid is able to exert mineralocorticoid-like effects, and this latter effect is mediated by glucocorticoid receptors. Because all parameters studied responded similarly to aldosterone and RU 28362, we speculate that in CCD cells glucocorticoids and mineralocorticoids might act by regulating the same gene(s). <\/jats:p>","DOI":"10.1152\/ajprenal.1990.259.4.f672","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T22:24:25Z","timestamp":1513981465000},"page":"F672-F678","source":"Crossref","is-referenced-by-count":13,"title":["Glucocorticoid receptors mediate mineralocorticoid-like effects in cultured collecting duct cells"],"prefix":"10.1152","volume":"259","author":[{"given":"A.","family":"Naray-Fejes-Toth","sequence":"first","affiliation":[{"name":"Hypertension Research Division, Henry Ford Hospital, Detroit, Michigan 48202."}]},{"given":"G.","family":"Fejes-Toth","sequence":"additional","affiliation":[{"name":"Hypertension Research Division, Henry Ford Hospital, Detroit, Michigan 48202."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1990.259.4.F672","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:17:18Z","timestamp":1567970238000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1990.259.4.F672"}},"issued":{"date-parts":[[1990,10,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1990,10,1]]}},"alternative-id":["10.1152\/ajprenal.1990.259.4.F672"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1990.259.4.f672","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1990,10,1]]}},{"indexed":{"date-parts":[[2025,8,24]],"date-time":"2025-08-24T01:34:42Z","timestamp":1755999282158},"reference-count":47,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2011,12]]},"abstract":"<jats:p>Fetal uninephrectomy (uni-x) in male sheep at 100 days of gestation (term = 150 days) reduces overall nephron endowment without affecting birth weight. Offspring have a lower glomerular filtration rate (GFR) and elevated mean arterial pressure (MAP) at 6 mo of age. This study investigated whether this reduction in renal function was associated with impaired urine-concentrating ability at 6 mo of age and exacerbated with ageing (4 yr) and examined response to 1) nonpressor dose of exogenous arginine vasopressin (AVP; 0.2 \u03bcg\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7h<jats:sup>\u22121<\/jats:sup>iv) and 2) 30 h of water deprivation. Basal MAP was higher in uni-x animals at both ages, and became further elevated with age compared with the sham group (elevation in MAP with age; sham: \u223c4 mmHg, uni-x: 9 mmHg, P<jats:sub>group \u00d7 age<\/jats:sub>&lt; 0.01). GFR declined with ageing in both groups with the decrease being greater with age in the uni-x group (further 26%, P<jats:sub>group \u00d7 age<\/jats:sub>&lt; 0.001). In response to AVP infusion, urine osmolality increased in both treatment groups; this response was significantly lower in the uni-x animals and became further reduced with ageing. Uni-x animals had reduced renal expression of vasopressin-2 receptor and aquaporin-2 at both ages ( P &lt; 0.01). The increase in plasma AVP levels in response to dehydration was similar between the treatment groups, suggesting the urine-concentrating defect was associated with these renal gene changes rather than defects in AVP secretion. Renal insufficiency due to a low-nephron endowment increases the risk of hypertension and chronic renal disease and may incur greater vulnerability to physiological challenges such as water deprivation as observed in the uni-x animals.<\/jats:p>","DOI":"10.1152\/ajprenal.00463.2011","type":"journal-article","created":{"date-parts":[[2011,9,15]],"date-time":"2011-09-15T09:56:34Z","timestamp":1316080594000},"page":"F1168-F1176","source":"Crossref","is-referenced-by-count":16,"title":["Urine-concentrating defects exacerbate with age in male offspring with a low-nephron endowment"],"prefix":"10.1152","volume":"301","author":[{"given":"Reetu R.","family":"Singh","sequence":"first","affiliation":[{"name":"Departments of 1Anatomy and Developmental Biology and"},{"name":"Physiology, Monash University, Victoria;"}]},{"given":"Kate M.","family":"Denton","sequence":"additional","affiliation":[{"name":"Physiology, Monash University, Victoria;"}]},{"given":"John F.","family":"Bertram","sequence":"additional","affiliation":[{"name":"Departments of 1Anatomy and Developmental Biology and"}]},{"given":"John","family":"Dowling","sequence":"additional","affiliation":[{"name":"Department of Anatomical Pathology, Monash Medical Centre, Clayton, Victoria; and"}]},{"given":"Karen M.","family":"Moritz","sequence":"additional","affiliation":[{"name":"School of Biomedical Sciences, University of Queensland, St. Lucia, Australia"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1007\/s11255-008-9494-9"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005020160"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-008-0498-1"},{"key":"B4","first-page":"S124","volume":"63","author":"Brenner BM","year":"1997","journal-title":"Kidney Int Suppl"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00167.2002"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00437.2007"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.0139.2001"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000036455.62159.7E"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1042\/cs0940149"},{"key":"B10","first-page":"232","volume":"314","author":"Donahue J","year":"1997","journal-title":"Am J Med Sci"},{"key":"B11","doi-asserted-by":"crossref","first-page":"96","DOI":"10.1111\/j.1651-2227.2007.00587.x","volume":"97","author":"Garcia Nieto VM","year":"2008","journal-title":"Acta Paediatr"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.110.166827"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00079.2006"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000081778.35370.1B"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.2527\/1996.74123052x"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00791.2010"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.275.5.F724"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/S0024-3205(99)00022-3"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.09712.x"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1995.269.3.C655"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1113\/expphysiol.1992.sp003646"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1007\/s004670050587"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00147.x"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000019131.77075.54"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1159\/000323984"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.1.F75"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1985.249.6.F799"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1186\/1471-2369-11-26"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1159\/000180731"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2004.078642"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.108.114058"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00721.x"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1983.244.1.R74"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1097\/HJH.0b013e32831bc778"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1042\/CS20090479"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00139.2011"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2006.125773"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1007\/BF00371114"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118044"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1530\/acta.0.1260357"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00403.2003"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1006\/dbio.1997.8629"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2003.042408"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007010015"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1203\/00006450-200104000-00005"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1203\/01.PDR.0000142589.08246.77"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00511.x"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00463.2011","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,4,11]],"date-time":"2024-04-11T16:23:25Z","timestamp":1712852605000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00463.2011"}},"issued":{"date-parts":[[2011,12]]},"references-count":47,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2011,12]]}},"alternative-id":["10.1152\/ajprenal.00463.2011"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00463.2011","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2011,12]]}},{"indexed":{"date-parts":[[2025,9,4]],"date-time":"2025-09-04T13:45:09Z","timestamp":1756993509334},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1986,3,1]]},"abstract":"<jats:p> The degree by which atrial natriuretic factor (ANF)-induced renal hemodynamic changes account for its natriuretic effect was determined by early clamp experiments in six anesthetized dogs. After control periods, perfusion pressure of the left kidney (LK) was reduced to 80-90 mmHg, and synthetic ANF (auriculin A) was infused intravenously (0.3 micrograms X min-1 X kg body wt). After recovery, furosemide (F) was administered as a bolus injection (1 mg\/kg body wt). In the right kidney (RK), which served as a time control, ANF increased (P less than 0.05) glomerular filtration rate (GFR) 16 +\/- 4% and Na excretion (UNa V) 261 +\/- 63%, whereas it decreased urine osmolality (Uosm) 36 +\/- 7% without changing free water clearance. ANF also increased diuresis (V) and kaliuresis (UKV). F produced qualitatively the same results without changing GFR. In the clamped LK, ANF failed to increase GFR (22 +\/- 4 vs. 26 +\/- 4 ml\/min), UNaV (30 +\/- 9 vs. 33 +\/- 11 mueq\/min), V, and UKV or to decrease Uosm (841 +\/- 97 vs. 840 +\/- 114 mosmol\/kg H2O). F had similar effects in LK as in RK. The data demonstrate that the natriuretic effect of ANF is abolished when its renal hemodynamic actions are impeded. In addition, the results demonstrate that ANF antagonizes renal vasoconstriction in the dog. The results are consistent with the view that the ANF-induced natriuresis is due in great part to an increase in the filtered load of Na into a washed-out inner medulla. <\/jats:p>","DOI":"10.1152\/ajprenal.1986.250.3.f520","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T01:24:13Z","timestamp":1513992253000},"page":"F520-F524","source":"Crossref","is-referenced-by-count":2,"title":["Relationship between renal hemodynamic and natriuretic effects of atrial natriuretic factor"],"prefix":"10.1152","volume":"250","author":[{"given":"R. E.","family":"Sosa","sequence":"first","affiliation":[]},{"given":"M.","family":"Volpe","sequence":"additional","affiliation":[]},{"given":"D. N.","family":"Marion","sequence":"additional","affiliation":[]},{"given":"S. A.","family":"Atlas","sequence":"additional","affiliation":[]},{"given":"J. H.","family":"Laragh","sequence":"additional","affiliation":[]},{"suffix":"Jr","given":"E. D.","family":"Vaughan","sequence":"additional","affiliation":[]},{"given":"T.","family":"Maack","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1986.250.3.F520","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:37:06Z","timestamp":1567971426000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1986.250.3.F520"}},"issued":{"date-parts":[[1986,3,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1986,3,1]]}},"alternative-id":["10.1152\/ajprenal.1986.250.3.F520"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1986.250.3.f520","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1986,3,1]]}},{"indexed":{"date-parts":[[2025,8,23]],"date-time":"2025-08-23T05:01:54Z","timestamp":1755925314397},"reference-count":37,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2006,3]]},"abstract":"<jats:p>During chronic metabolic acidosis, increased expression of renal glutaminase (GA) results from selective stabilization of the GA mRNA. This response is mediated by a direct repeat of an 8-base adenylate-uridylate (AU) sequence that binds \u03b6-crystallin and functions as a pH response element (pH-RE). A tetracycline-responsive promoter system was developed in LLC-PK<jats:sub>1<\/jats:sub>-F<jats:sup>+<\/jats:sup>cells to perform pulse-chase analysis of the turnover of a chimeric \u03b2-globin (\u03b2G) mRNA that contains 960 bp of the 3\u2032-UTR of GA mRNA including the pH-RE. The \u03b2G-GA mRNA exhibits a 14-fold increase in half-life when the LLC-PK<jats:sub>1<\/jats:sub>-F<jats:sup>+<\/jats:sup>cells are transferred to acidic medium. RNase H cleavage and Northern blot analysis of the 3\u2032-ends established that rapid deadenylation occurred concomitantly with the rapid decay of the \u03b2G-GA mRNA in cells grown in normal medium. Stabilization of the \u03b2G-GA mRNA in acidic medium is associated with a pronounced decrease in the rate of deadenylation. Mutation of the pH-RE within the \u03b2G-GA mRNA blocked the pH-responsive stabilization, but not the rapid decay, whereas insertion of only a 29-bp segment containing the pH-RE was sufficient to produce both a rapid decay and a pH-responsive stabilization. Various kidney cells express multiple isoforms of AUF1, an AU-binding protein that enhances mRNA turnover. RNA gel-shift assays demonstrated that the recombinant p40 isoform of AUF1 binds to the pH-RE with high affinity and specificity. Thus AUF1 may mediate the rapid turnover of the GA mRNA, whereas increased binding of \u03b6-crystallin during acidosis may inhibit degradation and result in selective stabilization.<\/jats:p>","DOI":"10.1152\/ajprenal.00250.2005","type":"journal-article","created":{"date-parts":[[2005,10,12]],"date-time":"2005-10-12T03:23:56Z","timestamp":1129087436000},"page":"F733-F740","source":"Crossref","is-referenced-by-count":18,"title":["Role of deadenylation and AUF1 binding in the pH-responsive stabilization of glutaminase mRNA"],"prefix":"10.1152","volume":"290","author":[{"given":"Jill M.","family":"Schroeder","sequence":"first","affiliation":[]},{"given":"Hend","family":"Ibrahim","sequence":"additional","affiliation":[]},{"given":"Lynn","family":"Taylor","sequence":"additional","affiliation":[]},{"given":"Norman P.","family":"Curthoys","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.7.8.2745"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1016\/S0968-0004(00)89102-1"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.281.3.F381"},{"key":"R4","doi-asserted-by":"crossref","unstructured":"Curthoys NPand Lowry OH.The distribution of glutaminase isoenzymes in the various structures of the nephron in normal, acidotic, and alkalotic rat kidney.J Biol Chem248: 162\u2013168, 1973.","DOI":"10.1016\/S0021-9258(19)44458-X"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.nu.15.070195.001025"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1021\/bi00516a024"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.21.12179"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00097.2002"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1016\/S1097-2765(00)80442-6"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1126\/science.6306768"},{"key":"R11","doi-asserted-by":"crossref","unstructured":"Gstraunthaler Gand Handler JS.Isolation, growth, and characterization of a gluconeogenic strain of renal cells.Am J Physiol Cell Physiol252: C232\u2013C238, 1987.","DOI":"10.1152\/ajpcell.1987.252.2.C232"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.1.F126"},{"key":"R13","doi-asserted-by":"crossref","unstructured":"Hopfer U, Jacobberger JW, Gruenert DC, Eckert RL, Jat PS, and Whitsett JA.Immortalization of epithelial cells.Am J Physiol Cell Physiol270: C1\u2013C11, 1996.","DOI":"10.1152\/ajpcell.1996.270.1.C1"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1021\/bi00244a022"},{"key":"R15","doi-asserted-by":"crossref","unstructured":"Kaiser Sand Curthoys NP.Effect of pH and bicarbonate on phosphoenolpyruvate carboxykinase and glutaminase mRNA levels in cultured renal epithelial cells.J Biol Chem266: 9397\u20139402, 1991.","DOI":"10.1016\/S0021-9258(18)92832-2"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1038\/sj.emboj.7600305"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M201377200"},{"key":"R18","doi-asserted-by":"crossref","unstructured":"Laterza OFand Curthoys NP.Effect of acidosis on the properties of the glutaminase mRNA pH-response element binding protein.J Am Soc Nephrol11: 1583\u20131588, 2000.","DOI":"10.1681\/ASN.V1191583"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.6.F970"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.36.22481"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.5.F866"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1172\/JCI200418046"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1006\/meth.1998.0702"},{"key":"R24","doi-asserted-by":"crossref","unstructured":"Lowry OH, Rosebrough NJ, Farr AL, and Randall RJ.Protein measurement with the Folin phenol reagent.J Biol Chem193: 265\u2013275, 1951.","DOI":"10.1016\/S0021-9258(19)52451-6"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1038\/nsmb724"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1006\/abio.1997.2059"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00422.2002"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M101941200"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1042\/bj2330139"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)81520-2"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1006\/geno.1997.5142"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1006\/meth.1998.0709"},{"key":"R33","doi-asserted-by":"crossref","unstructured":"Wilson GMand Brewer G.The search fortrans-acting factors controlling messenger RNA decay.Prog Nucleic Acid Res Mol Biol62: 257\u2013291, 1999.","DOI":"10.1016\/S0079-6603(08)60510-3"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M305775200"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.47.33374"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.259.6.F961"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.13.12.7652"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00250.2005","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,7,18]],"date-time":"2021-07-18T14:11:37Z","timestamp":1626617497000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00250.2005"}},"issued":{"date-parts":[[2006,3]]},"references-count":37,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2006,3]]}},"alternative-id":["10.1152\/ajprenal.00250.2005"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00250.2005","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2006,3]]}},{"indexed":{"date-parts":[[2025,8,23]],"date-time":"2025-08-23T05:15:52Z","timestamp":1755926152073,"version":"3.41.0"},"reference-count":35,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2001,2,1]]},"abstract":"<jats:p>We have used the patch-clamp technique to study the effect of dietary K intake on the apical K channels in the medullary thick ascending limb (mTAL) of rat kidneys. The channel activity, defined by the number of channels in a patch and the open probability ( NP<jats:sub>o<\/jats:sub>), of the 30- and 70-pS K channels, was 0.18 and 0.11, respectively, in the mTAL from rats on a K-deficient diet. In contrast, NP<jats:sub>o<\/jats:sub>of the 30- and 70-pS K channels increased to 0.60 and 0.80, respectively, in the tubules from animals on a high-K diet. The concentration of 20-hydroxyeicosatetraenoic acid (20-HETE) measured with gas chromatography-mass spectrometry was 0.8 pg\/\u03bcg protein in the mTAL from rats on a high-K diet and increased significantly to 4.6 pg\/\u03bcg protein in the tubules from rats on a K-deficient diet. Addition of N-methylsulfonyl-12,12-dibromododec-11-enamide (DDMS) or 17-octadecynoic acid (17-ODYA), agents that inhibit the formation of 20-HETE, had no significant effect on the activity of the 30-pS K channels. However, DDMS\/17-ODYA significantly increased the activity of the apical 70-pS K channel from 0.11 to 0.91 in the mTAL from rats on a K-deficient diet. In contrast, inhibition of the cytochrome P-450 metabolism of arachidonic acid increased NP<jats:sub>o<\/jats:sub>from 0.64 to 0.81 in the tubules from animals on a high-K diet. Furthermore, the sensitivity of the 70-pS K channel to 20-HETE was the same between rats on a high-K diet and on a K-deficient diet. Finally, the pretreatment of the tubules with DDMS increased NP<jats:sub>o<\/jats:sub>of the 70-pS K channels in the mTAL from rats on a K-deficient diet to 0.76. We conclude that an increase in 20-HETE production is involved in reducing the activity of the apical 70-pS K channels in the mTAL from rats on a K-deficient diet.<\/jats:p>","DOI":"10.1152\/ajprenal.2001.280.2.f223","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T13:20:15Z","timestamp":1514035215000},"page":"F223-F230","source":"Crossref","is-referenced-by-count":21,"title":["Role of 20-HETE in mediating the effect of dietary K intake on the apical K channels in the mTAL"],"prefix":"10.1152","volume":"280","author":[{"given":"Ruimin","family":"Gu","sequence":"first","affiliation":[{"name":"Department of Pharmacology, New York Medical College, Valhalla, New York 10595"}]},{"given":"Yuan","family":"Wei","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, New York Medical College, Valhalla, New York 10595"}]},{"given":"Houli","family":"Jiang","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, New York Medical College, Valhalla, New York 10595"}]},{"given":"Michael","family":"Balazy","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, New York Medical College, Valhalla, New York 10595"}]},{"given":"Wenhui","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, New York Medical College, Valhalla, New York 10595"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1007\/BF00373623"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.268.6.F1132"},{"key":"B3","doi-asserted-by":"crossref","first-page":"21720","DOI":"10.1016\/S0021-9258(19)36671-2","volume":"267","author":"Capdevila JH","year":"1992","journal-title":"J Biol Chem"},{"key":"B4","doi-asserted-by":"crossref","first-page":"12306","DOI":"10.1016\/S0021-9258(18)98897-6","volume":"266","author":"Carroll MA","year":"1991","journal-title":"J Biol Chem"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1172\/JCI110915"},{"key":"B6","doi-asserted-by":"crossref","first-page":"933","DOI":"10.1152\/ajplegacy.1970.219.4.933","volume":"219","author":"Eknoyan G","year":"1970","journal-title":"Am J Physiol"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1126\/science.1846705"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1994.266.6.C1568"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.270.6.F978"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.5.F726"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1985.65.3.760"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1172\/JCI111314"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1984.246.6.F745"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1981.241.4.F432"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.80.6.877"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.108.6.537"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1985.248.5.F682"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1978.146"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1994.267.2.R579"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.6.F916"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1999.276.6.R1691"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1984.107"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1172\/JCI104448"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1038\/314620a0"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.27.6.1329"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1172\/JCI108733"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1172\/JCI105146"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.257.3.F347"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.371"},{"key":"B30","doi-asserted-by":"crossref","first-page":"966","DOI":"10.1016\/S0022-3565(24)37347-1","volume":"284","author":"Wang MH","year":"1998","journal-title":"J Pharmacol Exp Ther"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.267.4.F599"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.59.1.413"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.1.F165"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.106.4.727"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1996.271.1.C103"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.2001.280.2.F223","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,6,29]],"date-time":"2025-06-29T04:37:28Z","timestamp":1751171848000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.2001.280.2.F223"}},"issued":{"date-parts":[[2001,2,1]]},"references-count":35,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2001,2,1]]}},"alternative-id":["10.1152\/ajprenal.2001.280.2.F223"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.2001.280.2.f223","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2001,2,1]]}},{"indexed":{"date-parts":[[2025,9,21]],"date-time":"2025-09-21T17:11:35Z","timestamp":1758474695543},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1987,7,1]]},"abstract":"<jats:p> Experiments were performed to investigate the effects of acute cyclooxygenase inhibition on renal hemodynamics in mid and late pregnant rats. In micropuncture studies in the control state, midterm pregnant rats exhibited increased single-nephron glomerular rate (SNGFR) and no change in glomerular or arterial blood pressures. In late pregnancy, SNGFR was no longer significantly elevated, glomerular pressure was similar, and arterial pressure was depressed compared with the virgin. Cyclooxygenase inhibition led to significant increases in single-nephron and whole-kidney filtration and flow in mid and late pregnant rats. This effect was also seen in the virgin control group, and all groups involved a selective renal vasodilation without change in blood pressure. In the absence of anesthesia and surgical stress, cyclooxygenase inhibition had little effect in virgin or pregnant chronically catheterized rats. These studies indicate that the cyclooxygenase-dependent arachidonic acid metabolites are not the agents directly responsible for the gestational rise in the glomerular filtration rate. <\/jats:p>","DOI":"10.1152\/ajprenal.1987.253.1.f158","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T21:11:34Z","timestamp":1513977094000},"page":"F158-F163","source":"Crossref","is-referenced-by-count":5,"title":["Renal effects of cyclooxygenase inhibition in the pregnant rat"],"prefix":"10.1152","volume":"253","author":[{"given":"C.","family":"Baylis","sequence":"first","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1987.253.1.F158","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:42:53Z","timestamp":1567957373000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1987.253.1.F158"}},"issued":{"date-parts":[[1987,7,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1987,7,1]]}},"alternative-id":["10.1152\/ajprenal.1987.253.1.F158"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1987.253.1.f158","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1987,7,1]]}},{"indexed":{"date-parts":[[2025,9,19]],"date-time":"2025-09-19T11:19:35Z","timestamp":1758280775415},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1992,4,1]]},"abstract":"<jats:p> We used the patch-clamp technique to study the effects of arachidonic acid (AA) on the 35-pS secretory K+ channel in the apical membrane of rat cortical collecting duct (CCD). Application of 10 microM AA reversibly reduced channel activity to 1% of the control value [sum of open probability (NPo) decreased from 3.8 to 0.04]. AA inhibits the apical 35-pS K+ channel directly, because application of indomethacin (an inhibitor of cyclooxygenase), nordihydroguaiaretic acid (an enzyme inhibitor of lipoxygenase), and clotrimazole (an inhibitor of epoxygenase) failed to antagonize the AA-induced blocking effect on K+ channel activity. Oleic acid, a cis-unsaturated acid, also blocks K+ channel activity. However, the inhibitory constant (Ki) of oleic acid (5.1 microM) is significantly higher than that of AA (2.6 microM). These results indicate that AA and cis-unsaturated fatty acids are involved in downregulating the apical secretory K+ channel of rat CCD. <\/jats:p>","DOI":"10.1152\/ajprenal.1992.262.4.f554","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T04:03:44Z","timestamp":1514001824000},"page":"F554-F559","source":"Crossref","is-referenced-by-count":7,"title":["Arachidonic acid inhibits the secretory K+ channel of cortical collecting duct of rat kidney"],"prefix":"10.1152","volume":"262","author":[{"given":"W.","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Cellular and Molecular Physiology, Yale UniversityMedical School, New Haven, Connecticut 06510."}]},{"given":"A.","family":"Cassola","sequence":"additional","affiliation":[{"name":"Department of Cellular and Molecular Physiology, Yale UniversityMedical School, New Haven, Connecticut 06510."}]},{"given":"G.","family":"Giebisch","sequence":"additional","affiliation":[{"name":"Department of Cellular and Molecular Physiology, Yale UniversityMedical School, New Haven, Connecticut 06510."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1992.262.4.F554","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:17:05Z","timestamp":1567959425000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1992.262.4.F554"}},"issued":{"date-parts":[[1992,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1992,4,1]]}},"alternative-id":["10.1152\/ajprenal.1992.262.4.F554"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1992.262.4.f554","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1992,4,1]]}},{"indexed":{"date-parts":[[2025,10,8]],"date-time":"2025-10-08T15:25:49Z","timestamp":1759937149955,"version":"3.41.0"},"reference-count":40,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2001,2,1]]},"abstract":"<jats:p>The present study was conducted to determine the metabolism of renal interstitial adenosine under resting conditions and during ischemia. By using a microdialysis method with HPLC-fluorometric analysis, renal interstitial concentrations of adenosine, inosine, and hypoxanthine were assessed in pentobarbital-anesthetized dogs. Average basal renal interstitial concentrations of adenosine, inosine, and hypoxanthine were 0.18 \u00b1 0.04, 0.31 \u00b1 0.05, and 0.35 \u00b1 0.05 \u03bcmol\/l, respectively. Local inhibition of adenosine kinase with iodotubercidin (10 \u03bcmol\/l in perfusate) or inhibition of adenosine deaminase with erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA; 100 \u03bcmol\/l in perfusate) did not change adenosine concentrations in the nonischemic kidneys (0.18 \u00b1 0.04 and 0.24 \u00b1 0.05 \u03bcmol\/l, respectively). On the other hand, treatment with iodotubercidin+EHNA significantly increased adenosine concentration (0.52 \u00b1 0.07 \u03bcmol\/l) with significant decreases in inosine and hypoxanthine levels (0.13 \u00b1 0.03 and 0.19 \u00b1 0.04 \u03bcmol\/l, respectively). During 30 min of ischemia, adenosine, inosine, and hypoxanthine were significantly increased to 0.76 \u00b1 0.29, 2.14 \u00b1 0.45, and 21.8 \u00b1 4.7 \u03bcmol\/l, respectively. The treatment with iodotubercidin did not alter ischemia-induced increase in adenosine (0.84 \u00b1 0.18 \u03bcmol\/l); however, EHNA alone markedly enhanced adenosine accumulation (13.54 \u00b1 2.16 \u03bcmol\/l), the value of which was not augmented by an addition of iodotubercidin (15.80 \u00b1 1.24 \u03bcmol\/l). In contrast, ischemia-induced increases in inosine and hypoxanthine were inversely diminished by the treatment with iodotubercidin+EHNA (0.90 \u00b1 0.20 and 9.86 \u00b1 1.96 \u03bcmol\/l, respectively). These results suggest that both adenosine kinase and adenosine deaminase contribute to the metabolism of renal interstitial adenosine under resting conditions, whereas adenosine produced during ischemia is mainly metabolized by adenosine deaminase and the rephosphorylation of adenosine by adenosine kinase is small.<\/jats:p>","DOI":"10.1152\/ajprenal.2001.280.2.f231","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T13:20:15Z","timestamp":1514035215000},"page":"F231-F238","source":"Crossref","is-referenced-by-count":24,"title":["Renal interstitial adenosine metabolism during ischemia in dogs"],"prefix":"10.1152","volume":"280","author":[{"given":"Akira","family":"Nishiyama","sequence":"first","affiliation":[{"name":"Department of Pharmacology and"}]},{"given":"Shoji","family":"Kimura","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and"}]},{"given":"Hong","family":"He","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and"}]},{"given":"Katsuyuki","family":"Miura","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Osaka City University Medical School, Osaka 545-8585, Japan"}]},{"given":"Matlubur","family":"Rahman","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and"}]},{"given":"Yoshihide","family":"Fujisawa","sequence":"additional","affiliation":[{"name":"Research Equipment Center, Kagawa Medical University, Kagawa 761-0793; and"}]},{"given":"Toshiki","family":"Fukui","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and"}]},{"given":"Youichi","family":"Abe","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.265.6.F802"},{"key":"B2","first-page":"461S","volume":"3","author":"Aki Y","year":"1997","journal-title":"Nephrology"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1159\/000139528"},{"key":"B4","first-page":"82","volume":"14","author":"Archi JRS","year":"1978","journal-title":"Essays Biochem"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.56.2.242"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.267.1.F174"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.1041570110"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1007\/BF01907228"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/0024-3205(95)00099-2"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1994.266.4.H1596"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.81.2.154"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1991.tb09233.x"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1096\/fasebj.8.3.8143938"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.263.5.F886"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1007\/BF00581533"},{"key":"B16","first-page":"150","volume":"108","author":"Lin JJ","year":"1986","journal-title":"J Lab Clin Med"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1139\/y87-233"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1988.4"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/S0008-6363(97)00213-7"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.43.3.390"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/0003-2697(91)90121-9"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.267.5.F783"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1996.76.2.425"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.86.6.656"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-2999(99)00716-5"},{"key":"B26","doi-asserted-by":"crossref","first-page":"988","DOI":"10.1016\/S0022-3565(24)35200-0","volume":"291","author":"Nishiyama A","year":"1999","journal-title":"J Pharmacol Exp Ther"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-2999(98)00978-9"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1007\/BF00580771"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/0028-3908(94)90142-2"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/0304-4165(92)90045-V"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.252.4.F678"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(95)00471-2"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1007\/BF01972265"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1038\/jcbfm.1993.24"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1016\/S0008-6363(96)88630-5"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.27.3.404"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.17.2.117"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1982.242.5.F423"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.266.2.F227"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1999.276.3.R790"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.2001.280.2.F231","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,6,29]],"date-time":"2025-06-29T04:37:29Z","timestamp":1751171849000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.2001.280.2.F231"}},"issued":{"date-parts":[[2001,2,1]]},"references-count":40,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2001,2,1]]}},"alternative-id":["10.1152\/ajprenal.2001.280.2.F231"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.2001.280.2.f231","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2001,2,1]]}},{"indexed":{"date-parts":[[2025,10,8]],"date-time":"2025-10-08T15:41:51Z","timestamp":1759938111307},"reference-count":50,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2016,3,1]]},"abstract":"<jats:p>Recently, we showed that renal afferent neurons exhibit a unique firing pattern, i.e., predominantly sustained firing, upon stimulation. Pathological conditions such as renal inflammation likely alter excitability of renal afferent neurons. Here, we tested whether the proinflammatory chemokine CXCL1 alters the firing pattern of renal afferent neurons. Rat dorsal root ganglion neurons (Th<jats:sub>11<\/jats:sub>-L<jats:sub>2<\/jats:sub>), retrogradely labeled with dicarbocyanine dye, were incubated with CXCL1 (20 h) or vehicle before patch-clamp recording. The firing pattern of neurons was characterized as tonic, i.e., sustained action potential (AP) firing, or phasic, i.e., &lt;5 APs following current injection. Of the labeled renal afferents treated with vehicle, 58.9% exhibited a tonic firing pattern vs. 7.8%, in unlabeled, nonrenal neurons ( P &lt; 0.05). However, after exposure to CXCL1, significantly more phasic neurons were found among labeled renal neurons; hence the occurrence of tonic neurons with sustained firing upon electrical stimulation decreased (35.6 vs. 58.9%, P &lt; 0.05). The firing frequency among tonic neurons was not statistically different between control and CXCL1-treated neurons. However, the lower firing frequency of phasic neurons was even further decreased with CXCL1 exposure [control: 1 AP\/600 ms (1\u20132) vs. CXCL1: 1 AP\/600 ms (1-1); P &lt; 0.05; median (25th-75th percentile)]. Hence, CXCL1 shifted the firing pattern of renal afferents from a predominantly tonic to a more phasic firing pattern, suggesting that CXCL1 reduced the sensitivity of renal afferent units upon stimulation.<\/jats:p>","DOI":"10.1152\/ajprenal.00189.2015","type":"journal-article","created":{"date-parts":[[2015,12,24]],"date-time":"2015-12-24T04:17:00Z","timestamp":1450930620000},"page":"F364-F371","source":"Crossref","is-referenced-by-count":8,"title":["Impaired excitability of renal afferent innervation after exposure to the inflammatory chemokine CXCL1"],"prefix":"10.1152","volume":"310","author":[{"given":"Tilmann","family":"Ditting","sequence":"first","affiliation":[{"name":"Department of Internal Medicine 4, Nephrology and Hypertension, Friedrich-Alexander University, Erlangen, Germany;"}]},{"given":"Wolfgang","family":"Freisinger","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine 1, Nephrology Johannes-Guttenberg University, Mainz, Germany;"}]},{"given":"Kristina","family":"Rodionova","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine 4, Nephrology and Hypertension, Friedrich-Alexander University, Erlangen, Germany;"}]},{"given":"Johannes","family":"Schatz","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine 4, Nephrology and Hypertension, Friedrich-Alexander University, Erlangen, Germany;"}]},{"given":"Nena","family":"Lale","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine 4, Nephrology and Hypertension, Friedrich-Alexander University, Erlangen, Germany;"}]},{"given":"Sonja","family":"Heinlein","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine 4, Nephrology and Hypertension, Friedrich-Alexander University, Erlangen, Germany;"}]},{"given":"Peter","family":"Linz","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine 4, Nephrology and Hypertension, Friedrich-Alexander University, Erlangen, Germany;"}]},{"given":"Christian","family":"Ott","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine 4, Nephrology and Hypertension, Friedrich-Alexander University, Erlangen, Germany;"}]},{"given":"Roland E.","family":"Schmieder","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine 4, Nephrology and Hypertension, Friedrich-Alexander University, Erlangen, Germany;"}]},{"given":"Karie E.","family":"Scrogin","sequence":"additional","affiliation":[{"name":"Department of Molecular Pharmacology and Therapeutics, Loyola University Chicago Stritch School of Medicine, Chicago, Illinois"}]},{"given":"Roland","family":"Veelken","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine 4, Nephrology and Hypertension, Friedrich-Alexander University, Erlangen, Germany;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00363.2010"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.22-23-10277.2002"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/0272-6386(95)90456-5"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/S0896-6273(00)81133-2"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/jn.00100.2011"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010050510"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199212313272704"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1997.77.1.75"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.111.185538"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90599.2008"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1007\/s00109-009-0498-4"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00427.2014"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00011.2012"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.63.1.871"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1113\/expphysiol.1991.sp003504"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfl065"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000034043.16664.96"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1161\/hc3601.095576"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000233356.10630.8a"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0611364104"},{"key":"B21","doi-asserted-by":"crossref","first-page":"731","DOI":"10.1002\/cphy.c100043","volume":"1","author":"Johns EJ","year":"2011","journal-title":"Compr Physiol"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1186\/1742-2094-9-189"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1139\/y92-099"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000097549.70134.D8"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000199984.78039.36"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1159\/000335582"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1084\/jem.171.5.1797"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.18-06-02174.1998"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1002\/jnr.20612"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/jn.2001.86.2.629"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMc0904179"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.89.21.10542"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1111\/j.1460-9568.2008.06267.x"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1016\/j.expneurol.2007.01.038"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1109\/TBME.2004.827531"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.4872-09.2010"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.2174\/157016110791330870"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.3389\/fphar.2011.00054"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(02)00838-3"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2014.59"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/jn.1996.76.3.1924"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/jn.01267.2004"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1186\/1744-8069-4-38"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1159\/000316528"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1186\/1744-8069-5-26"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.103"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1016\/S0895-7061(02)02959-X"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1007\/BF02088322"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.166.9.5755"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1016\/j.pain.2013.07.002"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00189.2015","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,5,30]],"date-time":"2022-05-30T17:36:57Z","timestamp":1653932217000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00189.2015"}},"issued":{"date-parts":[[2016,3,1]]},"references-count":50,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2016,3,1]]}},"alternative-id":["10.1152\/ajprenal.00189.2015"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00189.2015","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2016,3,1]]}},{"indexed":{"date-parts":[[2025,10,28]],"date-time":"2025-10-28T18:36:48Z","timestamp":1761676608768},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1983,12,1]]},"abstract":"<jats:p> The mechanism of inhibition of active Cl- secretion by 1 mM furosemide and 0.1 mM bumetanide was characterized in the isolated frog corneal epithelium. Transepithelial and transmembrane cell electrical parameters as well as transmembrane Cl- electrochemical potential difference were measured with conventional glass microelectrodes and Cl- selective microelectrodes. Furosemide caused the potential difference across the apical membrane to hyperpolarize by 20 mV while the transepithelial potential difference declined by 13 mV. The apical-to-basolateral membrane resistance ratio increased 3-4 times after furosemide or bumetanide addition. Preincubation with furosemide prevented a 30-mV depolarization of the apical membrane potential difference normally observed when Cl- was removed from the tear side bathing solution. In control conditions, intracellular Cl- activity was above equilibrium. Bumetanide further increased the Cl- electrochemical gradient between the cell compartment and the bathing solutions even though intracellular Cl- activity fell from 18 to 12 mM. In contrast, perfusion with Cl- -free Ringer in the stromal side bathing solution decreased the Cl- electrochemical gradient across the apical membrane to zero, indicating an equilibrium distribution. Adenosine, which selectively increases Cl- permeability of the apical membrane, also decreased the Cl- electrochemical gradient across the apical membrane. These results suggest that the diuretics inhibit active Cl- transport primarily by decreasing the Cl- permeability of the apical membrane. <\/jats:p>","DOI":"10.1152\/ajprenal.1983.245.6.f660","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T15:02:26Z","timestamp":1513954946000},"page":"F660-F669","source":"Crossref","is-referenced-by-count":2,"title":["Mode of inhibition of active chloride transport in the frog cornea by furosemide"],"prefix":"10.1152","volume":"245","author":[{"given":"R.","family":"Patarca","sequence":"first","affiliation":[]},{"given":"O. A.","family":"Candia","sequence":"additional","affiliation":[]},{"given":"P. S.","family":"Reinach","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1983.245.6.F660","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:25:26Z","timestamp":1567967126000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1983.245.6.F660"}},"issued":{"date-parts":[[1983,12,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1983,12,1]]}},"alternative-id":["10.1152\/ajprenal.1983.245.6.F660"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1983.245.6.f660","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1983,12,1]]}},{"indexed":{"date-parts":[[2025,10,28]],"date-time":"2025-10-28T18:31:15Z","timestamp":1761676275519},"reference-count":44,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2003,10]]},"abstract":"<jats:p> Extracellular nucleotides, acting through the P2Y<jats:sub>2<\/jats:sub> receptor and the associated phosphoinositide-Ca<jats:sup>2<\/jats:sup><jats:sup>+<\/jats:sup> signaling pathway, inhibit AVP-stimulated osmotic water permeability in rat inner medullary collecting duct (IMCD). Because a rise in intracellular Ca<jats:sup>2<\/jats:sup><jats:sup>+<\/jats:sup> is frequently associated with enhanced arachidonic acid metabolism, we examined the effect of activation of the P2Y<jats:sub>2<\/jats:sub> receptor on release of PGE<jats:sub>2<\/jats:sub> in freshly prepared rat IMCD suspensions. Unstimulated IMCD released moderate, but significant, amounts of PGE<jats:sub>2<\/jats:sub>, which were more sensitive to cyclooxygenase (COX)-2 than COX-1 inhibition. Agonist activation of P2Y<jats:sub>2<\/jats:sub> receptor by adenosine 5\u2032- O-(3-thiotriphosphate) enhanced release of PGE<jats:sub>2<\/jats:sub> from IMCD in a time- and concentration-dependent fashion. Purinergic-stimulated release of PGE<jats:sub>2<\/jats:sub> was completely blocked by nonspecific COX inhibitors (flurbiprofen and 2-acetoxyphenylhept-2-ynyl sulfide). Differential COX inhibition studies revealed that purinergic-stimulated release of PGE<jats:sub>2<\/jats:sub> was more sensitive to a COX-1-specific inhibitor (valeroyl salicylate) than a COX-2-specific inhibitor (NS-398). Thus purinergic stimulation resulted in significantly more release of PGE<jats:sub>2<\/jats:sub> in the presence of COX-2 inhibitor than COX-1 inhibitor. If it is assumed that increased release of PGE<jats:sub>2<\/jats:sub> is related to its increased production, our results suggest that purinergic stimulation of IMCD results in enhanced production and release of PGE<jats:sub>2<\/jats:sub> in a COX-1-dependent fashion. Because PGE<jats:sub>2<\/jats:sub> is known to affect transport of water, salt, and urea in IMCD, interaction of the purinergic system with the prostanoid system in IMCD can modulate handling of water, salt, and urea by IMCD and, thus, may constitute an AVP-independent regulatory mechanism. <\/jats:p>","DOI":"10.1152\/ajprenal.00096.2003","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T15:39:30Z","timestamp":1425397170000},"page":"F711-F721","source":"Crossref","is-referenced-by-count":33,"title":["P2Y<sub>2<\/sub> receptor-stimulated release of prostaglandin  E<sub>2<\/sub> by rat inner medullary collecting duct preparations"],"prefix":"10.1152","volume":"285","author":[{"given":"Brett D.","family":"Welch","sequence":"first","affiliation":[]},{"given":"Noel G.","family":"Carlson","sequence":"additional","affiliation":[]},{"given":"Huihui","family":"Shi","sequence":"additional","affiliation":[]},{"given":"Leslie","family":"Myatt","sequence":"additional","affiliation":[]},{"given":"Bellamkonda K.","family":"Kishore","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"REF1","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0703848"},{"key":"REF2","doi-asserted-by":"publisher","DOI":"10.1165\/ajrcmb.13.4.7546770"},{"key":"REF3","doi-asserted-by":"publisher","DOI":"10.1016\/S0165-1838(00)00125-9"},{"key":"REF4","doi-asserted-by":"crossref","unstructured":"Bao Y, Pucci  ML, Chan BS, Lu R, Ito S, and Schuster VL. Prostaglandin transporter PGT  is expressed in cell types that synthesize and release prostanoids.  Am J Physiol Renal Physiol 282:  F1103\u2013F1110, 2002.","DOI":"10.1152\/ajprenal.00152.2001"},{"key":"REF5","doi-asserted-by":"publisher","DOI":"10.1016\/0167-4838(94)90148-1"},{"key":"REF6","doi-asserted-by":"publisher","DOI":"10.1006\/abbi.1995.1130"},{"key":"REF7","unstructured":"Bonventre JV. The 85-kD cytosolic phospholipase  A2 knockout mouse: a new tool for physiology and cell biology.  J Am Soc Nephrol 10:  404\u2013412, 1999."},{"key":"REF8","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1097-4695(199804)35:1<29::AID-NEU3>3.0.CO;2-D"},{"key":"REF9","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.1988.tb11754.x"},{"key":"REF10","doi-asserted-by":"publisher","DOI":"10.1016\/S0898-6568(00)00083-8"},{"key":"REF11","doi-asserted-by":"publisher","DOI":"10.1016\/0014-2999(88)90526-2"},{"key":"REF12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.267.6.F998"},{"key":"REF13","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00048.x"},{"key":"REF14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00150.2001"},{"key":"atypb1","unstructured":"Gaion RM and  Trento M. The role of adrenergic, purinergic and opiate receptors in the  control of prostacyclin-induced contraction in the guinea-pig ileum.  Arch Int Pharmacodyn Ther 271:  33\u201344, 1984."},{"key":"REF16","doi-asserted-by":"publisher","DOI":"10.1007\/BF00165638"},{"key":"REF17","doi-asserted-by":"crossref","unstructured":"Harris RC and  Breyer MD. Physiological regulation of cyclooxygenase-2 in the kidney.  Am J Physiol Renal Physiol 281:  F1\u2013F11, 2001.","DOI":"10.1152\/ajprenal.2001.281.1.F1"},{"key":"REF18","doi-asserted-by":"publisher","DOI":"10.1016\/S1388-1981(00)00115-3"},{"key":"REF19","doi-asserted-by":"publisher","DOI":"10.1046\/j.1440-1681.2001.03450.x"},{"key":"REF20","doi-asserted-by":"publisher","DOI":"10.1111\/j.2042-7158.1997.tb06835.x"},{"key":"REF21","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.1041290109"},{"key":"REF22","doi-asserted-by":"publisher","DOI":"10.1126\/science.280.5367.1268"},{"key":"REF23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.6.F863"},{"key":"REF24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.1.F43"},{"key":"atypb2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00216.x"},{"key":"REF26","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1998.275.1.H131"},{"key":"REF27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00075.2002"},{"key":"REF28","doi-asserted-by":"publisher","DOI":"10.1006\/cimm.1998.1343"},{"key":"REF29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.262.2.F229"},{"key":"REF30","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-1759(98)00175-6"},{"key":"REF31","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00015.2002"},{"key":"REF32","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.pharmtox.40.1.563"},{"key":"REF33","doi-asserted-by":"publisher","DOI":"10.1042\/bj2140273"},{"key":"REF34","doi-asserted-by":"publisher","DOI":"10.1111\/j.1432-1033.1989.tb15236.x"},{"key":"REF35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1981.241.1.F53"},{"key":"REF36","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.2.F294"},{"key":"REF37","doi-asserted-by":"publisher","DOI":"10.1046\/j.1440-1681.2001.03451.x"},{"key":"REF38","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.6.F945"},{"key":"REF39","doi-asserted-by":"publisher","DOI":"10.1007\/BF00370763"},{"key":"REF40","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.263.6.F985"},{"key":"REF41","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00615.x"},{"key":"REF42","doi-asserted-by":"publisher","DOI":"10.1007\/s002100000310"},{"key":"REF43","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119227"},{"key":"REF44","doi-asserted-by":"publisher","DOI":"10.1016\/S0304-3959(02)00027-1"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00096.2003","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T17:39:05Z","timestamp":1567964345000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00096.2003"}},"issued":{"date-parts":[[2003,10]]},"references-count":44,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2003,10]]}},"alternative-id":["10.1152\/ajprenal.00096.2003"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00096.2003","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2003,10]]}},{"indexed":{"date-parts":[[2025,12,3]],"date-time":"2025-12-03T17:52:35Z","timestamp":1764784355725},"reference-count":8,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2020,2,1]]},"DOI":"10.1152\/ajprenal.00534.2019","type":"journal-article","created":{"date-parts":[[2020,2,11]],"date-time":"2020-02-11T18:45:26Z","timestamp":1581446726000},"page":"F506-F506","source":"Crossref","is-referenced-by-count":1,"title":["Bacteria-mediated TRPV5 activity promote kidney CaOx stones: a story too good to be true?"],"prefix":"10.1152","volume":"318","author":[{"given":"Ling-Yue","family":"An","sequence":"first","affiliation":[{"name":"Department of Urology and Guangdong Key Laboratory of Urology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China"}]},{"given":"Zhi-Can","family":"He","sequence":"additional","affiliation":[{"name":"Department of Urology and Guangdong Key Laboratory of Urology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China"}]},{"given":"Zheng-Lin","family":"Chang","sequence":"additional","affiliation":[{"name":"Department of Urology and Guangdong Key Laboratory of Urology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China"}]},{"given":"Ya-Peng","family":"Huang","sequence":"additional","affiliation":[{"name":"Department of Urology and Guangdong Key Laboratory of Urology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China"}]},{"given":"Shi-Ke","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Urology and Guangdong Key Laboratory of Urology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China"}]},{"given":"Wen-Qi","family":"Wu","sequence":"additional","affiliation":[{"name":"Department of Urology and Guangdong Key Laboratory of Urology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00199.2019"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/s41585-018-0120-z"},{"key":"B3","doi-asserted-by":"crossref","first-page":"1315","DOI":"10.1681\/ASN.V1291971","volume":"12","author":"Hostetter TH","year":"2001","journal-title":"J Am Soc Nephrol"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/ncomms8975"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.2174\/0929867323666161028154545"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.21037\/atm.2016.11.73"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2019.05.029"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1016\/j.intimp.2016.12.022"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00534.2019","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,10,15]],"date-time":"2022-10-15T08:11:11Z","timestamp":1665821471000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00534.2019"}},"issued":{"date-parts":[[2020,2,1]]},"references-count":8,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2020,2,1]]}},"alternative-id":["10.1152\/ajprenal.00534.2019"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00534.2019","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2020,2,1]]}},{"indexed":{"date-parts":[[2025,12,6]],"date-time":"2025-12-06T16:57:19Z","timestamp":1765040239564},"reference-count":41,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2010,4]]},"abstract":"<jats:p>Ascending urinary tract infections, a significant cause of kidney damage, are predominantly caused by uropathogenic Escherichia coli (UPEC). However, the role and mechanism of changes in ureteric function during infection are poorly understood. We therefore investigated the effects of UPEC on Ca signaling and contractions in rat ( n = 17) and human ( n = 6) ureters. Ca transients and force were measured and effects of UPEC on the urothelium were monitored in live tissues. In both species, luminal exposure of ureters to UPEC strains J96 and 536 caused significant time-dependent decreases in phasic and high K depolarization-induced contractility, associated with decreases in the amplitude and duration of the Ca transients. These changes were significant after 3\u20135 h and irreversible over the next 5 h. The infection causes increased activity of K channels, causing inhibition of voltage-gated Ca entry, and K channel blockers could reverse the effects of UPEC on ureteric function. A smaller direct effect on Ca entry also occurs. Nonpathogenic E. coli (TG2) or abluminal application of UPEC did not produce changes in Ca signaling or contractility. UPEC exposure also caused significant impairment of urothelial barrier function; luminal application of the Ca channel blocker nifedipine caused a reduction in contractions as it entered the tissue, an effect not observed in untreated ureters. Thus, UPEC impairs ureteric contractility in a Ca-dependent manner, largely caused by stimulation of potassium channels and this mechanism is dependent on host-urothelium interaction.<\/jats:p>","DOI":"10.1152\/ajprenal.00468.2009","type":"journal-article","created":{"date-parts":[[2010,2,4]],"date-time":"2010-02-04T02:56:45Z","timestamp":1265252205000},"page":"F900-F908","source":"Crossref","is-referenced-by-count":10,"title":["Modulation of ureteric Ca signaling and contractility in humans and rats by uropathogenic E. coli"],"prefix":"10.1152","volume":"298","author":[{"given":"Rachel V.","family":"Floyd","sequence":"first","affiliation":[{"name":"Physiological Laboratory, School of Biomedical Sciences, University of Liverpool, Liverpool;"}]},{"given":"Craig","family":"Winstanley","sequence":"additional","affiliation":[{"name":"Division of Medical Microbiology and Genitourinary Medicine, University of Liverpool, Liverpool; and"}]},{"given":"Ali","family":"Bakran","sequence":"additional","affiliation":[{"name":"Royal Liverpool University Hospital, Liverpool, United Kingdom"}]},{"given":"Susan","family":"Wray","sequence":"additional","affiliation":[{"name":"Physiological Laboratory, School of Biomedical Sciences, University of Liverpool, Liverpool;"}]},{"given":"Theodor V.","family":"Burdyga","sequence":"additional","affiliation":[{"name":"Physiological Laboratory, School of Biomedical Sciences, University of Liverpool, Liverpool;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"crossref","first-page":"1241","DOI":"10.1128\/jb.152.3.1241-1247.1982","volume":"152","author":"Berger H","year":"1982","journal-title":"J Bacteriol"},{"key":"B2","doi-asserted-by":"crossref","first-page":"63","DOI":"10.1128\/IAI.52.1.63-69.1986","volume":"52","author":"Bhakdi S","year":"1986","journal-title":"Infect Immun"},{"key":"B3","first-page":"189","volume":"126","author":"Blum G","year":"1995","journal-title":"FEMS Microbiol Lett"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/nature03834"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1995.sp021054"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.1999.00867.x"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.1999.0855s.x"},{"key":"B8","first-page":"208","volume-title":"What is the Role of the SR in Smooth Muscle","author":"Burdyga TV","year":"2002"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1097\/01.ju.0000091870.51841.ae"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1038\/386855a0"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1038\/31960"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1016\/j.juro.2008.02.045"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/S0891-5520(03)00005-9"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(17)62746-0"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0703068"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1136\/bmj.318.7186.770"},{"key":"B18","doi-asserted-by":"crossref","first-page":"933","DOI":"10.1128\/IAI.33.3.933-938.1981","volume":"33","author":"Hull RA","year":"1981","journal-title":"Infect Immun"},{"key":"B19","doi-asserted-by":"crossref","first-page":"613","DOI":"10.1128\/IAI.54.3.613-620.1986","volume":"54","author":"Hultgren SJ","year":"1986","journal-title":"Infect Immun"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1128\/CMR.4.1.80"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0308125100"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(17)60844-9"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.00376-06"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0607898104"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1016\/j.femsle.2005.08.028"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1046\/j.1462-5822.2002.00166.x"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1097\/01.ju.0000083492.80217.20"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1016\/j.juro.2007.03.099"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.97.16.8829"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M110560200"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1016\/j.micinf.2006.02.029"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00101.2002"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2004.070615"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1111\/j.1574-695X.2006.00140.x"},{"key":"B35","first-page":"81P","volume":"543","author":"Smith RD","year":"2002","journal-title":"J Physiol"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.74.1.750-757.2006"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.00075-08"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1371\/journal.ppat.0030060"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(17)62778-2"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(01)69137-7"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1371\/journal.ppat.1000415"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1038\/35015091"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00468.2009","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,10,21]],"date-time":"2021-10-21T15:00:36Z","timestamp":1634828436000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00468.2009"}},"issued":{"date-parts":[[2010,4]]},"references-count":41,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2010,4]]}},"alternative-id":["10.1152\/ajprenal.00468.2009"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00468.2009","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2010,4]]}},{"indexed":{"date-parts":[[2025,12,31]],"date-time":"2025-12-31T07:58:51Z","timestamp":1767167931089,"version":"build-2238731810"},"update-to":[{"DOI":"10.1152\/ajprenal.00385.2019","type":"correction","label":"Correction","source":"publisher","updated":{"date-parts":[[2022,1,21]],"date-time":"2022-01-21T00:00:00Z","timestamp":1642723200000}}],"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2022,2,1]]},"DOI":"10.1152\/ajprenal.00385.2019_cor","type":"journal-article","created":{"date-parts":[[2022,1,21]],"date-time":"2022-01-21T10:35:55Z","timestamp":1642761355000},"page":"F193-F194","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Corrigendum for Fu et al., volume 317, 2019, p. F1582\u2013F1592"],"prefix":"10.1152","volume":"322","member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00385.2019_COR","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,1,21]],"date-time":"2022-01-21T10:35:55Z","timestamp":1642761355000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00385.2019_COR"}},"issued":{"date-parts":[[2022,2,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2022,2,1]]}},"alternative-id":["10.1152\/ajprenal.00385.2019_COR"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00385.2019_cor","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2022,2,1]]},"assertion":[{"value":"2022-01-21","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,1,8]],"date-time":"2026-01-08T03:10:34Z","timestamp":1767841834024,"version":"3.49.0"},"reference-count":42,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2000,7,1]]},"abstract":"<jats:p>The fractional clearances (\u03b8) for FITC-Ficoll and albumin were estimated in isolated perfused rat kidneys in which the tubular activity was inhibited by low temperature (8\u00b0C) and\/or 10 mM NH<jats:sub>4<\/jats:sub>Cl. The Ficoll data were analyzed according to a two-pore model giving small and large pore radii of 46 \u00c5 and 80\u201387 \u00c5, respectively. The estimated negative charge density was 35\u201345 meq\/l at 8\u00b0C. Perfusion with erythrocyte-free solutions of kidneys at 37\u00b0C reduced glomerular size and charge permselectivity. Thus the large pore fraction of the glomerular filtrate (f<jats:sub>L<\/jats:sub>) was 1.64% at 37\u00b0C compared with 0.94% at 8\u00b0C. The \u03b8 for albumin was four times higher at 37\u00b0C than at 8\u00b0C (0.86% vs. 0.19%, respectively). NH<jats:sub>4<\/jats:sub>Cl caused further irreversible damage to the glomerular barrier. We conclude that there are no deleterious effects on the glomerular barrier of a reduction in temperature from 37\u00b0C to 8\u00b0C. Therefore our data seem to disprove the hypothesis of low glomerular permselectivity and transtubular uptake of intact albumin and support the classic concept of a highly selective glomerular barrier.<\/jats:p>","DOI":"10.1152\/ajprenal.2000.279.1.f84","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T12:43:17Z","timestamp":1514032997000},"page":"F84-F91","source":"Crossref","is-referenced-by-count":76,"title":["Glomerular size and charge selectivity in the rat as revealed by FITC-Ficoll and albumin"],"prefix":"10.1152","volume":"279","author":[{"given":"Maria","family":"Ohlson","sequence":"first","affiliation":[{"name":"Departments of Physiology and"}]},{"given":"Jenny","family":"S\u00f6rensson","sequence":"additional","affiliation":[{"name":"Departments of Physiology and"}]},{"given":"B\u00f6rje","family":"Haraldsson","sequence":"additional","affiliation":[{"name":"Departments of Physiology and"},{"name":"Nephrology, G\u00f6teborg University, SE-405 30 G\u00f6teborg, Sweden"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1981.63"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1007\/BF00870142"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.273.3.F430"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1984.9"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1975.104"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-3495(75)85863-2"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-3495(75)85862-0"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1016\/0003-9861(71)90528-5"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1007\/BF00788496"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1985.249.3.F374"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1981.241.2.F162"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2736(88)90504-4"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1983.tb07186.x"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1986.tb07973.x"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1992.43"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.132"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1993.264.5.H1428"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1992.tb09268.x"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1994.tb09676.x"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1994.tb09677.x"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1006\/mvre.1999.2146"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.147"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-201X.1998.0316f.x"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5320(66)80108-9"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.27.2.305"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1993.264.4.C810"},{"key":"B27","doi-asserted-by":"crossref","first-page":"214","DOI":"10.1681\/ASN.V32214","volume":"3","author":"Oliver JD","year":"1992","journal-title":"J Am Soc Nephrol"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.267.6.F917"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1797.1996.tb00088.x"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1978.41"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1978.tb06212.x"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1994.74.1.163"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1979.tb06329.x"},{"key":"B34","first-page":"1481","volume":"137","author":"Russo PA","year":"1990","journal-title":"Am J Pathol"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1976.5"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1986.102"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-201x.1998.00315.x"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.263.4.F601"},{"key":"B39","first-page":"61","volume":"3","author":"van Hinsbergh VWM","year":"1997","journal-title":"Vascular Endothelium. Physiology, Pathology and Therapeutic Opportunities"},{"key":"B40","first-page":"1241","volume":"19","author":"Vassiliou P","year":"1989","journal-title":"Biochem Int"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1093\/cvr\/27.3.384"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-201X.1996.553306000.x"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.2000.279.1.F84","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:39:43Z","timestamp":1660189183000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.2000.279.1.F84"}},"issued":{"date-parts":[[2000,7,1]]},"references-count":42,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2000,7,1]]}},"alternative-id":["10.1152\/ajprenal.2000.279.1.F84"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.2000.279.1.f84","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2000,7,1]]}},{"indexed":{"date-parts":[[2026,1,8]],"date-time":"2026-01-08T07:34:04Z","timestamp":1767857644962,"version":"3.49.0"},"reference-count":49,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2010,3]]},"abstract":"<jats:p>Nitroalkene derivatives of nitro-oleic acid (OA-NO<jats:sub>2<\/jats:sub>) are endogenous lipid products with potent anti-inflammatory properties in vitro. The present study was undertaken to evaluate the in vivo anti-inflammatory effect of OA-NO<jats:sub>2<\/jats:sub>in mice given LPS. Two days before LPS administration, C57BL\/6J mice were chronically infused with vehicle (LPS vehicle) or OA-NO<jats:sub>2<\/jats:sub>(LPS OA-NO<jats:sub>2<\/jats:sub>) at 200 \u03bcg\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7day<jats:sup>\u22121<\/jats:sup>via osmotic minipumps; LPS was administered via a single intraperitoneal (ip) injection (10 mg\/kg in saline). A third group received an ip injection of saline without LPS or OA-NO<jats:sub>2<\/jats:sub>and served as controls. At 18 h of LPS administration, LPS vehicle mice displayed multiorgan dysfunction as evidenced by elevated plasma urea and creatinine (kidney), aspartate aminotransferase (AST) and alanine aminotransferase (ALT; liver), and lactate dehydrogenase (LDH) and reduced ejection fraction (heart). In contrast, the severity of multiorgan dysfunction was less in LPS OA-NO<jats:sub>2<\/jats:sub>animals. The levels of circulating TNF-\u03b1 and renal TNF-\u03b1 mRNA expression, together with renal mRNA expression of monocyte chemoattractant protein-1, ICAM-1, and VCAM-1, and with renal mRNA and protein expression of inducible nitric oxide synthase and cyclooxygenase 2, and renal cGMP and PGE<jats:sub>2<\/jats:sub>contents, were greater in LPS vehicle vs. control mice, but were attenuated in LPS OA-NO<jats:sub>2<\/jats:sub>animals. Similar patterns of changes in the expression of inflammatory mediators were observed in the liver. Together, pretreatment with OA-NO<jats:sub>2<\/jats:sub>ameliorated the inflammatory response and multiorgan injury in endotoxin-induced endotoxemia in mice.<\/jats:p>","DOI":"10.1152\/ajprenal.00439.2009","type":"journal-article","created":{"date-parts":[[2009,12,24]],"date-time":"2009-12-24T02:45:46Z","timestamp":1261622746000},"page":"F754-F762","source":"Crossref","is-referenced-by-count":52,"title":["Nitro-oleic acid protects against endotoxin-induced endotoxemia and multiorgan injury in mice"],"prefix":"10.1152","volume":"298","author":[{"given":"Haiping","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, University of Utah and Salt Lake Veterans Affairs Medical Center, Salt Lake City, Utah; and"},{"name":"Department of Nephrology, 2nd Affiliated Hospital, Shandong University, Jinan, China"}]},{"given":"Haiying","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Utah and Salt Lake Veterans Affairs Medical Center, Salt Lake City, Utah; and"}]},{"given":"Zhunjun","family":"Jia","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Utah and Salt Lake Veterans Affairs Medical Center, Salt Lake City, Utah; and"}]},{"given":"Curtis","family":"Olsen","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Utah and Salt Lake Veterans Affairs Medical Center, Salt Lake City, Utah; and"}]},{"given":"Sheldon","family":"Litwin","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Utah and Salt Lake Veterans Affairs Medical Center, Salt Lake City, Utah; and"}]},{"given":"Guangju","family":"Guan","sequence":"additional","affiliation":[{"name":"Department of Nephrology, 2nd Affiliated Hospital, Shandong University, Jinan, China"}]},{"given":"Tianxin","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Utah and Salt Lake Veterans Affairs Medical Center, Salt Lake City, Utah; and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajplung.2000.279.6.L1137"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1001\/jama.1997.03540430043031"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M504212200"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M602814200"},{"key":"B5","first-page":"419","volume":"134","author":"Bertani T","year":"1989","journal-title":"Am J Pathol"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1126\/science.3895437"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90609.2008"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1097\/00003246-199609000-00002"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000032114.68919.EF"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M105209200"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M603357200"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.168.11.5817"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00319.x"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.172.4.2629"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1096\/fj.02-1078fje"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1089\/ars.2004.6.850"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199606273342603"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/14.4.853"},{"key":"B19","volume-title":"Deaths: Final Data for 1999.","author":"Hoyert D"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.2005.04155.x"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1210\/en.2007-1639"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajplung.1999.277.2.L310"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.2006.04320.x"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1016\/j.ccc.2005.01.002"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00740.x"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.232409599"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90236.2008"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa022139"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1093\/oxfordjournals.ndt.a027256"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1021\/tx980207u"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199305203282008"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-113-3-227"},{"key":"B33","doi-asserted-by":"crossref","first-page":"943","DOI":"10.4049\/jimmunol.160.2.943","volume":"160","author":"Peschon JJ","year":"1998","journal-title":"J Immunol"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.105.088062"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1038\/364798a0"},{"key":"B36","doi-asserted-by":"crossref","first-page":"26066","DOI":"10.1016\/S0021-9258(18)47160-8","volume":"269","author":"Rubbo H","year":"1994","journal-title":"J Biol Chem"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra043632"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M414689200"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0408384102"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra032401"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119551"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00512.x"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1038\/330662a0"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjc.6690067"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00323.2002"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.106.117184"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00445.2006"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1084\/jem.180.1.95"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0501744102"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00439.2009","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,5,29]],"date-time":"2023-05-29T00:57:40Z","timestamp":1685321860000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00439.2009"}},"issued":{"date-parts":[[2010,3]]},"references-count":49,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2010,3]]}},"alternative-id":["10.1152\/ajprenal.00439.2009"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00439.2009","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2010,3]]}},{"indexed":{"date-parts":[[2026,1,8]],"date-time":"2026-01-08T08:05:47Z","timestamp":1767859547444,"version":"3.49.0"},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1995,12,1]]},"abstract":"<jats:p> We recently reported that elevations in the intracellular Ca2+ concentration ([Ca2+]i) enhance low-voltage-activated, T-type, Ca2+ channel activity via Ca2+\/calmodulin-dependent protein kinase II (CaMKII). Here, we document CaMKII activity in bovine adrenal glomerulosa (AG) cells and assess the importance of CaMKII in depolarization-induced Ca2+ signaling. AG cell extracts exhibited kinase activity toward a CaMKII-selective peptide substrate that was dependent on both Ca2+ [half-maximal concentration for Ca2+ activation (K0.5) = 1.5 microM] and calmodulin (K0.5 = 46 nM) and was sensitive to a calmodulin antagonist and a CaMKII peptide inhibitor. On cell treatment with elevated extracellular potassium (10-60 mM) or angiotensin II, Ca(2+)-independent CaMKII activity increased to 133-205% of basal activity. Ca(2+)-independent kinase activity in agonist-stimulated extracts was inhibited by the CaMKII inhibitor peptide, 1(-)[N,O-bis(1,5- isoquinolinesulfonyl)-N-methyl-L-tyrosyl]-4-phenylpiperazine (KN-62), a cell-permeable inhibitor of CaMKII, reduced the agonist-induced stimulation of Ca(2+)-independent CaMKII activity. KN-62 also diminished depolarization-induced increases in [Ca2+]i without affecting the membrane potential. These observations suggest that CaMKII is activated in situ by aldosterone secretagogues and augments Ca2+ signaling through voltage-gated Ca2+ channels. <\/jats:p>","DOI":"10.1152\/ajprenal.1995.269.6.f751","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T05:21:03Z","timestamp":1514006463000},"page":"F751-F760","source":"Crossref","is-referenced-by-count":11,"title":["Ca2+\/calmodulin-dependent protein kinase II activation and regulation of adrenal glomerulosa Ca2+ signaling"],"prefix":"10.1152","volume":"269","author":[{"given":"R. J.","family":"Fern","sequence":"first","affiliation":[{"name":"Department of Pharmacology, University of Virginia Health SciencesCenter, Charlottesville 22908, USA."}]},{"given":"M. S.","family":"Hahm","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, University of Virginia Health SciencesCenter, Charlottesville 22908, USA."}]},{"given":"H. K.","family":"Lu","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, University of Virginia Health SciencesCenter, Charlottesville 22908, USA."}]},{"given":"L. P.","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, University of Virginia Health SciencesCenter, Charlottesville 22908, USA."}]},{"given":"F. S.","family":"Gorelick","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, University of Virginia Health SciencesCenter, Charlottesville 22908, USA."}]},{"given":"P. Q.","family":"Barrett","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, University of Virginia Health SciencesCenter, Charlottesville 22908, USA."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1995.269.6.F751","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:58:02Z","timestamp":1567972682000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1995.269.6.F751"}},"issued":{"date-parts":[[1995,12,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1995,12,1]]}},"alternative-id":["10.1152\/ajprenal.1995.269.6.F751"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1995.269.6.f751","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1995,12,1]]}},{"indexed":{"date-parts":[[2026,1,11]],"date-time":"2026-01-11T17:16:25Z","timestamp":1768151785296,"version":"3.49.0"},"reference-count":41,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2001,7,1]]},"abstract":"<jats:p>Recent studies have suggested that subtle microvascular and tubulointerstitial injury in the kidney can cause salt-sensitive hypertension. To test this hypothesis, we determined whether the mild renal disease induced by transient blockade of nitric oxide (NO) synthesis would result in salt-sensitive hypertension and whether prevention of the renal injury by coadministration of the immunosuppressive agent mycophenolate mofetil (MMF) would block the development of salt sensitivity. N<jats:sup>\u03c9<\/jats:sup>-nitro-l-arginine-methyl ester (l-NAME; 70 mg\/100 ml in the drinking water) was administered for 3 wk to rats with or without MMF (30 mg \u00b7 kg<jats:sup>\u22121<\/jats:sup>\u00b7 day<jats:sup>\u22121<\/jats:sup>by gastric gavage), followed by a 1-wk \u201cwashout\u201d period in which the MMF was continued, which was followed in turn by placement on a high-salt (4% NaCl) diet for an additional 4 wk. Renal histology was examined at 3 and 8 wk, and blood pressure was measured serially.l-NAME treatment resulted in acute hypertension and the development of mild renal injury. During the washout period, blood pressure returned to normal, only to return to the hypertensive range on exposure of the animals to a high-salt diet. MMF treatment prevented the development of hypertension in response to a high-salt diet. This correlated with the ability of MMF to inhibit specific aspects of the renal injury, including the development of segmental glomerulosclerosis, the infiltration of T cells and ANG II-positive cells, and the thickening of afferent arterioles.<\/jats:p>","DOI":"10.1152\/ajprenal.2001.281.1.f38","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T14:16:05Z","timestamp":1514038565000},"page":"F38-F47","source":"Crossref","is-referenced-by-count":136,"title":["Mycophenolate mofetil prevents salt-sensitive hypertension resulting from nitric oxide synthesis inhibition"],"prefix":"10.1152","volume":"281","author":[{"given":"Yasmir","family":"Quiroz","sequence":"first","affiliation":[{"name":"Renal Service and Department of Immunobiology (INBIOMED), Hospital Universitario de la Universidad del Zulia, Maracaibo 4001-A, Venezuela;"}]},{"given":"H\u00e9ctor","family":"Pons","sequence":"additional","affiliation":[{"name":"Renal Service and Department of Immunobiology (INBIOMED), Hospital Universitario de la Universidad del Zulia, Maracaibo 4001-A, Venezuela;"}]},{"given":"Katherine L.","family":"Gordon","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Baylor College of Medicine, Houston, Texas 77030;"}]},{"given":"Jaimar","family":"Rinc\u00f3n","sequence":"additional","affiliation":[{"name":"Renal Service and Department of Immunobiology (INBIOMED), Hospital Universitario de la Universidad del Zulia, Maracaibo 4001-A, Venezuela;"}]},{"given":"Maribel","family":"Ch\u00e1vez","sequence":"additional","affiliation":[{"name":"Renal Service and Department of Immunobiology (INBIOMED), Hospital Universitario de la Universidad del Zulia, Maracaibo 4001-A, Venezuela;"}]},{"given":"Gustavo","family":"Parra","sequence":"additional","affiliation":[{"name":"Renal Service and Department of Immunobiology (INBIOMED), Hospital Universitario de la Universidad del Zulia, Maracaibo 4001-A, Venezuela;"}]},{"given":"Jaime","family":"Herrera-Acosta","sequence":"additional","affiliation":[{"name":"Nephrology Department, Instituto Nacional de Cardiolog\u0131\u0301a, Mexico City 4080, Mexico; and"}]},{"given":"Dulcenombre","family":"G\u00f3mez-Garre","sequence":"additional","affiliation":[{"name":"Laboratorio de Nefrolog\u0131\u0301a, Fundaci\u00f3n Jim\u00e9nez D\u0131\u0301az, Aut\u00f3mona University, Madrid 28040, Spain"}]},{"given":"Raquel","family":"Largo","sequence":"additional","affiliation":[{"name":"Laboratorio de Nefrolog\u0131\u0301a, Fundaci\u00f3n Jim\u00e9nez D\u0131\u0301az, Aut\u00f3mona University, Madrid 28040, Spain"}]},{"given":"Jesus","family":"Egido","sequence":"additional","affiliation":[{"name":"Laboratorio de Nefrolog\u0131\u0301a, Fundaci\u00f3n Jim\u00e9nez D\u0131\u0301az, Aut\u00f3mona University, Madrid 28040, Spain"}]},{"given":"Richard J.","family":"Johnson","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Baylor College of Medicine, Houston, Texas 77030;"}]},{"given":"Bernardo","family":"Rodr\u00edguez-Iturbe","sequence":"additional","affiliation":[{"name":"Renal Service and Department of Immunobiology (INBIOMED), Hospital Universitario de la Universidad del Zulia, Maracaibo 4001-A, Venezuela;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/S0162-3109(00)00188-0"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00140.x"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115849"},{"key":"B4","first-page":"1333","volume":"101","author":"Chatziantoniou C","year":"1996","journal-title":"J Clin Invest"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1042\/bj2900033"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1093\/ajh\/6.9.806"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118074"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00138.x"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.266.5.F697"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1947.27.1.120"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.27.1.19"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.33.1.340"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0701517"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/14.1.58"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.34.1.151"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.442"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.21.6.944"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.4.F727"},{"key":"B19","doi-asserted-by":"crossref","first-page":"616","DOI":"10.1681\/ASN.V114616","volume":"11","author":"Kashiwagi M","year":"2000","journal-title":"J Am Soc Nephrol"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.83.7.743"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.1995.tb44647.x"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/0925-4439(94)90052-3"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1016\/S0008-6363(96)00073-9"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.33.4.1013"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1996.271.2.H806"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1006\/clin.1996.4314"},{"key":"B27","doi-asserted-by":"crossref","first-page":"1186","DOI":"10.1681\/ASN.V641186","volume":"6","author":"Pichler R","year":"1995","journal-title":"J Am Soc Nephrol"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1984.147"},{"key":"B29","doi-asserted-by":"crossref","first-page":"1542","DOI":"10.1681\/ASN.V1071542","volume":"10","author":"Remuzzi G","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.20.3.298"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2249.1991.tb05670.x"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2249.2000.01251.x"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.055003945.x"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1016\/S0021-9150(99)00458-X"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.26.4.691"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1002\/jlb.63.6.732"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.32.2.273"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.101.3.305"},{"key":"B39","doi-asserted-by":"crossref","first-page":"755","DOI":"10.1681\/ASN.V95755","volume":"9","author":"Verhagen AMG","year":"1998","journal-title":"J Am Soc Nephrol"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1016\/0008-8749(84)90195-3"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.32.6.958"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.2001.281.1.F38","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:44:58Z","timestamp":1660189498000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.2001.281.1.F38"}},"issued":{"date-parts":[[2001,7,1]]},"references-count":41,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2001,7,1]]}},"alternative-id":["10.1152\/ajprenal.2001.281.1.F38"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.2001.281.1.f38","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2001,7,1]]}},{"indexed":{"date-parts":[[2026,1,13]],"date-time":"2026-01-13T06:20:37Z","timestamp":1768285237459,"version":"3.49.0"},"reference-count":58,"publisher":"American Physiological Society","issue":"2","funder":[{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health","doi-asserted-by":"publisher","award":["R01DK111380"],"award-info":[{"award-number":["R01DK111380"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health","doi-asserted-by":"publisher","award":["R01DK29857"],"award-info":[{"award-number":["R01DK29857"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health","doi-asserted-by":"publisher","award":["R01117650"],"award-info":[{"award-number":["R01117650"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2023,8,1]]},"abstract":"<jats:p> In rats fed a diet rich in K<jats:sup>+<\/jats:sup>, proximal tubules reabsorbed less fluid, Na<jats:sup>+<\/jats:sup>, and K<jats:sup>+<\/jats:sup> compared with those in animals on a control diet. Glomerular filtration rates also decreased, probably due to glomerulotubular feedback. These reductions may help to maintain balance of the two ions simultaneously by shifting Na<jats:sup>+<\/jats:sup> reabsorption to K<jats:sup>+<\/jats:sup>-secreting nephron segments. <\/jats:p>","DOI":"10.1152\/ajprenal.00013.2023","type":"journal-article","created":{"date-parts":[[2023,6,15]],"date-time":"2023-06-15T16:45:15Z","timestamp":1686847515000},"page":"F224-F234","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":6,"title":["High dietary K<sup>+<\/sup> intake inhibits proximal tubule transport"],"prefix":"10.1152","volume":"325","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7054-2540","authenticated-orcid":false,"given":"Tong","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Molecular and Cellular Physiology, Yale University School of Medicine, New Haven, Connecticut, United States"}]},{"given":"Tommy","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Molecular and Cellular Physiology, Yale University School of Medicine, New Haven, Connecticut, United States"}]},{"given":"Shuhua","family":"Xu","sequence":"additional","affiliation":[{"name":"Department of Molecular and Cellular Physiology, Yale University School of Medicine, New Haven, Connecticut, United States"}]},{"given":"Gustavo","family":"Frindt","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, Weill-Cornell Medicine, New York, New York, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3192-1297","authenticated-orcid":false,"given":"Alan M.","family":"Weinstein","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, Weill-Cornell Medicine, New York, New York, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7702-4703","authenticated-orcid":false,"given":"Lawrence G.","family":"Palmer","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, Weill-Cornell Medicine, New York, New York, United States"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/B978-012088488-9.50050-4"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/physiol.00022.2016"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.05920613"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2013.04.002"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1113\/JP272504"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2013.14"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2014.12.006"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1817220116"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2015.289"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajplegacy.1972.222.2.421"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00536.2016"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1172\/jci110609"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00501.2005"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00323.2010"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00502.2009"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00117.2018"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00125.2019"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00608.2007"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.102.043380"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.16.9660"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajplegacy.1964.206.4.674"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajplegacy.1966.211.3.529"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajplegacy.1961.200.3.581"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00668.2016"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.200809989"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.201511533"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00401.2009"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00422.2005"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00505.2014"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00504.2014"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00046.2020"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00082.2004"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-020-02433-x"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00023.2012"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2021030286"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00057.2019"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00176.2013"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00011.2016"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1161\/01.cir.52.1.146"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00454.2003"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1016\/B978-0-12-381462-3.00033-1"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00002.2010"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00174.2014"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00042.2007"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00515.2014"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90235.2008"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1973.123"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.267.2.F223"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1983.245.5.F584"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1038\/299161a0"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00413.2021"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.104.4.693"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.15252\/emmm.202114273"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00044.2018"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-022-02718-3"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-014-1673-1"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00044.2005"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1152\/ajplegacy.1971.221.2.437"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00013.2023","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,7,24]],"date-time":"2023-07-24T13:15:31Z","timestamp":1690204531000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00013.2023"}},"issued":{"date-parts":[[2023,8,1]]},"references-count":58,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2023,8,1]]}},"alternative-id":["10.1152\/ajprenal.00013.2023"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00013.2023","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2023,8,1]]},"assertion":[{"value":"2023-01-27","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2023-05-15","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2023-06-14","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2023-07-24","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,1,15]],"date-time":"2026-01-15T21:04:29Z","timestamp":1768511069288,"version":"3.49.0"},"reference-count":68,"publisher":"American Physiological Society","issue":"1","funder":[{"DOI":"10.13039\/501100000024","name":"Gouvernement du Canada | Canadian Institutes of Health Research (Instituts de recherche en sant\u00e9 du Canada)","doi-asserted-by":"publisher","award":["OSO-115895"],"award-info":[{"award-number":["OSO-115895"]}],"id":[{"id":"10.13039\/501100000024","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000024","name":"Gouvernement du Canada | Canadian Institutes of Health Research (Instituts de recherche en sant\u00e9 du Canada)","doi-asserted-by":"publisher","award":["MOP-133484"],"award-info":[{"award-number":["MOP-133484"]}],"id":[{"id":"10.13039\/501100000024","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000191","name":"Kidney Foundation of Canada (La Fondation canadienne du rein)","doi-asserted-by":"publisher","award":["Krescent New Investigator award"],"award-info":[{"award-number":["Krescent New Investigator award"]}],"id":[{"id":"10.13039\/501100000191","id-type":"DOI","asserted-by":"publisher"}]},{"name":"St. Joseph's Healthcare Hamilton","award":["Father Sean O'Sullivan Research Studentship Award"],"award-info":[{"award-number":["Father Sean O'Sullivan Research Studentship Award"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2017,1,1]]},"abstract":"<jats:p> Proteinuria is one of the primary risk factors for the progression of chronic kidney disease (CKD) and has been implicated in the induction of endoplasmic reticulum (ER) stress. We hypothesized that the suppression of ER stress with a low molecular weight chemical chaperone, 4-phenylbutyric acid (4-PBA), would reduce the severity of CKD and proteinuria in the Dahl salt-sensitive (SS) hypertensive rat. To induce hypertension and CKD, 12-wk-old male rats were placed on a high-salt (HS) diet for 4 wk with or without 4-PBA treatment. We assessed blood pressure and markers of CKD, including proteinuria, albuminuria, and renal pathology. Furthermore, we determined if HS feeding resulted in an impaired myogenic response, subsequent to ER stress. 4-PBA treatment reduced salt-induced hypertension, proteinuria, and albuminuria and preserved myogenic constriction. Furthermore, renal pathology was reduced with 4-PBA treatment, as indicated by lowered expression of profibrotic markers and fewer intratubular protein casts. In addition, ER stress in the glomerulus was reduced, and the integrity of the glomerular filtration barrier was preserved. These results suggest that 4-PBA treatment protects against proteinuria in the SS rat by preserving the myogenic response and by preventing ER stress, which led to a breakdown in the glomerular filtration barrier. As such, alleviating ER stress serves as a viable therapeutic strategy to preserve kidney function and to delay the progression of CKD in the animal model under study. <\/jats:p>","DOI":"10.1152\/ajprenal.00119.2016","type":"journal-article","created":{"date-parts":[[2016,11,10]],"date-time":"2016-11-10T08:53:55Z","timestamp":1478768035000},"page":"F230-F244","source":"Crossref","is-referenced-by-count":33,"title":["Endoplasmic reticulum stress inhibition limits the progression of chronic kidney disease in the Dahl salt-sensitive rat"],"prefix":"10.1152","volume":"312","author":[{"given":"Victoria","family":"Yum","sequence":"first","affiliation":[{"name":"Department of Medicine, Division of Nephrology, McMaster University and St. Joseph\u2019s Healthcare Hamilton, Hamilton, Ontario, Canada; and"}]},{"given":"Rachel E.","family":"Carlisle","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Nephrology, McMaster University and St. Joseph\u2019s Healthcare Hamilton, Hamilton, Ontario, Canada; and"}]},{"given":"Chao","family":"Lu","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Nephrology, McMaster University and St. Joseph\u2019s Healthcare Hamilton, Hamilton, Ontario, Canada; and"}]},{"given":"Elise","family":"Brimble","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Nephrology, McMaster University and St. Joseph\u2019s Healthcare Hamilton, Hamilton, Ontario, Canada; and"}]},{"given":"Jasmine","family":"Chahal","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Nephrology, McMaster University and St. Joseph\u2019s Healthcare Hamilton, Hamilton, Ontario, Canada; and"}]},{"given":"Chandak","family":"Upagupta","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Nephrology, McMaster University and St. Joseph\u2019s Healthcare Hamilton, Hamilton, Ontario, Canada; and"}]},{"given":"Kjetil","family":"Ask","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Respirology, McMaster University, St. Joseph\u2019s Healthcare Hamilton, Hamilton, Ontario, Canada"}]},{"given":"Jeffrey G.","family":"Dickhout","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Nephrology, McMaster University and St. Joseph\u2019s Healthcare Hamilton, Hamilton, Ontario, Canada; and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)64495-1"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2010.550"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2006.040774"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1986.212"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(86)80051-8"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.265"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM198209093071104"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0084663"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00481.2011"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1097\/HJH.0000000000000943"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2012121149"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.2119\/molmed.2011.00131"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1016\/S0008-6363(00)00314-X"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1155\/2012\/146987"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1001\/jama.298.17.2038"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.37.2.456"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00194.2006"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M500729200"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.110.226803"},{"key":"B20","first-page":"5","volume":"1","author":"Dickhout JG","year":"2016","journal-title":"J Pharmacol Rep"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.29.3.781"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1096\/fj.10-159319"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfg533"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00208.x"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1038\/ncomms10330"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1038\/ncomms8841"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1038\/ajh.2008.301"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.1998.771bs.x"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.01097.2010"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1186\/1471-2121-11-59"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1981.241.1.F85"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1001\/archinternmed.2008.605"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00736.x"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004070600"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00868.x"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005091012"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-139-4-200308190-00006"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1007\/BF01002772"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1161\/ATVBAHA.112.249318"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfn583"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2007.12.098"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.43.27345"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00482.2011"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1016\/B978-0-12-385116-1.00002-9"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1161\/ATVBAHA.112.300606"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007121313"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2008.04.031"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gft267"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1503\/cmaj.121468"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1007\/s00125-009-1268-0"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1007\/s11010-008-9991-2"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfm446"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.3109\/00365518609083660"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007121271"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00786.x"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5001704"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119163"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00537.2009"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1177\/002215540305100902"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.6064\/2012\/857516"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00952.2012"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.71.2.471"},{"key":"B63","first-page":"R189","volume":"276","author":"Van Dokkum RP","year":"1999","journal-title":"Am J Physiol Renal Physiol"},{"key":"B64","first-page":"R855","volume":"276","author":"van Dokkum RP","year":"1999","journal-title":"Am J Physiol Renal Physiol"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/13.4.893"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.110.5.1501"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00485.2015"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.09220.x"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00119.2016","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T02:06:53Z","timestamp":1567994813000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00119.2016"}},"issued":{"date-parts":[[2017,1,1]]},"references-count":68,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2017,1,1]]}},"alternative-id":["10.1152\/ajprenal.00119.2016"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00119.2016","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2017,1,1]]}},{"indexed":{"date-parts":[[2026,1,23]],"date-time":"2026-01-23T16:09:37Z","timestamp":1769184577631,"version":"3.49.0"},"reference-count":40,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2008,7]]},"abstract":"<jats:p> A mutation in the human FXYD2 polypeptide (Na-K-ATPase \u03b3 subunit) that changes a conserved transmembrane glycine to arginine is linked to dominant renal hypomagnesemia. Xenopus laevis oocytes injected with wild-type FXYD2 or the mutant G41R cRNAs expressed large nonselective ion currents. However, in contrast to the wild-type FXYD2 currents, inward rectifying cation currents were induced by hyperpolarization pulses in oocytes expressing the G41R mutant. Injection of EDTA into the oocyte removed inward rectification in the oocytes expressing the mutant, but did not alter the nonlinear current-voltage relationship of the wild-type FXYD2 pseudo-steady-state currents. Extracellular divalent ions, Ca<jats:sup>2+<\/jats:sup> and Ba<jats:sup>2+<\/jats:sup>, and trivalent cations, La<jats:sup>3+<\/jats:sup>, blocked both the wild-type and mutant FXYD2 currents. Site-directed mutagenesis of G41 demonstrated that a positive charge at this site is required for the inward rectification. When the wild-type FXYD2 was expressed in Madin-Darby canine kidney cells, the cells in the presence of a large apical-to-basolateral Mg<jats:sup>2+<\/jats:sup> gradient and at negative potentials had an increase in transepithelial current compared with cells expressing the G41R mutant or control transfected cells. Moreover, this current was inhibited by extracellular Ba<jats:sup>2+<\/jats:sup> at the basolateral surface. These results suggest that FXYD2 can mediate basolateral extrusion of magnesium from cultured renal epithelial cells and provide new insights into the understanding of the possible physiological roles of FXYD2 wild-type and mutant proteins. <\/jats:p>","DOI":"10.1152\/ajprenal.00519.2007","type":"journal-article","created":{"date-parts":[[2008,4,30]],"date-time":"2008-04-30T21:07:09Z","timestamp":1209589629000},"page":"F91-F99","source":"Crossref","is-referenced-by-count":26,"title":["Human FXYD2 G41R mutation responsible for renal hypomagnesemia behaves as an inward-rectifying cation channel"],"prefix":"10.1152","volume":"295","author":[{"given":"Qun","family":"Sha","sequence":"first","affiliation":[]},{"given":"Wade","family":"Pearson","sequence":"additional","affiliation":[]},{"given":"Lauren C.","family":"Burcea","sequence":"additional","affiliation":[]},{"given":"Darian A.","family":"Wigfall","sequence":"additional","affiliation":[]},{"given":"Paul H.","family":"Schlesinger","sequence":"additional","affiliation":[]},{"given":"Colin G.","family":"Nichols","sequence":"additional","affiliation":[]},{"given":"Robert W.","family":"Mercer","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M414703200"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.47.33183"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.13.6092"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/16.14.4250"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(91)91527-8"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbamem.2007.10.009"},{"key":"R7","unstructured":"Chen ZH, Jones LR, Moorman JR. Ion currents through mutant phospholemman channel molecules. Receptors Channels 6: 435\u2013447, 1999."},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-005-1470-y"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M611117200"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M609872200"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1021\/bi00610a037"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.68.040104.131852"},{"key":"R13","unstructured":"Geering K. FXYD proteins: new regulators of Na-K-ATPase. J Bioenerg Biochem 37: 387\u2013392, 2005."},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00555.2004"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1993.sp019681"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2006.01.046"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M500697200"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.103.2.217"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.00377.2005"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1038\/81543"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.11.6521"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1038\/377737a0"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1016\/S0167-4889(00)00023-9"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1016\/S0167-4889(01)00082-9"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.5.2176"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.17.10279"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M010836200"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M201009200"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.2741\/A544"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1006\/jmbi.1999.3489"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1038\/ng889"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(03)00556-7"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.2001.t01-1-00407.x"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-3495(95)80052-4"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.00014.2002"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1006\/geno.2000.6274"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-2836(02)00781-7"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.18.12252"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-3495(95)79964-7"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1038\/ng901"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00519.2007","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:53:13Z","timestamp":1567968793000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00519.2007"}},"issued":{"date-parts":[[2008,7]]},"references-count":40,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2008,7]]}},"alternative-id":["10.1152\/ajprenal.00519.2007"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00519.2007","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2008,7]]}},{"indexed":{"date-parts":[[2025,9,26]],"date-time":"2025-09-26T22:23:48Z","timestamp":1758925428146},"reference-count":39,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2008,7]]},"abstract":"<jats:p> Recent studies have implicated epithelial Na<jats:sup>+<\/jats:sup> channels (ENaC) in myogenic signaling. The present study was undertaken to determine if ENaC and\/or Na<jats:sup>+<\/jats:sup> entry are involved in the myogenic response of the rat afferent arteriole. Myogenic responses were assessed in the in vitro hydronephrotic kidney model. ENaC expression and membrane potential responses were evaluated with afferent arterioles isolated from normal rat kidneys. Our findings do not support a role of ENaC, in that ENaC channel blockers did not reduce myogenic responses and ENaC expression could not be demonstrated in this vessel. Reducing extracellular Na<jats:sup>+<\/jats:sup> concentration ([Na<jats:sup>+<\/jats:sup>]<jats:sub>o<\/jats:sub>; 100 mmol\/l) did not attenuate myogenic responses, and amiloride had no effect on membrane potential. Benzamil, an inhibitor of ENaC that also blocks Na<jats:sup>+<\/jats:sup>\/Ca<jats:sup>2+<\/jats:sup> exchange (NCX), potentiated myogenic vasoconstriction. Benzamil and low [Na<jats:sup>+<\/jats:sup>]<jats:sub>o<\/jats:sub> elicited vasoconstriction; however, these responses were attenuated by diltiazem and were associated with significant membrane depolarization, suggesting a contribution of mechanisms other than a reduction in NCX. Na<jats:sup>+<\/jats:sup> repletion induced a vasodilation in pressurized afferent arterioles preequilibrated in low [Na<jats:sup>+<\/jats:sup>]<jats:sub>o<\/jats:sub>, a hallmark of NCX, and this response was reduced by 10 \u03bcmol\/l benzamil. The dilation was eliminated, however, by a combination of benzamil plus ouabain, suggesting an involvement of the electrogenic Na<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-ATPase. In concert, these findings refute the premise that ENaC plays a significant role in the rat afferent arteriole and instead suggest that reducing [Na<jats:sup>+<\/jats:sup>]<jats:sub>o<\/jats:sub> and\/or Na<jats:sup>+<\/jats:sup> entry is coupled to membrane depolarization. The mechanisms underlying these unexpected and paradoxical effects of Na<jats:sup>+<\/jats:sup> are not resolved at the present time. <\/jats:p>","DOI":"10.1152\/ajprenal.00200.2007","type":"journal-article","created":{"date-parts":[[2008,5,22]],"date-time":"2008-05-22T00:54:26Z","timestamp":1211417666000},"page":"F272-F282","source":"Crossref","is-referenced-by-count":29,"title":["Effects of amiloride, benzamil, and alterations in extracellular Na<sup>+<\/sup> on the rat afferent arteriole and its myogenic response"],"prefix":"10.1152","volume":"295","author":[{"given":"Xuemei","family":"Wang","sequence":"first","affiliation":[]},{"given":"Kosuke","family":"Takeya","sequence":"additional","affiliation":[]},{"given":"Philip I.","family":"Aaronson","sequence":"additional","affiliation":[]},{"given":"Kathy","family":"Loutzenhiser","sequence":"additional","affiliation":[]},{"given":"Rodger","family":"Loutzenhiser","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-201x.2000.00671.x"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1007\/BFb0036122"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.265.6.F743"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1977.sp011989"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.88.2.152"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.275.1.F126"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000144465.56360.ad"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1007\/s004240100594"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2736(92)90239-I"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.506"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1042\/bj20021375"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.6.F1093"},{"key":"R13","unstructured":"Hayashi K, Epstein M, Loutzenhiser R. Pressure-induced vasoconstriction of renal microvessels in normotensive and hypertensive rats: studies in the isolated perfused hydronephrotic kidney. Circ Res 65: 475\u20131484, 1989."},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.67.1.1"},{"key":"R15","unstructured":"Hayashi K, Epstein M, Loutzenhiser R, Forster H. Impaired myogenic responsiveness of the renal afferent arteriole in streptozotocin-induced diabetic rats: role of eicosanoid derangements. J Am Soc Nephrol 2: 1578\u20131586, 1992."},{"key":"R16","doi-asserted-by":"crossref","unstructured":"Jernigan NL, Drummond HA. Vascular ENaC proteins are required for renal myogenic constriction. Am J Physiol Renal Physiol 289: F891\u2013F901, 2005.","DOI":"10.1152\/ajprenal.00019.2005"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00177.2006"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00571.2007"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1998.275.2.H467"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1007\/BF01871102"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-007-0341-0"},{"key":"R22","doi-asserted-by":"crossref","unstructured":"Li C, Wang W, Norregaard R, Knepper MA, Nielsen S, Fr\u00f6kiaer J. Altered expression of epithelial sodium channel in rats with bilateral or unilateral ureteral obstruction. Am J Physiol Renal Physiol 293: F333\u2013F341, 2007.","DOI":"10.1152\/ajprenal.00372.2006"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000024262.11534.18"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.273.2.F307"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1016\/0002-9149(87)90180-9"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00402.2005"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.87.7.551"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.1999.0203o.x"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1016\/0076-6879(92)07008-C"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.510"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00179.2001"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.2000.279.1.H351"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1007\/s004240100591"},{"key":"R34","doi-asserted-by":"crossref","unstructured":"Schweda F, Seebauer H, Kramer BK, Kurtz A. Functional role of sodium-calcium exchange in the regulation of renal vascular resistance. Am J Physiol Renal Physiol 280: F155\u2013F161, 2001.","DOI":"10.1152\/ajprenal.2001.280.1.F155"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.91.3.445"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.71.2.471"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.86.6.663"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1161\/hy1201.096817"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1161\/01.STR.16.6.990"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00200.2007","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T22:54:03Z","timestamp":1567983243000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00200.2007"}},"issued":{"date-parts":[[2008,7]]},"references-count":39,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2008,7]]}},"alternative-id":["10.1152\/ajprenal.00200.2007"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00200.2007","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2008,7]]}},{"indexed":{"date-parts":[[2025,9,26]],"date-time":"2025-09-26T16:45:29Z","timestamp":1758905129740},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1994,10,1]]},"abstract":"<jats:p> We have characterized the integrins present on cultured tubule epithelial cells from human renal cortexes, enriched for proximal cells, using fluorescence microscopy, immunoprecipitation, and cell adhesion assays. By immunofluorescence, the alpha 3-integrin subunit stained most intensely and was present on all cells predominantly at cell-cell contacts. The alpha 6-subunit was present on all cells in a pattern consistent with extracellular matrix contacts. The alpha 5-subunit was present on most cells in a cell-matrix contact pattern; alpha V-subunit was weakly positive and occasionally seen in cell-matrix contacts. The alpha 2-subunit was present on clusters of distal tubule cells, predominantly at cell-cell contacts. Immunoprecipitation revealed the predominant integrin to be alpha 3 beta 1 with some alpha 2 beta 1, presumably contributed by distal cells. The alpha 5 beta 1-, alpha 6 beta 1-, alpha 6 beta 4-, and alpha V beta 3-integrins, as well as trace amounts of alpha 1 beta 1-integrins, were also present. The alpha 4 beta 1-integrin was not detected. Initial attachment to fibronectin was mediated by alpha V beta 3- and alpha 5 beta 1-integrins; initial attachment to laminin was mediated by the alpha 6 beta 1- and alpha 3 beta 1- integrins and, in some preparations, by an unidentified integrin; and initial attachment to collagen type IV was mediated by alpha V beta 3-integrin and an unidentified beta 1-integrin. After extensively immunodepleting membrane extracts with anti-alpha 1, -alpha 2, -alpha 3, -alpha 4, -alpha 5, -alpha 6, and -alpha V antibodies, an anti-beta 1 antibody still precipitated an integrin. Its electrophoretic mobility differs from the laminin-binding alpha 7 beta 1-integrin. Thus we have identified many of the integrins on cortical tubule cells and their role in mediating initial attachment to extracellular matrix. However, the cell adhesion assays and immunoprecipitations suggest the presence of an unidentified beta 1-integrin that may mediate renal tubule cell attachment to laminin and collagen. <\/jats:p>","DOI":"10.1152\/ajprenal.1994.267.4.f612","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T23:37:30Z","timestamp":1513985850000},"page":"F612-F623","source":"Crossref","is-referenced-by-count":1,"title":["Characterization of integrins in cultured human renal cortical tubule epithelial cells"],"prefix":"10.1152","volume":"267","author":[{"given":"E. E.","family":"Simon","sequence":"first","affiliation":[{"name":"Renal Division, Jewish Hospital, Washington University, St. Louis,Missouri 63110."}]},{"given":"C. H.","family":"Liu","sequence":"additional","affiliation":[{"name":"Renal Division, Jewish Hospital, Washington University, St. Louis,Missouri 63110."}]},{"given":"M.","family":"Das","sequence":"additional","affiliation":[{"name":"Renal Division, Jewish Hospital, Washington University, St. Louis,Missouri 63110."}]},{"given":"S.","family":"Nigam","sequence":"additional","affiliation":[{"name":"Renal Division, Jewish Hospital, Washington University, St. Louis,Missouri 63110."}]},{"given":"T. J.","family":"Broekelmann","sequence":"additional","affiliation":[{"name":"Renal Division, Jewish Hospital, Washington University, St. Louis,Missouri 63110."}]},{"given":"J. A.","family":"McDonald","sequence":"additional","affiliation":[{"name":"Renal Division, Jewish Hospital, Washington University, St. Louis,Missouri 63110."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1994.267.4.F612","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:55:33Z","timestamp":1567958133000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1994.267.4.F612"}},"issued":{"date-parts":[[1994,10,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1994,10,1]]}},"alternative-id":["10.1152\/ajprenal.1994.267.4.F612"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1994.267.4.f612","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1994,10,1]]}},{"indexed":{"date-parts":[[2025,10,3]],"date-time":"2025-10-03T09:34:57Z","timestamp":1759484097908},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1985,3,1]]},"abstract":"<jats:p> Immunologic models of renal injury are useful in the study of pathophysiology. Some of these models have already been used in glomerular micropuncture studies and were shown to be approachable with the same techniques that were developed to study normal renal function. The typical decrease in the glomerular permeability coefficient found in such studies is countered by an increase in the hydrostatic pressure gradient, minimizing decreases in single nephron filtration rate. Antibody mechanisms involving either direct glomerular (and tubular) fixation of antibody or accumulation of immune complex materials provide an array of acute and chronic lesions for evaluation with relevance to the bulk of immune glomerular and tubular lesions in humans. The influences of varied and overlapping immune mediator systems are also useful areas for physiologic assessment. The tools of the renal immunopathologist may be useful to the physiologist in identifying and localizing the effects of transport systems central to renal function. The collaborative interaction of investigators skilled in immunology, pathology, and physiology is necessary to achieve optimum scientific value. <\/jats:p>","DOI":"10.1152\/ajprenal.1985.248.3.f319","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T00:29:47Z","timestamp":1513988987000},"page":"F319-F331","source":"Crossref","is-referenced-by-count":0,"title":["Nephroimmunopathology and pathophysiology"],"prefix":"10.1152","volume":"248","author":[{"given":"C. B.","family":"Wilson","sequence":"first","affiliation":[]},{"given":"R. C.","family":"Blantz","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1985.248.3.F319","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:31:22Z","timestamp":1567971082000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1985.248.3.F319"}},"issued":{"date-parts":[[1985,3,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1985,3,1]]}},"alternative-id":["10.1152\/ajprenal.1985.248.3.F319"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1985.248.3.f319","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1985,3,1]]}},{"indexed":{"date-parts":[[2025,10,5]],"date-time":"2025-10-05T12:08:41Z","timestamp":1759666121632,"version":"3.37.3"},"reference-count":44,"publisher":"American Physiological Society","issue":"2","funder":[{"DOI":"10.13039\/501100000191","name":"Kidney Foundation of Canada (La Fondation canadienne du rein)","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100000191","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2018,8,1]]},"abstract":"<jats:p> Loss of ubiquitin COOH-terminal hydrolase L1 (UCHL1), a deubiquitinating enzyme required for neuronal function, led to hyperphosphatemia accompanied by phosphaturia in mice, while calcium homeostasis remained intact. We therefore investigated the mechanisms underlying the phosphate imbalance in Uchl1<jats:sup>\u2212\/\u2212<\/jats:sup> mice. Interestingly, phosphaturia was not a result of lower renal brush border membrane sodium-phosphate cotransporter expression as sodium-phosphate cotransporter 2a and 2c expression levels was similar to wild-type levels. Plasma parathyroid hormone and fibroblast growth factor 23 levels were not different; however, fibroblast growth factor 23 mRNA levels were significantly increased in femur homogenates from Uchl1<jats:sup>\u2212\/\u2212<\/jats:sup> mice. Full-length and soluble \u03b1-klotho levels were comparable in kidneys from wild-type and Uchl1<jats:sup>\u2212\/\u2212<\/jats:sup> mice; however, soluble \u03b1-klotho was reduced in Uchl1<jats:sup>\u2212\/\u2212<\/jats:sup> mice urine. Consistent with unchanged components of 1,25(OH)<jats:sub>2<\/jats:sub>D<jats:sub>3<\/jats:sub> metabolism (i.e., CYP27B1 and CYP24A1), sodium-phosphate cotransporter 2b protein levels were not different in ileum brush borders from Uchl1<jats:sup>\u2212\/\u2212<\/jats:sup> mice, suggesting that the intestine is not the source of hyperphosphatemia. Nonetheless, when Uchl1<jats:sup>\u2212\/\u2212<\/jats:sup> mice were fed a low-phosphate diet, plasma phosphate, urinary phosphate, and fractional excretion of phosphate were significantly attenuated and comparable to levels of low-phosphate diet-fed wild-type mice. Our findings demonstrate that Uchl1-deleted mice exhibit perturbed phosphate homeostasis, likely consequent to decreased urinary soluble \u03b1-klotho, which can be rescued with a low-phosphate diet. Uchl1<jats:sup>\u2212\/\u2212<\/jats:sup> mice may provide a useful mouse model to study mild perturbations in phosphate homeostasis. <\/jats:p>","DOI":"10.1152\/ajprenal.00411.2017","type":"journal-article","created":{"date-parts":[[2018,4,18]],"date-time":"2018-04-18T10:21:50Z","timestamp":1524046910000},"page":"F353-F363","source":"Crossref","is-referenced-by-count":3,"title":["Ubiquitin COOH-terminal hydrolase L1 deletion is associated with urinary \u03b1-klotho deficiency and perturbed phosphate homeostasis"],"prefix":"10.1152","volume":"315","author":[{"given":"Naomi C.","family":"Boisvert","sequence":"first","affiliation":[{"name":"Kidney Research Centre, The Ottawa Hospital, Ottawa, Ontario, Canada"},{"name":"Ottawa Hospital Research Institute, The Ottawa Hospital, Ottawa, Ontario, Canada"},{"name":"Faculty of Medicine, Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, Ontario, Canada"}]},{"given":"Chet E.","family":"Holterman","sequence":"additional","affiliation":[{"name":"Kidney Research Centre, The Ottawa Hospital, Ottawa, Ontario, Canada"},{"name":"Ottawa Hospital Research Institute, The Ottawa Hospital, Ottawa, Ontario, Canada"}]},{"given":"Alexey","family":"Gutsol","sequence":"additional","affiliation":[{"name":"Kidney Research Centre, The Ottawa Hospital, Ottawa, Ontario, Canada"},{"name":"Ottawa Hospital Research Institute, The Ottawa Hospital, Ottawa, Ontario, Canada"}]},{"given":"Jos\u00e9e","family":"Coulombe","sequence":"additional","affiliation":[{"name":"Ottawa Hospital Research Institute, The Ottawa Hospital, Ottawa, Ontario, Canada"}]},{"given":"Wanling","family":"Pan","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Alberta, Edmonton, Alberta, Canada"}]},{"given":"R. Todd","family":"Alexander","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Alberta, Edmonton, Alberta, Canada"},{"name":"Membrane Protein Disease Research Group, University of Alberta, Edmonton, Alberta, Canada"},{"name":"Department of Pediatrics, University of Alberta, Edmonton, Alberta, Canada"}]},{"given":"Douglas A.","family":"Gray","sequence":"additional","affiliation":[{"name":"Ottawa Hospital Research Institute, The Ottawa Hospital, Ottawa, Ontario, Canada"},{"name":"Faculty of Medicine, Department of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, Ontario, Canada"}]},{"given":"Chris R.","family":"Kennedy","sequence":"additional","affiliation":[{"name":"Kidney Research Centre, The Ottawa Hospital, Ottawa, Ontario, Canada"},{"name":"Ottawa Hospital Research Institute, The Ottawa Hospital, Ottawa, Ontario, Canada"},{"name":"Faculty of Medicine, Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, Ontario, Canada"}]}],"member":"24","reference":[{"doi-asserted-by":"publisher","key":"B1","DOI":"10.1073\/pnas.95.9.5372"},{"doi-asserted-by":"publisher","key":"B2","DOI":"10.1038\/nprot.2007.156"},{"doi-asserted-by":"publisher","key":"B2a","DOI":"10.1042\/CS20180085"},{"doi-asserted-by":"publisher","key":"B3","DOI":"10.1126\/science.1114245"},{"doi-asserted-by":"publisher","key":"B4","DOI":"10.1073\/pnas.0911516107"},{"doi-asserted-by":"publisher","key":"B5","DOI":"10.3389\/fnagi.2014.00129"},{"doi-asserted-by":"publisher","key":"B6","DOI":"10.1152\/ajprenal.00003.2008"},{"doi-asserted-by":"publisher","key":"B7","DOI":"10.1038\/bonekey.2013.231"},{"doi-asserted-by":"publisher","key":"B8","DOI":"10.1152\/ajprenal.00232.2013"},{"doi-asserted-by":"publisher","key":"B9","DOI":"10.1056\/NEJMoa0706130"},{"doi-asserted-by":"publisher","key":"B10","DOI":"10.1096\/fj.10-154765"},{"doi-asserted-by":"publisher","key":"B11","DOI":"10.1681\/ASN.2009121311"},{"doi-asserted-by":"publisher","key":"B12","DOI":"10.1016\/j.kint.2016.04.009"},{"doi-asserted-by":"publisher","key":"B13","DOI":"10.1001\/jama.2011.826"},{"doi-asserted-by":"publisher","key":"B14","DOI":"10.1681\/ASN.2007121360"},{"doi-asserted-by":"publisher","key":"B15","DOI":"10.1038\/nrneph.2013.111"},{"doi-asserted-by":"publisher","key":"B16","DOI":"10.1038\/36285"},{"doi-asserted-by":"publisher","key":"B17","DOI":"10.1074\/jbc.C500457200"},{"doi-asserted-by":"publisher","key":"B18","DOI":"10.1681\/ASN.2013111209"},{"doi-asserted-by":"publisher","key":"B19","DOI":"10.1084\/jem.61.3.319"},{"doi-asserted-by":"publisher","key":"B20","DOI":"10.1161\/01.HYP.0000013734.33441.EA"},{"doi-asserted-by":"publisher","key":"B21","DOI":"10.1016\/j.neuint.2010.04.015"},{"doi-asserted-by":"publisher","key":"B22","DOI":"10.1111\/j.1365-2990.1992.tb00789.x"},{"doi-asserted-by":"publisher","key":"B23","DOI":"10.1161\/CIRCGENETICS.108.847814"},{"doi-asserted-by":"publisher","key":"B24","DOI":"10.1681\/ASN.2012010048"},{"doi-asserted-by":"publisher","key":"B25","DOI":"10.1097\/MAJ.0b013e318167410c"},{"doi-asserted-by":"publisher","key":"B26","DOI":"10.1093\/hmg\/ddg211"},{"doi-asserted-by":"publisher","key":"B27","DOI":"10.1210\/en.2005-0777"},{"doi-asserted-by":"publisher","key":"B28","DOI":"10.1016\/j.kint.2017.05.016"},{"doi-asserted-by":"publisher","key":"B29","DOI":"10.1016\/j.bbadis.2014.03.009"},{"doi-asserted-by":"publisher","key":"B30","DOI":"10.1097\/01.ASN.0000141960.01035.28"},{"doi-asserted-by":"publisher","key":"B31","DOI":"10.1681\/ASN.2009050559"},{"doi-asserted-by":"publisher","key":"B32","DOI":"10.1038\/12647"},{"doi-asserted-by":"publisher","key":"B33","DOI":"10.1152\/ajprenal.00156.2009"},{"doi-asserted-by":"publisher","key":"B34","DOI":"10.1016\/j.jsps.2015.01.009"},{"doi-asserted-by":"publisher","key":"B35","DOI":"10.1038\/nrneph.2010.191"},{"doi-asserted-by":"publisher","key":"B36","DOI":"10.1359\/JBMR.0301264"},{"doi-asserted-by":"publisher","key":"B37","DOI":"10.1172\/JCI200419081"},{"doi-asserted-by":"publisher","key":"B38","DOI":"10.1681\/ASN.2008101106"},{"doi-asserted-by":"publisher","key":"B39","DOI":"10.1038\/sj.ki.5002163"},{"doi-asserted-by":"publisher","key":"B40","DOI":"10.1038\/nature05315"},{"doi-asserted-by":"publisher","key":"B41","DOI":"10.1038\/nrneph.2016.164"},{"doi-asserted-by":"publisher","key":"B42","DOI":"10.1126\/science.2530630"},{"doi-asserted-by":"publisher","key":"B43","DOI":"10.1210\/endo.143.2.8657"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00411.2017","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,21]],"date-time":"2019-09-21T01:46:26Z","timestamp":1569030386000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00411.2017"}},"issued":{"date-parts":[[2018,8,1]]},"references-count":44,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2018,8,1]]}},"alternative-id":["10.1152\/ajprenal.00411.2017"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00411.2017","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2018,8,1]]}},{"indexed":{"date-parts":[[2025,10,5]],"date-time":"2025-10-05T11:48:29Z","timestamp":1759664909684},"reference-count":45,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2012,7,1]]},"abstract":"<jats:p> While elevated plasma prorenin levels are commonly found in diabetic patients and correlate with diabetic nephropathy, the pathological role of prorenin, if any, remains unclear. Prorenin binding to the (pro)renin receptor [(p)RR] unmasks prorenin catalytic activity. We asked whether elevated prorenin could be activated at the site of renal mesangial cells (MCs) through receptor binding without being proteolytically converted to renin. Recombinant inactive rat prorenin and a mutant prorenin that is noncleavable, i.e., cannot be activated proteolytically, are produced in 293 cells. After MCs were incubated with 10<jats:sup>\u22127<\/jats:sup> M native or mutant prorenin for 6 h, cultured supernatant acquired the ability to generate angiotensin I (ANG I) from angiotensinogen, indicating both prorenins were activated. Small interfering RNA (siRNA) against the (p)RR blocked their activation. Furthermore, either native or mutant rat prorenin at 10<jats:sup>\u22127<\/jats:sup> M alone similarly and significantly induced transforming growth factor-\u03b2<jats:sub>1<\/jats:sub>, plasminogen activator inhibitor-1 (PAI-1), and fibronectin mRNA expression, and these effects were blocked by (p)RR siRNA, but not by the ANG II receptor antagonist, saralasin. When angiotensinogen was also added to cultured MCs with inactive native or mutant prorenin, PAI-1 and fibronectin were further increased significantly compared with prorenin or mutant prorenin alone. This effect was blocked partially by treatment with (p)RR siRNA or saralasin. We conclude that prorenin binds the (p)RR on renal MCs and is activated nonproteolytically. This activation leads to increased expression of PAI-1 and transforming growth factor-\u03b2<jats:sub>1<\/jats:sub> via ANG II-independent and ANG II-dependent mechanisms. These data provide a mechanism by which elevated prorenin levels in diabetes may play a role in the development of diabetic nephropathy. <\/jats:p>","DOI":"10.1152\/ajprenal.00050.2012","type":"journal-article","created":{"date-parts":[[2012,4,25]],"date-time":"2012-04-25T22:51:06Z","timestamp":1335394266000},"page":"F11-F20","source":"Crossref","is-referenced-by-count":15,"title":["Receptor-mediated nonproteolytic activation of prorenin and induction of TGF-\u03b2<sub>1<\/sub> and PAI-1 expression in renal mesangial cells"],"prefix":"10.1152","volume":"303","author":[{"given":"Jiandong","family":"Zhang","sequence":"first","affiliation":[{"name":"Fibrosis Research Laboratory, Division of Nephrology and Hypertension, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City, Utah"}]},{"given":"Jie","family":"Wu","sequence":"additional","affiliation":[{"name":"Fibrosis Research Laboratory, Division of Nephrology and Hypertension, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City, Utah"}]},{"given":"Chunyan","family":"Gu","sequence":"additional","affiliation":[{"name":"Fibrosis Research Laboratory, Division of Nephrology and Hypertension, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City, Utah"}]},{"given":"Nancy A.","family":"Noble","sequence":"additional","affiliation":[{"name":"Fibrosis Research Laboratory, Division of Nephrology and Hypertension, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City, Utah"}]},{"given":"Wayne A.","family":"Border","sequence":"additional","affiliation":[{"name":"Fibrosis Research Laboratory, Division of Nephrology and Hypertension, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City, Utah"}]},{"given":"Yufeng","family":"Huang","sequence":"additional","affiliation":[{"name":"Fibrosis Research Laboratory, Division of Nephrology and Hypertension, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City, Utah"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.109.128645"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1097\/HJH.0b013e3282f05bae"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00127.x"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.31.1.181"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.108.127258"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000186329.92187.2e"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/14.8.1904"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.107.101444"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007091030"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1210\/jcem-71-4-1008"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1038\/hr.2009.206"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/j.regpep.2009.11.006"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.2011.05486.x"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00017.2008"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1007\/s11906-007-0024-4"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002243"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000011"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1172\/JCI21398"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005121278"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000215838.48170.0b"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006010029"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.96"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.3181\/0705-MR-134"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.30.2.259"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.110.224667"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199311113292004"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM198505303122202"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1136\/bjo.82.8.939"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.84.9.1067"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.107.101493"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.511"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1172\/JCI0214276"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1172\/JCI114731"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2011020202"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000019242.51541.99"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2011020200"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1291\/hypres.30.1139"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1038\/ajh.2009.273"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.2001.280.4.H1706"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000240064.19301.1b"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1161\/hy0202.103002"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2009.10.121"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1016\/j.mce.2008.09.010"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.90264.2008"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00271.2011"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00050.2012","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:20:00Z","timestamp":1567974000000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00050.2012"}},"issued":{"date-parts":[[2012,7,1]]},"references-count":45,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2012,7,1]]}},"alternative-id":["10.1152\/ajprenal.00050.2012"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00050.2012","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2012,7,1]]}},{"indexed":{"date-parts":[[2025,10,24]],"date-time":"2025-10-24T16:42:11Z","timestamp":1761324131498},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1992,11,1]]},"abstract":"<jats:p> We have recently isolated cDNAs encoding a Na(+)-H+ exchanger isoform, referred to as NHE-1, from rabbit kidney and LLC-PK1 cells. To identify the NHE-1 protein and to establish its cellular and subcellular localization in the rabbit kidney, we prepared antibodies to a NHE-1 fusion protein. cDNA encoding the COOH-terminal 41 amino acids of NHE-1 was subcloned into a maltose-binding protein vector and the purified fusion protein (FP347A) used to immunize guinea pigs. To identify the NHE-1 protein, we performed Western blot analysis against membrane fractions prepared from rabbit renal cortex. Anti-FP347A antibody specifically reacted with a polypeptide with an apparent molecular mass of 100\u2013110 kDa that was enriched in basolateral membrane fractions. When indirect immunofluorescence was performed on semithin (0.5 micron) cryosections of paraformaldehyde-lysine-periodate-fixed rabbit kidney, anti-FP347A specifically stained the basolateral plasma membrane of cells of the proximal tubule, thick ascending limb, and distal convoluted tubule. Anti-FP347A similarly stained connecting tubule cells and principal cells. No staining was detected on the apical membrane of any cells of the rabbit nephron. We conclude that NHE-1 is a 100- to 110-kDa protein expressed on the basolateral membrane of multiple nephron segments. <\/jats:p>","DOI":"10.1152\/ajprenal.1992.263.5.f833","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T05:05:20Z","timestamp":1514005520000},"page":"F833-F840","source":"Crossref","is-referenced-by-count":37,"title":["Immunocytochemical characterization of Na(+)-H+ exchanger isoform NHE-1 in rabbit kidney"],"prefix":"10.1152","volume":"263","author":[{"given":"D.","family":"Biemesderfer","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06510."}]},{"given":"R. F.","family":"Reilly","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06510."}]},{"given":"M.","family":"Exner","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06510."}]},{"given":"P.","family":"Igarashi","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06510."}]},{"given":"P. S.","family":"Aronson","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06510."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1992.263.5.F833","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:24:45Z","timestamp":1567959885000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1992.263.5.F833"}},"issued":{"date-parts":[[1992,11,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1992,11,1]]}},"alternative-id":["10.1152\/ajprenal.1992.263.5.F833"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1992.263.5.f833","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1992,11,1]]}},{"indexed":{"date-parts":[[2025,10,23]],"date-time":"2025-10-23T16:49:33Z","timestamp":1761238173088},"reference-count":57,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2003,4,1]]},"abstract":"<jats:p>The renin-angiotensin system (RAS) plays a central role in body physiology, controlling blood pressure and blood electrolyte composition. ACE.1 (null) mice are null for all expression of angiotensin-converting enzyme (ACE). These mice have low blood pressure, the inability to concentrate urine, and a maldevelopment of the kidney. In contrast, ACE.2 (tissue null) mice produce one-third normal plasma ACE but no tissue ACE. They also have low blood pressure and cannot concentrate urine, but they have normal indices of renal function. These mice, while very informative, show that the null approach to creating knockout mice has intrinsic limitations given the many different physiological systems that no longer operate in an animal without a functioning RAS. To investigate the fine control of body physiology by the RAS, we developed a novel promoter swapping approach to generate a more selective tissue knockout of ACE expression. We used this to create ACE.3 (liver ACE) mice that selectively express ACE in the liver but lack all ACE within the vasculature. Evaluation of these mice shows that endothelial expression of ACE is not required for blood pressure control or normal renal function. Targeted homologous recombination has the power to create new strains of mice expressing the RAS in selected subsets of tissues. Not only will these new genetic models be useful for studying blood pressure regulation but also they show great promise for the investigation of the function of the RAS in complicated disease models.<\/jats:p>","DOI":"10.1152\/ajprenal.00308.2002","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:37:40Z","timestamp":1425415060000},"page":"F599-F607","source":"Crossref","is-referenced-by-count":11,"title":["New approaches to genetic manipulation of mice: tissue-specific expression of ACE"],"prefix":"10.1152","volume":"284","author":[{"given":"Justin M.","family":"Cole","sequence":"first","affiliation":[{"name":"Department of Pathology, Emory University, Atlanta, Georgia 30322"}]},{"given":"Hong","family":"Xiao","sequence":"additional","affiliation":[{"name":"Department of Pathology, Emory University, Atlanta, Georgia 30322"}]},{"given":"Jonathan W.","family":"Adams","sequence":"additional","affiliation":[{"name":"Department of Pathology, Emory University, Atlanta, Georgia 30322"}]},{"given":"Kevin M.","family":"Disher","sequence":"additional","affiliation":[{"name":"Department of Pathology, Emory University, Atlanta, Georgia 30322"}]},{"given":"Hui","family":"Zhao","sequence":"additional","affiliation":[{"name":"Department of Pathology, Emory University, Atlanta, Georgia 30322"}]},{"given":"Kenneth E.","family":"Bernstein","sequence":"additional","affiliation":[{"name":"Department of Pathology, Emory University, Atlanta, Georgia 30322"}]}],"member":"24","reference":[{"key":"B2","doi-asserted-by":"crossref","first-page":"26428","DOI":"10.1016\/S0021-9258(19)74332-4","volume":"268","author":"Beldent V","year":"1993","journal-title":"J Biol Chem"},{"key":"B3","doi-asserted-by":"crossref","first-page":"11945","DOI":"10.1016\/S0021-9258(18)80158-2","volume":"264","author":"Bernstein KE","year":"1989","journal-title":"J Biol Chem"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/scientificamerican0394-52"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/0306-4522(87)90114-X"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.272.3.F299"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.29.18185"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1172\/JCI10557"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1161\/hh0102.102360"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2744(71)90142-2"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.94.11.2756"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.44.28142"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M003892200"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.37.4.1047"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.86.20.7741"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/14.8.1912"},{"key":"B17","first-page":"953","volume":"74","author":"Esther CR","year":"1996","journal-title":"Lab Invest"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119419"},{"key":"B19","doi-asserted-by":"crossref","first-page":"1958","DOI":"10.1681\/ASN.V1291958","volume":"12","author":"Glicklich D","year":"2001","journal-title":"J Am Soc Nephrol"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1038\/377744a0"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.10.8.4294"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/377748a0"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.8.3521"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.93.17.9126"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.7.2735"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00326.2001"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1038\/375146a0"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.29.1.150"},{"key":"B29","doi-asserted-by":"crossref","first-page":"16754","DOI":"10.1016\/S0021-9258(19)84769-5","volume":"264","author":"Kumar RS","year":"1989","journal-title":"J Biol Chem"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(89)80897-X"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1038\/35093537"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1101\/gad.10.2.154"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/14.8.1836"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1038\/375247a0"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1038\/5036"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1006\/geno.2000.6113"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118988"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1210\/mend-1-8-535"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00420.x"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1172\/JCI4401"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.29.1.98"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)81168-X"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118366"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.26.15496"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1101\/gad.1.3.268"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1172\/JCI3545"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1210\/endo.137.2.8593824"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.28.6.1126"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.21.6.827"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.85.24.9386"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.32.18719"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1007\/BF02715664"},{"key":"B53","doi-asserted-by":"crossref","first-page":"31334","DOI":"10.1016\/S0021-9258(18)31697-1","volume":"269","author":"Tanimoto K","year":"1994","journal-title":"J Biol Chem"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1172\/JCI1899"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9343(98)00390-8"},{"key":"B56","doi-asserted-by":"crossref","first-page":"9002","DOI":"10.1016\/S0021-9258(18)31543-6","volume":"266","author":"Wei L","year":"1991","journal-title":"J Biol Chem"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(95)90234-1"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.275.1.5"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00308.2002","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,5,1]],"date-time":"2022-05-01T09:36:44Z","timestamp":1651397804000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00308.2002"}},"issued":{"date-parts":[[2003,4,1]]},"references-count":57,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2003,4,1]]}},"alternative-id":["10.1152\/ajprenal.00308.2002"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00308.2002","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2003,4,1]]}},{"indexed":{"date-parts":[[2025,10,21]],"date-time":"2025-10-21T14:46:05Z","timestamp":1761057965089},"reference-count":47,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2004,9]]},"abstract":"<jats:p>The mammalian kidney bumetanide-sensitive Na<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-2Cl<jats:sup>\u2212<\/jats:sup>and thiazide-sensitive Na<jats:sup>+<\/jats:sup>-Cl<jats:sup>\u2212<\/jats:sup>cotransporters are the major pathways for salt reabsorption in the thick ascending limb of Henle's loop and distal convoluted tubule, respectively. These cotransporters serve as receptors for the loop- and thiazide-type diuretics, and inactivating mutations of corresponding genes are associated with development of Bartter's syndrome type I and Gitleman's disease, respectively. Structural requirements for ion translocation and diuretic binding specificity are unknown. As an initial approach for analyzing structural determinants conferring ion or diuretic preferences in these cotransporters, we exploited functional differences and structural similarities between Na<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-2Cl<jats:sup>\u2212<\/jats:sup>and Na<jats:sup>+<\/jats:sup>-Cl<jats:sup>\u2212<\/jats:sup>cotransporters to design and study chimeric proteins in which the NH<jats:sub>2<\/jats:sub>-terminal and\/or COOH-terminal domains were switched between each other. Thus six chimeric proteins were produced. Using the heterologous expression system of Xenopus laevis oocytes, we observed that four chimeras exhibited functional activity. Our results revealed that, in the Na<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-2Cl<jats:sup>\u2212<\/jats:sup>cotransporter, ion translocation and diuretic binding specificity are determined by the central hydrophobic domain. Thus NH<jats:sub>2<\/jats:sub>-terminal and COOH-terminal domains do not play a role in defining these properties. A similar conclusion can be suggested for the Na<jats:sup>+<\/jats:sup>-Cl<jats:sup>\u2212<\/jats:sup>cotransporter.<\/jats:p>","DOI":"10.1152\/ajprenal.00124.2004","type":"journal-article","created":{"date-parts":[[2004,5,25]],"date-time":"2004-05-25T00:13:27Z","timestamp":1085444007000},"page":"F570-F577","source":"Crossref","is-referenced-by-count":20,"title":["Ion and diuretic specificity of chimeric proteins between apical Na<sup>+<\/sup>-K<sup>+<\/sup>-2Cl<sup>\u2212<\/sup>and Na<sup>+<\/sup>-Cl<sup>\u2212<\/sup>cotransporters"],"prefix":"10.1152","volume":"287","author":[{"given":"Claudia","family":"Tovar-Palacio","sequence":"first","affiliation":[]},{"given":"Norma A.","family":"Bobadilla","sequence":"additional","affiliation":[]},{"given":"Paulina","family":"Cort\u00e9s","sequence":"additional","affiliation":[]},{"given":"Consuelo","family":"Plata","sequence":"additional","affiliation":[]},{"given":"Paola","family":"de los Heros","sequence":"additional","affiliation":[]},{"given":"Norma","family":"V\u00e1zquez","sequence":"additional","affiliation":[]},{"given":"Gerardo","family":"Gamba","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1021\/bi962210n"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M107118200"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.10.6548"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.49.32595"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1001\/jama.289.19.2560"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1002\/jmor.1051360203"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(12)70272-X"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.253.3.F546"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1986.250.1.F176"},{"key":"R10","doi-asserted-by":"crossref","unstructured":"Gamba G, Miyanoshita A, Lombardi M, Lytton J, Lee WS, Hediger MA, and Hebert SC.Molecular cloning, primary structure and characterization of two members of the mammalian electroneutral sodium-(potassium)-chloride cotransporter family expressed in kidney.J Biol Chem269: 17713\u201317722, 1994.","DOI":"10.1016\/S0021-9258(17)32499-7"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.90.7.2749"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.C200021200"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1007\/BF00584588"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1981.241.4.F443"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000043903.93452.D0"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.39.24556"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1016\/S1095-6433(01)00420-2"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.112.5.549"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.12.7179"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.18.11295"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.275.11.8133"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1177\/002215540004801105"},{"key":"R23","doi-asserted-by":"crossref","unstructured":"Ji HL, Chalfant ML, Jovov B, Lockhart JP, Parker SB, Fuller CM, Stanton BA, and Benos DJ.The cytosolic termini of the beta- and gamma-ENaC subunits are involved in the functional interactions between cystic fibrosis transmembrane conductance regulator and epithelial sodium channel.J Biol Chem275: 27947\u201327956, 2000.","DOI":"10.1074\/jbc.M002848200"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.6"},{"key":"R25","unstructured":"Kurtz CL, Karolyi L, Seyberth HW, Koch MC, Vargas R, Feldmann D, Vollmer M, Knoers NV, Madrigal G, and Guay-Woodford LM.A common NKCC2 mutation in Costa Rican Bartter's syndrome patients: evidence for a founder effect.J Am Soc Nephrol8: 1706\u20131711, 1997."},{"key":"R26","unstructured":"Mastroianni N, Bettinelli A, Bianchetti M, Colussi G, de Fusco M, Sereni F, Ballabio A, and Casari G.Novel molecular variants of the Na-Cl cotransporter gene are responsible for Gitelman syndrome.Am J Hum Genet59: 1019\u20131026, 1996."},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00421.2002"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.1.F161"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M400602200"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.3.F347"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1021\/bi9630624"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.1999.041ad.x"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.4.F574"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1999.276.2.H359"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M110442200"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.300"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1172\/JCI200318232"},{"key":"R38","unstructured":"Sabath S, Meade P, Berkman J, de los Heron P, Moreno E, Bobadilla NA, Vazquez N, Ellison DH, and Gamba G.Pathophysiology of functional mutations of the thiazide-sensitive Na-Cl cotransporter in Gitelman disease.Am J Physiol Renal Physiol10.1152\/ajprenal.00044.2004."},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1038\/ng0696-183"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1038\/ng0196-24"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1007\/BF01868594"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.7.4137"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1172\/JCI10366"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1126\/science.1062844"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.242735399"},{"key":"R46","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.19-13-05255.1999"},{"key":"R47","doi-asserted-by":"publisher","DOI":"10.1172\/JCI17443"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00124.2004","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,6,17]],"date-time":"2021-06-17T22:47:27Z","timestamp":1623970047000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00124.2004"}},"issued":{"date-parts":[[2004,9]]},"references-count":47,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2004,9]]}},"alternative-id":["10.1152\/ajprenal.00124.2004"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00124.2004","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2004,9]]}},{"indexed":{"date-parts":[[2025,11,2]],"date-time":"2025-11-02T23:11:59Z","timestamp":1762125119801},"reference-count":46,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2004,11]]},"abstract":"<jats:p>2,3,5-Tris-(glutathion- S-yl)hydroquinone (TGHQ), a reactive metabolite of the nephrotoxicant hydroquinone, induces the ROS-dependent activation of MAPKs, followed by histone H3 phosphorylation and oncotic cell death in renal proximal tubule epithelial cells (LLC-PK<jats:sub>1<\/jats:sub>). Cell death and histone H3 phosphorylation are attenuated by pharmacological inhibition of p38 MAPK or ERK1\/2 pathways. Because TGHQ, but not epidermal growth factor (EGF), induces histone H3 phosphorylation and cell death in LLC-PK<jats:sub>1<\/jats:sub>cells, we hypothesized that there are differences in the mechanisms by which TGHQ and EGF induce activation of the EGF receptor (EGFR). We therefore compared the relative ability of TGHQ, H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>, and EGF to activate EGFR and MAPKs and found that p38 MAPK activation is EGFR independent, whereas ERK1\/2 activation occurs mainly through EGFR activation. TGHQ, H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>, and EGF induce different EGFR tyrosine phosphorylation profiles that likely influence the subsequent differential kinetics of MAPK activation. We next transfected LLC-PK<jats:sub>1<\/jats:sub>cells with a dominant negative p38 MAPK-expressing plasmid (pcDNA3-DNp38). TGHQ failed to induce phosphorylation of p38 MAPK and its substrate, MK-2, in pcDNA3-DNp38-transfected cells, indicating loss of function of p38 MAPK. In untransfected, pcDNA3 or pcDNA3-p38 (native)-transfected LLC-PK<jats:sub>1<\/jats:sub>cells, Hsp27 was intensively phosphorylated after TGHQ treatment, whereas in pcDNA3-DNp38-transfected cells, TGHQ failed to induce Hsp27 phosphorylation. Thus EGFR-independent p38 MAPK and EGFR-dependent ERK1\/2 activation by TGHQ lead to the activation of two downstream signaling factors, i.e., histone H3 and Hsp27 phosphorylation, which have in common the potential ability to remodel chromatin.<\/jats:p>","DOI":"10.1152\/ajprenal.00132.2004","type":"journal-article","created":{"date-parts":[[2004,6,30]],"date-time":"2004-06-30T00:53:53Z","timestamp":1088556833000},"page":"F1049-F1058","source":"Crossref","is-referenced-by-count":79,"title":["EGFR-independent activation of p38 MAPK and EGFR-dependent activation of ERK1\/2 are required for ROS-induced renal cell death"],"prefix":"10.1152","volume":"287","author":[{"given":"Jing","family":"Dong","sequence":"first","affiliation":[]},{"given":"Sampath","family":"Ramachandiran","sequence":"additional","affiliation":[]},{"given":"Kulbhushan","family":"Tikoo","sequence":"additional","affiliation":[]},{"given":"Zhe","family":"Jia","sequence":"additional","affiliation":[]},{"given":"Serrine S.","family":"Lau","sequence":"additional","affiliation":[]},{"given":"Terrence J.","family":"Monks","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1046\/j.1471-4159.1999.0720112.x"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.12.8335"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.10.3.525"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1021\/tx9902082"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M011766200"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.18.9.5178"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1016\/S0079-6107(98)00056-X"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1023\/A:1006820214072"},{"key":"R8A","unstructured":"Dong J, Person M, Hensley SC, Shen JJ, Lau SS, and Monks TJ.Coordinate regulation of the cytoskeletal and nuclear stress response by reactive oxygen species (Abstract).FASEB J17: A615\u2013A616, 2003."},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.7.4079"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1038\/sj.cdd.4401005"},{"key":"R11","doi-asserted-by":"crossref","unstructured":"Guyton KZ, Gorospe M, Wang X, Mock YD, Kokkonen GC, Liu Y, Roth GS, and Holbrook NJ.Age-related changes in activation of mitogen-activated protein kinase cascades by oxidative stress.J Investig Dermatol Symp Proc3: 23\u201327, 1998.","DOI":"10.1038\/jidsp.1998.7"},{"key":"R12","doi-asserted-by":"crossref","unstructured":"Helin Kand Beguinot L.Internalization and down-regulation of the human epidermal growth factor receptor are regulated by the carboxyl-terminal tyrosines.J Biol Chem266: 8363\u20138368, 1991.","DOI":"10.1016\/S0021-9258(18)92984-4"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.143.5.1361"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1006\/abbi.1997.9969"},{"key":"R15","doi-asserted-by":"crossref","unstructured":"Jia Z, Person J, Dong J, Shen J, Hensley SC, Stevens JL, Monks TJ, and Lau SS.GRP78 is essential for 11-deoxy,16,16,dimethyl prostaglandin E2mediated cytoprotection in renal epithelial cells.Am J Physiol Renal Physiol; first published June 29, 2004; 10.1152\/ajprenal.00138.2004.","DOI":"10.1152\/ajprenal.00138.2004"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1152\/ajplung.1997.273.5.L1029"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1016\/S0024-3205(01)00990-0"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1002\/j.1460-2075.1996.tb00916.x"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1139\/o95-078"},{"key":"R20","unstructured":"Lau SS, Hill BA, Highet RJ, and Monks TJ.Sequential oxidation and glutathione addition to 1,4-benzoquinone: correlation of toxicity with increased glutathione substitution.Mol Pharmacol34: 829\u2013836, 1988."},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1021\/tx000161g"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1016\/S1097-2765(00)80231-2"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1101\/gad.12.23.3663"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.10119"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1006\/abbi.1995.1341"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1016\/S0378-4274(01)00359-9"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1021\/tx9700937"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.pharmtox.38.1.229"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-291X(03)00623-5"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M107525200"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1016\/S0898-6568(97)00042-9"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1021\/tx0200663"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M303417200"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M204677200"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.44.27456"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(94)90272-0"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1210\/mend.12.4.0094"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)00114-8"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1038\/35010517"},{"key":"R40","doi-asserted-by":"crossref","unstructured":"Sorkin A, Helin K, Waters CM, Carpenter G, and Beguinot L.Multiple autophosphorylation sites of the epidermal growth factor receptor are essential for receptor kinase activity and internalization. Contrasting significance of tyrosine 992 in the native and truncated receptors.J Biol Chem267: 8672\u20138678, 1992.","DOI":"10.1016\/S0021-9258(18)42495-7"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1124\/mol.60.2.394"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.16.11178"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M206837200"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-5793(01)02117-2"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1021\/tx000190r"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00132.2004","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,6,23]],"date-time":"2021-06-23T21:26:26Z","timestamp":1624483586000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00132.2004"}},"issued":{"date-parts":[[2004,11]]},"references-count":46,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2004,11]]}},"alternative-id":["10.1152\/ajprenal.00132.2004"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00132.2004","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2004,11]]}},{"indexed":{"date-parts":[[2025,11,4]],"date-time":"2025-11-04T10:29:58Z","timestamp":1762252198162},"reference-count":48,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2003,5,1]]},"abstract":"<jats:p>Ischemia-reperfusion injury (IRI) is the major cause of acute renal failure in native and allograft kidneys. Identifying the molecules and pathways involved in the pathophysiology of renal IRI will yield valuable new diagnostic and therapeutic information. To identify differentially regulated genes in renal IRI, RNA from rat kidneys subjected to an established renal IRI protocol (bilateral occlusion of renal pedicles for 30 min followed by reperfusion) and time-matched kidneys from sham-operated animals was subjected to suppression subtractive hybridization. The level of spermidine\/spermine N<jats:sup>1<\/jats:sup>-acetyltransferase (SSAT) mRNA, an essential enzyme for the catabolism of polyamines, increased in renal IRI. SSAT expression was found throughout normal kidney tubules, as detected by nephron segment RT-PCR. Northern blots demonstrated that the mRNA levels of SSAT are increased by greater than threefold in the renal cortex and by fivefold in the renal medulla at 12 h and returned to baseline at 48 h after ischemia. The increase in SSAT mRNA was paralleled by an increase in SSAT protein levels as determined by Western blot analysis. The concentration of putrescine in the kidney increased by \u223c4- and \u223c7.5-fold at 12 and 24 h of reperfusion, respectively, consistent with increased functional activity of SSAT. To assess the specificity of SSAT for tubular injury, a model of acute renal failure from Na<jats:sup>+<\/jats:sup>depletion (without tubular injury) was studied; SSAT mRNA levels remained unchanged in rats subjected to Na<jats:sup>+<\/jats:sup>depletion. To distinguish SSAT increases from the effects of tubular injury vs. uremic toxins, SSAT was increased in cis-platinum-treated animals before the onset of renal failure. The expression of SSAT mRNA and protein increased by \u223c3.5- and &gt;10-fold, respectively, in renal tubule epithelial cells subjected to ATP depletion and metabolic poisoning (an in vitro model of kidney IRI). Our results suggest that SSAT is likely a new marker of tubular cell injury that distinguishes acute prerenal from intrarenal failure.<\/jats:p>","DOI":"10.1152\/ajprenal.00318.2002","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:38:06Z","timestamp":1425415086000},"page":"F1046-F1055","source":"Crossref","is-referenced-by-count":68,"title":["Expression of SSAT, a novel biomarker of tubular cell damage, increases in kidney ischemia-reperfusion injury"],"prefix":"10.1152","volume":"284","author":[{"given":"Kamyar","family":"Zahedi","sequence":"first","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Pediatrics, Children's Hospital Medical Center,"}]},{"given":"Zhaohui","family":"Wang","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Medicine, University of Cincinnati, and"}]},{"given":"Sharon","family":"Barone","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Medicine, University of Cincinnati, and"}]},{"given":"Anne E.","family":"Prada","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Pediatrics, Children's Hospital Medical Center,"}]},{"given":"Caitlin N.","family":"Kelly","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Pediatrics, Children's Hospital Medical Center,"}]},{"given":"Robert A.","family":"Casero","sequence":"additional","affiliation":[{"name":"Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21218; and"}]},{"given":"Naoko","family":"Yokota","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, and"}]},{"given":"Carl W.","family":"Porter","sequence":"additional","affiliation":[{"name":"Roswell Park Cancer Institute, Buffalo, New York 14263"}]},{"given":"Hamid","family":"Rabb","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, and"}]},{"given":"Manoocher","family":"Soleimani","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Medicine, University of Cincinnati, and"},{"name":"Veterans Affairs Medical Center, Cincinnati, Ohio 45267;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.4.1964"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.140122097"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1042\/bj3620149"},{"key":"B4","doi-asserted-by":"crossref","first-page":"281","DOI":"10.1016\/S0959-8049(00)00389-0","volume":"37","author":"Bettuzzi S","year":"2001","journal-title":"Eur J Cancer"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(95)01359-8"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1993.163"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-2952(97)00601-1"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1042\/bj3160697"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.10.6175"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1097-4652(199801)174:1<125::AID-JCP14>3.0.CO;2-E"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1021\/bi9612273"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1042\/bj20020156"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1016\/S0168-8278(01)00153-2"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00433.x"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(95)00591-V"},{"key":"B16","doi-asserted-by":"crossref","first-page":"65","DOI":"10.1016\/S0304-3940(98)00780-0","volume":"256","author":"Hatcher JF","year":"1998","journal-title":"Neurosci Lett"},{"key":"B17","doi-asserted-by":"crossref","first-page":"697","DOI":"10.1002\/(SICI)1097-4547(19991201)58:5<697::AID-JNR11>3.0.CO;2-B","volume":"58","author":"Hatcher JF","year":"1999","journal-title":"J Neurosci Res"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1046\/j.0014-2956.2001.02744.x"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.7.4135"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.2000.2601"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.3109\/07853899109148056"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1124\/mol.59.2.231"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.pa.35.040195.000415"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M100751200"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1093\/carcin\/21.12.2151"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.272.4.F430"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1007\/s004670050385"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00633.x"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/S0304-3940(01)01538-5"},{"key":"B30","doi-asserted-by":"crossref","first-page":"231","DOI":"10.1124\/mol.59.2.231","volume":"59","author":"Niiranen K","year":"2001","journal-title":"Mol Pharmacol"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1006\/excr.2002.5517"},{"key":"B32","first-page":"759","volume":"48","author":"Pegg AE.","year":"1988","journal-title":"Cancer Res"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.30.18746"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.46.29372"},{"key":"B35","first-page":"3715","volume":"51","author":"Porter CW","year":"1991","journal-title":"Cancer Res"},{"key":"B36","doi-asserted-by":"crossref","first-page":"605","DOI":"10.1681\/ASN.V94605","volume":"9","author":"Rabb H","year":"1998","journal-title":"J Am Soc Nephrol"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.267.6.F1052"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1995.1779"},{"key":"B39","first-page":"156","volume":"162","author":"Sacchi N","year":"1987","journal-title":"Anal Biochem"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(93)80103-2"},{"key":"B41","doi-asserted-by":"crossref","first-page":"2297","DOI":"10.1681\/ASN.V102315","volume":"10","author":"Shih T","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.2.F356"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1042\/bj3580343"},{"key":"B44","doi-asserted-by":"crossref","first-page":"F347","DOI":"10.1152\/ajprenal.1997.272.3.F347","volume":"272","author":"Wang YH","year":"1997","journal-title":"Am J Physiol Renal Physiol"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.0590041405.x"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117214"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1016\/0169-328X(95)00339-T"},{"key":"B48","doi-asserted-by":"crossref","first-page":"18532","DOI":"10.1016\/S0021-9258(17)46660-9","volume":"268","author":"Zweier JL","year":"1993","journal-title":"J Biol Chem"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00318.2002","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,5,1]],"date-time":"2022-05-01T09:37:26Z","timestamp":1651397846000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00318.2002"}},"issued":{"date-parts":[[2003,5,1]]},"references-count":48,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2003,5,1]]}},"alternative-id":["10.1152\/ajprenal.00318.2002"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00318.2002","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2003,5,1]]}},{"indexed":{"date-parts":[[2025,11,2]],"date-time":"2025-11-02T16:48:50Z","timestamp":1762102130928},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1992,9,1]]},"abstract":"<jats:p> Using the patch-clamp technique, we studied the effect of insulin on an amiloride-blockable Na channel in the apical membrane of a distal nephron cell line (A6) cultured on permeable collagen films for 10-14 days. NPo (N, number of channels per patch membrane; Po, average value of open probability of individual channels in the patch) under baseline conditions was 0.88 +\/- 0.12 (SE)(n = 17). After making cell-attached patches on the apical membrane which contained Na channels, insulin (1 mU\/ml) was applied to the serosal bath. While maintaining the cell-attached patch, NPo significantly increased to 1.48 +\/- 0.19 (n = 17; P less than 0.001) after 5-10 min of insulin application. The open probability of Na channels was 0.39 +\/- 0.01 (n = 38) under baseline condition, and increased to 0.66 +\/- 0.03 (n = 38, P less than 0.001) after addition of insulin. The baseline single-channel conductance was 4pS, and neither the single-channel conductance nor the current-voltage relationship was significantly changed by insulin. These results indicate that insulin increases Na absorption in the distal nephron by increasing the open probability of the amiloride-blockable Na channel. <\/jats:p>","DOI":"10.1152\/ajprenal.1992.263.3.f392","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T09:57:08Z","timestamp":1514023028000},"page":"F392-F400","source":"Crossref","is-referenced-by-count":26,"title":["Insulin activates single amiloride-blockable Na channels in a distal nephron cell line (A6)"],"prefix":"10.1152","volume":"263","author":[{"given":"Y.","family":"Marunaka","sequence":"first","affiliation":[{"name":"Hospital for Sick Children Research Institute, Ontario, Canada."}]},{"given":"N.","family":"Hagiwara","sequence":"additional","affiliation":[{"name":"Hospital for Sick Children Research Institute, Ontario, Canada."}]},{"given":"H.","family":"Tohda","sequence":"additional","affiliation":[{"name":"Hospital for Sick Children Research Institute, Ontario, Canada."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1992.263.3.F392","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:24:32Z","timestamp":1567974272000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1992.263.3.F392"}},"issued":{"date-parts":[[1992,9,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1992,9,1]]}},"alternative-id":["10.1152\/ajprenal.1992.263.3.F392"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1992.263.3.f392","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1992,9,1]]}},{"indexed":{"date-parts":[[2025,12,25]],"date-time":"2025-12-25T19:03:05Z","timestamp":1766689385752,"version":"3.37.3"},"reference-count":62,"publisher":"American Physiological Society","issue":"4","funder":[{"DOI":"10.13039\/100000060","name":"HHS | NIH | National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["F31 AI106357"],"award-info":[{"award-number":["F31 AI106357"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["U01 DK82343"],"award-info":[{"award-number":["U01 DK82343"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2020,4,1]]},"abstract":"<jats:p>Corticotropin-releasing factor (CRF) regulates diverse physiological functions, including bladder control. We recently reported that Crf expression is under genetic control of Aoah, the locus encoding acyloxyacyl hydrolase (AOAH), suggesting that AOAH may also modulate voiding. Here, we examined the role of AOAH in bladder function. AOAH-deficient mice exhibited enlarged bladders relative to wild-type mice and had decreased voiding frequency and increased void volumes. AOAH-deficient mice had increased nonvoiding contractions and increased peak voiding pressure in awake cystometry. AOAH-deficient mice also exhibited increased bladder permeability and higher neuronal firing rates of bladder afferents in response to stretch. In wild-type mice, AOAH was expressed in bladder projecting neurons and colocalized in CRF-expressing neurons in Barrington\u2019s nucleus, an important brain area for voiding behavior, and Crf was elevated in Barrington\u2019s nucleus of AOAH-deficient mice. We had previously identified aryl hydrocarbon receptor (AhR) and peroxisome proliferator-activated receptor-\u03b3 as transcriptional regulators of Crf, and conditional knockout of AhR or peroxisome proliferator-activated receptor-\u03b3 in Crf-expressing cells restored normal voiding in AOAH-deficient mice. Finally, an AhR antagonist improved voiding in AOAH-deficient mice. Together, these data demonstrate that AOAH regulates bladder function and that the AOAH- Crf axis is a therapeutic target for treating voiding dysfunction.<\/jats:p>","DOI":"10.1152\/ajprenal.00442.2019","type":"journal-article","created":{"date-parts":[[2020,1,31]],"date-time":"2020-01-31T16:29:56Z","timestamp":1580488196000},"page":"F1006-F1016","source":"Crossref","is-referenced-by-count":8,"title":["Acyloxyacyl hydrolase regulates voiding activity"],"prefix":"10.1152","volume":"318","author":[{"given":"Lizath M.","family":"Aguiniga","sequence":"first","affiliation":[{"name":"Department of Urology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois"}]},{"given":"Timothy J.","family":"Searl","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois"}]},{"given":"Afrida","family":"Rahman-Enyart","sequence":"additional","affiliation":[{"name":"Department of Urology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois"}]},{"given":"Ryan E.","family":"Yaggie","sequence":"additional","affiliation":[{"name":"Department of Urology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois"}]},{"given":"Wenbin","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Urology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois"}]},{"given":"Anthony J.","family":"Schaeffer","sequence":"additional","affiliation":[{"name":"Department of Urology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1237-8364","authenticated-orcid":false,"given":"David J.","family":"Klumpp","sequence":"additional","affiliation":[{"name":"Department of Urology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois"},{"name":"Department of Microbiology-Immunology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00029.2019"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1002\/nau.22549"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1007\/978-3-642-16499-6_8"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00072.2015"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/S0304-3940(98)00382-6"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/j.physbeh.2017.09.020"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1111\/j.1742-1241.2006.01183.x"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90259.2008"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1007\/s11255-014-0908-6"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1097\/FBP.0b013e328331b9bf"},{"key":"B11","doi-asserted-by":"crossref","first-page":"16444","DOI":"10.1016\/S0021-9258(17)46242-9","volume":"265","author":"Erwin AL","year":"1990","journal-title":"J Biol Chem"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/j.bcp.2010.04.033"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1038\/nrn2401"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.12740\/PP\/OnlineFirst\/59162"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1038\/nrurol.2015.266"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.3389\/fnins.2018.00931"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1021\/bi00098a020"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/j.juro.2015.01.086"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1002\/cphy.c150015"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1002\/cphy.c130045"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2016.08.073"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.3978\/j.issn.2223-4683.2015.10.03"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.18-23-10016.1998"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1007\/s12325-019-0880-8"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1016\/j.urology.2005.04.061"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1124\/mol.105.021832"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1097\/01.ju.0000144142.26242.f3"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1186\/s12894-015-0009-6"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1038\/nrurol.2016.227"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1006\/meth.2001.1262"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1016\/j.chom.2008.06.009"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1520-6777(2000)19:1<87:AID-NAU9>3.0.CO;2-O"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1111\/j.1460-9568.2012.08250.x"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1002\/nau.23421"},{"key":"B35","first-page":"11","volume":"15","author":"Miyazato M","year":"2013","journal-title":"Rev Urol"},{"key":"B36","doi-asserted-by":"crossref","first-page":"10116","DOI":"10.1016\/S0021-9258(19)50207-1","volume":"267","author":"Munford RS","year":"1992","journal-title":"J Biol Chem"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(05)67204-7"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1111\/j.1464-410X.2010.09843.x"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1016\/0304-3940(95)11873-U"},{"key":"B40","volume-title":"Paxinos and Franklin\u2019s the Mouse Brain in Stereotaxic Coordinates","author":"Paxinos G","year":"2019","edition":"5"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1016\/j.urology.2019.01.015"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1089\/neu.1998.15.375"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1002\/cne.20719"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1111\/bju.13039"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1002\/1096-9861(20010122)429:4<631:AID-CNE9>3.0.CO;2-M"},{"key":"B46","doi-asserted-by":"crossref","first-page":"383","DOI":"10.31887\/DCNS.2006.8.4\/ssmith","volume":"8","author":"Smith SM","year":"2006","journal-title":"Dialogues Clin Neurosci"},{"key":"B47","doi-asserted-by":"crossref","first-page":"23736","DOI":"10.1016\/S0021-9258(17)31577-6","volume":"269","author":"Staab JF","year":"1994","journal-title":"J Biol Chem"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1016\/j.amjmed.2005.12.011"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.3978\/j.issn.2223-4683.2016.01.08"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1002\/nau.20552"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1053\/j.gastro.2013.02.038"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1038\/nrurol.2010.203"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.91013.2008"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00257.2012"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1097\/ALN.0b013e318271606a"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00075.2017"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00239.2017"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.3389\/fnins.2019.00663"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.19-11-04644.1999"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1111\/iju.12308"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1016\/S0090-4295(01)01639-9"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00074.2014"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00442.2019","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,2,25]],"date-time":"2021-02-25T04:49:45Z","timestamp":1614228585000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00442.2019"}},"issued":{"date-parts":[[2020,4,1]]},"references-count":62,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2020,4,1]]}},"alternative-id":["10.1152\/ajprenal.00442.2019"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00442.2019","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2020,4,1]]}},{"indexed":{"date-parts":[[2026,1,2]],"date-time":"2026-01-02T17:20:42Z","timestamp":1767374442544,"version":"3.41.0"},"reference-count":64,"publisher":"American Physiological Society","issue":"10","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2016,5,15]]},"abstract":"<jats:p>Long-term angiotensin II (ANG II) infusion significantly increases ANG II levels in the kidney through two major mechanisms: AT<jats:sub>1<\/jats:sub>receptor-mediated augmentation of angiotensinogen (AGT) expression and uptake of circulating ANG II by the proximal tubules. However, it is not known whether intracellular ANG II stimulates AGT expression in the proximal tubule. In the present study, we overexpressed an intracellular cyan fluorescent ANG II fusion protein (Ad-sglt2-ECFP\/ANG II) selectively in the proximal tubule of rats and mice using the sodium and glucose cotransporter 2 (sglt2) promoter. AGT mRNA and protein expression in the renal cortex and 24-h urinary AGT excretion were determined 4 wk following overexpression of ECFP\/ANG II in the proximal tubule. Systolic blood pressure was significantly increased with a small antinatriuretic effect in rats and mice with proximal tubule-selective expression of ECFP\/ANG II ( P &lt; 0.01). AGT mRNA and protein expression in the cortex were increased by &gt;1.5-fold and 61 \u00b1 16% ( P &lt; 0.05), whereas urinary AGT excretion was increased from 48.7 \u00b1 5.7 ( n = 13) to 102 \u00b1 13.5 ( n = 13) ng\/24 h ( P &lt; 0.05). However, plasma AGT, renin activity, and ANG II levels remained unaltered by ECFP\/ANG II. The increased AGT mRNA and protein expressions in the cortex by ECFP\/ANG II were blocked in AT<jats:sub>1a<\/jats:sub>-knockout (KO) mice. Studies in cultured mouse proximal tubule cells demonstrated involvement of AT<jats:sub>1a<\/jats:sub>receptor\/MAP kinases\/NF-\u043aB signaling pathways. These results indicate that intracellular ANG II stimulates AGT expression in the proximal tubules, leading to increased AGT formation and secretion into the tubular fluid, which contributes to ANG II-dependent hypertension.<\/jats:p>","DOI":"10.1152\/ajprenal.00350.2015","type":"journal-article","created":{"date-parts":[[2016,2,11]],"date-time":"2016-02-11T03:33:17Z","timestamp":1455161597000},"page":"F1103-F1112","source":"Crossref","is-referenced-by-count":24,"title":["Augmentation of angiotensinogen expression in the proximal tubule by intracellular angiotensin II via AT<sub>1a<\/sub>\/MAPK\/NF-\u043aB signaling pathways"],"prefix":"10.1152","volume":"310","author":[{"given":"Jia L.","family":"Zhuo","sequence":"first","affiliation":[{"name":"Laboratory of Receptor and Signal Transduction, Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi; and"}]},{"given":"H.","family":"Kobori","sequence":"additional","affiliation":[{"name":"Department of Physiology and Hypertension and Renal Center of Excellence, Tulane University School of Medicine, New Orleans, Louisiana"}]},{"given":"Xiao C.","family":"Li","sequence":"additional","affiliation":[{"name":"Laboratory of Receptor and Signal Transduction, Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi; and"}]},{"given":"R.","family":"Satou","sequence":"additional","affiliation":[{"name":"Department of Physiology and Hypertension and Renal Center of Excellence, Tulane University School of Medicine, New Orleans, Louisiana"}]},{"given":"A.","family":"Katsurada","sequence":"additional","affiliation":[{"name":"Department of Physiology and Hypertension and Renal Center of Excellence, Tulane University School of Medicine, New Orleans, Louisiana"}]},{"given":"L. Gabriel","family":"Navar","sequence":"additional","affiliation":[{"name":"Department of Physiology and Hypertension and Renal Center of Excellence, Tulane University School of Medicine, New Orleans, Louisiana"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1101507108"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.110.165464"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.264.5.F891"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2736(91)90187-D"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000036452.28493.74"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/j.yjmcc.2003.09.021"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0605545103"},{"key":"B8","doi-asserted-by":"crossref","first-page":"415","DOI":"10.1016\/S0031-6997(24)01458-3","volume":"52","author":"de Gasparo M","year":"2000","journal-title":"Pharmacol Rev"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.1.F54"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00243.2004"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00019.2008"},{"volume":"20","journal-title":"Hypertension","author":"Guan S","key":"B12"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00525.2011"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.0335.2000"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.2.F303"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.37.5.1329"},{"key":"B17","doi-asserted-by":"crossref","first-page":"431","DOI":"10.1681\/ASN.V123431","volume":"12","author":"Kobori H","year":"2001","journal-title":"J Am Soc Nephrol"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00588.2007"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000056768.03657.B4"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000050102.90932.CF"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00146.2007"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00351.2011"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00402.2003"},{"key":"B24","first-page":"252","volume":"10","author":"Li J","year":"1996","journal-title":"Mol Endocrinol"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00329.2010"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00199.2014"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90734.2008"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00219.2012"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00489.2006"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.26.6.989"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00463.2006"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00398.2007"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00432.2007"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0b013e3282f2903c"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2011.161"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00338.2012"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00693.2013"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1556\/APhysiol.89.2002.4.3"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2011121159"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.273.2.F246"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00464.2013"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1038\/344541a0"},{"key":"B43","first-page":"412","volume":"17","author":"Navar LG","year":"1997","journal-title":"Semin Nephrol"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.110.163519"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2012050493"},{"key":"B46","first-page":"170","volume":"13","author":"Navar LG","year":"1998","journal-title":"News Physiol Sci"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00317.2005"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M110.150284"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000133023.89251.01"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000210"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00047.2008"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1096\/fj.11-195198"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90596.2008"},{"key":"B54","first-page":"37","volume":"13","author":"Singh A","year":"2013","journal-title":"Ochsner J"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00049.x"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.266.1.F120"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1290\/0511076.1"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1038\/ajh.2012.16"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.33.1.347"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1196\/annals.1378.078"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1161\/hy0102.100780"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00269.2005"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.27.3.658"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1016\/S0895-7061(97)00410-X"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00350.2015","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,6,1]],"date-time":"2025-06-01T10:37:04Z","timestamp":1748774224000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00350.2015"}},"issued":{"date-parts":[[2016,5,15]]},"references-count":64,"journal-issue":{"issue":"10","published-print":{"date-parts":[[2016,5,15]]}},"alternative-id":["10.1152\/ajprenal.00350.2015"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00350.2015","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2016,5,15]]}},{"indexed":{"date-parts":[[2026,1,8]],"date-time":"2026-01-08T18:54:21Z","timestamp":1767898461282,"version":"3.49.0"},"reference-count":46,"publisher":"American Physiological Society","issue":"4","funder":[{"name":"AP Moller Foundation","award":["12-263"],"award-info":[{"award-number":["12-263"]}]},{"name":"The Danish Research Council for Health and Disease","award":["DFF-1331-00162"],"award-info":[{"award-number":["DFF-1331-00162"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2015,8,15]]},"abstract":"<jats:p> While there is evidence that sex hormones influence multiple systems involved in salt and water homeostasis, the question of whether sex hormones regulate aquaporin-2 (AQP2) and thus water handling by the collecting duct has been largely ignored. Accordingly, the present study investigated AQP2 expression, localization and renal water handling in intact and ovariectomized (OVX) female rats, with and without estradiol or progesterone replacement. OVX resulted in a significant increase in urine osmolality and increase in p256-AQP2 in the renal cortex at 7 days post-OVX, as well as induced body weight changes. Relative to OVX alone, estradiol repletion produced a significant increase in urine output, normalized urinary osmolality and reduced both total AQP2 (protein and mRNA) and p256-AQP2 expression, whereas progesterone repletion had little effect. Direct effects of estradiol on AQP2 mRNA and protein levels were further tested in vitro using the mpkCCD principal cell line. Estradiol treatment of mpkCCD cells reduced AQP2 at both the mRNA and protein level in the absence of deamino-8-d-AVP (dDAVP) and significantly blunted the dDAVP-induced increase in AQP2 at the protein level only. We determined that mpkCCD and native mouse collecting ducts express both estrogen receptor (ER)\u03b1 and ER\u03b2 and that female mice lacking ER\u03b1 displayed significant increases in AQP2 protein compared with wild-type littermates, implicating ER\u03b1 in mediating the inhibitory effect of estradiol on AQP2 expression. These findings suggest that changes in estradiol levels, such as during menopause or following reproductive surgeries, may contribute to dysregulation of water homeostasis in women. <\/jats:p>","DOI":"10.1152\/ajprenal.00685.2014","type":"journal-article","created":{"date-parts":[[2015,6,11]],"date-time":"2015-06-11T07:22:07Z","timestamp":1434007327000},"page":"F305-F317","source":"Crossref","is-referenced-by-count":36,"title":["Estradiol regulates AQP2 expression in the collecting duct: a novel inhibitory role for estrogen receptor \u03b1"],"prefix":"10.1152","volume":"309","author":[{"given":"Muhammad Umar","family":"Cheema","sequence":"first","affiliation":[{"name":"Institute of Clinical Medicine, Aarhus University, Aarhus, Denmark;"}]},{"given":"Debra L.","family":"Irsik","sequence":"additional","affiliation":[{"name":"Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska; and"}]},{"given":"Yan","family":"Wang","sequence":"additional","affiliation":[{"name":"Institute of Clinical Medicine, Aarhus University, Aarhus, Denmark;"}]},{"given":"William","family":"Miller-Little","sequence":"additional","affiliation":[{"name":"Institute of Clinical Medicine, Aarhus University, Aarhus, Denmark;"}]},{"given":"Kelly A.","family":"Hyndman","sequence":"additional","affiliation":[{"name":"Division of Nephrology, University of Alabama at Birmingham, Birmingham, Alabama"}]},{"given":"Eileen S.","family":"Marks","sequence":"additional","affiliation":[{"name":"Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska; and"}]},{"given":"J\u00f8rgen","family":"Fr\u00f8ki\u00e6r","sequence":"additional","affiliation":[{"name":"Institute of Clinical Medicine, Aarhus University, Aarhus, Denmark;"}]},{"given":"Erika I.","family":"Boesen","sequence":"additional","affiliation":[{"name":"Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska; and"}]},{"given":"Rikke","family":"Norregaard","sequence":"additional","affiliation":[{"name":"Institute of Clinical Medicine, Aarhus University, Aarhus, Denmark;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1023\/A:1025601304345"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/j.amjmed.2006.05.009"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00095.2008"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/j.mce.2013.11.005"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.1.F29"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.107.095265"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/19.17.4688"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1677\/joe.0.1170397"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/j.febslet.2009.04.032"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.16-11-03620.1996"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M111880200"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1677\/JOE-09-0066"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00368.2014"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1096\/fj.10-163428"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1016\/j.juro.2007.07.123"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00534.2010"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0070926"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1095\/biolreprod.103.019927"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00950.2006"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00741.2010"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1007\/s00345-011-0674-3"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M110.207878"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1210\/endo.138.3.4979"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.5049\/EBP.2009.7.1.1"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.111.175174"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00199.2010"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009111190"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1007\/978-3-540-79885-9_6"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00291.2004"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00158.2005"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.4.1013"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00024.2001"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1172\/JCI649"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1677\/joe.0.1240277"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1038\/nrendo.2011.122"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1016\/j.yfrne.2007.08.005"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1998.274.1.R187"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1152\/jappl.2001.91.4.1893"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1152\/ajplung.00023.2012"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-59745-352-3_2"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1981.241.4.F403"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2005.08.226"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0603339103"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1016\/S1550-8579(05)80052-X"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1007\/s10157-013-0789-5"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1210\/jc.2011-0426"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00685.2014","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T21:20:31Z","timestamp":1567977631000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00685.2014"}},"issued":{"date-parts":[[2015,8,15]]},"references-count":46,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2015,8,15]]}},"alternative-id":["10.1152\/ajprenal.00685.2014"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00685.2014","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2015,8,15]]}},{"indexed":{"date-parts":[[2026,1,8]],"date-time":"2026-01-08T05:02:06Z","timestamp":1767848526239,"version":"3.49.0"},"reference-count":39,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2011,9]]},"abstract":"<jats:p>The renal extracellular 2\u2032,3\u2032-cAMP-adenosine and 3\u2032,5\u2032-cAMP-adenosine pathways (extracellular cAMPs\u2192AMPs\u2192adenosine) may contribute to renal adenosine production. Because mouse kidneys provide opportunities to investigate renal adenosine production in genetically modified kidneys, it is important to determine whether mouse kidneys express these cAMP-adenosine pathways. We administered (renal artery) 2\u2032,3\u2032-cAMP and 3\u2032,5\u2032-cAMP to isolated, perfused mouse kidneys and measured renal venous secretion rates of 2\u2032,3\u2032-cAMP, 3\u2032,5\u2032-cAMP, 2\u2032-AMP, 3\u2032-AMP, 5\u2032-AMP, adenosine, and inosine. Arterial infusions of 2\u2032,3\u2032-cAMP increased ( P &lt; 0.0001) the mean venous secretion of 2\u2032-AMP (390-fold), 3\u2032-AMP (497-fold), adenosine (18-fold), and inosine (adenosine metabolite; 7-fold), but they did not alter 5\u2032-AMP secretion. Infusions of 3\u2032,5\u2032-cAMP did not affect venous secretion of 2\u2032-AMP or 3\u2032-AMP, but they increased ( P &lt; 0.0001) secretion of 5\u2032-AMP (5-fold), adenosine (17-fold), and inosine (6-fold). Energy depletion (metabolic inhibitors) increased the secretion of 2\u2032,3\u2032-cAMP (8-fold, P = 0.0081), 2\u2032-AMP (4-fold, P = 0.0028), 3\u2032-AMP (4-fold, P = 0.0270), 5\u2032-AMP (3-fold, P = 0.0662), adenosine (2-fold, P = 0.0317), and inosine (7-fold, P = 0.0071), but it did not increase 3\u2032,5\u2032-cAMP secretion. The 2\u2032,3\u2032-cAMP-adenosine pathway was quantitatively similar in CD73 \u2212\/\u2212 vs. +\/+ kidneys. However, 3\u2032,5\u2032-cAMP induced a 6.7-fold greater increase in 5\u2032-AMP, an attenuated increase (61% reduction) in inosine and a similar increase in adenosine in CD73 \u2212\/\u2212 vs. CD73 +\/+ kidneys. In mouse kidneys, 1) 2\u2032,3\u2032-cAMP and 3\u2032,5\u2032-cAMP are metabolized to their corresponding AMPs, which are subsequently metabolized to adenosine; 2) energy depletion activates the 2\u2032,3\u2032-cAMP-adenosine, but not the 3\u2032,5\u2032-cAMP-adenosine, pathway; and 3) although CD73 is involved in the 3\u2032,5\u2032-AMP-adenosine pathway, alternative pathways of 5\u2032-AMP metabolism and reduced metabolism of adenosine to inosine compensate for life-long deficiency of CD73.<\/jats:p>","DOI":"10.1152\/ajprenal.00094.2011","type":"journal-article","created":{"date-parts":[[2011,6,9]],"date-time":"2011-06-09T03:32:54Z","timestamp":1307590374000},"page":"F565-F573","source":"Crossref","is-referenced-by-count":23,"title":["Extracellular cAMP-adenosine pathways in the mouse kidney"],"prefix":"10.1152","volume":"301","author":[{"given":"Edwin K.","family":"Jackson","sequence":"first","affiliation":[{"name":"Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania"}]},{"given":"Jin","family":"Ren","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania"}]},{"given":"Dongmei","family":"Cheng","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania"}]},{"given":"Zaichuan","family":"Mi","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00006.2009"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI21851"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0707648"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1021\/ac60052a025"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbabio.2005.11.005"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.31.1.296"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.36.3.337"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.37.4.1095"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.110.166371"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.35.1.262"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.28.5.765"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1053\/j.gastro.2008.01.030"},{"key":"B13","doi-asserted-by":"crossref","first-page":"23","DOI":"10.1016\/S0022-3565(24)38864-0","volume":"295","author":"Jackson EK","year":"2000","journal-title":"J Pharmacol Exp Ther"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.106.112748"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.106.119164"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.66.032102.111604"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.110.152454"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M109.053876"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.106.119057"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.106.101360"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/0006-291X(67)90510-4"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/0020-711X(87)90130-3"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1007\/BF02138128"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1016\/0003-9861(68)90351-2"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1016\/S0926-6593(65)80227-2"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/0024-3205(94)00846-9"},{"key":"B27","doi-asserted-by":"crossref","first-page":"926","DOI":"10.1016\/S0022-3565(24)37882-6","volume":"287","author":"Mi Z","year":"1998","journal-title":"J Pharmacol Exp Ther"},{"key":"B28","doi-asserted-by":"crossref","first-page":"728","DOI":"10.1016\/S0022-3565(25)09492-3","volume":"273","author":"Mi Z","year":"1995","journal-title":"J Pharmacol Exp Ther"},{"key":"B29","doi-asserted-by":"crossref","first-page":"1321","DOI":"10.1016\/S0022-3565(25)39381-X","volume":"266","author":"Oellerich WF","year":"1993","journal-title":"J Pharmacol Exp Ther"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00073.2007"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1021\/ac101975k"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1097\/TP.0b013e3182003d9b"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2010.06.107"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.108.146712"},{"key":"B35","first-page":"235","volume":"4","author":"Sprinkle TJ","year":"1989","journal-title":"Crit Rev Neurobiol"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00031.2005"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-4159.1988.tb02461.x"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.109.204529"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1002\/9780470032244.ch10"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00094.2011","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,3,6]],"date-time":"2025-03-06T01:38:41Z","timestamp":1741225121000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00094.2011"}},"issued":{"date-parts":[[2011,9]]},"references-count":39,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2011,9]]}},"alternative-id":["10.1152\/ajprenal.00094.2011"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00094.2011","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2011,9]]}},{"indexed":{"date-parts":[[2026,1,8]],"date-time":"2026-01-08T10:55:53Z","timestamp":1767869753481,"version":"3.49.0"},"reference-count":48,"publisher":"American Physiological Society","issue":"11","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,12,1]]},"abstract":"<jats:p> Diabetic nephropathy (DN) is a leading cause of end-stage renal disease (ESRD). The inhibitors of renin-angiotensin-aldosterone system (RAAS) can alleviate some of the symptoms of DN but fail to stop the progression to ESRD. Our previous studies demonstrate renoprotective action of nitro-oleic acid (OA-NO<jats:sub>2<\/jats:sub>) in several rodent models of renal disease. Here we examined the therapeutic potential and the underlying mechanism of combination of losartan and OA-NO<jats:sub>2<\/jats:sub> in db\/db mice. OA-NO<jats:sub>2<\/jats:sub> was infused at 5 mg\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7day<jats:sup>\u22121<\/jats:sup> via osmotic minipump, and losartan was incorporated into diet at 10 mg\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7day<jats:sup>\u22121<\/jats:sup>, each administered alone or in combination for 2 wk. Diabetic db\/db mice developed progressive albuminuria and glomerulosclerosis, accompanied by podocytes loss, increased indexes of renal fibrosis, oxidative stress, and inflammation. Treatment of the diabetic mice with OA-NO<jats:sub>2<\/jats:sub> or losartan alone moderately ameliorated kidney injury; however, the combined treatment remarkably reduced albuminuria, restored glomerular filtration barrier structure, and attenuated glomerulosclerosis, accompanied with significant suppression of renal oxidative stress and inflammation. These data demonstrate that combination of losartan and OA-NO<jats:sub>2<\/jats:sub> effectively reverses renal injury in DN. <\/jats:p>","DOI":"10.1152\/ajprenal.00157.2013","type":"journal-article","created":{"date-parts":[[2013,8,15]],"date-time":"2013-08-15T08:07:46Z","timestamp":1376554066000},"page":"F1555-F1562","source":"Crossref","is-referenced-by-count":38,"title":["Combined losartan and nitro-oleic acid remarkably improves diabetic nephropathy in mice"],"prefix":"10.1152","volume":"305","author":[{"given":"Ying","family":"Liu","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, University of Utah and Salt Lake Veterans Affairs Medical Center, Salt Lake City, Utah;"}]},{"given":"Zhanjun","family":"Jia","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Utah and Salt Lake Veterans Affairs Medical Center, Salt Lake City, Utah;"}]},{"given":"Shanshan","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Utah and Salt Lake Veterans Affairs Medical Center, Salt Lake City, Utah;"}]},{"given":"Maicy","family":"Downton","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Utah and Salt Lake Veterans Affairs Medical Center, Salt Lake City, Utah;"}]},{"given":"Gang","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Utah and Salt Lake Veterans Affairs Medical Center, Salt Lake City, Utah;"}]},{"given":"Yaomin","family":"Du","sequence":"additional","affiliation":[{"name":"Guangdong Provincial People's Hospital and Guangdong Academy of Medical Sciences, Guangzhou, China; and"}]},{"given":"Tianxin","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Utah and Salt Lake Veterans Affairs Medical Center, Salt Lake City, Utah;"},{"name":"Institute of Hypertension, Sun Yat-sen University School of Medicine, Guangzhou, China"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90449.2008"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00880.x"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1289\/ehp.94102s1053"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M504212200"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/j.freeradbiomed.2008.11.021"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa011161"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1038\/414813a"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2249.1991.tb05806.x"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(98)01346-4"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M603357200"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.107.092296"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2010.22"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M510595200"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000034509.14906.AE"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.2337\/db08-0057"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.2174\/157339908783502361"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.R800004200"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/0952-7915(92)90124-W"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/j.tice.2003.08.002"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/j.reprotox.2003.10.001"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1991.308"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M109.064873"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1016\/j.coph.2009.11.003"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1016\/j.freeradbiomed.2009.10.046"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000077412.07578.44"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa011303"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1155\/2012\/146154"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90236.2008"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.4239\/wjd.v3.i1.7"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.2337\/diab.42.3.450"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.09918.x"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(99)70182-4"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(99)70035-1"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M109.091512"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0408384102"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00028.2010"},{"key":"B37","first-page":"17","volume":"4","author":"Seibert K","year":"1994","journal-title":"Receptor"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.91.25.12013"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000410"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1007\/s001250051241"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000054498.83125.90"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00261.2007"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1155\/2010\/601562"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00439.2009"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1042\/BJ20090339"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0501744102"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.110.218404"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002572"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00157.2013","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T23:50:15Z","timestamp":1567986615000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00157.2013"}},"issued":{"date-parts":[[2013,12,1]]},"references-count":48,"journal-issue":{"issue":"11","published-print":{"date-parts":[[2013,12,1]]}},"alternative-id":["10.1152\/ajprenal.00157.2013"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00157.2013","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2013,12,1]]}},{"indexed":{"date-parts":[[2026,1,9]],"date-time":"2026-01-09T01:32:45Z","timestamp":1767922365193,"version":"3.49.0"},"reference-count":33,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2001,3,1]]},"abstract":"<jats:p>Cyclooxygenase-2 (COX-2) is expressed in macula densa (MD) and surrounding cortical thick ascending limb of the loop of Henle (cTALH) and is involved in regulation of renin production. We and others have previously found that selective COX-2 inhibitors can inhibit renal renin production (Cheng HF, Wang JL, Zhang MZ, Miyazaki Y, Ichikawa I, McKanna JA, and Harris RC. J Clin Invest 103: 953\u2013961, 1999; Harding P, Sigmon DH, Alfie ME, Huang PL, Fishman MC, Beierwaltes WH, and Carretero OA. Hypertension 29: 297\u2013302, 1997; Traynor TR, Smart A, Briggs JP, and Schnermann J. Am J Physiol Renal Physiol 277: F706\u2013F710, 1999; Wang JL, Cheng HF, and Harris RC. Hypertension 34: 96\u2013101, 1999). In the present studies, we utilized mice with genetic deletions of the COX-2 gene in order to investigate further the potential role of COX-2 in mediation of the renin-angiotensin system (RAS). Age-matched wild-type (+\/+), heterozygotes (+\/\u2212), and homozygous null mice (\u2212\/\u2212) were administered the angiotensin-converting enzyme inhibitor (ACEI), captopril, for 7 days. ACEI failed to significantly increase plasma renin activity, renal renin mRNA expression, and renal renin activity in (\u2212\/\u2212) mice. ACEI increased the number of cells expressing immunoreactive renin in the (+\/+) mice both by inducing more juxtaglomerular cells to express immunoreactive renin and by recruiting additional renin-expressing cells in the more proximal afferent arteriole. In contrast, there was minimal recruitment of renin-expressing cells in the more proximal afferent arteriole of the \u2212\/\u2212 mice. In summary, these results indicate that ACEI-mediated increases in renal renin production were defective in COX-2 knockout (K\/O) mice and provide further indication that MD COX-2 is an important mediator of the renin-angiotensin system.<\/jats:p>","DOI":"10.1152\/ajprenal.2001.280.3.f449","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T13:15:32Z","timestamp":1514034932000},"page":"F449-F456","source":"Crossref","is-referenced-by-count":76,"title":["Genetic deletion of COX-2 prevents increased renin expression in response to ACE inhibition"],"prefix":"10.1152","volume":"280","author":[{"given":"Hui-Fang","family":"Cheng","sequence":"first","affiliation":[{"name":"George M. O'Brien Kidney and Urologic Diseases Center and Divisionof Nephrology, Department of Medicine and"}]},{"given":"Jun-Ling","family":"Wang","sequence":"additional","affiliation":[{"name":"George M. O'Brien Kidney and Urologic Diseases Center and Divisionof Nephrology, Department of Medicine and"}]},{"given":"Ming-Zhi","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Cell Biology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232"}]},{"given":"Su-Wan","family":"Wang","sequence":"additional","affiliation":[{"name":"George M. O'Brien Kidney and Urologic Diseases Center and Divisionof Nephrology, Department of Medicine and"}]},{"given":"James. A.","family":"McKanna","sequence":"additional","affiliation":[{"name":"Department of Cell Biology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232"}]},{"given":"Raymond C.","family":"Harris","sequence":"additional","affiliation":[{"name":"George M. O'Brien Kidney and Urologic Diseases Center and Divisionof Nephrology, Department of Medicine and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.18.6.763"},{"key":"B2","doi-asserted-by":"crossref","first-page":"343A","DOI":"10.1681\/ASN.V1071566","volume":"10","author":"Cheng HF","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1172\/JCI5505"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/378406a0"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1982.243.6.F537"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.259.4.F660"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1988.254.6.F900"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1988.254.4.F582"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.265.4.F578"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1990.70.4.1067"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.29.1.297"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117620"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.31.1.201"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1989.102"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.449"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.3.F659"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/S0085-2538(15)46757-2"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1984.246.6.F811"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118988"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(95)90125-6"},{"key":"B21","first-page":"S39","volume":"32","author":"Persson AEG","year":"1991","journal-title":"Kidney Int"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1007\/BF00584628"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1007\/s004240050379"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1978.235.5.F451"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1007\/BF01716726"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1007\/BF00493286"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.5.F706"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.34.1.96"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/0090-6980(77)90287-8"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.5.F819"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.3.F481"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.26.15280"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.273.6.F994"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.2001.280.3.F449","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:42:19Z","timestamp":1660189339000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.2001.280.3.F449"}},"issued":{"date-parts":[[2001,3,1]]},"references-count":33,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2001,3,1]]}},"alternative-id":["10.1152\/ajprenal.2001.280.3.F449"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.2001.280.3.f449","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2001,3,1]]}},{"indexed":{"date-parts":[[2026,1,9]],"date-time":"2026-01-09T22:28:53Z","timestamp":1767997733344,"version":"3.49.0"},"reference-count":43,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2011,11]]},"abstract":"<jats:p> Matricellular proteins in the kidney have been associated with the development of tubulointerstitial fibrogenesis and the progression of renal disease. This study investigated potential antifibrotic effects of the cytokine oncostatin M (OSM) in human proximal tubule cells (PTC), particularly with regard to inhibition of profibrotic events initiated by TGF-\u03b21. In human PTC, OSM diminished transforming growth factor (TGF)-\u03b21-induced expression of the transcriptional epithelial-mesenchymal transition mediator FoxC2. Furthermore, exposure to OSM attenuated basal and TGF-\u03b21-induced expression of the matricellular proteins SPARC, TSP-1, TNC, and CTGF regardless of the sequence of ligand administration. OSM was shown to result in rapid and sustained phosphorylation of both Stat1 and Stat3 and also in transient phosphorylation of Smad2\/3 in contrast to TGF-\u03b21, which demonstrated a gradually building phosphorylation of Smad2\/3 and a brief phosphorylation of Smad1\/5\/8. Utilizing receptor-blocking molecules, we found the inhibitory effect of OSM on TGF-\u03b21-induced CTGF mRNA expression occurs independently of Smad2\/3 signaling and present evidence that this effect may be partially driven by OSM receptor-mediated Stat1 and\/or Stat3 signaling pathways, thereby providing a mechanism whereby OSM can contribute to tubulointerstitial protection. <\/jats:p>","DOI":"10.1152\/ajprenal.00123.2011","type":"journal-article","created":{"date-parts":[[2011,8,4]],"date-time":"2011-08-04T00:24:58Z","timestamp":1312417498000},"page":"F1014-F1025","source":"Crossref","is-referenced-by-count":32,"title":["Oncostatin M is a novel inhibitor of TGF-\u03b21-induced matricellular protein expression"],"prefix":"10.1152","volume":"301","author":[{"given":"Rita","family":"Sark\u00f6zi","sequence":"first","affiliation":[{"name":"Department of Internal Medicine IV, Nephrology and Hypertension, Innsbruck Medical University, Innsbruck;"}]},{"given":"Christine","family":"Hauser","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine IV, Nephrology and Hypertension, Innsbruck Medical University, Innsbruck;"}]},{"given":"Susie-Jane","family":"Noppert","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine IV, Nephrology and Hypertension, Innsbruck Medical University, Innsbruck;"}]},{"given":"Andreas","family":"Kronbichler","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine IV, Nephrology and Hypertension, Innsbruck Medical University, Innsbruck;"}]},{"given":"Markus","family":"Pirklbauer","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine IV, Nephrology and Hypertension, Innsbruck Medical University, Innsbruck;"}]},{"given":"Viktoria Maria","family":"Haller","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine IV, Nephrology and Hypertension, Innsbruck Medical University, Innsbruck;"}]},{"given":"Johannes","family":"Grillari","sequence":"additional","affiliation":[{"name":"Aging and Immortalization Research, Institute of Applied Microbiology, Department of Biotechnology, BOKU-University of Natural Resources and Applied Life Sciences, and"},{"name":"Evercyte, Vienna, Austria"}]},{"given":"Regina","family":"Grillari-Voglauer","sequence":"additional","affiliation":[{"name":"Aging and Immortalization Research, Institute of Applied Microbiology, Department of Biotechnology, BOKU-University of Natural Resources and Applied Life Sciences, and"},{"name":"Evercyte, Vienna, Austria"}]},{"given":"Gert","family":"Mayer","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine IV, Nephrology and Hypertension, Innsbruck Medical University, Innsbruck;"}]},{"given":"Herbert","family":"Schramek","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine IV, Nephrology and Hypertension, Innsbruck Medical University, Innsbruck;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1007\/s12079-009-0069-z"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000033611.79556.AE"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/j.biocel.2008.07.025"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1006\/excr.2001.5364"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejca.2005.02.014"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1002\/biof.30"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1007\/s10555-010-9221-8"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.01192-08"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1354\/vp.37-4-328"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00007.2002"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1016\/S1097-2765(03)00386-1"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/21.7.1743"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1096\/fj.06-6713com"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90521.2008"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfn399"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfg159"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1124\/mol.62.1.65"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.1998.00820.x"},{"key":"B19","first-page":"423","volume":"5","author":"Jyo Y","year":"1997","journal-title":"Exp Nephrol"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00528.2009"},{"key":"B21","first-page":"4752","volume":"58","author":"Liu X","year":"1998","journal-title":"Cancer Res"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008121226"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0703900104"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1007\/s12079-009-0038-6"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000102479.92582.43"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1159\/000262316"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.520"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00130.2007"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/j.biocel.2007.01.006"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.6"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M313408200"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1016\/j.canlet.2008.03.027"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1038\/nrm2297"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1016\/j.yexmp.2005.01.010"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000054498.83125.90"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1159\/000188943"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00776.x"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90405.2008"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)62533-3"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002722"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000130565.69170.85"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1038\/nchembio.2007.54"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1016\/j.cellbi.2004.09.003"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00123.2011","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:12:57Z","timestamp":1567973577000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00123.2011"}},"issued":{"date-parts":[[2011,11]]},"references-count":43,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2011,11]]}},"alternative-id":["10.1152\/ajprenal.00123.2011"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00123.2011","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2011,11]]}},{"indexed":{"date-parts":[[2026,2,26]],"date-time":"2026-02-26T21:48:56Z","timestamp":1772142536588,"version":"3.50.1"},"reference-count":33,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2009,9]]},"abstract":"<jats:p> GLUT9 (SLC2A9) is a newly described urate transporter whose function, characteristics, and localization have just started to be elucidated. Some transport properties of human GLUT9 have been studied in the Xenopus laevis oocyte expression system, but the type of transport (uniport, coupled transport system, stoichiometry \u2026 .) is still largely unknown. We used the same experimental system to characterize in more detail the transport properties of mouse GLUT9, its sensitivity to several uricosuric drugs, and the specificities of two splice variants, mGLUT9a and mGLUT9b. [<jats:sup>14<\/jats:sup>C]urate uptake measurements show that both splice variants are high-capacity urate transporters and have a K<jats:sub>m<\/jats:sub> of \u223c650 \u03bcM. The well-known uricosuric agents benzbromarone (500 \u03bcM) and losartan (1 mM) inhibit GLUT9-mediated urate uptake by 90 and 50%, respectively. Surprisingly, phloretin, a glucose-transporter blocker, inhibits [<jats:sup>14<\/jats:sup>C]urate uptake by \u223c50% at 1 mM. Electrophysiological measurements suggest that urate transport by mouse GLUT9 is electrogenic and voltage dependent, but independent of the Na<jats:sup>+<\/jats:sup> and Cl<jats:sup>\u2212<\/jats:sup> transmembrane gradients. Taken together, our results suggest that GLUT9 works as a urate (anion) uniporter. Finally, we show by RT-PCR performed on RNA from mouse kidney microdissected tubules that GLUT9a is expressed at low levels in proximal tubules, while GLUT9b is specifically expressed in distal convoluted and connecting tubules. Expression of mouse GLUT9 in the kidney differs from that of human GLUT9, which could account for species differences in urate handling. <\/jats:p>","DOI":"10.1152\/ajprenal.00139.2009","type":"journal-article","created":{"date-parts":[[2009,7,8]],"date-time":"2009-07-08T21:51:52Z","timestamp":1247089912000},"page":"F612-F619","source":"Crossref","is-referenced-by-count":105,"title":["Mouse GLUT9: evidences for a urate uniporter"],"prefix":"10.1152","volume":"297","author":[{"given":"St\u00e9phanie","family":"Bibert","sequence":"first","affiliation":[]},{"given":"Solange Kharoubi","family":"Hess","sequence":"additional","affiliation":[]},{"given":"Dmitri","family":"Firsov","sequence":"additional","affiliation":[]},{"given":"Bernard","family":"Thorens","sequence":"additional","affiliation":[]},{"given":"K\u00e4thi","family":"Geering","sequence":"additional","affiliation":[]},{"given":"Jean-Daniel","family":"Horisberger","sequence":"additional","affiliation":[]},{"given":"Olivier","family":"Bonny","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.C800156200"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M312226200"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1016\/S0955-0674(99)80072-6"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1978.sp012311"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.2337\/dc08-0349"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.268"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1210\/en.2003-1264"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pmed.0050197"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(08)61343-4"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1172\/JCI107323"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1038\/ng.107"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1038\/nature742"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra0800885"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.133.6.1193"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1152\/physiol.00039.2004"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2001.013201"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000107560.80107.19"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1210\/me.2005-0010"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pgen.0030194"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1080\/09687680701298143"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1038\/nature04516"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M405674200"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1097\/01.mnh.0000232876.04975.33"},{"key":"R24","doi-asserted-by":"crossref","unstructured":"Roch-Ramel F, Guisan B. Renal transport of urate in humans. News Physiol Sci 14: 80\u201384, 1999.","DOI":"10.1152\/physiologyonline.1999.14.2.80"},{"key":"R25","unstructured":"Roch-Ramel F, Peters G. Urinary excretion of uric acid in nonhuman mammalian species. In: Uric Acid, edited by Kelley WN and Weiner IM. Berlin: Springer-Verlag, 1978, p. 211\u2013255."},{"key":"R26","unstructured":"Roch-Ramel F, Weiner IM. Inhibition of urate excretion by pyrazinoate: a micropuncture study. Am J Physiol 229: 1604\u20131608, 1975."},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00439.2004"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0001948"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(88)90051-7"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-5793(02)03058-2"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1038\/ng.106"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1016\/j.ajhg.2007.11.001"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1979.237.2.F85"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00139.2009","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:09:51Z","timestamp":1567973391000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00139.2009"}},"issued":{"date-parts":[[2009,9]]},"references-count":33,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2009,9]]}},"alternative-id":["10.1152\/ajprenal.00139.2009"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00139.2009","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2009,9]]}},{"indexed":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T05:54:58Z","timestamp":1772171698685,"version":"3.50.1"},"reference-count":43,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2008,8]]},"abstract":"<jats:p>Urinary tract obstruction impairs renal function and is often associated with a urinary acidification defect caused by diminished net H<jats:sup>+<\/jats:sup>secretion and\/or HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup>reabsorption. To identify the molecular mechanisms of these defects, protein expression of key acid-base transporters were examined along the renal nephron and collecting duct of kidneys from rats subjected to 24-h bilateral ureteral obstruction (BUO), 4 days after release of BUO (BUO-R), or BUO-R rats with experimentally induced metabolic acidosis (BUO-A). Semiquantitative immunoblotting revealed that BUO caused a significant reduction in the expression of the type 3 Na<jats:sup>+<\/jats:sup>\/H<jats:sup>+<\/jats:sup>exchanger (NHE3) in the cortex (21 \u00b1 4%), electrogenic Na<jats:sup>+<\/jats:sup>\/HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup>cotransporter (NBC1; 71 \u00b1 5%), type 1 bumetanide-sensitive Na<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-2Cl<jats:sup>\u2212<\/jats:sup>cotransporter (NKCC2; 3 \u00b1 1%), electroneutral Na<jats:sup>+<\/jats:sup>\/HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup>cotransporter (NBCn1; 46 \u00b1 7%), and anion exchanger (pendrin; 87 \u00b1 2%). The expression of H<jats:sup>+<\/jats:sup>-ATPase increased in the inner medullary collecting duct (152 \u00b1 13%). These changes were confirmed by immunocytochemistry. In BUO-R rats, there was a persistent downregulation of all the acid-base transporters including H<jats:sup>+<\/jats:sup>-ATPase. Two days of NH<jats:sub>4<\/jats:sub>Cl loading reduced plasma pH and HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup>levels in BUO-A rats. The results demonstrate that the expression of multiple renal acid-base transporters are markedly altered in response to BUO, which may be responsible for development of metabolic acidosis and contribute to the urinary acidification defect after release of the obstruction.<\/jats:p>","DOI":"10.1152\/ajprenal.00425.2007","type":"journal-article","created":{"date-parts":[[2008,5,29]],"date-time":"2008-05-29T00:44:26Z","timestamp":1212021866000},"page":"F497-F506","source":"Crossref","is-referenced-by-count":23,"title":["Ureter obstruction alters expression of renal acid-base transport proteins in rat kidney"],"prefix":"10.1152","volume":"295","author":[{"given":"Guixian","family":"Wang","sequence":"first","affiliation":[]},{"given":"Chunling","family":"Li","sequence":"additional","affiliation":[]},{"given":"Soo Wan","family":"Kim","sequence":"additional","affiliation":[]},{"given":"Troels","family":"Ring","sequence":"additional","affiliation":[]},{"given":"Jianguo","family":"Wen","sequence":"additional","affiliation":[]},{"given":"Jens Christian","family":"Djurhuus","sequence":"additional","affiliation":[]},{"given":"Weidong","family":"Wang","sequence":"additional","affiliation":[]},{"given":"S\u00f8ren","family":"Nielsen","sequence":"additional","affiliation":[]},{"given":"J\u00f8rgen","family":"Fr\u00f8ki\u00e6r","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.86.14.5429"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM198102123040701"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1016\/0002-9343(73)90228-3"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.81.1.29"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1172\/JCI113833"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1172\/JCI109243"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1038\/35014615"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M406591200"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.3.F619"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00254.2002"},{"key":"R11","unstructured":"Fr\u00f8ki\u00e6r J, Zeidel ML.Urinary tract obstruction. In:Brenner & Rector's, The Kidney, edited by Brenner BM. Philadelphia, PA: Saunders, 2008, p. 1239\u20131264."},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.270.4.F657"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M607041200"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1988.255.1.F78"},{"key":"R15","unstructured":"Hamm LL, Nakhoul NL.Renal acidification. In:Brenner & Rector's The Kidney, edited by Brenner BM. Philadelphia, PA: Saunders, 2008, p. 248\u2013279."},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004080667"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1038\/15440"},{"key":"R18","doi-asserted-by":"crossref","unstructured":"Kim GH, Ecelbarger C, Knepper MA, Packer RK.Regulation of thick ascending limb ion transporter abundance in response to altered acid\/base intake.J Am Soc Nephrol10: 935\u2013942, 1999.","DOI":"10.1681\/ASN.V105935"},{"key":"R19","doi-asserted-by":"crossref","unstructured":"Kim J, Kim YH, Cha JH, Tisher CC, Madsen KM.Intercalated cell subtypes in connecting tubule and cortical collecting duct of rat and mouse.J Am Soc Nephrol10: 1\u201312, 1999.","DOI":"10.1681\/ASN.V1011"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00176.2003"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00037.2002"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.2169\/internalmedicine.39.355"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00104.2001"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00453.2003"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.281.1.F163"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00170.2003"},{"key":"R27","doi-asserted-by":"crossref","unstructured":"Maunsbach AB, Vorum H, Kwon TH, Nielsen S, Simonsen B, Choi I, Schmitt BM, Boron WF, Aalkjaer C.Immunoelectron microscopic localization of the electrogenic Na\/HCO3cotransporter in rat and ambystoma kidney.J Am Soc Nephrol11: 2179\u20132189, 2000.","DOI":"10.1681\/ASN.V11122179"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1097\/00008480-200404000-00014"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.275.6.F885"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2003.046474"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.261.3.F365"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1986.123"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000023430.92674.E5"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.071516798"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1038\/969"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.44"},{"key":"R37","doi-asserted-by":"crossref","unstructured":"Thirakomen K, Kozlov N, Arruda JA, Kurtzman NA.Renal hydrogen ion secretion after release of unilateral ureteral obstruction.Am J Physiol231: 1233\u20131239, 1976.","DOI":"10.1152\/ajplegacy.1976.231.4.1233"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(01)61987-6"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.2000.279.3.H901"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1097\/01.mnh.0000168390.04520.06"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1975.43"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.2.F298"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.69.040705.142215"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00425.2007","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,9,11]],"date-time":"2021-09-11T07:17:34Z","timestamp":1631344654000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00425.2007"}},"issued":{"date-parts":[[2008,8]]},"references-count":43,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2008,8]]}},"alternative-id":["10.1152\/ajprenal.00425.2007"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00425.2007","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2008,8]]}},{"indexed":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T12:40:42Z","timestamp":1772196042986,"version":"3.50.1"},"reference-count":30,"publisher":"American Physiological Society","issue":"6","funder":[{"name":"None"},{"name":"None"},{"name":"None"},{"name":"None"},{"name":"None"},{"name":"None"},{"name":"None"},{"name":"None"},{"name":"None"}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2023,12,1]]},"abstract":"<jats:p> Aging rats can be useful models for studying the natural progression of age-related lower urinary tract dysfunctions, for which impaired nitric oxide-mediated transmitter function is likely to be an important mechanism. <\/jats:p>","DOI":"10.1152\/ajprenal.00092.2023","type":"journal-article","created":{"date-parts":[[2023,9,28]],"date-time":"2023-09-28T08:00:22Z","timestamp":1695888022000},"page":"F750-F756","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":3,"title":["Impaired nitric oxide mechanisms underlying lower urinary tract dysfunction in aging rats"],"prefix":"10.1152","volume":"325","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6056-3820","authenticated-orcid":false,"given":"Daisuke","family":"Gotoh","sequence":"first","affiliation":[{"name":"Department of Urology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, United States"},{"name":"Department of Urology, Nara Medical University, Kashihara, Japan"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2870-0466","authenticated-orcid":false,"given":"Kazumasa","family":"Torimoto","sequence":"additional","affiliation":[{"name":"Department of Urology, Nara Medical University, Kashihara, Japan"}]},{"given":"Kenta","family":"Onishi","sequence":"additional","affiliation":[{"name":"Department of Urology, Nara Medical University, Kashihara, Japan"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7142-5901","authenticated-orcid":false,"given":"Yosuke","family":"Morizawa","sequence":"additional","affiliation":[{"name":"Department of Urology, Nara Medical University, Kashihara, Japan"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9514-9964","authenticated-orcid":false,"given":"Shunta","family":"Hori","sequence":"additional","affiliation":[{"name":"Department of Urology, Nara Medical University, Kashihara, Japan"}]},{"given":"Yasushi","family":"Nakai","sequence":"additional","affiliation":[{"name":"Department of Urology, Nara Medical University, Kashihara, Japan"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9503-7356","authenticated-orcid":false,"given":"Makito","family":"Miyake","sequence":"additional","affiliation":[{"name":"Department of Urology, Nara Medical University, Kashihara, Japan"}]},{"given":"Kiyohide","family":"Fujimoto","sequence":"additional","affiliation":[{"name":"Department of Urology, Nara Medical University, Kashihara, Japan"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8070-1664","authenticated-orcid":false,"given":"Naoki","family":"Yoshimura","sequence":"additional","affiliation":[{"name":"Department of Urology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, United States"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM198901053200101"},{"key":"B2","first-page":"109","volume":"43","author":"Moncada S","year":"1991","journal-title":"Pharmacol Rev"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1046\/j.1464-410x.2000.00459.x"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2013.262410"},{"key":"B5","first-page":"253","volume":"45","author":"Anderson KE","year":"1993","journal-title":"Pharmacol Rev"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1002\/nau.20999"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1002\/nau.23481"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.14814\/phy2.14643"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/j.lfs.2021.119690"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1177\/1756287216675778"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1002\/nau.23372"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1002\/nau.23158"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1111\/luts.12272"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/j.lfs.2020.117537"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00450.2015"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00566.2019"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1002\/nau.23066"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/j.lfs.2021.120001"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1002\/nau.22849"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/j.juro.2016.05.104"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-018-20406-0"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00508.2011"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1016\/j.urology.2006.12.018"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1007\/s002400000135"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1016\/S0090-4295(99)80013-2"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1002\/(sici)1097-0045(19970915)33:1<1::aid-pros1>3.0.co;2-p"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1986.251.2.R250"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1111\/jth.15844"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00105.2022"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2013.262634"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00092.2023","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,11,21]],"date-time":"2023-11-21T15:54:59Z","timestamp":1700582099000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00092.2023"}},"issued":{"date-parts":[[2023,12,1]]},"references-count":30,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2023,12,1]]}},"alternative-id":["10.1152\/ajprenal.00092.2023"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00092.2023","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2023,12,1]]},"assertion":[{"value":"2023-04-13","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2023-09-25","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2023-09-25","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2023-11-21","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,2,21]],"date-time":"2026-02-21T06:58:21Z","timestamp":1771657101948,"version":"3.50.1"},"reference-count":32,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2004,12]]},"abstract":"<jats:p>Thiazide diuretics are specific inhibitors of the Na-Cl cotransporter in the distal convoluted tubule (DCT). In addition to producing diuresis and natriuresis, they have a hypocalciuric effect. Recently, two apical calcium channels have been identified, transient receptor potential vanilloid 5 (TRPV5) and TRPV6; both are expressed in the DCT. We studied the effects of thiazides on mouse renal calcium handling and renal gene expression of TRPV5 and TRPV6, as well as calbindin-D<jats:sub>28k<\/jats:sub>and calbindin-D<jats:sub>9k<\/jats:sub>, both of which are calcium transport facilitators located in the DCT. Upregulation of renal TRPV5 was found 4 h after intraperitoneal injection of chlorothiazide (CTZ) at both 25 and 50 mg\/kg, but not at 100 mg\/kg. Chronic treatment with CTZ at 25 mg\/kg twice daily for 3 days, with or without salt supplementation of 0.8% NaCl and 0.1% KCl in the drinking water, caused hypocalciuria, but the gene expression patterns were different. Without salt supplementation, mice developed volume contraction and there were no changes in gene expression. When volume contraction was prevented by salt supplementation, there was a significant increase in gene expression of TRPV5, calbindin-D<jats:sub>28k<\/jats:sub>, and calbindin-D<jats:sub>9k<\/jats:sub>. Salt supplementation alone also induced significant upregulation of TRPV5, TRPV6, and both calbindins. The upregulation of TRPV5 by CTZ and salt supplementation and salt alone was further confirmed with immunofluorescent staining studies. Our studies suggest that thiazides induce hypocalciuria through different mechanisms depending on volume status. With volume contraction, increased calcium reabsorption in the proximal tubule plays the major role. Without volume contraction, hypocalciuria is probably achieved through increased calcium reabsorption in the DCT by the activation of a transcellular calcium transport system and upregulation of apical calcium channel TRPV5, calbindin-D<jats:sub>28k<\/jats:sub>, and calbindin-D<jats:sub>9k<\/jats:sub>.<\/jats:p>","DOI":"10.1152\/ajprenal.00437.2003","type":"journal-article","created":{"date-parts":[[2004,7,21]],"date-time":"2004-07-21T01:11:09Z","timestamp":1090372269000},"page":"F1164-F1170","source":"Crossref","is-referenced-by-count":56,"title":["Effect of thiazide on renal gene expression of apical calcium channels and calbindins"],"prefix":"10.1152","volume":"287","author":[{"given":"Chien-Te","family":"Lee","sequence":"first","affiliation":[]},{"given":"Shuhua","family":"Shang","sequence":"additional","affiliation":[]},{"given":"Li-Wen","family":"Lai","sequence":"additional","affiliation":[]},{"given":"Kim-Chong","family":"Yong","sequence":"additional","affiliation":[]},{"given":"Yeong-Hau H.","family":"Lien","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1976.91"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1002\/jat.2550100509"},{"key":"R3","unstructured":"Costanzo LS.Mechanism of action of thiazide diuretics.Semin Nephrol8: 234\u2013241, 1988."},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1172\/JCI107800"},{"key":"R5","unstructured":"Costanzo LSand Weiner IM.Relationship between clearance of Ca and Na: effect of distal diuretics and PTH.Am J Physiol230: 67\u201373, 1976."},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1978.235.5.F492"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1172\/JCI107432"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(12)70272-X"},{"key":"R9","unstructured":"Friedman PAand Bushinsky DA.Diuretic effects on calcium metabolism.Semin Nephrol19: 551\u2013556, 1999."},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115878"},{"key":"R11","doi-asserted-by":"crossref","unstructured":"Hoenderop JG, Muller D, van der Kemp AW, Hartog A, Suzuki M, Ishibashi K, Imai M, Sweep F, Willems PH, Van Os CH, and Bindels RJ.Calcitriol controls the epithelial calcium channel in kidney.J Am Soc Nephrol12: 1342\u20131349, 2001.","DOI":"10.1681\/ASN.V1271342"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.64.081501.155921"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.13.8375"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1999.1059"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00670.x"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.426"},{"key":"R17","doi-asserted-by":"crossref","unstructured":"Massry SG, Coburn JW, Chapman LW, and Kleeman CR.Role of serum Ca, parathyroid hormone, and NaCl infusion on renal Ca and Na clearance.Am J Physiol214: 1403\u20131409, 1968.","DOI":"10.1152\/ajplegacy.1968.214.6.1403"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1016\/0026-0495(73)90264-3"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.261.1.F137"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00227.2002"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00128.x"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-003-1038-7"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000094081.78893.E8"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200103000-00008"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.32.22739"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.2000.80.1.277"},{"key":"R27","doi-asserted-by":"crossref","unstructured":"Rizzo M, Capasso G, Bleich M, Pica A, Grimaldi D, Bindels RJ, and Greger R.Effects of chronic metabolic acidosis on calbindin expression along the rat distal tubule.J Am Soc Nephrol11: 203\u2013210, 2000.","DOI":"10.1681\/ASN.V112203"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.261.1.F36"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200007000-00004"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.231474698"},{"key":"R31","doi-asserted-by":"crossref","unstructured":"Velazquez H.Thiazide diuretics.Renal Physiol10: 184\u2013197, 1987.","DOI":"10.1159\/000173129"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.2001.6121"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00437.2003","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,6,24]],"date-time":"2021-06-24T09:38:14Z","timestamp":1624527494000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00437.2003"}},"issued":{"date-parts":[[2004,12]]},"references-count":32,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2004,12]]}},"alternative-id":["10.1152\/ajprenal.00437.2003"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00437.2003","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2004,12]]}},{"indexed":{"date-parts":[[2026,2,21]],"date-time":"2026-02-21T08:03:11Z","timestamp":1771660991868,"version":"3.50.1"},"reference-count":44,"publisher":"American Physiological Society","issue":"5","funder":[{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)","doi-asserted-by":"publisher","award":["F30DK109605"],"award-info":[{"award-number":["F30DK109605"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2019,5,1]]},"abstract":"<jats:p> The proximal tubule (PT) is responsible for the majority of calcium reabsorption by the kidney. Most PT calcium transport appears to be passive, although the molecular facilitators have not been well established. Emerging evidence supports a major role for PT calcium transport in idiopathic hypercalciuria and the development of kidney stones. This review will cover recent developments in our understanding of PT calcium transport and the role of the PT in kidney stone formation. <\/jats:p>","DOI":"10.1152\/ajprenal.00519.2018","type":"journal-article","created":{"date-parts":[[2019,3,6]],"date-time":"2019-03-06T07:47:00Z","timestamp":1551858420000},"page":"F966-F969","source":"Crossref","is-referenced-by-count":11,"title":["Paracellular calcium transport in the proximal tubule and the formation of kidney stones"],"prefix":"10.1152","volume":"316","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7364-964X","authenticated-orcid":false,"given":"Joshua N.","family":"Curry","sequence":"first","affiliation":[{"name":"Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, Kansas"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1776-2533","authenticated-orcid":false,"given":"Alan S. L.","family":"Yu","sequence":"additional","affiliation":[{"name":"Jared Grantham Kidney Institute, University of Kansas Medical Center, Kansas City, Kansas"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajplegacy.1973.224.5.1143"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.00165"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1007\/BF01871104"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013101085"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00129.2018"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1172\/JCI107432"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.0021.2001"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1001\/jama.1939.02800410016004"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.e07-09-0973"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.141.7.1539"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.153.2.263"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200110122"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.257.4.F658"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.040113"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1086\/427887"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1146\/annurev-physiol-030212-183705"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/S0171-9335(99)80086-7"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfq006"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00071.2015"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1007\/s00018-012-0949-x"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014111067"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1984.247.5.F816"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.8.4296"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbamem.2010.07.014"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(06)68071-9"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1007\/BF00586037"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0912901107"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1172\/JCI111500"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1979.237.6.F415"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa020028"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1053\/gast.2001.21736"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1097\/00000658-193706000-00014"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1983.244.5.F461"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.060665"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1210\/jcem-61-5-825"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00342.2013"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1139\/y75-136"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM198003273021302"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1007\/BF00581759"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pgen.1002541"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00138.2006"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2017030295"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90404.2008"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.200810154"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00519.2018","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,24]],"date-time":"2019-09-24T00:45:33Z","timestamp":1569285933000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00519.2018"}},"issued":{"date-parts":[[2019,5,1]]},"references-count":44,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2019,5,1]]}},"alternative-id":["10.1152\/ajprenal.00519.2018"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00519.2018","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2019,5,1]]}},{"indexed":{"date-parts":[[2026,2,24]],"date-time":"2026-02-24T22:14:30Z","timestamp":1771971270631,"version":"3.50.1"},"reference-count":35,"publisher":"American Physiological Society","issue":"7","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2015,4,1]]},"abstract":"<jats:p>Angiotensin II (ANG II) increases thiazide-sensitive sodium-chloride cotransporter (NCC) activity both acutely and chronically. ANG II has been implicated as a switch that turns WNK4 from an inhibitor of NCC into an activator of NCC, and ANG II's effect on NCC appears to require WNK4. Chronically, ANG II stimulation of NCC results in an increase in total and phosphorylated NCC, but the role of NCC phosphorylation in acute ANG II actions is unclear. Here, using a mammalian cell model with robust native NCC activity, we corroborate the role that ANG II plays in WNK4 regulation and clarify the role of Ste20-related proline alanine-rich kinase (SPAK)-induced NCC phosphorylation in ANG II action. ANG II was noted to have a biphasic effect on NCC, with a peak increase in NCC activity in the physiologic range of 10<jats:sup>\u221211<\/jats:sup>M ANG II. This effect was apparent as early as 15 min and remained sustained through 120 min. These changes correlated with significant increases in NCC surface protein expression. Knockdown of WNK4 expression sharply attenuated the effect of ANG II. SPAK knockdown did not affect ANG II action at early time points (15 and 30 min), but it did attenuate the response at 60 min. Correspondingly, NCC phosphorylation did not increase at 15 or 30 min, but increased significantly at 60 min. We therefore conclude that within minutes of an increase in ANG II, NCC is rapidly trafficked to the cell surface in a phosphorylation-independent but WNK4-dependent manner. Then, after 60 min, ANG II induces SPAK-dependent phosphorylation of NCC.<\/jats:p>","DOI":"10.1152\/ajprenal.00465.2014","type":"journal-article","created":{"date-parts":[[2015,1,29]],"date-time":"2015-01-29T05:31:17Z","timestamp":1422509477000},"page":"F720-F727","source":"Crossref","is-referenced-by-count":26,"title":["Mechanisms of angiotensin II stimulation of NCC are time-dependent in mDCT15 cells"],"prefix":"10.1152","volume":"308","author":[{"given":"Benjamin","family":"Ko","sequence":"first","affiliation":[{"name":"Department of Medicine, University of Chicago, Chicago, Illinois;"}]},{"given":"Abinash","family":"Mistry","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Emory University, Atlanta, Georgia; and"}]},{"given":"Lauren","family":"Hanson","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Chicago, Chicago, Illinois;"}]},{"given":"Rickta","family":"Mallick","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Emory University, Atlanta, Georgia; and"}]},{"given":"Robert S.","family":"Hoover","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Emory University, Atlanta, Georgia; and"},{"name":"Atlanta Veteran's Administration Medical Center, Decatur, Georgia"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2011020132"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00121.2011"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000333"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1200947109"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0b013e32835571a4"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1001\/jama.289.19.2560"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.37.6.1458"},{"key":"B8","first-page":"468","volume":"26","author":"Freis EWI","year":"1957","journal-title":"Med Ann DC"},{"key":"B9","doi-asserted-by":"crossref","first-page":"17713","DOI":"10.1016\/S0021-9258(17)32499-7","volume":"269","author":"Gamba G","year":"1994","journal-title":"J Biol Chem"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00468.2005"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1007\/BF00581370"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2012.07.124"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.464"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.24.14552"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00139.2012"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00053.2013"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-011-1062-y"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1038\/ng1877"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00287.2012"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00016.2002"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M603773200"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.3.F374"},{"key":"B23","first-page":"657","volume":"123","author":"Ronzaud C","year":"2013","journal-title":"J Clin Invest"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M113.543710"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0813238106"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00064.2007"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1038\/ng0196-24"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2013.14"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M109.008185"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2010.02.096"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2010.290"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.270.1.F211"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.242735399"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1172\/JCI17443"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008121275"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00465.2014","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,4,27]],"date-time":"2022-04-27T22:21:32Z","timestamp":1651098092000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00465.2014"}},"issued":{"date-parts":[[2015,4,1]]},"references-count":35,"journal-issue":{"issue":"7","published-print":{"date-parts":[[2015,4,1]]}},"alternative-id":["10.1152\/ajprenal.00465.2014"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00465.2014","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2015,4,1]]}},{"indexed":{"date-parts":[[2026,3,2]],"date-time":"2026-03-02T14:32:00Z","timestamp":1772461920845,"version":"3.50.1"},"reference-count":48,"publisher":"American Physiological Society","issue":"5","funder":[{"DOI":"10.13039\/100000968","name":"American Heart Association","doi-asserted-by":"publisher","award":["POST903198"],"award-info":[{"award-number":["POST903198"]}],"id":[{"id":"10.13039\/100000968","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100017618","name":"HHS | NIH | NIDDK | Division of Diabetes, Endocrinology, and Metabolic Diseases","doi-asserted-by":"publisher","award":["R01DK119274"],"award-info":[{"award-number":["R01DK119274"]}],"id":[{"id":"10.13039\/100017618","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"HHS | NIH | National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["R01HL148597"],"award-info":[{"award-number":["R01HL148597"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"HHS | NIH | National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["R01HL149704"],"award-info":[{"award-number":["R01HL149704"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2022,11,1]]},"abstract":"<jats:p> Creation of an arteriovenous fistula (AVF) is the preferred approach for dialysis access, but some patients experience hand dysfunction after AVF creation. In this study, we provide a detailed metabolomic analysis of the limb muscle in a murine model of AVF. AVF creation resulted in metabolite changes associated with an energetic crisis and myosteatosis that associated with limb function. <\/jats:p>","DOI":"10.1152\/ajprenal.00156.2022","type":"journal-article","created":{"date-parts":[[2022,8,26]],"date-time":"2022-08-26T00:20:20Z","timestamp":1661473220000},"page":"F577-F589","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":6,"title":["Metabolomic profiling reveals muscle metabolic changes following iliac arteriovenous fistula creation in mice"],"prefix":"10.1152","volume":"323","author":[{"given":"Ram B.","family":"Khattri","sequence":"first","affiliation":[{"name":"Department of Applied Physiology and Kinesiology, University of Florida, Gainesville, Florida"}]},{"given":"Kyoungrae","family":"Kim","sequence":"additional","affiliation":[{"name":"Department of Applied Physiology and Kinesiology, University of Florida, Gainesville, Florida"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8957-5932","authenticated-orcid":false,"given":"Erik M.","family":"Anderson","sequence":"additional","affiliation":[{"name":"Division of Vascular Surgery and Endovascular Therapy, University of Florida, Gainesville, Florida"},{"name":"Malcom Randall Veterans Affairs Medical Center, Gainesville, Florida"}]},{"given":"Brian","family":"Fazzone","sequence":"additional","affiliation":[{"name":"Division of Vascular Surgery and Endovascular Therapy, University of Florida, Gainesville, Florida"},{"name":"Malcom Randall Veterans Affairs Medical Center, Gainesville, Florida"}]},{"given":"Kenneth C.","family":"Harland","sequence":"additional","affiliation":[{"name":"Division of Vascular Surgery and Endovascular Therapy, University of Florida, Gainesville, Florida"},{"name":"Malcom Randall Veterans Affairs Medical Center, Gainesville, Florida"}]},{"given":"Qiongyao","family":"Hu","sequence":"additional","affiliation":[{"name":"Division of Vascular Surgery and Endovascular Therapy, University of Florida, Gainesville, Florida"},{"name":"Malcom Randall Veterans Affairs Medical Center, Gainesville, Florida"}]},{"given":"Victoria R.","family":"Palzkill","sequence":"additional","affiliation":[{"name":"Department of Applied Physiology and Kinesiology, University of Florida, Gainesville, Florida"}]},{"given":"Tomas A.","family":"Cort","sequence":"additional","affiliation":[{"name":"Department of Applied Physiology and Kinesiology, University of Florida, Gainesville, Florida"}]},{"given":"Kerri A.","family":"O\u2019Malley","sequence":"additional","affiliation":[{"name":"Division of Vascular Surgery and Endovascular Therapy, University of Florida, Gainesville, Florida"},{"name":"Malcom Randall Veterans Affairs Medical Center, Gainesville, Florida"}]},{"given":"Scott A.","family":"Berceli","sequence":"additional","affiliation":[{"name":"Division of Vascular Surgery and Endovascular Therapy, University of Florida, Gainesville, Florida"},{"name":"Malcom Randall Veterans Affairs Medical Center, Gainesville, Florida"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8128-3203","authenticated-orcid":false,"given":"Salvatore T.","family":"Scali","sequence":"additional","affiliation":[{"name":"Division of Vascular Surgery and Endovascular Therapy, University of Florida, Gainesville, Florida"},{"name":"Malcom Randall Veterans Affairs Medical Center, Gainesville, Florida"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0780-029X","authenticated-orcid":false,"given":"Terence E.","family":"Ryan","sequence":"additional","affiliation":[{"name":"Department of Applied Physiology and Kinesiology, University of Florida, Gainesville, Florida"},{"name":"Center for Exercise Science, University of Florida, Gainesville, Florida"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2021.01.002"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.24272\/j.issn.2095-8137.2017.055"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/j.ekir.2016.11.006"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/j.jvs.2016.04.041"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.3390\/metabo11010045"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00117.2021"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1172\/jci.insight.139826"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-019-52107-7"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.00578.2013"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1111\/acel.12707"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.7554\/eLife.49874"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.3390\/cells9010197"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1016\/j.jvir.2009.03.044"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/j.jvir.2010.02.043"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00590.2013"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00288.2015"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.3791\/53294"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/j.jvssci.2021.09.022"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00098.2019"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.3390\/cells10123282"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00324.2003"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1186\/s13395-018-0171-0"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1016\/S0021-9258(18)64849-5"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.3390\/jcm10030548"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0132873"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1039\/c9mo00192a"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1002\/nbm.4266"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1002\/nbm.1419"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/gkm957"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/j.cca.2011.12.014"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00562.2012"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1042\/bj3040509"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1007\/BF02578242"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1016\/j.celrep.2018.04.104"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1038\/nature13909"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.10320819"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1172\/jci.insight.133289"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1096\/fj.201901936RR"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1111\/nep.13606"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1002\/jcsm.12646"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.086629"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1002\/jcsm.12901"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.2337\/dbi18-0042"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.2337\/dbi19-0006"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00221.2006"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1213\/ANE.0b013e3182121d37"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbabio.2013.11.006"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1016\/j.bja.2018.01.036"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00156.2022","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,10,19]],"date-time":"2022-10-19T17:47:44Z","timestamp":1666201664000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00156.2022"}},"issued":{"date-parts":[[2022,11,1]]},"references-count":48,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2022,11,1]]}},"alternative-id":["10.1152\/ajprenal.00156.2022"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00156.2022","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2022,11,1]]},"assertion":[{"value":"2022-06-08","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2022-08-22","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2022-08-22","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2022-10-19","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,3,6]],"date-time":"2026-03-06T13:01:52Z","timestamp":1772802112075,"version":"3.50.1"},"reference-count":21,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2004,5]]},"abstract":"<jats:p> Edelman et al. have empirically shown that plasma water sodium concentration ([Na<jats:sup>+<\/jats:sup>]<jats:sub>pw<\/jats:sub>) is equal to 1.11(Na<jats:sub>e<\/jats:sub> + K<jats:sub>e<\/jats:sub>)\/TBW - 25.6 (Edelman IS, Leibman J, O'Meara MP, Birkenfeld LW. J Clin Invest 37: 1236\u20131256, 1958). However, the physiological significance of the slope and y-intercept in this equation has not been previously considered. Our analysis demonstrates that there are several clinically relevant parameters determining the magnitude of the y-intercept that independently alter [Na<jats:sup>+<\/jats:sup>]<jats:sub>pw<\/jats:sub>: 1) osmotically inactive exchangeable Na<jats:sup>+<\/jats:sup> and K<jats:sup>+<\/jats:sup>; 2) plasma water K<jats:sup>+<\/jats:sup> concentration; and 3) osmotically active non-Na<jats:sup>+<\/jats:sup> and non-K<jats:sup>+<\/jats:sup> osmoles. In addition, we demonstrate quantitatively the physiological significance of the slope in the Edelman equation and its role in modulating [Na<jats:sup>+<\/jats:sup>]<jats:sub>pw<\/jats:sub>. The slope of 1.11 in this equation which Edelman et al. determined empirically can be theoretically predicted by considering the combined effect of the osmotic coefficient of Na<jats:sup>+<\/jats:sup> salts at physiological concentrations and Gibbs-Donnan equilibrium. In addition, our results demonstrate that the slope has an independent quantitative impact on the magnitude of the y-intercept in the Edelman equation. From a physiological standpoint, the components of both the slope and the y-intercept need to be addressed when considering the factors that modulate [Na<jats:sup>+<\/jats:sup>]<jats:sub>pw<\/jats:sub>. <\/jats:p>","DOI":"10.1152\/ajprenal.00393.2003","type":"journal-article","created":{"date-parts":[[2004,3,31]],"date-time":"2004-03-31T22:23:05Z","timestamp":1080771785000},"page":"F828-F837","source":"Crossref","is-referenced-by-count":67,"title":["Determinants of plasma water sodium concentration as reflected in the Edelman equation: role of osmotic and Gibbs-Donnan equilibrium"],"prefix":"10.1152","volume":"286","author":[{"given":"Minhtri K.","family":"Nguyen","sequence":"first","affiliation":[{"name":"Division of Nephrology, David Geffen School of Medicine at UCLA, Los Angeles, California 90095-1689"}]},{"given":"Ira","family":"Kurtz","sequence":"additional","affiliation":[{"name":"Division of Nephrology, David Geffen School of Medicine at UCLA, Los Angeles, California 90095-1689"}]}],"member":"24","reference":[{"key":"REF1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI103199"},{"key":"REF2","doi-asserted-by":"publisher","DOI":"10.1016\/0002-9343(67)90096-4"},{"key":"REF3","unstructured":"Cameron IL, Hardman WE, Hunter KE, Haskin C, Smith NKR, and Fullerton GD. Evidence that a major portion of cellular potassium is \u201cbound\u201d. Scanning Microsc 4: 89-102, 1990."},{"key":"REF4","doi-asserted-by":"publisher","DOI":"10.1172\/JCI102878"},{"key":"atypb1","unstructured":"Edelman IS, James AH, Brooks L, and Moore FD. Body sodium and potassium\u2014the normal total exchangeable sodium; its measurement and magnitude. Metabolism 3: 530-538, 1954."},{"key":"REF6","doi-asserted-by":"publisher","DOI":"10.1172\/JCI103712"},{"key":"REF7","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-75-6-853"},{"key":"REF8","doi-asserted-by":"publisher","DOI":"10.1016\/0002-9343(62)90255-3"},{"key":"REF9","unstructured":"Guyton AC and Hall JE. The body fluid compartments: extracellular and intracellular fluids, interstitial fluid and edema. In: Textbook of Medical Physiology, edited by Guyton AC and Hall JE. Philadelphia, PA: Saunders, 2000, p. 264-278."},{"key":"REF10","unstructured":"Halperin ML and Goldstein MB. Hyponatremia. In: Fluid, Electrolyte and Acid-Base Physiology\u2014A Problem-Based Approach, edited by Halperin ML and Goldstein MB. Philadelphia, PA: Saunders, 1994, p. 253-288."},{"key":"REF11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.4.F585"},{"key":"REF12","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM197310182891607"},{"key":"REF13","unstructured":"Kutchai HC. Cellular membranes and transmembrane transport of solutes and water. In: Physiology, edited by Berne RM, Levy MN, Koeppen BM, and Stanton BA. St. Louis, MO: Mosby, 2004, p. 3-21."},{"key":"REF14","doi-asserted-by":"publisher","DOI":"10.1172\/JCI102952"},{"key":"REF15","doi-asserted-by":"publisher","DOI":"10.1007\/s10157-003-0233-3"},{"key":"REF16","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfg112"},{"key":"REF17","unstructured":"Pitts RF. Volume and composition of the body fluids. In: Physiology of the Kidney and Body Fluids, edited by Pitts RF. Chicago, IL: Year Book Medical Publishers, 1974, p. 11-34."},{"key":"REF18","unstructured":"Rose BD. The total body water and the plasma sodium concentration. Introduction to disorders of osmolality. In: Clinical Physiology of Acid-Base and Electrolyte Disorders, edited by Rose BD. New York: McGrawHill, 1994, p. 219-234, 638-650."},{"key":"REF19","doi-asserted-by":"publisher","DOI":"10.1016\/0002-9343(57)90224-3"},{"key":"REF20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00323.2001"},{"key":"REF21","doi-asserted-by":"publisher","DOI":"10.1053\/ajkd.2002.34908"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00393.2003","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T21:41:17Z","timestamp":1567978877000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00393.2003"}},"issued":{"date-parts":[[2004,5]]},"references-count":21,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2004,5]]}},"alternative-id":["10.1152\/ajprenal.00393.2003"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00393.2003","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2004,5]]}},{"indexed":{"date-parts":[[2026,3,6]],"date-time":"2026-03-06T10:20:12Z","timestamp":1772792412762,"version":"3.50.1"},"reference-count":45,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2007,10]]},"abstract":"<jats:p> Hyperglycemia-induced oxidative stress is a key mediator of renal tubular hypertrophy in diabetic nephropathy (DN). The molecular mechanisms of antioxidants responsible for inhibition of renal tubular hypertrophy in DN are incompletely characterized. We now aim at verifying the effects of N-acetylcysteine (NAC) and taurine on cellular hypertrophy in renal tubular epithelial cells under high ambient glucose. We found that NAC and taurine treatments significantly attenuated high glucose (HG)-inhibited cellular growth and HG-induced hypertrophy. HG-induced Raf-1, p42\/p44 mitogen-activated protein kinase (MAPK), Janus kinase 2 (JAK2), and signal transducer and activator of transcription 1 (STAT1) and STAT3 (but not STAT5) activation was markedly blocked by NAC and taurine. Moreover, NAC and taurine increased cyclin D1\/cdk4 activation and suppressed p21<jats:sup>Waf1\/Cip1<\/jats:sup> and p27<jats:sup>Kip1<\/jats:sup> expression in HG-treated cells. It seems that apoptosis was not observed in these treatments. There were no changes in bcl-2 and poly(ADP-ribose) polymerase expression, and mitochondrial cytochrome c release. However, NAC or taurine markedly inhibited the stimulation by HG of fibronectin and type IV collagen protein levels. It is concluded that both NAC and taurine significantly attenuated HG-induced activation of the Raf-1\/MAPK and the JAK2-STAT1\/STAT3 signaling pathways and hypertrophic growth in renal tubular epithelial cells. <\/jats:p>","DOI":"10.1152\/ajprenal.00020.2007","type":"journal-article","created":{"date-parts":[[2007,6,28]],"date-time":"2007-06-28T04:44:45Z","timestamp":1183005885000},"page":"F1072-F1082","source":"Crossref","is-referenced-by-count":60,"title":["Antioxidants attenuate high glucose-induced hypertrophic growth in renal tubular epithelial cells"],"prefix":"10.1152","volume":"293","author":[{"given":"Jau-Shyang","family":"Huang","sequence":"first","affiliation":[]},{"given":"Lea-Yea","family":"Chuang","sequence":"additional","affiliation":[]},{"given":"Jinn-Yuh","family":"Guh","sequence":"additional","affiliation":[]},{"given":"Yann-Jia","family":"Huang","sequence":"additional","affiliation":[]},{"given":"Min-Shyang","family":"Hsu","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1016\/j.jnutbio.2005.06.007"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1097\/01.mnh.0000191912.65281.e9"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1016\/j.febslet.2005.03.024"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1042\/BST0340837"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.54.suppl_2.S97"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.2174\/1570161043385538"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejphar.2006.05.039"},{"key":"R8","unstructured":"Ferrario F, Rastaldi MP. Histopathological atlas of renal diseases: diabetic nephropathy. J Nephrol 19: 1\u20135, 2006."},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1016\/j.yjmcc.2004.07.008"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1097\/01.mco.0000196141.65362.46"},{"key":"R11","unstructured":"Giunti S, Barit D, Cooper ME. Diabetic nephropathy: from mechanisms to rational therapies. Minerva Med 97: 241\u2013262, 2006."},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000240331.32352.0c"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbabio.2006.03.016"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.00355.2002"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005010030"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1042\/bj3420231"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1007\/s007950200011"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1097\/01.cad.0000176502.40810.b0"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1186\/1475-2840-4-5"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00274.x"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1016\/j.nbd.2006.01.012"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M411863200"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1016\/j.jacc.2005.10.041"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00181.2005"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000065640.77499.D7"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1161\/hy09t1.094234"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejpain.2005.08.006"},{"key":"R28","unstructured":"Nangaku M. Chronic hypoxia and tubulointerstitial injury: a final common pathway to end-stage renal failure. J Am Soc Nephrol 17: 17\u201325, 2003."},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.2169\/internalmedicine.43.9"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1016\/j.febslet.2006.05.072"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1385\/CBB:43:2:289"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2005.05.032"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1007\/s00380-005-0841-9"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1159\/000025912"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1053\/meta.2002.35579"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1016\/j.taap.2006.01.003"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1210\/er.2003-0018"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1097\/01.shk.0000226341.32786.b9"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1097\/01.mjt.0000178769.52610.69"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1053\/j.ackd.2005.01.001"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1136\/jim-50-06-04"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.2174\/1570161054368625"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1038\/sj.cdd.4401992"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5001846"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1999.277.6.C1229"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00020.2007","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T22:45:17Z","timestamp":1567982717000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00020.2007"}},"issued":{"date-parts":[[2007,10]]},"references-count":45,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2007,10]]}},"alternative-id":["10.1152\/ajprenal.00020.2007"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00020.2007","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2007,10]]}},{"indexed":{"date-parts":[[2026,3,3]],"date-time":"2026-03-03T15:48:07Z","timestamp":1772552887202,"version":"3.50.1"},"reference-count":41,"publisher":"American Physiological Society","issue":"2","funder":[{"name":"Moorhead Trust"},{"DOI":"10.13039\/501100004543","name":"China Scholarship Council","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100004543","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2020,8,1]]},"abstract":"<jats:p> In proteinuric renal diseases, excessive plasma nonesterified free fatty acids bound to albumin can leak across damaged glomeruli to be reabsorbed by renal proximal tubular cells and cause inflammatory tubular cells damage by as yet unknown mechanisms. The present study was designed to investigate these mechanisms induced by palmitic acid (PA; one of the nonesterified free fatty acids) overload. Our results show that excess PA stimulates ATP release through the pannexin 1 channel in human renal tubule epithelial cells (HK-2), increasing extracellular ATP concentration approximately threefold compared with control. The ATP release is dependent on caspase-3\/7 activation induced by mitochondrial reactive oxygen species. Furthermore, extracellular ATP aggravates PA-induced monocyte chemoattractant protein-1 secretion and monocyte infiltration of tubular cells, enlarging the inflammatory response in both macrophages and HK-2 cells via the purinergic P2X7 receptor-mammalian target of rapamycin-forkhead box O1-thioredoxin-interacting protein\/NOD-like receptor protein 3 inflammasome pathway. Hence, PA increases mitochondrial reactive oxygen species-induced ATP release and inflammatory stress, which cause a \u201cfirst hit,\u201d while ATP itself is a \u201csecond hit\u201d in amplifying the renal tubular inflammatory response. Thus, inhibition of ATP release or the purinergic P2X7 receptor may be an approach to reduce renal inflammation and improve renal function. <\/jats:p>","DOI":"10.1152\/ajprenal.00098.2020","type":"journal-article","created":{"date-parts":[[2020,7,20]],"date-time":"2020-07-20T10:59:10Z","timestamp":1595242750000},"page":"F292-F303","source":"Crossref","is-referenced-by-count":25,"title":["Nonesterified free fatty acids enhance the inflammatory response in renal tubules by inducing extracellular ATP release"],"prefix":"10.1152","volume":"319","author":[{"given":"Hong","family":"Sun","sequence":"first","affiliation":[{"name":"Department of Endocrinology and Metabolism, The First Affiliated Hospital of Soochow University, Suzhou, China"},{"name":"Department of Endocrinology and Metabolism, Zhongda Hospital, Institute of Diabetes, Medical School, Southeast University, Nanjing, China"}]},{"given":"Zilin","family":"Sun","sequence":"additional","affiliation":[{"name":"Department of Endocrinology and Metabolism, Zhongda Hospital, Institute of Diabetes, Medical School, Southeast University, Nanjing, China"}]},{"given":"Zac","family":"Varghese","sequence":"additional","affiliation":[{"name":"John Moorhead Research Laboratory, Department of Renal Medicine, University College London Medical School, Royal Free Campus, London, United Kingdom"}]},{"given":"Yinfeng","family":"Guo","sequence":"additional","affiliation":[{"name":"Department of Endocrinology and Metabolism, Zhongda Hospital, Institute of Diabetes, Medical School, Southeast University, Nanjing, China"}]},{"given":"John F.","family":"Moorhead","sequence":"additional","affiliation":[{"name":"John Moorhead Research Laboratory, Department of Renal Medicine, University College London Medical School, Royal Free Campus, London, United Kingdom"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7839-6031","authenticated-orcid":false,"given":"Robert John","family":"Unwin","sequence":"additional","affiliation":[{"name":"John Moorhead Research Laboratory, Department of Renal Medicine, University College London Medical School, Royal Free Campus, London, United Kingdom"},{"name":"Early Cardiovascular, Renal & Metabolism, AstraZeneca Biopharmaceutical\u2019s R&D, Cambridge, United Kingdom"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5199-4971","authenticated-orcid":false,"given":"Xiong Z.","family":"Ruan","sequence":"additional","affiliation":[{"name":"John Moorhead Research Laboratory, Department of Renal Medicine, University College London Medical School, Royal Free Campus, London, United Kingdom"},{"name":"Centre for Lipid Research and Key Laboratory of Molecular Biology for Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, Department of Infectious Diseases, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, People\u2019s Republic of China"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M114.567537"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1111\/eci.12230"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00021.2012"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0060184"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1038\/nature09413"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0129663"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.4.F562"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1098\/rstb.2014.0191"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.00490.2010"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0000000000000087"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1016\/j.clim.2017.12.006"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0099596"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.176.7.3877"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.3969\/j.issn.1672-7347.2014.08.010"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.3390\/nu11040722"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/j.trre.2011.10.002"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.4161\/isl.3.5.15935"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1111\/bph.13326"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/j.phrs.2014.02.007"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M113.473082"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/j.freeradbiomed.2011.05.028"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1186\/s40360-015-0040-y"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1021\/bi902083n"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2012.07.007"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1210\/ME.2015-1090"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-4419-1599-3_18"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1007\/s12026-015-8751-0"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1093\/cvr\/cvs426"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1159\/000314656"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/j.freeradbiomed.2008.04.029"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1016\/j.jsbmb.2014.10.014"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1186\/cc13092"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2010.10.012"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1016\/j.freeradbiomed.2015.10.414"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1159\/000168653"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.2133\/dmpk.24.300"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1007\/s11302-015-9456-5"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00175.2012"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1186\/1471-2407-13-468"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1186\/s12906-015-0826-x"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1038\/ni.1831"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00098.2020","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2020,8,7]],"date-time":"2020-08-07T14:34:42Z","timestamp":1596810882000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00098.2020"}},"issued":{"date-parts":[[2020,8,1]]},"references-count":41,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2020,8,1]]}},"alternative-id":["10.1152\/ajprenal.00098.2020"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00098.2020","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2020,8,1]]}},{"indexed":{"date-parts":[[2026,3,3]],"date-time":"2026-03-03T23:36:07Z","timestamp":1772580967222,"version":"3.50.1"},"reference-count":37,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2000,9,1]]},"abstract":"<jats:p>We determined alterations in renal aquaporin-2 (AQP2) gene expression in association with impaired water excretion in glucocorticoid-deficient rats. After adrenalectomy, Sprague-Dawley rats were administered aldosterone alone by osmotic pumps (glucocorticoid-deficient rats). As a control, both aldosterone and dexamethasone were administered. These animals were subjected to the studies on days 7\u201314. The expressions of AQP2 mRNA and protein in kidney of the glucocorticoid-deficient rats were increased by 1.6- and 1.4-fold compared with the control rats, respectively. An acute oral water load test verified the marked impairment in water excretion in the glucocorticoid-deficient rats. One hour after the water load, the expressions of AQP2 mRNA and protein were significantly reduced in the control rats, but they remained unchanged in the glucocorticoid-deficient rats. However, there was no alteration in [<jats:sup>3<\/jats:sup>H]arginine vasopressin (AVP) receptor binding and AVP V<jats:sub>2<\/jats:sub>receptor mRNA expression in the glucocorticoid-deficient rats. A V<jats:sub>2<\/jats:sub>-receptor antagonist abolished the increased expressions of AQP2 mRNA and protein in the glucocorticoid-deficient rats. These results indicate that augmented expression of AQP2 participates in impaired water excretion, dependent on AVP, in glucocorticoid deficiency.<\/jats:p>","DOI":"10.1152\/ajprenal.2000.279.3.f502","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T12:20:10Z","timestamp":1514031610000},"page":"F502-F508","source":"Crossref","is-referenced-by-count":56,"title":["Vasopressin-dependent upregulation of aquaporin-2 gene expression in glucocorticoid-deficient rats"],"prefix":"10.1152","volume":"279","author":[{"given":"Takako","family":"Saito","sequence":"first","affiliation":[{"name":"Division of Endocrinology and Metabolism, Department of Medicine, Jichi Medical School, Tochigi 329-0498; and"}]},{"given":"San-E","family":"Ishikawa","sequence":"additional","affiliation":[{"name":"Division of Endocrinology and Metabolism, Department of Medicine, Jichi Medical School, Tochigi 329-0498; and"}]},{"given":"Fumiko","family":"Ando","sequence":"additional","affiliation":[{"name":"Division of Endocrinology and Metabolism, Department of Medicine, Jichi Medical School, Tochigi 329-0498; and"}]},{"given":"Minori","family":"Higashiyama","sequence":"additional","affiliation":[{"name":"Division of Endocrinology and Metabolism, Department of Medicine, Jichi Medical School, Tochigi 329-0498; and"}]},{"given":"Shoichiro","family":"Nagasaka","sequence":"additional","affiliation":[{"name":"Division of Endocrinology and Metabolism, Department of Medicine, Jichi Medical School, Tochigi 329-0498; and"}]},{"given":"Sei","family":"Sasaki","sequence":"additional","affiliation":[{"name":"Second Department of Internal Medicine, Tokyo Medical and Dental University, Tokyo 113-0034, Japan"}]},{"given":"Toshikazu","family":"Saito","sequence":"additional","affiliation":[{"name":"Division of Endocrinology and Metabolism, Department of Medicine, Jichi Medical School, Tochigi 329-0498; and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI105504"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1002\/hep.1840210128"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/0003-2697(87)90021-2"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.258.4.F812"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.6.F926"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1038\/361549a0"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1172\/JCI106390"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1002\/cne.903630103"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1996.270.6.C1695"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1507\/endocrj.40.373"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1507\/endocrj1954.38.325"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1986.149"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1982.216"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.253.1.F41"},{"key":"B15","first-page":"1584","volume":"77","author":"Kamoi K","year":"1993","journal-title":"J Clin Endocrinol Metab"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1980.110"},{"key":"B18","doi-asserted-by":"crossref","first-page":"861","DOI":"10.1681\/ASN.V86861","volume":"8","author":"Matsumura Y","year":"1997","journal-title":"J Am Soc Nephrol"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.90.24.11663"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.94.10.5450"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.1993.tb55621.x"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1987.252.4.R635"},{"key":"B23","doi-asserted-by":"crossref","first-page":"1357","DOI":"10.1681\/ASN.V891357","volume":"8","author":"Rai T","year":"1997","journal-title":"J Am Soc Nephrol"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1210\/endo-101-1-1"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1159\/000123479"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1007\/BF00233445"},{"key":"B27","first-page":"4034","volume":"83","author":"Saito T","year":"1998","journal-title":"J Clin Endocrinol Metab"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.272.2.F183"},{"key":"B29","first-page":"1823","volume":"82","author":"Saito T","year":"1997","journal-title":"J Clin Endocrinol Metab"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117079"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1210\/endo-103-4-1009"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1210\/jcem-11-7-700"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.265"},{"key":"B34","doi-asserted-by":"crossref","first-page":"23451","DOI":"10.1016\/S0021-9258(17)31537-5","volume":"269","author":"Uchida S","year":"1994","journal-title":"J Biol Chem"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119312"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1995.268.6.C1546"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.1992.tb09058.x"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.2.F461"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.2000.279.3.F502","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:38:55Z","timestamp":1660189135000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.2000.279.3.F502"}},"issued":{"date-parts":[[2000,9,1]]},"references-count":37,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2000,9,1]]}},"alternative-id":["10.1152\/ajprenal.2000.279.3.F502"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.2000.279.3.f502","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2000,9,1]]}},{"indexed":{"date-parts":[[2026,3,4]],"date-time":"2026-03-04T00:23:53Z","timestamp":1772583833792,"version":"3.50.1"},"reference-count":30,"publisher":"American Physiological Society","issue":"11","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2016,6,1]]},"abstract":"<jats:p>Autonomic and somatic motor neurons that innervate the urinary bladder and urethra control the highly coordinated functions of the lower urinary tract, the storage, and the emptying of urine. ACh is the primary excitatory neurotransmitter in the bladder. Here, we aimed to determine whether PKA regulates neuronal ACh release and related nerve-evoked detrusor smooth muscle (DSM) contractions in the guinea pig urinary bladder. Isometric DSM tension recordings were used to measure spontaneous phasic and electrical field stimulation (EFS)- and carbachol-induced DSM contractions with a combination of pharmacological tools. The colorimetric method was used to measure ACh released by the parasympathetic nerves in DSM isolated strips. The pharmacological inhibition of PKA with H-89 (10 \u03bcM) increased the spontaneous phasic contractions, whereas it attenuated the EFS-induced DSM contractions. Intriguingly, H-89 (10 \u03bcM) attenuated the (primary) cholinergic component, whereas it simultaneously increased the (secondary) purinergic component of the nerve-evoked contractions in DSM isolated strips. The acetylcholinesterase inhibitor, eserine (10 \u03bcM), increased EFS-induced DSM contractions, and the subsequent addition of H-89 attenuated the contractions. H-89 (10 \u03bcM) significantly increased DSM phasic contractions induced by the cholinergic agonist carbachol. The inhibition of PKA decreased the neuronal release of ACh in DSM tissues. This study revealed that PKA-mediated signaling pathways differentially regulate nerve-evoked and spontaneous phasic contractions of guinea pig DSM. Constitutively active PKA in the bladder nerves controls synaptic ACh release, thus regulating the nerve-evoked DSM contractions, whereas PKA in DSM cells controls the spontaneous phasic contractility.<\/jats:p>","DOI":"10.1152\/ajprenal.00026.2016","type":"journal-article","created":{"date-parts":[[2016,3,31]],"date-time":"2016-03-31T02:24:30Z","timestamp":1459391070000},"page":"F1377-F1384","source":"Crossref","is-referenced-by-count":5,"title":["Constitutively active PKA regulates neuronal acetylcholine release and contractility of guinea pig urinary bladder smooth muscle"],"prefix":"10.1152","volume":"310","author":[{"given":"Wenkuan","family":"Xin","sequence":"first","affiliation":[{"name":"Department of Drug Discovery and Biomedical Sciences, South Carolina College of Pharmacy, University of South Carolina, Columbia, South Carolina"}]},{"given":"Ning","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Drug Discovery and Biomedical Sciences, South Carolina College of Pharmacy, University of South Carolina, Columbia, South Carolina"}]},{"given":"Vitor S.","family":"Fernandes","sequence":"additional","affiliation":[{"name":"Department of Drug Discovery and Biomedical Sciences, South Carolina College of Pharmacy, University of South Carolina, Columbia, South Carolina"}]},{"given":"Georgi V.","family":"Petkov","sequence":"additional","affiliation":[{"name":"Department of Drug Discovery and Biomedical Sciences, South Carolina College of Pharmacy, University of South Carolina, Columbia, South Carolina"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"crossref","first-page":"458","DOI":"10.1016\/S0022-3565(25)10643-5","volume":"274","author":"Alberts P","year":"1995","journal-title":"J Pharmacol Exp Ther"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00038.2003"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1007\/978-3-642-16499-6_8"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1002\/nau.20837"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00440.2007"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/j.pneurobio.2010.04.006"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1007\/978-3-540-79090-7_4"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1002\/nau.22634"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.3644-09.2010"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1111\/j.1464-410X.2008.07935.x"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuroscience.2007.10.016"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2004.077826"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.2001.00507.x"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.04520413"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1209185109"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1038\/nrurol.2015.193"},{"key":"B17","doi-asserted-by":"crossref","first-page":"337","DOI":"10.1016\/S0031-6997(25)06843-7","volume":"32","author":"Langer SZ","year":"1980","journal-title":"Pharmacol Rev"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/S0024-3205(00)00588-9"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.3321-06.2006"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00180.2010"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1111\/apha.12010"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/j.nlm.2014.05.005"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1016\/j.mcn.2009.11.007"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1002\/jnr.21885"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1111\/j.1460-9568.2006.04753.x"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1111\/ejn.12922"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.0944-14.2015"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1996.sp021681"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1046\/j.1464-410x.2000.00562.x"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00167.2014"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00026.2016","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,6,2]],"date-time":"2025-06-02T01:40:13Z","timestamp":1748828413000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00026.2016"}},"issued":{"date-parts":[[2016,6,1]]},"references-count":30,"journal-issue":{"issue":"11","published-print":{"date-parts":[[2016,6,1]]}},"alternative-id":["10.1152\/ajprenal.00026.2016"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00026.2016","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2016,6,1]]}},{"indexed":{"date-parts":[[2026,3,5]],"date-time":"2026-03-05T16:24:52Z","timestamp":1772727892953,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1989,11,1]]},"abstract":"<jats:p> Renal calcium transport is described as the result of two processes, a paracellular, gradient-dependent process that predominates in most segments of the nephron and a transcellular, energy-dependent step that characterizes calcium transport in the distal convoluted tubule (DCT). Transcellular calcium transport involves entry into the DCT cell, possibly via channels, intracellular movement which appears to be facilitated by the presence of the vitamin D-dependent, cytosolic calcium-binding protein (CaBPr, calbindin D28k, mol mass approximately 28 kDa), and extrusion via the Ca-ATPase. Although much is known about calcium channels, their presence in renal tissue has only been demonstrated by preliminary studies. Quantitative data on CaBPr content of rat DCT are also unavailable, but theoretical analysis and early experimental values of intracellular self-diffusion of calcium have confirmed the need for an intracellular calcium \"ferry,\" i.e., a molecule like CaBPr to amplify intracellular calcium movement. Available data on the plasma membrane Ca-ATPase are consistent with the extrusion kinetics attributed to the renal Ca-ATPase, but it has not been isolated, nor has its gene been cloned. Regulation and disorders of renal calcium transport are likely to involve one of the three transcellular steps, but indirect regulation by modification of the cell walls and molecules constituting the paracellular pathway cannot be excluded. <\/jats:p>","DOI":"10.1152\/ajprenal.1989.257.5.f707","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T22:07:26Z","timestamp":1513980446000},"page":"F707-F711","source":"Crossref","is-referenced-by-count":6,"title":["Renal calcium transport: mechanisms and regulation--an overview"],"prefix":"10.1152","volume":"257","author":[{"given":"F.","family":"Bronner","sequence":"first","affiliation":[{"name":"Department of BioStructure and Function, University of ConnecticutHealth Center, Farmington 06032."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1989.257.5.F707","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:14:54Z","timestamp":1567970094000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1989.257.5.F707"}},"issued":{"date-parts":[[1989,11,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1989,11,1]]}},"alternative-id":["10.1152\/ajprenal.1989.257.5.F707"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1989.257.5.f707","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1989,11,1]]}},{"indexed":{"date-parts":[[2026,3,3]],"date-time":"2026-03-03T00:42:51Z","timestamp":1772498571067,"version":"3.50.1"},"reference-count":37,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2007,9]]},"abstract":"<jats:p>Accelerated medial calcification is a major cause of premature cardiovascular mortality in patients with chronic kidney disease (CKD). Evidence suggests that extracellular concentration of Ca<jats:sup>2+<\/jats:sup>and vascular smooth muscle cells may play a pivotal role in the pathogenesis of vascular calcification. The calcium-sensing receptor (CaSR) is a G protein-coupled receptor that is expressed in a range of tissues, but characterization of its expression and function in the cardiovascular system is limited. Here we report the expression of CaSR mRNA (RT-PCR) and protein (Western blotting and immunocytochemistry) in human aortic smooth muscle cells (HAoSMC). Treatment of HAoSMC with Ca<jats:sup>2+<\/jats:sup>(0\u20135 mM; 0\u201330 min) or the CaSR agonists gentamycin and neomycin (0\u2013300 \u03bcM; 0\u201330 min) resulted in a dose- and time-dependent phosphorylation of ERK1\/2. Gentamycin- and neomycin-mediated ERK1\/2 stimulation was inhibited by pretreatment with PD-98059, an ERK-activating kinase 1 (MEK1) inhibitor, confirming specificity of the observed effects. ERK1\/2 activation was inhibited in HAoSMC, with CaSR expression knocked down by transfection with specific small-interference RNA, which confirmed that the observed neomycin\/gentamycin-induced MEK1\/ERK1\/2 activation was mediated via the CaSR. CaSR mRNA and protein were also expressed in large and small arteries from normal subjects (kidney donors) and patients with end-stage renal disease (ESRD). The CaSR was detected in smooth muscle and endothelial cells. Expression was significantly lower in arteries from ESRD patients. In conclusion, these data not only demonstrate the presence of a functional CaSR in human artery but show a correlation between CaSR expression and progression of CKD.<\/jats:p>","DOI":"10.1152\/ajprenal.00474.2006","type":"journal-article","created":{"date-parts":[[2007,5,31]],"date-time":"2007-05-31T01:04:40Z","timestamp":1180573480000},"page":"F946-F955","source":"Crossref","is-referenced-by-count":108,"title":["Extracellular calcium-sensing receptor is functionally expressed in human artery"],"prefix":"10.1152","volume":"293","author":[{"given":"Guerman","family":"Molostvov","sequence":"first","affiliation":[]},{"given":"Sean","family":"James","sequence":"additional","affiliation":[]},{"given":"Simon","family":"Fletcher","sequence":"additional","affiliation":[]},{"given":"Jeanette","family":"Bennett","sequence":"additional","affiliation":[]},{"given":"Hendrik","family":"Lehnert","sequence":"additional","affiliation":[]},{"given":"Rosemary","family":"Bland","sequence":"additional","affiliation":[]},{"given":"Daniel","family":"Zehnder","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1210\/endo.140.5.6683"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000133041.27682.A2"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1172\/JCI116391"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1038\/366575a0"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.2001.81.1.239"},{"key":"R6","unstructured":"Brown EM, Vassilev PM, Quinn S, Hebert SC.G-protein-coupled, extracellular Ca2+-sensing receptor: a versatile regulator of diverse cellular functions.Vitam Horm55: 1\u201371, 1999."},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.29.20561"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1210\/en.2003-1127"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1210\/en.2004-1281"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000145894.57533.C4"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00344.2005"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1038\/nrm1154"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M010921200"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.2.F291"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000141775.67189.98"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1038\/ncb822"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.36.23344"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00510.2004"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1172\/JCI9799"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000141960.01035.28"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.3.F611"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.1.131"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.100.21.2168"},{"key":"R24","unstructured":"Sheehan D, Hrapchak B.Theory and Practice of Histotechnology(2nd ed.). Columbus, OH: Battelle, 1980, p. 226\u2013227."},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1161\/01.ATV.15.11.2003"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2006.07.192"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1080\/10408360590886606"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00821.2005"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M107122200"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1161\/01.ATV.0000059406.92165.31"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1046\/j.1432-1033.2003.03645.x"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000015623.73739.B8"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000178787.59594.a0"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1007\/s00232001068"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.66015.x"},{"key":"R36","doi-asserted-by":"crossref","unstructured":"Zehnder D, Bland R, Walker EA, Bradwell AR, Howie AJ, Hewison M, Stewart PM.Expression of 25-hydroxyvitamin D31\u03b1-hydroxylase in the human kidney.J Am Soc Nephrol10: 2465\u20132473, 1999.","DOI":"10.1681\/ASN.V10122465"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2006.01.135"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00474.2006","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,5,12]],"date-time":"2023-05-12T02:45:10Z","timestamp":1683859510000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00474.2006"}},"issued":{"date-parts":[[2007,9]]},"references-count":37,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2007,9]]}},"alternative-id":["10.1152\/ajprenal.00474.2006"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00474.2006","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2007,9]]}},{"indexed":{"date-parts":[[2026,2,14]],"date-time":"2026-02-14T09:31:22Z","timestamp":1771061482453,"version":"3.50.1"},"reference-count":28,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2004,1]]},"abstract":"<jats:p>Digital three-dimensional (3-D) functional reconstructions of inner medullary nephrons were performed. Antibodies against aquaporins (AQP)-1 and -2 and the chloride channel ClC-K1 identified descending thin limbs (DTLs), collecting ducts (CDs), and ascending thin limbs (ATLs), respectively, through indirect immunofluorescence. Tubules were labeled in transverse sections and assembled into 3-D arrays, permitting individual tubule or combined surface representations to depths of 3.3 mm to be viewed in an interactive digital model. Surface representations of 75 tubules positioned near the central region of the inner medulla were reconstructed. In most DTL segments that form loops below 1 mm from the inner medullary base, AQP1 expression begins at the base, becomes intermittent for variable lengths, and continues nearly midway to the loop. The terminal DTL segment exhibiting undetectable AQP1 represents nearly 60% of the distance from the medullary base to the tip of the loop. AQP1 expression was entirely undetectable in shorter long-looped DTLs. ClC-K1 is expressed continuously along the terminal portion of all DTLs reconstructed here, beginning with a prebend region \u223c164 \u03bcm before the bend in all tubules and continuing through the entire ascent of the ATLs to the base of the inner medulla. CDs express AQP2 continuously and extensive branching patterns are illustrated. 3-D functional reconstruction of inner medullary nephrons is capable of showing axial distribution of membrane proteins in tubules of the inner medulla and can contribute to further development and refinement of models that attempt to elucidate the concentrating mechanism.<\/jats:p>","DOI":"10.1152\/ajprenal.00285.2003","type":"journal-article","created":{"date-parts":[[2004,1,31]],"date-time":"2004-01-31T00:56:49Z","timestamp":1075510609000},"page":"F38-F45","source":"Crossref","is-referenced-by-count":83,"title":["Three-dimensional functional reconstruction of inner medullary thin limbs of Henle's loop"],"prefix":"10.1152","volume":"286","author":[{"given":"Thomas L.","family":"Pannabecker","sequence":"first","affiliation":[{"name":"Department of Physiology, College of Medicine, University of Arizona, Tucson, Arizona 85724-5051"}]},{"given":"Diane E.","family":"Abbott","sequence":"additional","affiliation":[{"name":"Department of Physiology, College of Medicine, University of Arizona, Tucson, Arizona 85724-5051"}]},{"given":"William H.","family":"Dantzler","sequence":"additional","affiliation":[{"name":"Department of Physiology, College of Medicine, University of Arizona, Tucson, Arizona 85724-5051"}]}],"member":"24","reference":[{"key":"atypb1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.2.F204"},{"key":"REF2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.263.3.F417"},{"key":"atypb2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.265.6.F863"},{"key":"REF4","doi-asserted-by":"publisher","DOI":"10.1007\/BF00317960"},{"key":"REF5","doi-asserted-by":"publisher","DOI":"10.1177\/38.1.2294148"},{"key":"atypb3","unstructured":"Kaissling Band Kriz W.Morphology of the loop of Henle, distal tubule, and collecting duct. In:Handbook of Physiology. Renal Physiology. Bethesda, MD: Am Physiol Soc, 1992, sect. 8, vol.I, chapt. 3, p. 109-168."},{"key":"REF7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00067.2002"},{"key":"REF8","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1972.97"},{"key":"REF9","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1988.1"},{"key":"atypb4","unstructured":"Kriz Wand Kaissling B.Structural organization of the mammalian kidney. In:The Kidney: Physiology and Pathophysiology, edited by Seldin DW and Giebisch G. New York: Raven, 1992."},{"key":"REF11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.270.1.F9"},{"key":"REF12","doi-asserted-by":"crossref","unstructured":"Maxwell MH.Two rapid and simple methods used for the removal of resins from 1.0 \u03bcm thick epoxy sections.J Microsc112: 253-255, 1977.","DOI":"10.1111\/j.1365-2818.1978.tb01174.x"},{"key":"REF13","doi-asserted-by":"publisher","DOI":"10.1177\/22.12.1077"},{"key":"REF14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00340.2000"},{"key":"atypb5","unstructured":"Moon C, Preston GM, Griffin CA, Jabs EW, and Agre P.The human aquaporin CHIP gene: structure, organization, and chromosomal localization.J Biol Chem268: 15772-15778, 1993."},{"key":"atypb6","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.389"},{"key":"REF17","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00024.2001"},{"key":"atypb7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.268.6.F1023"},{"key":"REF19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.2.F202"},{"key":"atypb8","unstructured":"Sands JMand Kokko JP.Current concepts of the countercurrent multiplication system.Kidney Int50,Suppl57: S93-S99, 1996."},{"key":"REF21","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1974.101"},{"key":"REF22","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1972.75"},{"key":"REF23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.5.F802"},{"key":"REF24","doi-asserted-by":"crossref","unstructured":"Uchida S, Sasaki S, Furukawa T, Hiraoka M, Imai T, Hirata Y, and Marumo F.Molecular cloning of a chloride channel that is regulated by dehydration and expressed predominantly in kidney medulla.J Biol Chem268: 3821-3824, 1999.","DOI":"10.1016\/S0021-9258(18)53545-6"},{"key":"atypb9","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117626"},{"key":"atypb10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.272.5.F678"},{"key":"REF27","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.123.3.605"},{"key":"REF28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.260.3.F368"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00285.2003","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,6,14]],"date-time":"2021-06-14T05:31:14Z","timestamp":1623648674000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00285.2003"}},"issued":{"date-parts":[[2004,1]]},"references-count":28,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2004,1]]}},"alternative-id":["10.1152\/ajprenal.00285.2003"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00285.2003","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2004,1]]}},{"indexed":{"date-parts":[[2026,2,17]],"date-time":"2026-02-17T04:47:48Z","timestamp":1771303668747,"version":"3.50.1"},"reference-count":175,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2006,8]]},"abstract":"<jats:p>In the renal collecting duct, water reabsorption is regulated by the antidiuretic hormone vasopressin (AVP). Binding of this hormone to the vasopressin V2 receptor (V2R) leads to insertion of aquaporin-2 (AQP2) water channels in the apical membrane, thereby allowing water reabsorption from the pro-urine to the interstitium. The disorder nephrogenic diabetes insipidus (NDI) is characterized by the kidney's inability to concentrate pro-urine in response to AVP, which is mostly acquired due to electrolyte disturbances or lithium therapy. Alternatively, NDI is inherited in an X-linked or autosomal fashion due to mutations in the genes encoding V2R or AQP2, respectively. This review describes the current knowledge of the cell biological causes of NDI and how these defects may explain the patients' phenotypes. Also, the increased understanding of these cellular defects in NDI has opened exciting initiatives in the development of novel therapies for NDI, which are extensively discussed in this review.<\/jats:p>","DOI":"10.1152\/ajprenal.00491.2005","type":"journal-article","created":{"date-parts":[[2006,7,6]],"date-time":"2006-07-06T17:10:09Z","timestamp":1152205809000},"page":"F257-F270","source":"Crossref","is-referenced-by-count":152,"title":["Cell biological aspects of the vasopressin type-2 receptor and aquaporin 2 water channel in nephrogenic diabetes insipidus"],"prefix":"10.1152","volume":"291","author":[{"given":"Joris H.","family":"Robben","sequence":"first","affiliation":[]},{"given":"Nine V. A. M.","family":"Knoers","sequence":"additional","affiliation":[]},{"given":"Peter M. T.","family":"Deen","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1038\/78107"},{"key":"R2","unstructured":"Ala Y, Morin D, Mouillac B, Sabatier N, Vargas R, Cotte N, Dechaux M, Antignac C, Arthus MF, Lonergan M, Turner MS, Balestre MN, Alonso G, Hibert M, Barberis C, Hendy GN, Bichet DG, and Jard S.Functional studies of twelve mutant V2 vasopressin receptors related to nephrogenic diabetes insipidus: molecular basis of a mild clinical phenotype.J Am Soc Nephrol9: 1861\u20131872, 1998."},{"key":"R3","unstructured":"Albertazzi E, Zanchetta D, Barbier P, Faranda S, Frattini A, Vezzoni P, Procaccio M, Bettinelli A, Guzzi F, Parenti M, and Chini B.Nephrogenic diabetes insipidus: functional analysis of new AVPR2 mutations identified in Italian families.J Am Soc Nephrol11: 1033\u20131043, 2000."},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1159\/000166896"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00569.x"},{"key":"R6","doi-asserted-by":"crossref","unstructured":"Arthus MF, Lonergan M, Crumley MJ, Naumova AK, Morin D, De Marco LA, Kaplan BS, Robertson GL, Sasaki S, Morgan K, Bichet DG, and Fujiwara TM.Report of 33 novel AVPR2 mutations and analysis of 117 families with X-linked nephrogenic diabetes insipidus.J Am Soc Nephrol11: 1044\u20131054, 2000.","DOI":"10.1681\/ASN.V1161044"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00049.x"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004121079"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1124\/mol.51.2.177"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.98.1.93"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1016\/S1357-2725(03)00139-0"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M403354200"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1016\/S0924-9338(01)00565-X"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1016\/j.tem.2004.05.003"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1210\/me.2004-0080"},{"key":"R16","doi-asserted-by":"crossref","unstructured":"Bernier V, Morello JP, Zarruk A, Debrand N, Salahpour A, Lonergan M, Arthus MF, Laperriere A, Brouard R, Bouvier M, and Bichet DG.Pharmacologic chaperones as a potential treatment for X-linked nephrogenic diabetes insipidus.J Am Soc Nephrol17: 232\u2013243, 2006.","DOI":"10.1681\/ASN.2005080854"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1172\/JCI116698"},{"key":"R18","unstructured":"Bichet DG, Birnbaumer M, Lonergan M, Arthus MF, and Rosenthal W.Nature and recurrence of AVPR2 mutations in X-linked nephrogenic.Am J Hum Genet55: 278\u2013286, 1994."},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1038\/357333a0"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000125248.85135.43"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1172\/JCI9594"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00337.2004"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/6.11.1865"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1007\/s100380200002"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00266.2003"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1172\/JCI111901"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1176\/appi.ajp.162.10.1805"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/ddh339"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005010104"},{"key":"R30","unstructured":"Deen PMand Brown D.Aquaporins: current topics in membranes. In:Trafficking of Native and Mutant Mammalian MIP Proteins, edited by Hohmann S, Agre P, and Nielsen S. San Diego, CA: Academic, 2001, p. 235\u2013276."},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117920"},{"key":"R32","doi-asserted-by":"crossref","unstructured":"Deen PM, van Aubel RA, van Lieburg AF, and van Os CH.Urinary content of aquaporin 1 and 2 in nephrogenic diabetes insipidus.J Am Soc Nephrol7: 836\u2013841, 1996.","DOI":"10.1681\/ASN.V76836"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1126\/science.8140421"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1159\/000133707"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1172\/JCI111805"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1172\/JCI104320"},{"key":"R37","doi-asserted-by":"crossref","unstructured":"Earm JH, Christensen BM, Fr\u00f8ki\u00e6r J, Marples D, Han JS, Knepper MA, and Nielsen S.Decreased aquaporin-2 expression and apical plasma membrane delivery in kidney collecting ducts of polyuric hypercalcemic rats.J Am Soc Nephrol9: 2181\u20132193, 1998.","DOI":"10.1681\/ASN.V9122181"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.1.F46"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00154.2002"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1016\/S0955-0674(00)00233-7"},{"key":"R41","doi-asserted-by":"crossref","unstructured":"Fr\u00f8ki\u00e6r J, Christensen BM, Marples D, Djurhuus JC, Jensen UB, Knepper MA, and Nielsen S.Downregulation of aquaporin-2 parallels changes in renal water excretion in unilateral ureteral obstruction.Am J Physiol Renal Physiol272: F213\u2013F223, 1997.","DOI":"10.1152\/ajprenal.1997.273.2.F213"},{"key":"R42","unstructured":"Fr\u00f8ki\u00e6r J, Li C, Shi Y, Jensen A, Praetorius H, Hansen H, Topcu O, Sardeli C, Wang W, Kwon TH, and Nielsen S.Renal aquaporins and sodium transporters with special focus on urinary tract obstruction.APMIS Suppl: 71\u201379, 2003."},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.270.4.F657"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005040371"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.23.14800"},{"key":"R46","unstructured":"Goji K, Kuwahara M, Gu Y, Matsuo M, Marumo F, and Sasaki S.Novel mutations in aquaporin-2 gene in female siblings with nephrogenic diabetes insipidus: evidence of disrupted water channel function.J Clin Endocrinol Metab83: 3205\u20133209, 1998."},{"key":"R47","unstructured":"Guyon C, Bissonnette P, Lussier Y, Arthus MF, Lonergan M, Bedoya Perez R, and Bichet D.Novel aquaporin-2(AQP2)mutations responsible for autosomal recessive nephrogenic diabetes insipidus (Abstract).J Am Soc Nephrol2004."},{"key":"R48","doi-asserted-by":"publisher","DOI":"10.1016\/S1043-2760(97)00157-4"},{"key":"R49","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M111880200"},{"key":"R50","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004110930"},{"key":"R51","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-0854.2004.00239.x"},{"key":"R52","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)63635-8"},{"key":"R53","doi-asserted-by":"crossref","unstructured":"Hochberg Z, van Lieburg AF, Even L, Brenner B, Lanir N, van Oost BA, and Knoers NV.Autosomal recessive nephrogenic diabetes insipidus caused by an aquaporin-2 mutation.J Clin Endocrinol Metab82: 686\u2013689, 1997.","DOI":"10.1210\/jcem.82.2.3781"},{"key":"R54","doi-asserted-by":"publisher","DOI":"10.1517\/13543784.9.5.1029"},{"key":"R55","doi-asserted-by":"publisher","DOI":"10.1210\/jcem.86.1.7165"},{"key":"R56","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.4.2486"},{"key":"R57","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.272.2.F235"},{"key":"R58","doi-asserted-by":"publisher","DOI":"10.1111\/j.1651-2227.1994.tb13072.x"},{"key":"R59","doi-asserted-by":"crossref","unstructured":"Jung JS, Preston GM, Smith BL, Guggino WB, and Agre P.Molecular structure of the water channel through aquaporin CHIP. The hourglass model.J Biol Chem269: 14648\u201314654, 1994.","DOI":"10.1016\/S0021-9258(17)36674-7"},{"key":"R60","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00111.2003"},{"key":"R61","doi-asserted-by":"publisher","DOI":"10.1053\/ajkd.2002.31993"},{"key":"R62","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200309017"},{"key":"R63","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.151.4.919"},{"key":"R64","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/18.9.2394"},{"key":"R65","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199506083322303"},{"key":"R66","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfh677"},{"key":"R67","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.270.3.F548"},{"key":"R68","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.272.6.F816"},{"key":"R69","doi-asserted-by":"publisher","DOI":"10.1042\/BC20040148"},{"key":"R70","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00176.2003"},{"key":"R71","doi-asserted-by":"publisher","DOI":"10.1136\/adc.80.6.548"},{"key":"R72","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.256"},{"key":"R73","doi-asserted-by":"publisher","DOI":"10.1159\/000185888"},{"key":"R74","doi-asserted-by":"crossref","unstructured":"Konoshita T, Kuroda M, Kawane T, Koni I, Miyamori I, Tofuku Y, Mabuchi H, and Takeda R.Treatment of congenital nephrogenic diabetes insipidus with hydrochlorothiazide and amiloride in an adult patient.Horm Res61: 63\u201367, 2004.","DOI":"10.1159\/000075241"},{"key":"R75","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00114.2004"},{"key":"R76","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1986.250.1.F151"},{"key":"R77","doi-asserted-by":"publisher","DOI":"10.2169\/internalmedicine.37.215"},{"key":"R78","doi-asserted-by":"publisher","DOI":"10.1086\/323643"},{"key":"R79","doi-asserted-by":"publisher","DOI":"10.1172\/JCI1694"},{"key":"R80","doi-asserted-by":"publisher","DOI":"10.1159\/000077593"},{"key":"R81","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.281.1.F163"},{"key":"R82","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00272.2002"},{"key":"R83","unstructured":"Li Y, Shaw S, Kamsteeg EJ, Vandewalle A, and Deen PM.Development of lithium-induced nephrogenic diabetes insipidus is dissociated from adenylyl cyclase activity.J Am Soc Nephrol. In press."},{"key":"R84","doi-asserted-by":"publisher","DOI":"10.1210\/jcem.87.6.8617"},{"key":"R85","doi-asserted-by":"publisher","DOI":"10.1038\/357336a0"},{"key":"R86","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.080499597"},{"key":"R87","unstructured":"MacDonald WB.Congenital nephrogenic diabetes insipidus.Med J Aust40: 32\u201333, 1953."},{"key":"R88","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117863"},{"key":"R89","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118628"},{"key":"R90","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000027355.41663.14"},{"key":"R91","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/11.7.779"},{"key":"R92","doi-asserted-by":"publisher","DOI":"10.1007\/s004240000498"},{"key":"R93","doi-asserted-by":"publisher","DOI":"10.1038\/5036"},{"key":"R94","doi-asserted-by":"crossref","unstructured":"McKinley MJand Johnson AK.The physiological regulation of thirst and fluid intake.News Physiol Sci19: 1\u20136, 2004.","DOI":"10.1152\/nips.01470.2003"},{"key":"R95","doi-asserted-by":"crossref","unstructured":"Mizuno H, Fujimoto S, Sugiyama Y, Kobayashi M, Ohro Y, Uchida S, Sasaki S, and Togari H.Successful treatment of partial nephrogenic diabetes insipidus with thiazide and desmopressin.Horm Res59: 297\u2013300, 2003.","DOI":"10.1159\/000070629"},{"key":"R96","doi-asserted-by":"publisher","DOI":"10.1385\/ENDO:24:1:055"},{"key":"R97","doi-asserted-by":"publisher","DOI":"10.1042\/cs0660709"},{"key":"R98","doi-asserted-by":"publisher","DOI":"10.1016\/S0165-6147(00)01575-3"},{"key":"R99","doi-asserted-by":"publisher","DOI":"10.1172\/JCI8688"},{"key":"R100","doi-asserted-by":"publisher","DOI":"10.1021\/bi002699r"},{"key":"R101","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0502236102"},{"key":"R102","doi-asserted-by":"publisher","DOI":"10.1210\/jcem-59-6-1044"},{"key":"R103","doi-asserted-by":"publisher","DOI":"10.1172\/JCI2605"},{"key":"R104","doi-asserted-by":"crossref","unstructured":"Mulders SM, Knoers NV, van Lieburg AF, Monnens LAH, Leumann E, Wuhl E, Schober E, Rijss JPL, van Os CH, and Deen PM.New mutations in the AQP2 gene in nephrogenic diabetes insipidus resulting in functional but misrouted water channels.J Am Soc Nephrol8: 242\u2013248, 1997.","DOI":"10.1681\/ASN.V82242"},{"key":"R105","doi-asserted-by":"publisher","DOI":"10.1038\/35036519"},{"key":"R106","doi-asserted-by":"publisher","DOI":"10.1530\/acta.0.0690434"},{"key":"R107","unstructured":"Nascimento L, Rademacher DR, Hamburger R, Arruda JA, and Kurtzman A.On the mechanism of lithium-induced renal tubular acidosis.J Lab Clin Med89: 455\u2013462, 1977."},{"key":"R108","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00321.2005"},{"key":"R109","doi-asserted-by":"crossref","unstructured":"Nielsen J, Kwon TH, Praetorius J, Kim YH, Fr\u00f8ki\u00e6r J, Knepper MA, and Nielsen S.Segment-specific ENaC downregulation in kidney of rats with lithium-induced NDI.Am J Physiol Renal Physiol285: F1198\u2013F1209, 2003.","DOI":"10.1152\/ajprenal.00118.2003"},{"key":"R110","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00024.2001"},{"key":"R111","doi-asserted-by":"publisher","DOI":"10.1016\/j.febslet.2004.05.021"},{"key":"R112","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118222"},{"key":"R113","doi-asserted-by":"crossref","unstructured":"Norregaard R, Jensen BL, Li C, Wang W, Knepper MA, Nielsen S, and Fr\u00f8ki\u00e6r J.COX-2 inhibition prevents downregulation of key renal water and sodium transport proteins in response to bilateral ureteral obstruction.Am J Physiol Renal Physiol289: F322\u2013F333, 2005.","DOI":"10.1152\/ajprenal.00061.2005"},{"key":"R114","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-5793(98)00140-9"},{"key":"R115","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1994.2700"},{"key":"R116","doi-asserted-by":"publisher","DOI":"10.1007\/s004390050264"},{"key":"R117","unstructured":"Oksche A, Schulein R, Rutz C, Liebenhoff U, Dickson J, Muller H, Birnbaumer M, and Rosenthal W.Vasopressin V2 receptor mutants that cause X-linked nephrogenic diabetes insipidus: analysis of expression, processing, and function.Mol Pharmacol50: 820\u2013828, 1996."},{"key":"R118","doi-asserted-by":"publisher","DOI":"10.1016\/S1043-2760(03)00048-1"},{"key":"R119","doi-asserted-by":"crossref","unstructured":"Pan Y, Wilson P, and Gitschier J.The effect of eight V2 vasopressin receptor mutations on stimulation.J Biol Chem269: 31933\u201331937, 1994.","DOI":"10.1016\/S0021-9258(18)31785-X"},{"key":"R120","doi-asserted-by":"crossref","unstructured":"Pasel K, Schulz A, Timmermann K, Linnemann K, Hoeltzenbein M, Jaaskelainen J, Gruters A, Filler G, and Schoneberg T.Functional characterization of the molecular defects causing nephrogenic diabetes insipidus in eight families.J Clin Endocrinol Metab85: 1703\u20131710, 2000.","DOI":"10.1210\/jcem.85.4.6507"},{"key":"R121","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-003-1195-0"},{"key":"R122","doi-asserted-by":"publisher","DOI":"10.1080\/003655902320131811"},{"key":"R123","unstructured":"Pollak MR.Disturbances of calcium metabolism. In:The Kidney, edited by Brenner BM. Philadelphia, PA: Saunders, 2000, p. 1037\u20131054."},{"key":"R124","doi-asserted-by":"publisher","DOI":"10.1016\/S0303-7207(00)00236-7"},{"key":"R125","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.66036.x"},{"key":"R126","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00287.2004"},{"key":"R127","doi-asserted-by":"publisher","DOI":"10.1007\/BF00849258"},{"key":"R128","doi-asserted-by":"publisher","DOI":"10.1210\/jcem.87.7.8677"},{"key":"R129","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00404.2004"},{"key":"R130","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1098-1004(1999)14:3<233::AID-HUMU6>3.0.CO;2-O"},{"key":"R131","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00305.2004"},{"key":"R132","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1976.40"},{"key":"R133","doi-asserted-by":"crossref","unstructured":"Rosenthal W, Antaramian A, Gilbert S, and Birnbaumer M.Nephrogenic diabetes insipidus. A V2 vasopressin receptor unable to stimulate adenylyl cyclase.J Biol Chem268: 13030\u201313033, 1993.","DOI":"10.1016\/S0021-9258(19)38614-4"},{"key":"R134","unstructured":"Rosenthal W, Seibold A, Antaramian A, Gilbert S, Birnbaumer M, Bichet DG, Arthus MF, and Lonergan M.Mutations in the vasopressin V2 receptor gene in families with nephrogenic diabetes insipidus and functional expression of the Q-2 mutant.Cell Mol Biol (Noisy-le-grand)40: 429\u2013436, 1994."},{"key":"R135","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M208999200"},{"key":"R136","doi-asserted-by":"publisher","DOI":"10.1210\/mend.11.12.0017"},{"key":"R137","doi-asserted-by":"publisher","DOI":"10.1210\/mend.11.6.9919"},{"key":"R138","doi-asserted-by":"publisher","DOI":"10.3109\/10799899709036619"},{"key":"R139","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-4615-4871-3_43"},{"key":"R140","doi-asserted-by":"publisher","DOI":"10.1159\/000133885"},{"key":"R141","doi-asserted-by":"publisher","DOI":"10.1007\/s00232-002-1053-1"},{"key":"R142","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119299"},{"key":"R143","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/ddh105"},{"key":"R144","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1098-1004(1998)12:3<196::AID-HUMU7>3.0.CO;2-F"},{"key":"R145","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M007045200"},{"key":"R146","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.275.4.2381"},{"key":"R147","doi-asserted-by":"publisher","DOI":"10.1210\/jc.2002-020286"},{"key":"R148","doi-asserted-by":"crossref","unstructured":"Singh D.Merck withdraws arthritis drug worldwide.BMJ329: 816, 2004.","DOI":"10.1136\/bmj.329.7470.816-a"},{"key":"R149","doi-asserted-by":"crossref","unstructured":"Smith BLand Agre P.ErythrocyteMr28,000 transmembrane protein exists as a multisubunit oligomer similar to channel proteins.J Biol Chem266: 6407\u20136415, 1991.","DOI":"10.1016\/S0021-9258(18)38133-X"},{"key":"R150","doi-asserted-by":"publisher","DOI":"10.3122\/15572625-12-1-43"},{"key":"R151","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00245.2002"},{"key":"R152","doi-asserted-by":"publisher","DOI":"10.1172\/JCI2303"},{"key":"R153","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M301888200"},{"key":"R154","doi-asserted-by":"publisher","DOI":"10.1080\/10408360590886606"},{"key":"R155","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118252"},{"key":"R156","unstructured":"Valtin H, Coffey AK, O'Sullivan DJ, Homma S, and Dousa TP.Causes of the urinary concentrating defect in mice with nephrogenic diabetes insipidus.Physiol Bohemoslov39: 103\u2013111, 1990."},{"key":"R157","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M207525200"},{"key":"R158","doi-asserted-by":"publisher","DOI":"10.1038\/ng1092-99"},{"key":"R159","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-291X(05)80028-2"},{"key":"R160","doi-asserted-by":"crossref","unstructured":"Van Lieburg AF, Knoers NV, and Monnens LA.Clinical presentation and follow-up of 30 patients with congenital nephrogenic diabetes insipidus.J Am Soc Nephrol10: 1958\u20131964, 1999.","DOI":"10.1681\/ASN.V1091958"},{"key":"R161","doi-asserted-by":"publisher","DOI":"10.1007\/BF00868270"},{"key":"R162","unstructured":"Van Lieburg AF, Verdijk MAJ, Knoers NV, van Essen AJ, Proesmans W, Mallmann R, Monnens LAH, van Oost BA, van Os CH, and Deen PM.Patients with autosomal nephrogenic diabetes insipidus homozygous for mutations in the aquaporin 2 water-channel gene.Am J Hum Genet55: 648\u2013652, 1994."},{"key":"R163","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-4615-4871-3_49"},{"key":"R164","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(95)90493-X"},{"key":"R165","unstructured":"Wang W, Li C, Kwon TH, Knepper MA, Fr\u00f8ki\u00e6r J, and Nielsen S.AQP3, p-AQP2, and AQP2 expression is reduced in polyuric rats with hypercalcemia: prevention by cAMP-PDE inhibitors.Am J Physiol Renal Physiol283: F1313\u2013F1325, 2002."},{"key":"R166","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00044.2003"},{"key":"R167","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00070.2005"},{"key":"R168","unstructured":"Wei J, Fish FA, Myerburg RJ, Roden DM, and George AL Jr.Novel KCNQ1 mutations associated with recessive and dominant congenital long QT syndromes: evidence for variable hearing phenotype associated with R518X.Hum Mutat15: 387\u2013388, 2000."},{"key":"R169","doi-asserted-by":"publisher","DOI":"10.1016\/S0303-7207(96)03926-3"},{"key":"R170","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00214.x"},{"key":"R171","unstructured":"Wingo CSand Weiner ID.Disorders of potassium balance. In:The Kidney, edited by Brenner BM. Philadelphia, PA: Saunders, 2000, p. 998\u20131035."},{"key":"R172","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M408154200"},{"key":"R173","doi-asserted-by":"crossref","unstructured":"Yang B, Gillespie A, Carlson EJ, Epstein CJ, and Verkman AS.Neonatal mortality in an aquaporin-2 knock-in mouse model of recessive nephrogenic diabetes insipidus.J Biol Chem276: 2775\u20132779, 2000.","DOI":"10.1074\/jbc.M008216200"},{"key":"R174","doi-asserted-by":"publisher","DOI":"10.1172\/JCI9154"},{"key":"R175","doi-asserted-by":"publisher","DOI":"10.1212\/WNL.47.4.993"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00491.2005","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,7,29]],"date-time":"2021-07-29T08:19:05Z","timestamp":1627546745000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00491.2005"}},"issued":{"date-parts":[[2006,8]]},"references-count":175,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2006,8]]}},"alternative-id":["10.1152\/ajprenal.00491.2005"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00491.2005","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2006,8]]}},{"indexed":{"date-parts":[[2026,2,13]],"date-time":"2026-02-13T10:54:44Z","timestamp":1770980084531,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1997,3,1]]},"abstract":"<jats:p> This study examined the hypothesis that certain immunoglobulin light chains directly altered mesangial cell calcium homeostasis. Intracellular Ca2+ concentration (intracellular [Ca2+]) signaling was determined in suspensions of rat mesangial cells using the acetoxymethyl ester of fura 2 with a calcium removal\/replacement protocol. Pretreatment of cultured rat mesangial cells with a glomerulopathic kappa-light chain (gle) produced reversible dose- and time-dependent attenuation of ATP- and thrombin-evoked [Ca2+] transients (189 +\/- 24 vs. 126 +\/- 10 nM, P &lt; 0.05 with ATP; 198 +\/- 5 vs. 117 +\/- 3 nM, P &lt; 0.05 with thrombin) and capacitative calcium influx (199 +\/- 14 vs. 142 +\/- 17 nM, P &lt; 0.05 for ATP; 252 +\/- 19 vs. 198 +\/- 18 nM, P &lt; 0.05 for thrombin). Mesangial cells treated with gle and supplemented with myo-inositol (450 microM) did not demonstrate the attenuation of the ATP-evoked [Ca2+] transient and capacitative calcium influx. Gle also decreased mean [Ca2+] transient (80 +\/- 7 vs. 56 +\/- 1 nM, P &lt; 0.05) and capacitative calcium influx (306 +\/- 10 vs. 241 +\/- 4 nM, P &lt; 0.05) in response to thapsigargin, a Ca2+-adenosinetriphosphatase inhibitor. This inhibition was not reversed by exogenous myo-inositol. Another kappa-light chain (10 microg\/ml) did not affect mesangial cell calcium signaling. Deranged mesangial cell calcium homeostasis by certain light chains may play a central pathogenetic role in glomerulosclerosis associated with deposition of immunoglobulin light chains. <\/jats:p>","DOI":"10.1152\/ajprenal.1997.272.3.f319","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T08:08:36Z","timestamp":1514016516000},"page":"F319-F324","source":"Crossref","is-referenced-by-count":4,"title":["Immunoglobulin light chain alters mesangial cell calcium homeostasis"],"prefix":"10.1152","volume":"272","author":[{"given":"L.","family":"Zhu","sequence":"first","affiliation":[{"name":"Department of Pathology, University of Alabama at Birmingham,35294-0007, USA."}]},{"given":"G. A.","family":"Herrera","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Alabama at Birmingham,35294-0007, USA."}]},{"given":"C. R.","family":"White","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Alabama at Birmingham,35294-0007, USA."}]},{"given":"P. W.","family":"Sanders","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Alabama at Birmingham,35294-0007, USA."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1997.272.3.F319","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:12:56Z","timestamp":1567973576000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1997.272.3.F319"}},"issued":{"date-parts":[[1997,3,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1997,3,1]]}},"alternative-id":["10.1152\/ajprenal.1997.272.3.F319"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1997.272.3.f319","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1997,3,1]]}},{"indexed":{"date-parts":[[2026,2,12]],"date-time":"2026-02-12T15:30:32Z","timestamp":1770910232804,"version":"3.50.1"},"reference-count":43,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2007,1]]},"abstract":"<jats:p>It is unknown if endothelin-A and -B receptors (ET<jats:sub>A<\/jats:sub>R and ET<jats:sub>B<\/jats:sub>R) activate the production of superoxide via NAD(P)H oxidase and subsequently stimulate the formation of cyclic adenine diphosphate ribose (cADPR) in afferent arterioles. Vessels were isolated from rat kidney and loaded with fura 2. Endothelin-1 (ET-1) rapidly increased cytosolic Ca<jats:sup>2+<\/jats:sup>concentration ([Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>) by 303 nM. The superoxide dismutase mimetic tempol, the NAD(P)H oxidase inhibitor apocynin, and nicotinamide, an inhibitor of ADPR cyclase, diminished the response by \u223c60%. The ET<jats:sub>B<\/jats:sub>R agonist sarafotoxin 6c (S6c) increased peak [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>by 117 nM. Subsequent addition of ET-1 in the continued presence of S6c caused an additional [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>peak of 225 nM. Neither nicotinamide or 8-bromo- (8-Br) cADPR nor apocynin decreased the [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>response to S6c, but inhibited the subsequent [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>response to ET-1. The ET<jats:sub>B<\/jats:sub>R blockers BQ-788 and A-192621 prevented the S6c [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>peak and reduced the ET-1 response by more than one-half, suggesting an ET<jats:sub>B<\/jats:sub>R\/ET<jats:sub>A<\/jats:sub>R interaction. In contrast, the ET<jats:sub>A<\/jats:sub>R blocker BQ-123 had no effect on the S6c [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>peak and obliterated the subsequent ET-1 response. ET-1 immediately stimulated superoxide formation (measured with TEMPO-9-AC, 68 arbitrary units) that was inhibited 95% by apocynin or diphenyl iodonium. S6c or IRL-1620 increased superoxide by 8% of that caused by subsequent ET-1 addition. We conclude that ET<jats:sub>A<\/jats:sub>R activation of afferent arterioles increases the formation of superoxide that accounts for \u223c60% of subsequent Ca<jats:sup>2+<\/jats:sup>signaling. ET<jats:sub>B<\/jats:sub>R activation appears to result in only minor increases in superoxide production. Nicotinamide and 8-Br-cADPR results suggest that ET-1 (and primarily ET<jats:sub>A<\/jats:sub>R) causes the activation of vascular smooth muscle cell-ADPR cyclase.<\/jats:p>","DOI":"10.1152\/ajprenal.00050.2006","type":"journal-article","created":{"date-parts":[[2006,6,21]],"date-time":"2006-06-21T04:13:21Z","timestamp":1150863201000},"page":"F175-F184","source":"Crossref","is-referenced-by-count":36,"title":["Endothelin-A and -B receptors, superoxide, and Ca<sup>2+<\/sup>signaling in afferent arterioles"],"prefix":"10.1152","volume":"292","author":[{"given":"Susan K.","family":"Fellner","sequence":"first","affiliation":[]},{"given":"William","family":"Arendshorst","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1096\/fj.01-0749com"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000039568.93355.85"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000126068.27125.42"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1016\/0167-0115(95)00112-1"},{"key":"R5","unstructured":"Edwards RMand Trizna W.Characterization of125I-endothelin-1 binding to rat and rabbit renal microvasculature.J Pharmacol Exp Ther274: 1084\u20131089, 1995."},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1996.sp021761"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1002\/1097-010X(20010415\/30)289:5<273::AID-JEZ1>3.0.CO;2-L"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00372.2004"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00579.x"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00144.2005"},{"key":"R11","unstructured":"Fellner SKand Parker L.Endothelin B Ca2+signaling inSqualus acanthiasvascular smooth muscle: participation of IP3and ryanodine receptors.Bull Mt Desert Isl Biol Lab Salisb Cove Maine43: 6\u20137, 2004."},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1242\/jeb.01506"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1242\/jeb.01134"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/15.3.339"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M403601200"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1016\/S0898-6568(99)00004-2"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1023\/A:1019822107048"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1023\/A:1022557717481"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0706412"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.91.11.4892"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00368.2003"},{"key":"R22","doi-asserted-by":"crossref","unstructured":"Kanzawa N, Poma CP, Takebayashi-Suzuki K, Diaz KG, Layliev J, and Mikawa T.Competency of embryonic cardiomyocytes to undergo Purkinje fiber differentiation is regulated by endothelin receptor expression.Development129: 3185\u20133194, 2002.","DOI":"10.1242\/dev.129.13.3185"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1097\/00005344-199100177-00133"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000084853.47326.F2"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0702846"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1998.274.3.H752"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00315.2004"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1006\/abio.1993.1295"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.5.F697"},{"key":"R29A","doi-asserted-by":"crossref","unstructured":"Sauvageau S, Thorin E, Caron A, Dupuis J.Evaluation of endothelin-1-induced pulmonary vasoconstriction following myocardial infarction.Exp Biol Med (Maywood)231: 840\u2013846, 2006.","DOI":"10.3181\/00379727-231-2310840"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000084372.91932.BA"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1242\/jeb.01834"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1097\/00005344-200408000-00009"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1161\/01.ATV.0000069236.27911.68"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-200406000-00015"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.10.5647"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1161\/hh1601.094983"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1369\/jhc.4A6474.2005"},{"key":"R38","unstructured":"Wu-Wong JR, Dixon DB, Chiou WJ, Sorensen BK, Liu G, Jae HS, Tasker A, von Geldern TW, Winn M, and Opgenorth TJ.Pharmacology of endothelin receptor antagonists ABT-627, ABT-546, A-182086 and A-192621: in vitro studies.Clin Sci (Lond)103,Suppl48: 107S\u2013111S, 2002."},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00174.2004"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1016\/j.mvr.2003.11.001"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00441.2005"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1016\/0041-0101(92)90540-L"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00050.2006","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,1,9]],"date-time":"2025-01-09T13:56:47Z","timestamp":1736431007000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00050.2006"}},"issued":{"date-parts":[[2007,1]]},"references-count":43,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2007,1]]}},"alternative-id":["10.1152\/ajprenal.00050.2006"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00050.2006","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2007,1]]}},{"indexed":{"date-parts":[[2026,2,16]],"date-time":"2026-02-16T02:51:15Z","timestamp":1771210275035,"version":"3.50.1"},"reference-count":50,"publisher":"American Physiological Society","issue":"2","funder":[{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health (NIH)","doi-asserted-by":"publisher","award":["R01DK069403"],"award-info":[{"award-number":["R01DK069403"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health (NIH)","doi-asserted-by":"publisher","award":["R01DK112652"],"award-info":[{"award-number":["R01DK112652"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health (NIH)","doi-asserted-by":"publisher","award":["1P30DK079307"],"award-info":[{"award-number":["1P30DK079307"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000097","name":"HHS | NIH | National Center for Research Resources (NCRR)","doi-asserted-by":"publisher","award":["1S10RR028478-01"],"award-info":[{"award-number":["1S10RR028478-01"]}],"id":[{"id":"10.13039\/100000097","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2018,8,1]]},"abstract":"<jats:p>Sepsis-associated acute kidney injury (S-AKI) independently predicts mortality among critically ill patients. The role of innate immunity in this process is unclear, and there is an unmet need for S-AKI models to delineate the pathophysiological response. Mammals and zebrafish ( Danio rerio) share a conserved nephron structure and homologous innate immune systems, making the latter suitable for S-AKI research. We introduced Edwardsiella tarda to the zebrafish. Systemic E. tarda bacteremia resulted in sustained bacterial infection and dose-dependent mortality. A systemic immune reaction was characterized by increased mRNA expressions of il1b, tnfa, tgfb1a, and cxcl8-l1 ( P\u2009&lt; 0.0001, P\u2009&lt; 0.001, P\u2009&lt; 0.001, and P\u2009&lt; 0.01, respectively). Increase of host stress response genes ccnd1 and tp53 was observed at 24 h postinjection ( P\u2009&lt; 0.0001 and P\u2009&lt; 0.05, respectively). Moderate E. tarda infection induced zebrafish mortality of over 50% in larvae and 20% in adults, accompanied by pericardial edema in larvae and renal dysfunction in both larval and adult zebrafish. Expression of AKI markers insulin-like growth factor-binding protein-7 (IGFBP7), tissue inhibitor of metalloproteinases 2 (TIMP-2), and kidney injury molecule-1 (KIM-1) was found to be significantly increased in the septic animals at the transcription level ( P\u2009&lt; 0.01, P\u2009&lt; 0.05, and P\u2009&lt; 0.05) and in nephric tubules compared with noninfected animals. In conclusion, we established a zebrafish model of S-AKI induced by E. tarda injection, with both larval and adult zebrafish showing nephron injury in the setting of infection.<\/jats:p>","DOI":"10.1152\/ajprenal.00328.2017","type":"journal-article","created":{"date-parts":[[2018,3,14]],"date-time":"2018-03-14T14:30:17Z","timestamp":1521037817000},"page":"F291-F299","source":"Crossref","is-referenced-by-count":38,"title":["A zebrafish model of infection-associated acute kidney injury"],"prefix":"10.1152","volume":"315","author":[{"given":"Xiaoyan","family":"Wen","sequence":"first","affiliation":[{"name":"Center for Critical Care Nephrology, Department of Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania"}]},{"given":"Liyan","family":"Cui","sequence":"additional","affiliation":[{"name":"Center for Critical Care Nephrology, Department of Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania"}]},{"given":"Seth","family":"Morrisroe","sequence":"additional","affiliation":[{"name":"Center for Critical Care Nephrology, Department of Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania"}]},{"suffix":"Jr","given":"Donald","family":"Maberry","sequence":"additional","affiliation":[{"name":"Center for Critical Care Nephrology, Department of Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania"}]},{"given":"David","family":"Emlet","sequence":"additional","affiliation":[{"name":"Center for Critical Care Nephrology, Department of Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania"}]},{"given":"Simon","family":"Watkins","sequence":"additional","affiliation":[{"name":"Center for Biologic Imaging, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania"}]},{"given":"Neil A.","family":"Hukriede","sequence":"additional","affiliation":[{"name":"Center for Critical Care Nephrology, Department of Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania"},{"name":"Department of Developmental Biology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania"}]},{"given":"John A.","family":"Kellum","sequence":"additional","affiliation":[{"name":"Center for Critical Care Nephrology, Department of Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.02954"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1002\/cphy.c110041"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1172\/JCI45161"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.63.3.883"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014111108"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.3791\/2079"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2012111055"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1186\/s40560-016-0146-3"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1172\/JCI39421"},{"key":"B10","doi-asserted-by":"crossref","first-page":"4655","DOI":"10.1242\/dev.125.23.4655","volume":"125","author":"Drummond IA","year":"1998","journal-title":"Development"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00271.2016"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1186\/cc9031"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1097\/SHK.0b013e3181e7e69e"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1038\/nrg892"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1038\/nm.3893"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00009.2007"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00386.2004"},{"key":"B18","doi-asserted-by":"crossref","first-page":"3735","DOI":"10.1242\/dev.126.17.3735","volume":"126","author":"Herbomel P","year":"1999","journal-title":"Development"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/S0925-4773(02)00094-1"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1038\/nature12813."},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/j.clim.2008.08.016"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2014.180"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.3791\/2845"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1001\/archinte.167.15.1655"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1097\/CCM.0000000000002206"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1093\/bioinformatics\/btt703"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/S0145-305X(03)00103-4"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.178.7.4385"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.02473-14"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1001\/jama.2014.5804"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2013.08.005"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.2174\/138945011795677809"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0041816"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1016\/j.dci.2004.10.007"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1016\/j.tox.2007.09.007"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1177\/1087057113495296"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.0801755"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1155\/2015\/504259"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2011.201"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.71.3.1343-1351.2003"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1186\/gb-2007-8-11-r251"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/advan.00058.2013"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M113.541953"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1371\/journal.ppat.1002349"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1242\/dmm.015594"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1155\/2012\/159807"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1186\/1471-2172-12-58"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1016\/j.jss.2010.11.923"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1089\/zeb.2014.1023"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010050484"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00328.2017","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,16]],"date-time":"2022-08-16T00:58:53Z","timestamp":1660611533000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00328.2017"}},"issued":{"date-parts":[[2018,8,1]]},"references-count":50,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2018,8,1]]}},"alternative-id":["10.1152\/ajprenal.00328.2017"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00328.2017","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2018,8,1]]}},{"indexed":{"date-parts":[[2026,2,12]],"date-time":"2026-02-12T12:15:52Z","timestamp":1770898552918,"version":"3.50.1"},"reference-count":27,"publisher":"American Physiological Society","issue":"6","funder":[{"DOI":"10.13039\/100005384","name":"American Physiological Society","doi-asserted-by":"publisher","award":["William Townsend Porter Predoctoral Fellowship"],"award-info":[{"award-number":["William Townsend Porter Predoctoral Fellowship"]}],"id":[{"id":"10.13039\/100005384","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health","doi-asserted-by":"publisher","award":["R25GM109441"],"award-info":[{"award-number":["R25GM109441"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100008717","name":"Sylvia and Charles Viertel Charitable Foundation","doi-asserted-by":"publisher","award":["Senior Medical Research Fellowship"],"award-info":[{"award-number":["Senior Medical Research Fellowship"]}],"id":[{"id":"10.13039\/100008717","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000925","name":"Department of Health, Australian Government | National Health and Medical Research Council","doi-asserted-by":"publisher","award":["GNT2017382"],"award-info":[{"award-number":["GNT2017382"]}],"id":[{"id":"10.13039\/501100000925","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK076169"],"award-info":[{"award-number":["DK076169"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK115255"],"award-info":[{"award-number":["DK115255"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000968","name":"American Heart Association","doi-asserted-by":"publisher","award":["Established Investigator Award"],"award-info":[{"award-number":["Established Investigator Award"]}],"id":[{"id":"10.13039\/100000968","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["R01DK137762"],"award-info":[{"award-number":["R01DK137762"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000925","name":"DHAC | National Health and Medical Research Council","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100000925","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2024,6,1]]},"abstract":"<jats:p> We explore the role of the gut microbiome in regulating aldosterone, a hormone closely linked to blood pressure and cardiovascular disease. Despite the recognized importance of the gut microbiome in host physiology, the relationship with circulating aldosterone remains largely unexplored. We demonstrate that suppression of gut microbiota leads to increased levels of plasma and urinary aldosterone. These findings underscore the potential of the gut microbiota to influence aldosterone regulation, suggesting new possibilities for treating hypertension. <\/jats:p>","DOI":"10.1152\/ajprenal.00051.2024","type":"journal-article","created":{"date-parts":[[2024,4,18]],"date-time":"2024-04-18T08:01:51Z","timestamp":1713427311000},"page":"F1032-F1038","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":4,"title":["Commensal microbiota regulate aldosterone"],"prefix":"10.1152","volume":"326","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2188-4629","authenticated-orcid":false,"given":"Brittni N.","family":"Moore","sequence":"first","affiliation":[{"name":"Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States"}]},{"given":"Alexandra D.","family":"Medcalf","sequence":"additional","affiliation":[{"name":"Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States"}]},{"given":"Rachel Q.","family":"Muir","sequence":"additional","affiliation":[{"name":"Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States"}]},{"ORCID":"https:\/\/orcid.org\/0009-0004-2918-9836","authenticated-orcid":false,"given":"Chudan","family":"Xu","sequence":"additional","affiliation":[{"name":"School of Biological Sciences, Faculty of Medicine, Monash University, Clayton, Victoria, Australia"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4920-9991","authenticated-orcid":false,"given":"Francine Z.","family":"Marques","sequence":"additional","affiliation":[{"name":"School of Biological Sciences, Faculty of Medicine, Monash University, Clayton, Victoria, Australia"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3621-2665","authenticated-orcid":false,"given":"Jennifer L.","family":"Pluznick","sequence":"additional","affiliation":[{"name":"Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.7326\/M20-0065"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1503\/cmaj.161486"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.00099.2021"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.121.17288"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/physiolgenomics.00089.2016"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2016.06.033"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1038\/s41581-022-00654-0"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/s41440-023-01334-7"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.26402\/jpp.2019.2.03"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/j.biopha.2022.114149"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1215927110"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00417.2015"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.119.316394"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00584.2018"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2021.01.020"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00303.2022"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00303.2022"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-84-6-639"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1161\/01.cir.95.1.39"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1159\/000505788"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.123.21983"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1007\/s00345-012-1011-1"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2017030295"},{"key":"B24","first-page":"87","volume":"77","author":"Kotchen TA","year":"1984","journal-title":"Arch Mal Coeur Vaiss"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1111\/j.1472-8206.2010.00854.x"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1126\/science.aad9378"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.4161\/gmic.23362"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00051.2024","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,5,30]],"date-time":"2024-05-30T14:59:25Z","timestamp":1717081165000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00051.2024"}},"issued":{"date-parts":[[2024,6,1]]},"references-count":27,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2024,6,1]]}},"alternative-id":["10.1152\/ajprenal.00051.2024"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00051.2024","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2024,6,1]]},"assertion":[{"value":"2024-02-20","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2024-03-22","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2024-04-09","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2024-05-30","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,2,18]],"date-time":"2026-02-18T00:09:30Z","timestamp":1771373370738,"version":"3.50.1"},"reference-count":40,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2010,1]]},"abstract":"<jats:p>Acute renal failure (ARF) is frequently associated with polyuria and urine concentration defects and it is a severe complication of sepsis because it increases the mortality rate. Inhibition of NF-\u03baB activation has been suggested to provide a useful strategy for the treatment of septic shock. However, the impact on sepsis-induced ARF is still unclear. Therefore, we examined the effect of pyrrolidine dithiocarbamate (PDTC) and of small interfering RNA (siRNA) silencing NF-\u03baB p50\/p105 on sepsis-induced downregulation of vasopressin V<jats:sub>2<\/jats:sub>receptors and aquaporin (AQP)-2 channels using a cecal ligation and puncture (CLP) mouse model. CLP caused a time-dependent downregulation of renal vasopressin V<jats:sub>2<\/jats:sub>receptor and of AQP2 expression without alterations in plasma vasopressin levels. Renal activation of NF-\u03baB in response to CLP was attenuated by PDTC pretreatment, which also attenuated the downregulation of V<jats:sub>2<\/jats:sub>receptor and AQP2 expression. Furthermore, a strong nuclear staining for the NF-\u03baB p50 subunit throughout the whole kidney in response to CLP was observed. siRNA against NF-\u03baB p50 attenuated the CLP-induced nuclear translocation of the p50 subunit and the CLP-induced downregulation of V<jats:sub>2<\/jats:sub>receptor and AQP2 expression. Additionally, PDTC and siRNA pretreatment inhibited the CLP-induced increase in renal TNF-\u03b1 and IL-1\u03b2 concentration and NOS-2 mRNA abundance. Moreover, PDTC and siRNA pretreatment ameliorated CLP-induced hypotension and ARF. Our findings suggest that NF-\u03baB activation is of importance for the downregulation of AQP2 channel and vasopressin V<jats:sub>2<\/jats:sub>receptor expression during sepsis. In addition, our data indicate that NF-\u03baB inhibition ameliorates sepsis-induced ARF.<\/jats:p>","DOI":"10.1152\/ajprenal.90607.2008","type":"journal-article","created":{"date-parts":[[2009,10,15]],"date-time":"2009-10-15T01:50:20Z","timestamp":1255571420000},"page":"F196-F204","source":"Crossref","is-referenced-by-count":74,"title":["Inhibition of NF-\u03baB ameliorates sepsis-induced downregulation of aquaporin-2\/V<sub>2<\/sub>receptor expression and acute renal failure in vivo"],"prefix":"10.1152","volume":"298","author":[{"given":"Klaus","family":"H\u00f6cherl","sequence":"first","affiliation":[{"name":"Institut f\u00fcr Physiologie and"}]},{"given":"Christoph","family":"Schmidt","sequence":"additional","affiliation":[{"name":"Klinik f\u00fcr An\u00e4sthesiologe, Universit\u00e4t Regensburg, Regensburg, Germany"}]},{"given":"Birg\u00fcl","family":"Kurt","sequence":"additional","affiliation":[{"name":"Institut f\u00fcr Physiologie and"}]},{"given":"Michael","family":"Bucher","sequence":"additional","affiliation":[{"name":"Klinik f\u00fcr An\u00e4sthesiologe, Universit\u00e4t Regensburg, Regensburg, Germany"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1097\/01.CCM.0000266684.17500.2F"},{"key":"B2","doi-asserted-by":"crossref","first-page":"923","DOI":"10.1681\/ASN.V105923","volume":"10","author":"Bens M","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1007\/s00134-003-1887-8"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1001\/archinte.1982.00340230128022"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.97"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1096\/fj.02-1078fje"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00378.x"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M708350200"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.1998.tb02258.x"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000059863.48590.E9"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.102.036194"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1521-4141(199906)29:06<1890::AID-IMMU1890>3.0.CO;2-F"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1001\/jama.1996.03530430033035"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajplung.00477.2005"},{"key":"B15","doi-asserted-by":"crossref","first-page":"3976","DOI":"10.4049\/jimmunol.159.8.3976","volume":"159","author":"Liu SF","year":"1997","journal-title":"J Immunol"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.100.12.1330"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa022139"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00513.2006"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1093\/oxfordjournals.ndt.a027256"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00024.2001"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199305203282008"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1081\/JDI-100108188"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1001\/jama.1995.03520260039030"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1172\/JCI200319523"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00460.2006"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00258.2006"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1097\/CCM.0b013e318180b51d"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1097\/01.ccm.0000281447.22966.8b"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006050454"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00178.x"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1084\/jem.175.5.1181"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00124.2005"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1097\/shk.0b013e3180ca9e53"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00439.2007"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.01249.2007"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1016\/0022-4804(80)90037-2"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000022"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00023.2005"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00072.2006"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00485.2005"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.90607.2008","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,3,17]],"date-time":"2024-03-17T04:05:38Z","timestamp":1710648338000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.90607.2008"}},"issued":{"date-parts":[[2010,1]]},"references-count":40,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2010,1]]}},"alternative-id":["10.1152\/ajprenal.90607.2008"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.90607.2008","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2010,1]]}},{"indexed":{"date-parts":[[2026,2,5]],"date-time":"2026-02-05T21:27:44Z","timestamp":1770326864852,"version":"3.49.0"},"reference-count":59,"publisher":"American Physiological Society","issue":"4","funder":[{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)","doi-asserted-by":"publisher","award":["R01DK099196"],"award-info":[{"award-number":["R01DK099196"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)","doi-asserted-by":"publisher","award":["R01DK084060"],"award-info":[{"award-number":["R01DK084060"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)","doi-asserted-by":"publisher","award":["P30-DK079307"],"award-info":[{"award-number":["P30-DK079307"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2018,10,1]]},"abstract":"<jats:p> Acid-sensing ion channels (ASICs) are trimeric proton-activated, cation-selective neuronal channels that are considered to play important roles in mechanosensation and nociception. Here we investigated the role of ASIC3, a subunit primarily expressed in sensory neurons, in bladder sensory signaling and function. We found that extracellular acidification evokes a transient increase in current, consistent with the kinetics of activation and desensitization of ASICs, in ~25% of the bladder sensory neurons harvested from both wild-type (WT) and ASIC3 knockout (KO) mice. The absence of ASIC3 increased the magnitude of the peak evoked by extracellular acidification and reduced the rate of decay of the ASIC-like currents. These findings suggest that ASICs are assembled as heteromers and that the absence of ASIC3 alters the composition of these channels in bladder sensory neurons. Consistent with the notion that ASIC3 serves as a proton sensor, 59% of the bladder sensory neurons harvested from WT, but none from ASIC3 KO mice, fired action potentials in response to extracellular acidification. Studies of bladder function revealed that ASIC3 deletion reduces voiding volume and the pressure required to trigger micturition. In summary, our findings indicate that ASIC3 plays a role in the control of bladder function by modulating the response of afferents to filling. <\/jats:p>","DOI":"10.1152\/ajprenal.00630.2017","type":"journal-article","created":{"date-parts":[[2018,3,21]],"date-time":"2018-03-21T10:57:08Z","timestamp":1521629828000},"page":"F870-F879","source":"Crossref","is-referenced-by-count":17,"title":["ASIC3 fine-tunes bladder sensory signaling"],"prefix":"10.1152","volume":"315","author":[{"given":"Nicolas","family":"Montalbetti","sequence":"first","affiliation":[{"name":"Renal-Electrolyte Division, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania"}]},{"given":"James G.","family":"Rooney","sequence":"additional","affiliation":[{"name":"Renal-Electrolyte Division, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania"}]},{"given":"Allison L.","family":"Marciszyn","sequence":"additional","affiliation":[{"name":"Renal-Electrolyte Division, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania"}]},{"given":"Marcelo D.","family":"Carattino","sequence":"additional","affiliation":[{"name":"Renal-Electrolyte Division, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania"},{"name":"Department of Cell Biology, University of Pittsburgh, Pittsburgh, Pennsylvania"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1097\/00001756-200007140-00031"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1600-0854.2003.00156.x"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002439"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1046\/j.1471-4159.1999.0720051.x"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1007\/BF00657509"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1007\/BF00580280"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M104030200"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2014.283119"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.032678399"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00030.2012"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1002\/nau.20837"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00072.2015"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.17.10240"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.122245999"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00618.2009"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1097\/MOU.0b013e3283476ea2"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/jn.00945.2012"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.5239-04.2005"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/jn.00211.2007"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1111\/apha.12014"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1007\/978-3-540-79090-7_4"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-5793(98)00916-8"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M112.441964"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1016\/0304-3959(96)02993-4"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1407018111"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1976.sp011476"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1038\/nrn2401"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1038\/nm.2844"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1023\/A:1006903507321"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.94.4.1459"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1096\/fj.12-220400"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1097\/00001756-200006050-00003"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1993.sp019604"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1016\/j.autneu.2015.06.002"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1016\/S0079-6123(08)62758-2"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.0703-05.2005"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00007.2002"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1124\/pr.114.009225"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1111\/j.1464-410X.2009.08658.x"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M113.504324"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1253\/circj.CJ-10-0607"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1038\/378730a0"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1186\/1744-8069-1-35"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00200.2015"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2013.261180"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1016\/S0896-6273(01)00547-5"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.14.7879"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1046\/j.1442-2042.10.s1.4.x"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1002\/mrd.22489"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1038\/nmeth.2089"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1152\/jn.1994.72.5.2420"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M110.202366"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.18.10433"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1172\/JCI24086"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-4899-1585-6_29"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1186\/1471-2105-13-134"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.19-11-04644.1999"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00175.2015"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0018704"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00630.2017","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,20]],"date-time":"2019-09-20T00:37:59Z","timestamp":1568939879000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00630.2017"}},"issued":{"date-parts":[[2018,10,1]]},"references-count":59,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2018,10,1]]}},"alternative-id":["10.1152\/ajprenal.00630.2017"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00630.2017","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2018,10,1]]}},{"indexed":{"date-parts":[[2026,2,5]],"date-time":"2026-02-05T09:21:26Z","timestamp":1770283286019,"version":"3.49.0"},"reference-count":125,"publisher":"American Physiological Society","issue":"6","funder":[{"DOI":"10.13039\/100000968","name":"American Heart Association (AHA)","doi-asserted-by":"crossref","award":["12BGIA9840020"],"award-info":[{"award-number":["12BGIA9840020"]}],"id":[{"id":"10.13039\/100000968","id-type":"DOI","asserted-by":"crossref"}]},{"name":"Diabetic Complications Consortium"},{"name":"HHS | NIH | National Institute of Mental Health (NIMH)","award":["R01 MH096979"],"award-info":[{"award-number":["R01 MH096979"]}]},{"name":"HHS | NIH | National Institute of Biomedical Imaging and Bioengineering (NIBIB)","award":["P41 EB015897"],"award-info":[{"award-number":["P41 EB015897"]}]},{"name":"HHS | National Institutes of Health (NIH)","award":["S10 OD010683"],"award-info":[{"award-number":["S10 OD010683"]}]},{"name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)","award":["DK091722"],"award-info":[{"award-number":["DK091722"]}]},{"name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)","award":["DK088375"],"award-info":[{"award-number":["DK088375"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2016,12,1]]},"abstract":"<jats:p>MRI can provide excellent detail of renal structure and function. Recently, novel MR contrast mechanisms and imaging tools have been developed to evaluate microscopic kidney structures including the tubules and glomeruli. Quantitative MRI can assess local tubular function and is able to determine the concentrating mechanism of the kidney noninvasively in real time. Measuring single nephron function is now a near possibility. In parallel to advancing imaging techniques for kidney microstructure is a need to carefully understand the relationship between the local source of MRI contrast and the underlying physiological change. The development of these imaging markers can impact the accurate diagnosis and treatment of kidney disease. This study reviews the novel tools to examine kidney microstructure and local function and demonstrates the application of these methods in renal pathophysiology.<\/jats:p>","DOI":"10.1152\/ajprenal.00134.2016","type":"journal-article","created":{"date-parts":[[2016,9,15]],"date-time":"2016-09-15T02:08:55Z","timestamp":1473905335000},"page":"F1109-F1124","source":"Crossref","is-referenced-by-count":30,"title":["MRI tools for assessment of microstructure and nephron function of the kidney"],"prefix":"10.1152","volume":"311","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3712-5558","authenticated-orcid":false,"given":"Luke","family":"Xie","sequence":"first","affiliation":[{"name":"Utah Center for Advanced Imaging Research, Department of Radiology, University of Utah, Salt Lake City, Utah;"}]},{"given":"Kevin M.","family":"Bennett","sequence":"additional","affiliation":[{"name":"Department of Biology, University of Hawaii at Manoa, Honolulu, Hawaii;"}]},{"given":"Chunlei","family":"Liu","sequence":"additional","affiliation":[{"name":"Center for In Vivo Microscopy, Department of Radiology, Duke University Medical Center, Durham, North Carolina; and"},{"name":"Brain Imaging and Analysis Center, Duke University Medical Center, Durham, North Carolina"}]},{"given":"G. Allan","family":"Johnson","sequence":"additional","affiliation":[{"name":"Center for In Vivo Microscopy, Department of Radiology, Duke University Medical Center, Durham, North Carolina; and"}]},{"given":"Jeff Lei","family":"Zhang","sequence":"additional","affiliation":[{"name":"Utah Center for Advanced Imaging Research, Department of Radiology, University of Utah, Salt Lake City, Utah;"}]},{"given":"Vivian S.","family":"Lee","sequence":"additional","affiliation":[{"name":"Utah Center for Advanced Imaging Research, Department of Radiology, University of Utah, Salt Lake City, Utah;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1364\/AO.46.006623"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2015.316"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1006\/jmrb.1996.0086"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00092.2014"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1002\/mrm.24619"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00044.2011"},{"key":"B7","first-page":"233","volume":"52","author":"Bekkevold CM","year":"2013","journal-title":"J Am Assoc Lab Anim Sci"},{"key":"B8","first-page":"67","volume":"1397","author":"Bennett KM","year":"2016","journal-title":"Mol Biol"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00714.2012"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1002\/mrm.21684"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1006\/nimg.2000.0567"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2015.219"},{"key":"B13","first-page":"R298","volume":"258","author":"Beuchat CA","year":"1990","journal-title":"Am J Physiol"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1002\/jmri.24365"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuroimage.2015.08.015"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1002\/mrm.25144"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000079785.13922.F6"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.me.44.020193.000331"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/j.zemedi.2015.12.008"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-014-2758-y"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1177\/0284185113498076"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1002\/cmmi.1578"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1016\/0022-5320(72)90087-1"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1002\/mrm.21710"},{"key":"B25","doi-asserted-by":"crossref","first-page":"194","DOI":"10.1002\/mrm.22187","volume":"63","author":"de Rochefort L","year":"2010","journal-title":"Magn Reson Med"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006010017"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1002\/mrm.20666"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1186\/s12968-015-0159-4"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1007\/BF00317960"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.3348\/kjr.2015.16.4.827"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0610821104"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.02900313"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1002\/mrm.21801"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1007\/BF01395707"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1016\/j.mri.2011.02.032"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00824.2011"},{"key":"B37","doi-asserted-by":"crossref","first-page":"281","DOI":"10.1007\/BF02889441","volume":"25","author":"Glaumann B","year":"1977","journal-title":"Virchows Arch B Cell Pathol Incl Mol Pathol"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1002\/mrm.1910280209"},{"key":"B39","first-page":"317","volume":"17","author":"Gurses B","year":"2011","journal-title":"Diagn Interv Radiol"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1002\/mrm.20198"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfr273"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1097\/RLI.0b013e31824f272d"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010111143"},{"key":"B44","unstructured":"Jamison RL.Urinary Concentrating Mechanism: Structure and Function. New York, NY: Oxford University, 1982, p. viii, 340."},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1177\/0192623310389622"},{"key":"B46","first-page":"1","volume":"9","author":"Johnson GA","year":"1993","journal-title":"Magnes Res"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1002\/jmri.10175"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuroimage.2011.10.078"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1007\/978-3-540-45243-0_4"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1148\/radiol.12112522"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00263.2011"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0910222107"},{"key":"B53","first-page":"17","volume":"14","author":"Lester DS","year":"1999","journal-title":"Spectroscopy"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1172\/JCI103853"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1002\/mrm.1276"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1002\/nbm.3056"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1002\/jmri.1880070209"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuroimage.2011.10.038"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuroimage.2010.11.088"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuroimage.2012.04.042"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1023\/A:1008045108935"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1002\/mrm.22482"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1002\/jmri.24768"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuroimage.2011.07.096"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuroimage.2011.08.082"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1002\/mrm.24272"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1109\/TMI.2011.2182523"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7580.2004.00264.x"},{"key":"B69","doi-asserted-by":"publisher","DOI":"10.1016\/0010-406X(69)92086-6"},{"key":"B70","doi-asserted-by":"publisher","DOI":"10.1007\/s11934-011-0229-6"},{"key":"B71","doi-asserted-by":"publisher","DOI":"10.1103\/PhysRevLett.35.397"},{"key":"B72","doi-asserted-by":"publisher","DOI":"10.1080\/01926230490451707"},{"key":"B73","doi-asserted-by":"publisher","DOI":"10.1002\/cmr.b.20034"},{"key":"B74","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuroimage.2009.02.023"},{"key":"B75","doi-asserted-by":"publisher","DOI":"10.1136\/bmj.2.4893.901"},{"key":"B76","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1522-2586(199906)9:6<832::AID-JMRI10>3.0.CO;2-1"},{"key":"B77","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005070757"},{"key":"B78","doi-asserted-by":"publisher","DOI":"10.1111\/apha.12393"},{"key":"B79","doi-asserted-by":"publisher","DOI":"10.1097\/RLI.0b013e31817d14e6"},{"key":"B80","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00114.2005"},{"key":"B81","doi-asserted-by":"publisher","DOI":"10.1148\/radiol.13121352"},{"key":"B82","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00326.2014"},{"key":"B83","doi-asserted-by":"publisher","DOI":"10.1002\/mrm.20868"},{"key":"B84","doi-asserted-by":"publisher","DOI":"10.1002\/jmri.10346"},{"key":"B85","doi-asserted-by":"publisher","DOI":"10.1002\/jmri.1149"},{"key":"B86","doi-asserted-by":"publisher","DOI":"10.1097\/00004728-200311000-00001"},{"key":"B87","doi-asserted-by":"publisher","DOI":"10.1002\/cmr.b.10083"},{"key":"B88","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2009.03.008"},{"key":"B89","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-3495(84)84196-X"},{"key":"B90","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuroimage.2010.10.070"},{"key":"B91","doi-asserted-by":"publisher","DOI":"10.1002\/mrm.24405"},{"key":"B92","doi-asserted-by":"publisher","DOI":"10.1148\/radiol.09091134"},{"key":"B93","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2011.16"},{"key":"B94","doi-asserted-by":"publisher","DOI":"10.1002\/mrm.22135"},{"key":"B95","first-page":"4175","volume":"24","author":"Squillaci E","year":"2004","journal-title":"Anticancer Res"},{"key":"B96","unstructured":"Suckow MA, Stevens KA, Wilson RP.The Laboratory Rabbit, Guinea Pig, Hamster, And Other Rodents. Boston, MA: Elsevier Academic, 2012, p. xvii, 1268."},{"key":"B97","doi-asserted-by":"publisher","DOI":"10.1148\/radiol.2353040554"},{"key":"B98","doi-asserted-by":"publisher","DOI":"10.1148\/radiol.100211"},{"key":"B99","doi-asserted-by":"publisher","DOI":"10.1002\/jmri.22645"},{"key":"B100","doi-asserted-by":"publisher","DOI":"10.1016\/j.mri.2014.07.012"},{"key":"B101","doi-asserted-by":"publisher","DOI":"10.1117\/1.JBO.20.3.036003"},{"key":"B102","doi-asserted-by":"publisher","DOI":"10.1002\/mrm.25358"},{"key":"B103","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00236.2015"},{"key":"B104","doi-asserted-by":"crossref","first-page":"1706","DOI":"10.1152\/ajplegacy.1970.219.6.1706","volume":"219","author":"Weisser F","year":"1970","journal-title":"Am J Physiol"},{"key":"B105","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuroimage.2012.12.050"},{"key":"B106","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.75.11.5475"},{"key":"B107","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuroimage.2011.07.019"},{"key":"B108","doi-asserted-by":"publisher","DOI":"10.1177\/0192623312441408"},{"key":"B109","doi-asserted-by":"publisher","DOI":"10.1002\/mrm.25219"},{"key":"B110","first-page":"463","volume-title":"ISMRM 23rd Annual Meeting and Exhibition","author":"Xie L","year":"2015"},{"key":"B111","first-page":"705","volume-title":"ISMRM 24th Annual Meeting and Exhibition","author":"Xie L","year":"2016"},{"key":"B112","first-page":"6670","volume-title":"ISMRM 24th Annual Meeting and Exhibition","author":"Xie L","year":"2016"},{"key":"B113","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00351.2015"},{"key":"B114","volume-title":"HHMI Image of the Week","author":"Xie L","year":"2016"},{"key":"B115","first-page":"6810","volume-title":"ISMRM 24th Annual Meeting and Exhibition","author":"Xie L","year":"2016"},{"key":"B116","doi-asserted-by":"publisher","DOI":"10.1002\/nbm.3039"},{"key":"B117","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0057691"},{"key":"B118","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfs381"},{"key":"B119","doi-asserted-by":"publisher","DOI":"10.1148\/radiol.2313021587"},{"key":"B120","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2013.361"},{"key":"B121","doi-asserted-by":"publisher","DOI":"10.1002\/jmri.21891"},{"key":"B122","doi-asserted-by":"publisher","DOI":"10.1002\/jmri.22412"},{"key":"B123","doi-asserted-by":"publisher","DOI":"10.1109\/TMI.2015.2509463"},{"key":"B124","doi-asserted-by":"publisher","DOI":"10.1109\/TBME.2014.2360154"},{"key":"B125","doi-asserted-by":"publisher","DOI":"10.1016\/j.compmedimag.2008.11.004"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00134.2016","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,7,8]],"date-time":"2022-07-08T14:20:01Z","timestamp":1657290001000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00134.2016"}},"issued":{"date-parts":[[2016,12,1]]},"references-count":125,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2016,12,1]]}},"alternative-id":["10.1152\/ajprenal.00134.2016"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00134.2016","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2016,12,1]]}},{"indexed":{"date-parts":[[2026,2,4]],"date-time":"2026-02-04T14:52:30Z","timestamp":1770216750124,"version":"3.49.0"},"reference-count":35,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2005,12]]},"abstract":"<jats:p>Acute administration of loop diuretics like furosemide leads to a stimulation of renin secretion, an effect thought to result from inhibition of Na-K-2Cl cotransporter (NKCC2)-mediated salt transport at the luminal surface of the macula densa (MD). However, loop diuretics also inhibit NKCC1, the second isoform of the Na-K-2Cl cotransporter, with similar potency. In the present study, we examined the influence of furosemide on renin secretion in NKCC1-deficient mice to distinguish between effects of the loop diuretic involving NKCC2 and, by implication, the MD pathway, and effects that might occur via inhibition of NKCC1. Baseline plasma renin concentration (PRC) was 1,212 \u00b1 211 in NKCC1+\/+ ( n = 13) and 3,851 \u00b1 579 ng ANG I\u00b7ml<jats:sup>\u22121<\/jats:sup>\u00b7h<jats:sup>\u22121<\/jats:sup>in NKCC1\u2212\/\u2212 mice ( n = 14; P = 0.00024). Acute administration of furosemide (50 mg\/kg i.p.) increased PRC significantly to 9,324 \u00b1 1,018 ng ANG I\u00b7ml<jats:sup>\u22121<\/jats:sup>\u00b7h<jats:sup>\u22121<\/jats:sup>in NKCC1+\/+ ( n = 13; P &lt; 0.0001 compared with basal) and to 14,188 \u00b1 2,274 ng ANG I\u00b7ml<jats:sup>\u22121<\/jats:sup>\u00b7h<jats:sup>\u22121<\/jats:sup>in NKCC1\u2212\/\u2212 mice [ n = 14; P = 0.0002 compared with basal; P = 0.034 compared with wild-type (WT) plus furosemide]. Renin mRNA expression was about threefold higher in NKCC1\u2212\/\u2212 compared with WT mice. There was considerable recruitment of granular cells to upstream regions of afferent arterioles in NKCC1\u2212\/\u2212 mice. Patch-clamp studies in single juxtaglomerular granular (JG) cells from WT mice showed an \u223c10% increase in membrane capacitance during incubation with furosemide (10<jats:sup>\u22124<\/jats:sup>M), indicating a direct effect of the loop diuretic on renin secretion. No effect of furosemide on membrane capacitance was observed in JG cells from NKCC1-deficient mice. Furosemide (10<jats:sup>\u22123<\/jats:sup>M) significantly stimulated renin release from primary cultures of JG cells from WT mice, whereas no response was observed in NKCC1\u2212\/\u2212 mice. Our data suggest that a functional NKCC1 suppresses basal renin release, at least in part, through a direct effect on JG cells.<\/jats:p>","DOI":"10.1152\/ajprenal.00455.2004","type":"journal-article","created":{"date-parts":[[2005,8,17]],"date-time":"2005-08-17T02:39:04Z","timestamp":1124246344000},"page":"F1185-F1192","source":"Crossref","is-referenced-by-count":64,"title":["Contribution of the basolateral isoform of the Na-K-2Cl<sup>\u2212<\/sup>cotransporter (NKCC1\/BSC2) to renin secretion"],"prefix":"10.1152","volume":"289","author":[{"given":"Hayo","family":"Castrop","sequence":"first","affiliation":[]},{"given":"John N.","family":"Lorenz","sequence":"additional","affiliation":[]},{"given":"Pernille B.","family":"Hansen","sequence":"additional","affiliation":[]},{"given":"Ulla","family":"Friis","sequence":"additional","affiliation":[]},{"given":"Diane","family":"Mizel","sequence":"additional","affiliation":[]},{"given":"Mona","family":"Oppermann","sequence":"additional","affiliation":[]},{"given":"Boye L.","family":"Jensen","sequence":"additional","affiliation":[]},{"given":"Josie","family":"Briggs","sequence":"additional","affiliation":[]},{"given":"Ole","family":"Sk\u00f8tt","sequence":"additional","affiliation":[]},{"given":"Jurgen","family":"Schnermann","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.265.1.F151"},{"key":"R2","doi-asserted-by":"crossref","unstructured":"Castrop H, Schweda F, Mizel D, Huang Y, Briggs J, Kurtz A, and Schnermann J.Permissive role of nitric oxide in macula densa control of renin secretion.Am J Physiol Renal Physiol286: F848\u2013F857, 2004.","DOI":"10.1152\/ajprenal.00272.2003"},{"key":"R3","doi-asserted-by":"crossref","unstructured":"Chomczynski Pand Sacchi N.Single-step method of RNA isolation by acid guanidinium thiocyanate-phenol-chloroform extraction.Anal Biochem162: 156\u2013159, 1987.","DOI":"10.1016\/0003-2697(87)90021-2"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.37.4.464"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1038\/9713"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.38.26946"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.84.8.929"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000017622.25365.71"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-201X.2004.01310.x"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000085041.70276.3D"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.62.1.515"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1990.70.4.1067"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1007\/s00210-001-0521-y"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00522.2002"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.26.1.137"},{"key":"R16","doi-asserted-by":"crossref","unstructured":"Ikebe M, Nonoguchi H, Nakayama Y, Tashima Y, and Tomita K.Upregulation of the secretory-type Na+\/K+\/2Cl\u2212cotransporter in the kidney by metabolic acidosis and dehydration in rats.J Am Soc Nephrol12: 423\u2013430, 2001.","DOI":"10.1681\/ASN.V123423"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.7.3_Pt_2.I49"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.3.F659"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.ph.58.030196.003245"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118844"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.258.5.F1466"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.260.4.F486"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00083.2002"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.79.21.6712"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.275.6.F885"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118834"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1172\/JCI114373"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1172\/JCI8553"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1007\/BF00584628"},{"key":"R30","unstructured":"Schnermann Jand Briggs JP.Function of the juxtaglomerular apparatus: control of glomerular hemodynamics and renin secretion. In:The Kidney: Physiology and Pathophysiology, edited by Seldin DW and Giebisch G. Philadelphia: Lippincott Williams &Wilkins, 2000, p. 945\u2013980."},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1967.47.3.359"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.1977.tb16749.x"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1152\/ajplung.1995.268.4.L642"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.4.F931"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M006218200"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00455.2004","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,7,15]],"date-time":"2021-07-15T21:54:56Z","timestamp":1626386096000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00455.2004"}},"issued":{"date-parts":[[2005,12]]},"references-count":35,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2005,12]]}},"alternative-id":["10.1152\/ajprenal.00455.2004"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00455.2004","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2005,12]]}},{"indexed":{"date-parts":[[2026,2,3]],"date-time":"2026-02-03T16:26:38Z","timestamp":1770135998312,"version":"3.49.0"},"reference-count":49,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2002,4,1]]},"abstract":"<jats:p>Epidermal growth factor (EGF) regulates cell proliferation, differentiation, and ion transport by using extracellular signal-regulated kinase (ERK)1\/2 as a downstream signal. Furthermore, the EGF-receptor (EGF-R) is involved in signaling by G protein-coupled receptors, growth hormone, and cytokines by means of transactivation. It has been suggested that steroids interact with peptide hormones, in part, by rapid, potentially nongenomic, mechanisms. Previously, we have shown that aldosterone modulates Na<jats:sup>+<\/jats:sup>\/H<jats:sup>+<\/jats:sup>exchange in Madin-Darby canine kidney (MDCK) cells by means of ERK1\/2 in a way similar to growth factors. Here, we tested the hypothesis that aldosterone uses the EGF-R as a heterologous signal transducer in MDCK cells. Nanomolar concentrations of aldosterone induce a rapid increase in ERK1\/2 phosphorylation, cellular Ca<jats:sup>2+<\/jats:sup>concentration, and Na<jats:sup>+<\/jats:sup>\/H<jats:sup>+<\/jats:sup>exchange activity similar to increases induced by EGF. Furthermore, aldosterone induced a rapid increase in EGF-R-Tyr phosphorylation, and inhibition of EGF-R kinase abolished aldosterone-induced signaling. Inhibition of ERK1\/2 phosphorylation reduced the Ca<jats:sup>2+<\/jats:sup>response, whereas prevention of Ca<jats:sup>2+<\/jats:sup>influx did not abolish ERK1\/2 phosphorylation. Our data show that aldosterone uses the EGF-R-ERK1\/2 signaling cascade to elicit its rapid effects in MDCK cells.<\/jats:p>","DOI":"10.1152\/ajprenal.00159.2001","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:34:49Z","timestamp":1425414889000},"page":"F669-F679","source":"Crossref","is-referenced-by-count":56,"title":["Aldosterone interaction with epidermal growth factor receptor signaling in MDCK cells"],"prefix":"10.1152","volume":"282","author":[{"given":"Michael","family":"Gekle","sequence":"first","affiliation":[{"name":"Physiologisches Institut, University of W\u00fcrzburg, 97070 W\u00fcrzburg, Germany"}]},{"given":"Ruth","family":"Freudinger","sequence":"additional","affiliation":[{"name":"Physiologisches Institut, University of W\u00fcrzburg, 97070 W\u00fcrzburg, Germany"}]},{"given":"Sigrid","family":"Mildenberger","sequence":"additional","affiliation":[{"name":"Physiologisches Institut, University of W\u00fcrzburg, 97070 W\u00fcrzburg, Germany"}]},{"given":"Stefan","family":"Silbernagl","sequence":"additional","affiliation":[{"name":"Physiologisches Institut, University of W\u00fcrzburg, 97070 W\u00fcrzburg, Germany"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00979.x"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.t01-1-00201.x"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1021\/jm9503613"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1988.255.1.F151"},{"key":"B5","first-page":"1452","volume":"77","author":"Christ M","year":"1993","journal-title":"J Clin Endocrinol Metab"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1994.sp020306"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0703272"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1998.275.1.C82"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.15.8763"},{"key":"B10","first-page":"S15","volume":"41","author":"El Nahas AM.","year":"1992","journal-title":"Kidney Int"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1007\/s004240000507"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.93.19.10500"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1997.273.5.C1673"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1007\/BF00374853"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.ph.52.030190.003111"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1021\/bi00797a004"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1038\/33176"},{"key":"B18","doi-asserted-by":"crossref","first-page":"3440","DOI":"10.1016\/S0021-9258(19)83641-4","volume":"260","author":"Grynkiewicz G","year":"1985","journal-title":"J Biol Chem"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/S0955-0674(99)80024-6"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00981.x"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1999.1771"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.42.27111"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.17.9919"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1994.266.2.C406"},{"key":"B25","first-page":"279","volume":"12","author":"Lovisolo D","year":"1997","journal-title":"NIPS"},{"key":"B26","first-page":"805","volume":"45","author":"Manegold JC","year":"1999","journal-title":"Cell Mol Biol (Noisy-le-grand)"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/S0955-0674(99)80025-8"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.6.F875"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1007\/BF01869208"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.84.5.1464"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1159\/000057444"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1007\/s002329900599"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1996.270.1.C40"},{"key":"B34","doi-asserted-by":"crossref","first-page":"1460","DOI":"10.1016\/S0022-3565(24)37174-5","volume":"283","author":"Schramek H","year":"1997","journal-title":"J Pharmacol Exp Ther"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.148.3.591"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.50.35449"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1042\/bj3250501"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1021\/bi00578a012"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.48.30505"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1996.sp021200"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1042\/bj3500717"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1007\/BF00381507"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1997.77.1.51"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.264.4.F670"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.59.1.365"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.1992.263.5.E974"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.76.6.973"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.256.5.F957"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1007\/s002329900534"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00159.2001","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,5,20]],"date-time":"2025-05-20T17:51:11Z","timestamp":1747763471000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00159.2001"}},"issued":{"date-parts":[[2002,4,1]]},"references-count":49,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2002,4,1]]}},"alternative-id":["10.1152\/ajprenal.00159.2001"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00159.2001","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2002,4,1]]}},{"indexed":{"date-parts":[[2026,1,30]],"date-time":"2026-01-30T02:09:00Z","timestamp":1769738940771,"version":"3.49.0"},"reference-count":35,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2007,8]]},"abstract":"<jats:p>The canonical WNT signaling pathway plays a crucial role in patterning of the embryo during development, but little is known about the specific developmental events which are under WNT control. To understand more about how the WNT pathway orchestrates mammalian organogenesis, we studied the canonical \u03b2-catenin-mediated WNT signaling pathway in kidneys of mice bearing a \u03b2-catenin-responsive TCF\/\u03b2Gal reporter transgene. In metanephric kidney, intense canonical WNT signaling was evident in epithelia of the branching ureteric bud and in nephrogenic mesenchyme during its transition into renal tubules. WNT signaling activity is rapidly downregulated in maturing nephrons and becomes undetectable in postnatal kidney. Sites of TCF\/\u03b2Gal activity are in proximity to the known sites of renal WNT2b and WNT4 expression, and these WNTs stimulate TCF reporter activity in kidney cell lines derived from ureteric bud and metanephric mesenchyme lineages. When fetal kidney explants from HoxB7\/GFP mice were exposed to the canonical WNT signaling pathway inhibitor, Dickkopf-1, arborization of the ureteric bud was significantly reduced. We conclude that restricted zones of intense canonical WNT signaling drive branching nephrogenesis in fetal kidney.<\/jats:p>","DOI":"10.1152\/ajprenal.00416.2006","type":"journal-article","created":{"date-parts":[[2007,5,10]],"date-time":"2007-05-10T00:43:59Z","timestamp":1178757839000},"page":"F494-F500","source":"Crossref","is-referenced-by-count":148,"title":["Canonical WNT signaling during kidney development"],"prefix":"10.1152","volume":"293","author":[{"given":"Diana M.","family":"Iglesias","sequence":"first","affiliation":[]},{"given":"Pierre-Alain","family":"Hueber","sequence":"additional","affiliation":[]},{"given":"LeeLee","family":"Chu","sequence":"additional","affiliation":[]},{"given":"Robert","family":"Campbell","sequence":"additional","affiliation":[]},{"given":"Anne-Marie","family":"Patenaude","sequence":"additional","affiliation":[]},{"given":"Alison J.","family":"Dziarmaga","sequence":"additional","affiliation":[]},{"given":"Jacklyn","family":"Quinlan","sequence":"additional","affiliation":[]},{"given":"Othman","family":"Mohamed","sequence":"additional","affiliation":[]},{"given":"Daniel","family":"Dufort","sequence":"additional","affiliation":[]},{"given":"Paul R.","family":"Goodyer","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1038\/35083081"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1207642"},{"key":"R3","unstructured":"Cadoret A, Ovejero C, Saadi-Kheddouci S, Souil E, Fabre M, Romagnolo B, Kahn A, Perret C.Hepatomegaly in transgenic mice expressing an oncogenic form of beta-catenin.Cancer Res61: 3245\u20133249, 2001."},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1016\/j.devcel.2005.05.016"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1242\/dev.01347"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1016\/j.ydbio.2004.09.023"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1016\/j.cub.2005.08.037"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005101074"},{"key":"R9","unstructured":"Giles RH, van Es JH, Clevers H.Caught up in a Wnt storm: Wnt signaling in cancer.Biochim Biophys Acta1653: 1\u201324, 2003."},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1016\/j.devcel.2005.02.017"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1242\/dev.01117"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1006\/dbio.1994.1360"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1002\/gene.10079"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2003.10.129"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.2001.6076"},{"key":"R16","doi-asserted-by":"crossref","unstructured":"Kispert A, Vainio S, Shen L, Rowitch DH, McMahon AP.Proteoglycans are required for maintenance of Wnt-11 expression in the ureter tips.Development122: 3627\u20133637, 1996.","DOI":"10.1242\/dev.122.11.3627"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1016\/S0925-4773(97)00041-5"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1002\/dvdy.1164"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1016\/j.yexcr.2004.04.036"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0434590100"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1111\/j.0021-8782.2004.00285.x"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1002\/dvdy.20135"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0500612102"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M305892200"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1038\/nature04888"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1242\/dev.02271"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1999.0379"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1016\/j.devcel.2004.11.008"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1038\/ng1552"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1520-6408(1999)24:3\/4<241::AID-DVG7>3.0.CO;2-R"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1038\/372679a0"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1016\/j.biocel.2004.12.010"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1016\/0012-1606(70)90077-1"},{"key":"R34","unstructured":"Vainio SJ.Nephrogenesis regulated by Wnt signaling.J Nephrol16: 279\u2013285, 2003."},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.25.12.5022-5030.2005"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00416.2006","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,5,11]],"date-time":"2023-05-11T19:28:40Z","timestamp":1683833320000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00416.2006"}},"issued":{"date-parts":[[2007,8]]},"references-count":35,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2007,8]]}},"alternative-id":["10.1152\/ajprenal.00416.2006"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00416.2006","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2007,8]]}},{"indexed":{"date-parts":[[2026,1,25]],"date-time":"2026-01-25T12:20:55Z","timestamp":1769343655595,"version":"3.49.0"},"reference-count":41,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2012,9,15]]},"abstract":"<jats:p> Tuberous sclerosis complex (TSC), an inherited tumor predisposition syndrome associated with mutations in TSC1 or TSC2, affects \u223c1 in 6,000 individuals. Eighty percent of TSC patients develop renal angiomyolipomas, and renal involvement is a major contributor to patient morbidity and mortality. Recent work has shown that mammalian target of rapamycin complex 1 (mTORC1) inhibition caused angiomyolipoma shrinkage but that this treatment may cause cytostatic not a cytotoxic effect. Endoplasmic reticulum (ER) stress can develop in TSC-associated cells due to mTORC1-driven protein translation. We hypothesized that renal angiomyolipoma cells experience ER stress that can be leveraged to result in targeted cytotoxicity. We used immortalized human angiomyolipoma cells stably transfected with empty vector or TSC2 (encoding tuberin). Using cell number quantification and cell death assays, we found that mTORC1 inhibition with RAD001 suppressed angiomyolipoma cell proliferation in a cytostatic manner. Angiomyolipoma cells exhibited enhanced sensitivity to proteasome inhibitor-induced ER stress compared with TSC2-rescued cells. After proteasome inhibition with MG-132, Western blot analyses showed greater induction of C\/EBP-homologous protein (CHOP) and more poly (ADP-ribose) polymerase (PARP) and caspase-3 cleavage, supporting ER stress-induced apoptosis. Live cell numbers also were decreased and cell death increased by MG-132 in angiomyolipoma cells compared with TSC2 rescued. Intriguingly, while pretreatment of angiomyolipoma cells with RAD001 attenuated CHOP and BiP induction, apoptotic markers cleaved PARP and caspase-3 and eukaryotic translation initiation factor 2\u03b1 phosphorylation were increased, along with evidence of increased autophagy. These results suggest that human angiomyolipoma cells are uniquely susceptible to agents that exacerbate ER stress and that additional synergy may be achievable with targeted combination therapy. <\/jats:p>","DOI":"10.1152\/ajprenal.00441.2011","type":"journal-article","created":{"date-parts":[[2012,7,12]],"date-time":"2012-07-12T04:24:03Z","timestamp":1342067043000},"page":"F831-F844","source":"Crossref","is-referenced-by-count":34,"title":["Human TSC-associated renal angiomyolipoma cells are hypersensitive to ER stress"],"prefix":"10.1152","volume":"303","author":[{"given":"Brian J.","family":"Siroky","sequence":"first","affiliation":[{"name":"Division of Nephrology and Hypertension, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio;"}]},{"given":"Hong","family":"Yin","sequence":"additional","affiliation":[{"name":"Division of Pathology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio; and"}]},{"given":"Justin T.","family":"Babcock","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, Indiana"}]},{"given":"Lu","family":"Lu","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio;"}]},{"given":"Anna R.","family":"Hellmann","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio;"}]},{"given":"Bradley P.","family":"Dixon","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio;"}]},{"given":"Lawrence A.","family":"Quilliam","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, Indiana"}]},{"given":"John J.","family":"Bissler","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio;"}]}],"member":"24","reference":[{"key":"B1","author":"Babcock JT","journal-title":"Curr Drug Targets"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa063564"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2006-04-016055"},{"key":"B5","first-page":"1316","volume":"146","author":"Cocciolone RA","journal-title":"Arch Dermatol"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2006-11-053728"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMc072500"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/cdd.2011.146"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.0778-09.2009"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/j.urology.2009.05.007"},{"key":"B11","first-page":"1763","volume":"148","author":"Furukawa T","year":"1996","journal-title":"Am J Pathol"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/j.it.2003.11.004"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1101\/gad.1212704"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1002\/gcc.2870130411"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2002-08-2543"},{"key":"B16","first-page":"3071","volume":"61","author":"Hideshima T","year":"2001","journal-title":"Cancer Res"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/j.molcel.2008.04.027"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1159\/000210573"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1038\/cdd.2010.82"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/S0962-8924(98)01346-4"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1172\/JCI26390"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/j.exphem.2008.06.005"},{"key":"B23","doi-asserted-by":"crossref","first-page":"551","DOI":"10.4161\/cbt.3.6.846","volume":"3","author":"Mimnaugh EG","year":"2004","journal-title":"Mol Cancer Ther"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1158\/1541-7786.MCR-06-0019"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.4161\/auto.4600"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.7.3963"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/j.molcel.2007.12.023"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1104361108"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.4161\/auto.6.2.11062"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/j.tibs.2007.09.003"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1016\/j.drup.2010.04.002"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.biochem.73.011303.074134"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200907074"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa0907419"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1016\/S0025-6196(12)61196-3"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-010-1689-5"},{"key":"B37","first-page":"1419","volume":"7","author":"Sunwoo JB","year":"2001","journal-title":"Clin Cancer Res"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1016\/S1535-6108(02)00068-5"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa1003491"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1038\/7410"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1042\/BST0340007"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/ajplung.00204.2003"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00441.2011","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T00:27:42Z","timestamp":1567988862000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00441.2011"}},"issued":{"date-parts":[[2012,9,15]]},"references-count":41,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2012,9,15]]}},"alternative-id":["10.1152\/ajprenal.00441.2011"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00441.2011","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2012,9,15]]}},{"indexed":{"date-parts":[[2026,1,31]],"date-time":"2026-01-31T17:11:55Z","timestamp":1769879515197,"version":"3.49.0"},"reference-count":25,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2004,2]]},"abstract":"<jats:p>Controversy exists regarding the effect of A<jats:sub>1<\/jats:sub>adenosine receptor (AR) activation in the kidney during ischemia and reperfusion (I\/R) injury. We sought to further characterize the role of A<jats:sub>1<\/jats:sub>ARs in modulating renal function after I\/R renal injury using both pharmacological and gene deletion approaches in mice. A<jats:sub>1<\/jats:sub>AR knockout mice (A<jats:sub>1<\/jats:sub>KO) or their wild-type littermate controls (A<jats:sub>1<\/jats:sub>WT) were subjected to 30 min of renal ischemia. Some A<jats:sub>1<\/jats:sub>WT mice were subjected to 30 min of renal ischemia with or without pretreatment with 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) or 2-chrolo-cyclopentyladenosine (CCPA), selective A<jats:sub>1<\/jats:sub>AR antagonist and agonist, respectively. Plasma creatinine and renal histology were compared 24 h after renal injury. A<jats:sub>1<\/jats:sub>KO mice exhibited significantly higher creatinines and worsened renal histology compared with A<jats:sub>1<\/jats:sub>WT controls following renal I\/R injury. A<jats:sub>1<\/jats:sub>WT mice pretreated with the A<jats:sub>1<\/jats:sub>AR antagonist or agonist demonstrated significantly worsened or improved renal function, respectively, after I\/R injury. In addition, A<jats:sub>1<\/jats:sub>WT mice pretreated with DPCPX or CCPA showed significantly increased or reduced markers of renal inflammation, respectively (renal myeloperoxidase activity, renal tubular neutrophil infiltration, ICAM-1, TNF-\u03b1, and IL-1\u03b2 mRNA expression), while demonstrating no differences in indicators of apoptosis. In conclusion, we demonstrate that endogenous or exogenous preischemic activation of A<jats:sub>1<\/jats:sub>ARs protects against renal I\/R injury in vivo via mechanisms leading to decreased necrosis and inflammation.<\/jats:p>","DOI":"10.1152\/ajprenal.00185.2003","type":"journal-article","created":{"date-parts":[[2004,1,31]],"date-time":"2004-01-31T01:13:21Z","timestamp":1075511601000},"page":"F298-F306","source":"Crossref","is-referenced-by-count":115,"title":["A<sub>1<\/sub>adenosine receptor knockout mice exhibit increased renal injury following ischemia and reperfusion"],"prefix":"10.1152","volume":"286","author":[{"given":"H. Thomas","family":"Lee","sequence":"first","affiliation":[]},{"given":"Hua","family":"Xu","sequence":"additional","affiliation":[]},{"given":"Samih H.","family":"Nasr","sequence":"additional","affiliation":[]},{"given":"Jurgen","family":"Schnermann","sequence":"additional","affiliation":[]},{"given":"Charles W.","family":"Emala","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"REF1","doi-asserted-by":"crossref","unstructured":"Alam J, Wicks C, Stewart D, Gong P, Touchard C, Otterbein S, Choi AM, Burow ME, and Tou J.Mechanism of heme oxygenase-1 gene activation by cadmium in MCF-7 mammary epithelial cells. Role of p38 kinase and Nrf2 transcription factor.J Biol Chem275: 27694-27702, 2000.","DOI":"10.1074\/jbc.M004729200"},{"key":"REF2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.1986.tb09488.x"},{"key":"REF3","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1999.277.3.R922"},{"key":"REF4","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00739.2002"},{"key":"REF5","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.1989.tb11956.x"},{"key":"REF6","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(99)70375-6"},{"key":"REF7","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.10.4666"},{"key":"REF8","doi-asserted-by":"publisher","DOI":"10.1097\/00007890-198303000-00002"},{"key":"REF9","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.71.5.1101"},{"key":"REF10","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.1989.tb14639.x"},{"key":"REF11","doi-asserted-by":"crossref","unstructured":"Lameire Nand Vanholder R.Pathophysiologic features and prevention of human and experimental acute tubular necrosis.J Am Soc Nephrol12,Suppl17: S20-S32, 2001.","DOI":"10.1681\/ASN.V12suppl_1s20"},{"key":"REF12","doi-asserted-by":"crossref","unstructured":"Lee HTand Emala CW.Protein kinase C and Gi\/oproteins are involved in adenosine- and ischemic preconditioning-mediated protection of renal ischemic-reperfusion injury.J Am Soc Nephrol12: 233-240, 2001.","DOI":"10.1681\/ASN.V122233"},{"key":"REF13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00195.2001"},{"key":"REF14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.3.F380"},{"key":"REF15","doi-asserted-by":"publisher","DOI":"10.1053\/ajkd.2001.26888"},{"key":"REF16","doi-asserted-by":"publisher","DOI":"10.1159\/000065306"},{"key":"REF17","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000032421.79225.6E"},{"key":"REF18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00271.2002"},{"key":"REF19","doi-asserted-by":"publisher","DOI":"10.1139\/y87-233"},{"key":"REF20","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1988.4"},{"key":"REF21","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00210.x"},{"key":"REF22","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.171317998"},{"key":"REF23","doi-asserted-by":"publisher","DOI":"10.1254\/jjp.65.167"},{"key":"REF24","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/15.10.1562"},{"key":"REF25","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.33.1.511"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00185.2003","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,6,14]],"date-time":"2021-06-14T05:34:38Z","timestamp":1623648878000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00185.2003"}},"issued":{"date-parts":[[2004,2]]},"references-count":25,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2004,2]]}},"alternative-id":["10.1152\/ajprenal.00185.2003"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00185.2003","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2004,2]]}},{"indexed":{"date-parts":[[2026,1,31]],"date-time":"2026-01-31T04:07:32Z","timestamp":1769832452156,"version":"3.49.0"},"reference-count":38,"publisher":"American Physiological Society","issue":"5","funder":[{"name":"NIH\/NIDDK","award":["NIH K08 DK084305"],"award-info":[{"award-number":["NIH K08 DK084305"]}]},{"name":"NIH\/NIDDK","award":["NIH R01 DK075048"],"award-info":[{"award-number":["NIH R01 DK075048"]}]},{"name":"NIH\/NIDDK","award":["NIH R01 DKo84184"],"award-info":[{"award-number":["NIH R01 DKo84184"]}]},{"name":"VA","award":["VA Merit BX002175"],"award-info":[{"award-number":["VA Merit BX002175"]}]},{"name":"VA","award":["VA Merit BX000277"],"award-info":[{"award-number":["VA Merit BX000277"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2015,9,1]]},"abstract":"<jats:p> Renal hypoxia contributes to chronic kidney disease (CKD) progression, as validated in experimental and human CKD. In the early stages, increased oxygen consumption causes oxygen demand\/supply mismatch, leading to hypoxia. Hence, early targeting of the determinants and regulators of oxygen consumption in CKD may alter the disease course before permanent damage ensues. Here, we focus on hypoxia inducible factor-1\u03b1 (HIF-1\u03b1) and AMP-activated protein kinase (AMPK) and on the mechanisms by which they may facilitate cellular hypoxia adaptation. We found that HIF-1\u03b1 activation in the subtotal nephrectomy (STN) model of CKD limits protein synthesis, inhibits apoptosis, and activates autophagy, presumably for improved cell survival. AMPK activation was diminished in the STN kidney and was remarkably restored by HIF-1\u03b1 activation, demonstrating a novel role for HIF-1\u03b1 in the regulation of AMPK activity. We also investigated the independent and combined effects of HIF-1\u03b1 and AMPK on cell survival and death pathways by utilizing pharmacological and knockdown approaches in cell culture models. We found that the effect of HIF-1\u03b1 activation on autophagy is independent of AMPK, but on apoptosis it is partially AMPK dependent. The effects of HIF-1\u03b1 and AMPK activation on inhibiting protein synthesis via the mTOR pathway appear to be additive. These various effects were also observed under hypoxic conditions. In conclusion, HIF-1\u03b1 and AMPK appear to be linked at a molecular level and may act as components of a concerted cellular response to hypoxic stress in the pathophysiology of CKD. <\/jats:p>","DOI":"10.1152\/ajprenal.00463.2014","type":"journal-article","created":{"date-parts":[[2015,7,1]],"date-time":"2015-07-01T22:41:05Z","timestamp":1435790465000},"page":"F414-F428","source":"Crossref","is-referenced-by-count":72,"title":["Interactions between HIF-1\u03b1 and AMPK in the regulation of cellular hypoxia adaptation in chronic kidney disease"],"prefix":"10.1152","volume":"309","author":[{"given":"Hui","family":"Li","sequence":"first","affiliation":[{"name":"Department of Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California;"}]},{"given":"Joseph","family":"Satriano","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Medicine, University of California and Veterans Affairs San Diego Healthcare System, San Diego, California; and"}]},{"given":"Joanna L.","family":"Thomas","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Medicine, University of California and Veterans Affairs San Diego Healthcare System, San Diego, California; and"}]},{"given":"Satoshi","family":"Miyamoto","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Medicine, University of California and Veterans Affairs San Diego Healthcare System, San Diego, California; and"},{"name":"Center for Renal Translational Medicine, University of California, San Diego, California"}]},{"given":"Kumar","family":"Sharma","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Medicine, University of California and Veterans Affairs San Diego Healthcare System, San Diego, California; and"},{"name":"Center for Renal Translational Medicine, University of California, San Diego, California"}]},{"given":"N\u00faria M.","family":"Pastor-Soler","sequence":"additional","affiliation":[{"name":"Department of Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California;"}]},{"given":"Kenneth R.","family":"Hallows","sequence":"additional","affiliation":[{"name":"Department of Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California;"}]},{"given":"Prabhleen","family":"Singh","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Medicine, University of California and Veterans Affairs San Diego Healthcare System, San Diego, California; and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-009-1310-y"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010030238"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.267.6.F1059"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.267.6.F1063"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2011010026"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00153.2010"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.481"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1159\/000070698"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006050503"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1172\/JCI19375"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008070804"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.00054-09"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00005.2010"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1988.254.2.F267"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1159\/000146075"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000034910.58454.FD"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.4161\/auto.19496"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.00166-06"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M306104200"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00278.2006"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.107.169201"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000125614.35046.10"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.2337\/db11-0402"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005070757"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1159\/000148256"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.258.5.F1354"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1038\/376037a0"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.2006.04476.x"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000017223.49823.2A"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00293.2013"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/physiol.00045.2008"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2011020130"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90722.2008"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1011498108"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1038\/labinvest.3700328"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.109.145896"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00485.2010"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1797.2011.01498.x"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00463.2014","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T21:20:39Z","timestamp":1567977639000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00463.2014"}},"issued":{"date-parts":[[2015,9,1]]},"references-count":38,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2015,9,1]]}},"alternative-id":["10.1152\/ajprenal.00463.2014"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00463.2014","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2015,9,1]]}},{"indexed":{"date-parts":[[2026,1,14]],"date-time":"2026-01-14T18:54:47Z","timestamp":1768416887835,"version":"3.49.0"},"reference-count":40,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,2,1]]},"abstract":"<jats:p>Hypertension affects one-third of the adult population of the world. The causes of hypertension are incompletely understood, but relative impairment of sodium excretion is central to its pathogenesis. Immune cell infiltration in the kidney is a constant finding in hypertension that in association with local angiotensin and oxidants causes a defect in sodium excretion. However, it is unclear if the T cell influx into the kidney responds to nonspecific chemokine cues or is due to antigen-driven immune attraction. We found that T cells in experimentally induced salt-driven hypertension present a CD4 clonal response to heat shock protein 70 (HSP70) that is overexpressed in the kidney. We used a highly preserved amino acid sequence within the HSP molecule to induce immune tolerance associated with the generation of IL-10 producing regulatory T cells. Immune tolerant rats to HSP70 developed minimal renal inflammation and were protected from the development of salt-sensitive hypertension. Adoptive transfer of T lymphocytes isolated from spleen of tolerized rats also reversed hypertension. HSP70 gene delivery to the renal vein of the kidneys of rats sensitized to HSP70 caused an increment in blood pressure in response to a high-salt diet. The HSP70 peptide used in this work induces a strong proliferative response in peripheral blood lymphocytes of patients with essential hypertension. These studies provide evidence that autoimmunity plays a role in salt-sensitive hypertension and identifies HSP70 expressed in the kidney as one key antigen. These findings raise the possibility of novel approaches to the treatment of this condition.<\/jats:p>","DOI":"10.1152\/ajprenal.00517.2012","type":"journal-article","created":{"date-parts":[[2012,10,25]],"date-time":"2012-10-25T02:52:45Z","timestamp":1351133565000},"page":"F289-F299","source":"Crossref","is-referenced-by-count":92,"title":["Immune reactivity to heat shock protein 70 expressed in the kidney is cause of salt-sensitive hypertension"],"prefix":"10.1152","volume":"304","author":[{"given":"H\u00e9ctor","family":"Pons","sequence":"first","affiliation":[{"name":"Hospital Universitario y Universidad del Zulia and"}]},{"given":"Atilio","family":"Ferrebuz","sequence":"additional","affiliation":[{"name":"Instituto Venezolano de Investigaciones Cient\u00edficas (IVIC)-Zulia, Maracaibo, Venezuela; and"}]},{"given":"Yasmir","family":"Quiroz","sequence":"additional","affiliation":[{"name":"Instituto Venezolano de Investigaciones Cient\u00edficas (IVIC)-Zulia, Maracaibo, Venezuela; and"}]},{"given":"Freddy","family":"Romero-Vasquez","sequence":"additional","affiliation":[{"name":"Instituto Venezolano de Investigaciones Cient\u00edficas (IVIC)-Zulia, Maracaibo, Venezuela; and"}]},{"given":"Gustavo","family":"Parra","sequence":"additional","affiliation":[{"name":"Hospital Universitario y Universidad del Zulia and"}]},{"given":"Richard J.","family":"Johnson","sequence":"additional","affiliation":[{"name":"the 3Division of Renal Diseases and Hypertension, University of Colorado, Denver, Colorado"}]},{"given":"Bernardo","family":"Rodriguez-Iturbe","sequence":"additional","affiliation":[{"name":"Hospital Universitario y Universidad del Zulia and"},{"name":"Instituto Venezolano de Investigaciones Cient\u00edficas (IVIC)-Zulia, Maracaibo, Venezuela; and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.110.162941"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.64.s86.9.x"},{"key":"B3","first-page":"34A","volume":"17","author":"Chavez M","year":"2006","journal-title":"J Am Soc Nephrol"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1186\/1471-2172-13-13"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00454.2010"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1172\/JCI27203"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00645.2006"},{"key":"B8","doi-asserted-by":"crossref","first-page":"2263","DOI":"10.1681\/ASN.V12112263","volume":"12","author":"Franco M","year":"2001","journal-title":"J Am Soc Nephrol"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/0002-9343(72)90050-2"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20070657"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.110.163576"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006080918"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1161\/hy1201.096818"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra011078"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.111.181123"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(05)17741-1"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1007\/s12192-008-0089-2"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.110.217299"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2008.04.097"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00264.2002"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/j.coph.2011.01.009"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1007\/s11906-010-0094-6"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.513"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-200209000-00027"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.167.8.4147"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.281.1.F38"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.105.088062"},{"key":"B28","first-page":"1440","volume":"10","author":"Rodr\u00edguez-Iturbe B","year":"2011","journal-title":"Clin Exp Pharmacol Physiol"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.0197.2001"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2007.05.025"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00269.2003"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0b013e3283360a2e"},{"key":"B33","first-page":"523","volume":"84","author":"Svendsen UG","year":"1976","journal-title":"Path Microbiol Scand Acta"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00981.2007"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2567.2003.01725.x"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1038\/ncpneph0283"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.172.10.5986"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.27.3.481"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.164.5.2711"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1159\/000279307"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00517.2012","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,1,30]],"date-time":"2022-01-30T14:21:27Z","timestamp":1643552487000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00517.2012"}},"issued":{"date-parts":[[2013,2,1]]},"references-count":40,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2013,2,1]]}},"alternative-id":["10.1152\/ajprenal.00517.2012"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00517.2012","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2013,2,1]]}},{"indexed":{"date-parts":[[2026,1,13]],"date-time":"2026-01-13T21:41:53Z","timestamp":1768340513741,"version":"3.49.0"},"reference-count":61,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2009,5]]},"abstract":"<jats:p>Injection of antisense oligonucleotide morpholinos to elicit selective gene knockdown of ammonia (Rhag, Rhbg, and Rhcg1) or urea transporters (UT) was used as a tool to assess the relative importance of each transporter to nitrogen excretion in developing zebrafish ( Danio rerio). Knockdown of UT caused urea excretion to decrease by \u223c90%, whereas each of the Rh protein knockdowns resulted in an \u223c50% reduction in ammonia excretion. Contrary to what has been hypothesized previously for adult fish, each of the Rh proteins appeared to have a similar effect on total ammonia excretion, and thus all are required to facilitate normal ammonia excretion in the zebrafish larva. As demonstrated in other teleosts, zebrafish embryos utilized urea to a much greater extent than adults and were effectively ureotelic until hatching. At that point, ammonia excretion rapidly increased and appeared to be triggered by a large increase in the mRNA expression of Rhag, Rhbg, and Rhcg1. Unlike the situation in the adult pufferfish ( 35 ), the various transporters are not specifically localized to the gills of the developing zebrafish, but each protein has a unique expression pattern along the skin, gills, and yolk sac. This disparate pattern of expression would appear to preclude interaction between the Rh proteins in zebrafish embryos. However, this may be a developmental feature of the delayed maturation of the gills, because as the embryos matured, expression of the transporters in and around the gills increased.<\/jats:p>","DOI":"10.1152\/ajprenal.90656.2008","type":"journal-article","created":{"date-parts":[[2009,3,12]],"date-time":"2009-03-12T01:49:46Z","timestamp":1236822586000},"page":"F994-F1005","source":"Crossref","is-referenced-by-count":120,"title":["Nitrogen excretion in developing zebrafish (<i>Danio rerio<\/i>): a role for Rh proteins and urea transporters"],"prefix":"10.1152","volume":"296","author":[{"given":"M. H.","family":"Braun","sequence":"first","affiliation":[]},{"given":"S. L.","family":"Steele","sequence":"additional","affiliation":[]},{"given":"M.","family":"Ekker","sequence":"additional","affiliation":[]},{"given":"S. F.","family":"Perry","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"crossref","unstructured":"Alsop DH, Wood CM.The interactive effects of feeding and exercise on oxygen consumption, swimming performance and protein usage in juvenile rainbow trout.J Exp Biol200: 2337\u20132346, 1997.","DOI":"10.1242\/jeb.200.17.2337"},{"key":"R2","doi-asserted-by":"crossref","unstructured":"Avent ND, Madgett TE, Lee ZE, Head DJ, Maddocks DG, Skinner LH.Molecular biology of Rh proteins and relevance to molecular medicine.Expert Rev Mol Med8: 1\u201320, 2006.","DOI":"10.1017\/S1462399406010969"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1999.276.2.R505"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1042\/bj0750082"},{"key":"R5","unstructured":"Chadwick TD, Wright PA.Nitrogen excretion and expression of urea cycle enzymes in the Atlantic cod (Gadus morhual.): a comparison of early life stages with adults.J Exp Biol202: 2653\u20132662, 1999."},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1016\/j.tracli.2006.02.005"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1038\/ng0296-168"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1242\/dev.001115"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000025280.02386.9D"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.90685.2008"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M412338200"},{"key":"R12","doi-asserted-by":"crossref","unstructured":"Felskie AK, Anderson PM, Wright PA.Expression and activity of carbamoyl phosphate synthetase III and ornithine urea cycle enzymes in various tissues of four fish species.Comp Biochem Physiol B119: 355\u2013364, 2008.","DOI":"10.1016\/S0305-0491(97)00361-1"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00053.2006"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.2001.280.1.R16"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1007\/BF00007454"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00578.2006"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.4.2207"},{"key":"R18","doi-asserted-by":"crossref","unstructured":"Hung CC, Nawata CM, Wood CM, Wright PA.Rhesus glycoprotein and urea transporter genes are expressed in early stages of development of rainbow trout (Oncorhynchus mykiss).J Exp Zool Part A Ecol Genet Physiol309: 262\u2013268, 2008.","DOI":"10.1002\/jez.456"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1242\/jeb.002568"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1016\/j.cbpa.2007.06.416"},{"key":"R21","doi-asserted-by":"crossref","unstructured":"Hyland CA, Cherif-Zahar B, Cowley N, Raynal V, Parkes J, Saul A, Cartron JP.A novel single missense mutation identified along the RH50 gene in a composite heterozygous Rhnull blood donor of the regulator type.Blood91: 1458\u20131463, 1998.","DOI":"10.1182\/blood.V91.4.1458"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.91.14.6269"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1002\/aja.1002030302"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1006\/abbi.1997.0522"},{"key":"R25","doi-asserted-by":"crossref","unstructured":"Kong H, Kahatapitiya N, Kingsley K, Salo WL, Anderson PM, Wang YS, Walsh PJ.Induction of carbamoyl phosphate synthetase III and glutamine synthetase mRNA during confinement stress in gulf toadfish (Opsanus beta).J Exp Biol203: 311\u2013320, 2000.","DOI":"10.1242\/jeb.203.2.311"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.10.6270"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1007\/BF02338293"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1172\/JCI107393"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1172\/JCI107317"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1016\/j.tracli.2006.03.002"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00896.2004"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.2001.281.5.R1594"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1242\/jeb.00555"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00248.2007"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1096\/fj.06-6834com"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-003-1142-8"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1152\/physiolgenomics.00061.2007"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/29.9.e45"},{"key":"R39","doi-asserted-by":"crossref","unstructured":"Pilley CM, Wright PA.The mechanisms of urea transport by early life stages of rainbow trout (Oncorhynchus mykiss).J Exp Biol203: 3199\u20133207, 2000.","DOI":"10.1242\/jeb.203.20.3199"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000050413.43662.55"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1016\/0009-8981(80)90407-6"},{"key":"R42","doi-asserted-by":"crossref","unstructured":"Rombough PJ.Gills are needed for ionoregulation before they are needed for O2uptake in developing zebrafish,Danio rerio.J Exp Biol205: 1787\u20131794, 2002.","DOI":"10.1242\/jeb.205.12.1787"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00255.2008"},{"key":"R44","unstructured":"Smith RR, Rumsey GL.Nutrient utilization by fish. In:First International Symposium: Feed Comparisons, Animal Nutrient Requirements, and Computerization of Diets, edited by Fonnesbeck PV, Harris LE, and Kearl LC. Logan, UT: Utah State University, 1976, p. 320."},{"key":"R45","doi-asserted-by":"crossref","unstructured":"Smith S.Studies in the development of the rainbow trout (Salmo irideus).J Exp Biol23: 357\u2013378, 1947.","DOI":"10.1242\/jeb.23.3-4.357"},{"key":"R46","doi-asserted-by":"crossref","unstructured":"Steele SL, Chadwick TD, Wright PA.Ammonia detoxification and localization of urea cycle enzyme activity in embryos of the rainbow trout (Oncorhynchus mykiss) in relation to early tolerance to high environmental ammonia levels.J Exp Biol204: 2145\u20132154, 2001.","DOI":"10.1242\/jeb.204.12.2145"},{"key":"R47","doi-asserted-by":"publisher","DOI":"10.1016\/S1095-6433(01)00290-2"},{"key":"R48","unstructured":"Toon MR, Solomon AK.Modulation of water and urea transport in human red cells: effects of pH and phloretin.J Membr Biol99: 1432\u20131442, 1987."},{"key":"R49","doi-asserted-by":"publisher","DOI":"10.1242\/jeb.021899"},{"key":"R50","doi-asserted-by":"publisher","DOI":"10.1016\/0043-1354(78)90107-0"},{"key":"R51","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00050.2002"},{"key":"R52","doi-asserted-by":"crossref","unstructured":"Walsh PJ, Wood CM, Perry SF, Thomas S.Urea transport by hepatocytes and red blood cells of selected elasmobranch and teleost fishes.J Exp Biol193: 321\u2013335, 1994.","DOI":"10.1242\/jeb.193.1.321"},{"key":"R53","doi-asserted-by":"publisher","DOI":"10.1016\/S0016-5085(03)00277-4"},{"key":"R54","unstructured":"Westerfield M.The Zebrafish Book.Eugene, OR: University of Oregon Press, 1995."},{"key":"R55","doi-asserted-by":"publisher","DOI":"10.1002\/jez.10123"},{"key":"R56","unstructured":"Wood C, Hopkins T, Hogstrand C, Walsh P.Pulsatile urea excretion in the ureagenic toadfishOpsanus beta: an analysis of rates and routes.J Exp Biol198: 1729\u20131741, 1995."},{"key":"R57","unstructured":"Wood CM.Ammonia and urea metabolism and excretion. In:The Physiology of Fishes, edited by Evans DE. Boca Raton, FL: CRC, 1993, p. 379\u2013427."},{"key":"R58","doi-asserted-by":"crossref","unstructured":"Wright PA, Felskie A, Anderson PM.Induction of ornithine-urea cycle enzymes and nitrogen metabolism and excretion in rainbow trout (Oncorhynchus mykiss) during early life stages.J Exp Biol198: 127\u2013135, 1995.","DOI":"10.1242\/jeb.198.1.127"},{"key":"R59","doi-asserted-by":"crossref","unstructured":"Wright PA, Heming T, Randall DJ.Downstream pH changes in water flowing over the gills of rainbow trout.J Exp Biol126: 499\u2013512, 1986.","DOI":"10.1242\/jeb.126.1.499"},{"key":"R60","doi-asserted-by":"publisher","DOI":"10.1038\/365844a0"},{"key":"R61","doi-asserted-by":"crossref","unstructured":"Zhao D, Bankir L, Qian L, Yang D, Yang B.Urea and urine concentrating ability in mice lacking AQP1 and AQP3.Am J Physiol Renal Physiol291: F429\u2013F438, 2006.","DOI":"10.1152\/ajprenal.00011.2006"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.90656.2008","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,10,3]],"date-time":"2021-10-03T03:58:01Z","timestamp":1633233481000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.90656.2008"}},"issued":{"date-parts":[[2009,5]]},"references-count":61,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2009,5]]}},"alternative-id":["10.1152\/ajprenal.90656.2008"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.90656.2008","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2009,5]]}},{"indexed":{"date-parts":[[2026,1,18]],"date-time":"2026-01-18T06:37:30Z","timestamp":1768718250960,"version":"3.49.0"},"reference-count":20,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2009,2]]},"abstract":"<jats:p> Activation of the CD40 receptor by its cognate ligand, CD154, results in interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1) production and increased intercellular adhesion molecule-1 (ICAM-1) expression in proximal tubule cells (PTCs). The independent role of these two proinflammatory chemokines, IL-8 and MCP-1, in inciting an inflammatory response in PTCs was explored. Exposure of primary cultures of human renal PTCs to recombinant IL-8 and MCP-1 resulted in increased ICAM-1 expression measured by quantitative real-time PCR, but confirmed only for IL-8 by immunoblot. The mechanism of action of IL-8 was explored in further detail. Immunohistochemistry identified both the CXCR-1 and CXCR-2 receptors, confirmed by RT-PCR, immunoprecipitation, immunoblot, and FACS analysis. IL-8 increased ICAM-1 expression only via the CXCR-1 receptor, which in turn resulted in activation of the p38 mitogen-activated protein kinase (MAPK) pathway; neither the extracellular signal-related kinase (ERK) 1\/2 MAPK pathway nor the stress-activated protein kinase (SAPK)\/c-Jun NH<jats:sub>2<\/jats:sub> terminal kinase (JNK) pathway was involved. CD154\/CD40-mediated ICAM-1 upregulation was not affected by preincubation of monolayers with the CXCR-1 blocking antibody, indicating that ICAM-1 expression occurs independent of CD154-mediated IL-8 production. Coincubation of monolayers with both CD154 and IL-8 resulted in a greater ICAM-1 response than either compound alone. We conclude that in human renal PTCs, IL-8 upregulates ICAM-1 production by engaging the CXCR-1 receptor and p38 MAPK signaling pathway. This cascade of events is independent of CD40\/CD154-mediated IL-8 stimulation and ICAM-1 production and serves to amplify the inflammatory response. <\/jats:p>","DOI":"10.1152\/ajprenal.90214.2008","type":"journal-article","created":{"date-parts":[[2008,7,31]],"date-time":"2008-07-31T00:48:58Z","timestamp":1217465338000},"page":"F438-F445","source":"Crossref","is-referenced-by-count":23,"title":["IL-8 amplifies CD40\/CD154-mediated ICAM-1 production via the CXCR-1 receptor and p38-MAPK pathway in human renal proximal tubule cells"],"prefix":"10.1152","volume":"296","author":[{"given":"Hongye","family":"Li","sequence":"first","affiliation":[]},{"given":"Edward P.","family":"Nord","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.266.1.F46"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI7286"},{"key":"R3","doi-asserted-by":"crossref","unstructured":"Chomczynski P, Sacchi N. Single-step method of RNA isolation by acid guanidinium thiocyanate-phenol-chloroform extraction. Anal Biochem 162: 156\u2013159, 1987.","DOI":"10.1016\/0003-2697(87)90021-2"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.3.F449"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M308192200"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.168.12.6244"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-291X(02)00829-X"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00291.2001"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00308.2003"},{"key":"R10","doi-asserted-by":"crossref","unstructured":"Li H, Nord EP. CD40\/CD154 ligation induces mononuclear cell adhesion to human renal proximal tubule cells via increased ICAM-1 expression. Am J Physiol Renal Physiol 288: F145\u2013F153, 2005.","DOI":"10.1152\/ajprenal.00317.2004"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1016\/j.earlhumdev.2004.10.022"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.48.32222"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.82.18.6133"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1986.250.3.F539"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.23.13585"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005020202"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.170.6.2904"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.17.11768"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.275.10.6868"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1097\/00062752-200005000-00009"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.90214.2008","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T22:58:23Z","timestamp":1567983503000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.90214.2008"}},"issued":{"date-parts":[[2009,2]]},"references-count":20,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2009,2]]}},"alternative-id":["10.1152\/ajprenal.90214.2008"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.90214.2008","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2009,2]]}},{"indexed":{"date-parts":[[2026,1,18]],"date-time":"2026-01-18T21:19:01Z","timestamp":1768771141974,"version":"3.49.0"},"reference-count":52,"publisher":"American Physiological Society","issue":"4","funder":[{"DOI":"10.13039\/100000738","name":"U.S. Department of Veterans Affairs","doi-asserted-by":"publisher","award":["BX000319"],"award-info":[{"award-number":["BX000319"]}],"id":[{"id":"10.13039\/100000738","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK058831"],"award-info":[{"award-number":["DK058831"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK087843"],"award-info":[{"award-number":["DK087843"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2020,4,1]]},"abstract":"<jats:p> Disruption of mitochondrial dynamics is an important pathogenic event in both acute and chronic kidney diseases, but the underlying mechanism remains poorly understood. Here, we report the regulation of mitofusin-2 (Mfn2; a key mitochondrial fusion protein) by microRNA-214 (miR-214) in renal ischemia-reperfusion that contributes to mitochondrial fragmentation, renal tubular cell death, and ischemic acute kidney injury (AKI). miR-214 was induced, whereas Mfn2 expression was decreased, in mouse ischemic AKI and cultured rat kidney proximal tubular cells (RPTCs) following ATP depletion treatment. Overexpression of miR-214 decreased Mfn2. Conversely, inhibition of miR-214 with anti-miR-214 prevented Mfn2 downregulation in RPTCs following ATP depletion. Anti-miR-214 further ameliorated mitochondrial fragmentation and apoptosis, whereas overexpression of miR-214 increased apoptosis, in ATP-depleted RPTCs. To test regulation in vivo, we established a mouse model with miR-214 specifically deleted from kidney proximal tubular cells (PT- miR-214<jats:sup>\u2212\/\u2212<\/jats:sup>). Compared with wild-type mice, PT- miR-214<jats:sup>\u2212\/\u2212<\/jats:sup> mice had less severe tissue damage, fewer apoptotic cells, and better renal function after ischemic AKI. miR-214 induction in ischemic AKI was suppressed in PT- miR-214<jats:sup>\u2212\/\u2212<\/jats:sup> mice, accompanied by partial preservation of Mfn2 in kidneys. These results unveil the miR-214\/Mfn2 axis that contributes to the disruption of mitochondrial dynamics and tubular cell death in ischemic AKI, offering new therapeutic targets. <\/jats:p>","DOI":"10.1152\/ajprenal.00567.2019","type":"journal-article","created":{"date-parts":[[2020,1,31]],"date-time":"2020-01-31T16:29:56Z","timestamp":1580488196000},"page":"F878-F887","source":"Crossref","is-referenced-by-count":48,"title":["miR-214 represses mitofusin-2 to promote renal tubular apoptosis in ischemic acute kidney injury"],"prefix":"10.1152","volume":"318","author":[{"given":"Yu","family":"Yan","sequence":"first","affiliation":[{"name":"Department of Nephrology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China"},{"name":"Department of Cellular Biology and Anatomy, Medical College of Georgia at Augusta University, Augusta, Georgia"},{"name":"Charlie Norwood Veterans Affairs Medical Center, Augusta, Georgia"}]},{"given":"Zhengwei","family":"Ma","sequence":"additional","affiliation":[{"name":"Department of Cellular Biology and Anatomy, Medical College of Georgia at Augusta University, Augusta, Georgia"},{"name":"Charlie Norwood Veterans Affairs Medical Center, Augusta, Georgia"}]},{"given":"Jiefu","family":"Zhu","sequence":"additional","affiliation":[{"name":"Department of Nephrology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China"}]},{"given":"Mengru","family":"Zeng","sequence":"additional","affiliation":[{"name":"Department of Nephrology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China"}]},{"given":"Hong","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Nephrology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China"}]},{"given":"Zheng","family":"Dong","sequence":"additional","affiliation":[{"name":"Department of Nephrology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China"},{"name":"Department of Cellular Biology and Anatomy, Medical College of Georgia at Augusta University, Augusta, Georgia"},{"name":"Charlie Norwood Veterans Affairs Medical Center, Augusta, Georgia"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI59327"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2015101096"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2018.12.028"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00081.2017"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2017.107"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014050463"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1172\/JCI45161"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1172\/JCI37829"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0703976104"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1146\/annurev-genet-110410-132529"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00571.2013"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2018111117"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013010072"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00035.2011"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014010126"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1172\/JCI127277"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1038\/s41581-018-0103-6"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1172\/JCI70911"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2017040381"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2016.07.017"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2011.120"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/s41581-019-0135-6"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejphar.2018.05.001"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014030262"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1016\/j.molimm.2018.12.028"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1038\/emm.2017.98"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbadis.2014.04.002"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00402.2018"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1172\/JCI77084"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2012.02.035"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.109.906610"},{"key":"B32","first-page":"1898","volume":"7","author":"Pan JS","year":"2019","journal-title":"Med Res Arch"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2015.01.011"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2017060659"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2016.01.005"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1158\/0008-5472.CAN-05-3241"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2011.16"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.3389\/fphys.2018.00790"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2018111126"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1038\/srep18351"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2017030247"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2012.01.009"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009070718"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2015080870"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1172\/JCI121859"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1159\/000479570"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1007\/s00018-016-2202-5"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1126\/science.1219855"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2012.441"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014050457"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1159\/000501038"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1186\/s40659-018-0179-2"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00567.2019","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2020,3,19]],"date-time":"2020-03-19T13:42:26Z","timestamp":1584625346000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00567.2019"}},"issued":{"date-parts":[[2020,4,1]]},"references-count":52,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2020,4,1]]}},"alternative-id":["10.1152\/ajprenal.00567.2019"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00567.2019","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2020,4,1]]}},{"indexed":{"date-parts":[[2026,1,18]],"date-time":"2026-01-18T21:08:37Z","timestamp":1768770517984,"version":"3.49.0"},"reference-count":51,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2006,3]]},"abstract":"<jats:p>Experimental and clinical studies impressively demonstrate that angiotensin-converting enzyme inhibitors (ACEI) and angiotensin receptor blockers (ARB) significantly reduce proteinuria and retard progression of glomerular disease. The underlying intraglomerular mechanisms are not yet fully elucidated. As podocyte injury constitutes a critical step in the pathogenesis of glomerular proteinuria, beneficial effects of ACEI and ARB may partially result from interference with a local renin-angiotensin system (RAS) in podocytes. The knowledge of expression and function of a local RAS in podocytes is limited. In this study, we demonstrate functional expression of key components of the RAS in differentiated human podocytes: podocytes express mRNA for angiotensinogen, renin, ACE type 1, and the AT<jats:sub>1<\/jats:sub>and AT<jats:sub>2<\/jats:sub>angiotensin receptor subtypes. In Western blot experiments and immunostainings, expression of the AT<jats:sub>1<\/jats:sub>and AT<jats:sub>2<\/jats:sub>receptor was demonstrated both in differentiated human podocytes and in human kidney cortex. ANG II induced a concentration-dependent increase in cytosolic Ca<jats:sup>2+<\/jats:sup>concentration via AT<jats:sub>1<\/jats:sub>receptors in differentiated human podocytes, whereas it did not increase cAMP. Furthermore, ANG II secretion was detected, which was blocked by neither the ACEI captopril nor the renin inhibitor remikiren nor the chymase inhibitor chymostatin. ANG II secretion of podocytes was not increased by mechanical stress. Finally, ANG II was found to increase staurosporine-induced apoptosis in podocytes. We speculate that ACEI and ARB exert their beneficial effects, in part, by interfering with a local RAS in podocytes. Further experiments are required to identify the underlying molecular mechanism(s) of podocyte protection.<\/jats:p>","DOI":"10.1152\/ajprenal.00475.2004","type":"journal-article","created":{"date-parts":[[2005,9,28]],"date-time":"2005-09-28T03:33:59Z","timestamp":1127878439000},"page":"F710-F719","source":"Crossref","is-referenced-by-count":97,"title":["Functional expression of the renin-angiotensin system in human podocytes"],"prefix":"10.1152","volume":"290","author":[{"given":"Max C.","family":"Liebau","sequence":"first","affiliation":[]},{"given":"D.","family":"Lang","sequence":"additional","affiliation":[]},{"given":"J.","family":"B\u00f6hm","sequence":"additional","affiliation":[]},{"given":"N.","family":"Endlich","sequence":"additional","affiliation":[]},{"given":"Martin J.","family":"Bek","sequence":"additional","affiliation":[]},{"given":"Ian","family":"Witherden","sequence":"additional","affiliation":[]},{"given":"Peter W.","family":"Mathieson","sequence":"additional","affiliation":[]},{"given":"Moin A.","family":"Saleem","sequence":"additional","affiliation":[]},{"given":"Hermann","family":"Pavenst\u00e4dt","sequence":"additional","affiliation":[]},{"given":"Karl-Georg","family":"Fischer","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1007\/s001090100210"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-200204000-00033"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1172\/JCI108293"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1159\/000052624"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1007\/s001250100546"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa011161"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.33.1.102"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-200301000-00031"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1042\/cs1000481"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.52.4.1023"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00362.x"},{"key":"R12","doi-asserted-by":"crossref","unstructured":"Endlich N, Kress KR, Reiser J, Uttenweiler D, Kriz W, Mundel P, and Endlich K.Podocytes respond to mechanical stress in vitro.J Am Soc Nephrol12: 413\u2013422, 2001.","DOI":"10.1681\/ASN.V123413"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119467"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00796.x"},{"key":"R15","doi-asserted-by":"crossref","unstructured":"Grynkiewicz G, Poenie M, and Tsien RY.A new generation of Ca2+indicators with greatly improved fluorescence properties.J Biol Chem260: 3340\u20133350, 1985.","DOI":"10.1016\/S0021-9258(19)83641-4"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.383"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000127988.42710.A7"},{"key":"R18","unstructured":"Inagami T.Molecular biology and signaling of angiotensin receptors: an overview.J Am Soc Nephrol10,Suppl11: S2\u2013S7, 1999."},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/17.7.1327"},{"key":"R20","unstructured":"Kim Sand Iwao H.Molecular and cellular mechanisms of angiotensin II-mediated cardiovascular and renal diseases.Pharmacol Rev52: 11\u201334, 2000."},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00421.x"},{"key":"R22","unstructured":"Kriz W, Elger M, Nagata M, Kretzler M, Uiker S, Koeppen-Hagemann I, Tenschert S, and Lemley KV.The role of podocytes in the development of glomerular sclerosis.Kidney Int45: S-64\u2013S-72, 1994."},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.47"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.168.12.6152"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1007\/s00125-002-0946-y"},{"key":"R26","doi-asserted-by":"crossref","unstructured":"Lapinski R, Perico N, Remuzzi A, Sangalli F, Benigni A, and Remuzzi G.Angiotensin II modulates glomerular capillary permselectivity in rat isolated perfused kidney.J Am Soc Nephrol7: 653\u2013660, 1996.","DOI":"10.1681\/ASN.V75653"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00536.x"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199311113292004"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa011303"},{"key":"R30","doi-asserted-by":"crossref","unstructured":"Macconi D, Ghilardi M, Bonassi ME, Mohamed EI, Abbate M, Colombi F, Remuzzi G, and Remuzzi A.Effect of angiotensin-converting enzyme inhibition on glomerular basement membrane permeability and distribution of zonula occludens-1 in MWF rats.J Am Soc Nephrol11: 477\u2013489, 2000.","DOI":"10.1681\/ASN.V113477"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199604113341502"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1007\/s001250100561"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1136\/bmj.321.7274.1440"},{"key":"R34","doi-asserted-by":"crossref","unstructured":"Mundel P, Reiser J, and Kriz W.Induction of differentiation in cultured rat and human podocytes.J Am Soc Nephrol8: 697\u2013705, 1997.","DOI":"10.1681\/ASN.V85697"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(03)12229-5"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1161\/hy0202.103821"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.00183.2004"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1007\/BF00372961"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00810.x"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00020.2002"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.35.6.1189"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199811123392007"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(98)10363-X"},{"key":"R44","doi-asserted-by":"crossref","unstructured":"Saleem MA, O'Hare MJ, Reiser J, Coward RJ, Inward CD, Farren T, Xing CY, Ni L, Mathieson PW, and Mundel P.A conditionally immortalized human podocyte cell line demonstrating nephrin and podocin expression.J Am Soc Nephrol13: 630\u2013638, 2002.","DOI":"10.1681\/ASN.V133630"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1172\/JCI114846"},{"key":"R46","doi-asserted-by":"crossref","unstructured":"Sharma M, Sharma R, Greene AS, McCarthy ET, and Savin VJ.Documentation of angiotensin II receptors in glomerular epithelial cells.Am J Physiol Renal Physiol274: F623\u2013F627, 1998.","DOI":"10.1152\/ajprenal.1998.274.3.F623"},{"key":"R47","doi-asserted-by":"crossref","unstructured":"Sharma R, Lovell HB, Wiegmann TB, and Savin VJ.Vasoactive substances induce cytoskeletal changes in cultured rat glomerular epithelial cells.J Am Soc Nephrol3: 1131\u20131138, 1992.","DOI":"10.1681\/ASN.V351131"},{"key":"R48","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000032549.36050.78"},{"key":"R49","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-2143(03)00139-2"},{"key":"R50","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0706166"},{"key":"R51","doi-asserted-by":"publisher","DOI":"10.1159\/000066656"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00475.2004","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,7,18]],"date-time":"2021-07-18T03:52:39Z","timestamp":1626580359000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00475.2004"}},"issued":{"date-parts":[[2006,3]]},"references-count":51,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2006,3]]}},"alternative-id":["10.1152\/ajprenal.00475.2004"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00475.2004","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2006,3]]}},{"indexed":{"date-parts":[[2026,1,15]],"date-time":"2026-01-15T21:44:17Z","timestamp":1768513457219,"version":"3.49.0"},"reference-count":30,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2016,7,1]]},"DOI":"10.1152\/ajprenal.00229.2016","type":"journal-article","created":{"date-parts":[[2016,5,5]],"date-time":"2016-05-05T03:38:36Z","timestamp":1462419516000},"page":"F68-F70","source":"Crossref","is-referenced-by-count":2,"title":["The evolving field of salt transport regulation in the Steve Hebert Lecture"],"prefix":"10.1152","volume":"311","author":[{"given":"Gerardo","family":"Gamba","sequence":"first","affiliation":[{"name":"Molecular Physiology Unit, Instituto de Investigaciones Biom\u00e9dicas, Universidad Nacional Aut\u00f3noma de M\u00e9xico and Instituto Nacional de Ciencias M\u00e9dicas y Nutrici\u00f3n Salvador Zubir\u00e1n, Mexico City, Mexico"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014050470"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/nature10814"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1038\/366575a0"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.114.04036"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00358.2015"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1042\/BJ20131478"},{"key":"B7","doi-asserted-by":"crossref","first-page":"17713","DOI":"10.1016\/S0021-9258(17)32499-7","volume":"269","author":"Gamba G","year":"1994","journal-title":"J Biol Chem"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.90.7.2749"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1038\/362031a0"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1038\/ng.2218"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00017.2010"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1172\/JCI76126"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1016\/j.str.2004.04.014"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M603773200"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1126\/scisignal.2005050"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M208108200"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.1.131"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.025312"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.077230"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00044.2004"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2012040404"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0901749106"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.15252\/emmm.201505444"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1304592110"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1038\/ng0196-24"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1042\/BJ20051180"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0808358106"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1126\/science.1062844"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.275.22.16795"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1411705111"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00229.2016","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,6,19]],"date-time":"2022-06-19T22:42:16Z","timestamp":1655678536000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00229.2016"}},"issued":{"date-parts":[[2016,7,1]]},"references-count":30,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2016,7,1]]}},"alternative-id":["10.1152\/ajprenal.00229.2016"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00229.2016","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2016,7,1]]}},{"indexed":{"date-parts":[[2026,1,16]],"date-time":"2026-01-16T09:37:06Z","timestamp":1768556226715,"version":"3.49.0"},"reference-count":59,"publisher":"American Physiological Society","issue":"6","funder":[{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)","doi-asserted-by":"publisher","award":["R01DK056903"],"award-info":[{"award-number":["R01DK056903"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"name":"US Department of Veterans Affairs Administration","award":["1I01BX002049"],"award-info":[{"award-number":["1I01BX002049"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2018,6,1]]},"abstract":"<jats:p>Expression of Tamm-Horsfall protein (THP or uromodulin) is highly restricted to the kidney thick ascending limb (TAL) of loop of Henle. Despite the unique location and recent association of THP gene mutations with hereditary uromodulin-associated kidney disease and THP single nucleotide polymorphisms with chronic kidney disease and hypertension, the physiological function(s) of THP and its pathological involvement remain incompletely understood. By studying age-dependent changes of THP knockout (KO) mice, we show here that young KO mice had significant salt and water wasting but were partially responsive to furosemide, due to decreased luminal translocation of Na-K-Cl cotransporter 2 (NKCC2) in the TAL. Aged THP KO mice were, however, markedly oliguric and unresponsive to furosemide, and their NKCC2 was localized primarily in the cytoplasm as evidenced by lipid raft floatation assay, cell fractionation, and confocal and immunoelectron microscopy. These aged KO mice responded to metolazone and acetazolamide, known to target distal and proximal tubules, respectively. They also had marked upregulation of renin in juxtaglomerular apparatus and serum, and they were hypertensive. Finally, the aged THP KO mice had significant upregulation of Na-coupled urate transporters Slc5a8 and Slc22a12 as well as sodium-hydrogen exchanger 3 (NHE3) in the proximal tubule and elevated serum uric acid and allantoin. Collectively, our results suggest that THP deficiency can cause progressive disturbances in renal functions via initially NKCC2 dysfunction and later compensatory responses, resulting in prolonged activation of the renin-angiotensin-aldosterone axis and hyperuricemia.<\/jats:p>","DOI":"10.1152\/ajprenal.00233.2017","type":"journal-article","created":{"date-parts":[[2018,1,10]],"date-time":"2018-01-10T13:59:07Z","timestamp":1515592747000},"page":"F1062-F1076","source":"Crossref","is-referenced-by-count":36,"title":["Tamm-Horsfall protein\/uromodulin deficiency elicits tubular compensatory responses leading to hypertension and hyperuricemia"],"prefix":"10.1152","volume":"314","author":[{"given":"Yan","family":"Liu","sequence":"first","affiliation":[{"name":"Department of Urology, New York University School of Medicine, New York, New York"}]},{"given":"David S.","family":"Goldfarb","sequence":"additional","affiliation":[{"name":"Department of Nephrology, New York University School of Medicine, New York, New York"},{"name":"Veterans Affairs New York Harbor Healthcare System, Manhattan Campus, New York, New York"}]},{"given":"Tarek M.","family":"El-Achkar","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Indiana University School of Medicine and Indianapolis Veterans Affairs, Indianapolis, Indiana"}]},{"given":"John C.","family":"Lieske","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota"}]},{"given":"Xue-Ru","family":"Wu","sequence":"additional","affiliation":[{"name":"Department of Urology, New York University School of Medicine, New York, New York"},{"name":"Veterans Affairs New York Harbor Healthcare System, Manhattan Campus, New York, New York"},{"name":"Department of Pathology, New York University School of Medicine, New York, New York"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1007\/s10157-011-0532-z"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1007\/BF00492456"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00143.2004"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00452.x"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/ddq205"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.12201115"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1159\/000320889"},{"key":"B8","doi-asserted-by":"crossref","first-page":"895","DOI":"10.1681\/ASN.V34895","volume":"3","author":"Brown D","year":"1992","journal-title":"J Am Soc Nephrol"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.7554\/eLife.08887"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2004.09.003"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.2174\/138161205774913219"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00432.2014"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M308821200"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2015.267"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00543.2012"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00621.2010"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2011.10.054"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00083.2008"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2015.192"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfk081"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pgen.1001039"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1023\/A:1020521308985"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00522.2009"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.2741\/1347"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1038\/ng.377"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009070725"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1990.128"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1159\/000320681"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M112.348243"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00243.2010"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.459"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1146\/annurev-physiol-021113-170343"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014070664"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00867.x"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00357.2003"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M111.222968"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013070781"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M008610200"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1078\/1438-4221-00151"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2011.09.009"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1007\/BF01746679"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1159\/000176450"},{"key":"B43","first-page":"423","volume":"17","author":"Quan A","year":"1997","journal-title":"Semin Nephrol"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1002\/nau.20693"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2013.162"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2011.134"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M110.149880"},{"key":"B48","doi-asserted-by":"crossref","first-page":"20784","DOI":"10.1016\/S0021-9258(17)45284-7","volume":"265","author":"Rindler MJ","year":"1990","journal-title":"J Biol Chem"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1194\/jlr.R062885"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1007\/s00418-004-0638-4"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2004.08.021"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009121283"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1977.1"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(03)00829-1"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1007\/s10719-005-2142-z"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1097\/MD.0000000000003011"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1248\/bpb.31.405"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1038\/nm.3384"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.91.2.742"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00233.2017","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,12]],"date-time":"2022-08-12T04:07:55Z","timestamp":1660277275000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00233.2017"}},"issued":{"date-parts":[[2018,6,1]]},"references-count":59,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2018,6,1]]}},"alternative-id":["10.1152\/ajprenal.00233.2017"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00233.2017","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2018,6,1]]}},{"indexed":{"date-parts":[[2026,1,18]],"date-time":"2026-01-18T21:49:26Z","timestamp":1768772966302,"version":"3.49.0"},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1988,9,1]]},"abstract":"<jats:p> The system of renal Ca transport in the rat is modeled in terms of two classes of processes: a nonsaturable flux that predominates in the proximal tubule, and an active, vitamin D-dependent flux with major expression in the distal convoluted tubule. There transport is against an electrochemical gradient, with much of the efflux probably mediated by the Ca\/Mg-ATPase. Calculations of the rate of free Ca diffusion in tubular cells indicate that an unaided flux would be only one-seventy-seventh of that found experimentally. It is suggested that the vitamin D-induced renal calcium binding protein, CaBPr, Mr approximately 28,000, in raising total cellular calcium by three orders of magnitude, increases the transcellular Ca flux and thus the free intracellular Ca ion concentration at the basolateral pole, allowing the Ca\/Mg-ATPase to function near its maximum. Analysis of the rate of nonsaturable Ca flux throughout the kidney tubule suggests a paracellular pathway via bulk flow, following water that is driven osmotically. Evaluation of whole animal data in terms of these two classes of calcium fluxes indicates that our model is consistent with experimental observations and assigns a functional role to active calcium transport. <\/jats:p>","DOI":"10.1152\/ajprenal.1988.255.3.f558","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T21:21:03Z","timestamp":1513977663000},"page":"F558-F562","source":"Crossref","is-referenced-by-count":6,"title":["CaBPr facilitates intracellular diffusion for Ca pumping in distal convoluted tubule"],"prefix":"10.1152","volume":"255","author":[{"given":"F.","family":"Bronner","sequence":"first","affiliation":[{"name":"Department of BioStructure and Function, University of Connecticut Health Center, Farmington 06032."}]},{"given":"W. D.","family":"Stein","sequence":"additional","affiliation":[{"name":"Department of BioStructure and Function, University of Connecticut Health Center, Farmington 06032."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1988.255.3.F558","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:09:32Z","timestamp":1567969772000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1988.255.3.F558"}},"issued":{"date-parts":[[1988,9,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1988,9,1]]}},"alternative-id":["10.1152\/ajprenal.1988.255.3.F558"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1988.255.3.f558","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1988,9,1]]}},{"indexed":{"date-parts":[[2026,1,22]],"date-time":"2026-01-22T05:25:09Z","timestamp":1769059509076,"version":"3.49.0"},"reference-count":96,"publisher":"American Physiological Society","issue":"3","funder":[{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)","doi-asserted-by":"publisher","award":["DK038217"],"award-info":[{"award-number":["DK038217"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2019,9,1]]},"abstract":"<jats:p>LPS inhibits [Formula: see text] absorption in the medullary thick ascending limb (MTAL) through a Toll-like receptor 4 (TLR4)-myeloid differentiation factor 88 (MyD88)-extracellular signal-regulated kinase (ERK) pathway that is upregulated by sepsis. Pretreatment with the nontoxic immunomodulator monophosphoryl lipid A (MPLA) prevents inhibition by LPS through activation of a TLR4-TIR-domain-containing adaptor-inducing interferon-\u03b2 (TRIF)-phosphatidylinositol 3-kinase (PI3K) pathway that prevents LPS-induced ERK activation. Here, we identified the molecular mechanisms that underlie the protective inhibitory interaction between the MPLA-PI3K and LPS-ERK pathways. Treatment of mouse MTALs with LPS in vitro increased phosphorylation of IL-1 receptor-associated kinase (IRAK)-1, a critical mediator of LPS signaling downstream of TLR4-MyD88. Activation of ERK by LPS was eliminated by a selective IRAK-1 inhibitor, establishing IRAK-1 as the upstream mediator of ERK activation. Pretreatment of MTALs with MPLA in vitro prevented LPS-induced IRAK-1 activation; this effect was dependent on PI3K. Treatment of MTALs with MPLA increased expression of Toll-interacting protein (Tollip), an inducible protein that negatively regulates LPS signaling by inhibiting IRAK-1. The MPLA-induced increase in Tollip protein level was prevented by PI3K inhibitors. In coimmunoprecipitation experiments, MPLA increased the amount of Tollip stably bound to IRAK-1, an interaction that inhibits IRAK-1 activation. These results support a mechanism whereby MPLA increases Tollip expression in the MTAL through a PI3K-dependent pathway. Tollip, in turn, inhibits LPS-induced TLR4 signaling by suppressing activation of IRAK-1, thereby preventing activation of ERK that inhibits [Formula: see text] absorption. These studies show that MPLA induces reprogramming of MTAL cells that protects against LPS stimulation and identify IRAK-1 and Tollip as new therapeutic targets to prevent renal tubule dysfunction in response to infectious and inflammatory stimuli.<\/jats:p>","DOI":"10.1152\/ajprenal.00170.2019","type":"journal-article","created":{"date-parts":[[2019,6,26]],"date-time":"2019-06-26T19:15:02Z","timestamp":1561576502000},"page":"F705-F719","source":"Crossref","is-referenced-by-count":10,"title":["Monophosphoryl lipid A induces protection against LPS in medullary thick ascending limb through induction of Tollip and negative regulation of IRAK-1"],"prefix":"10.1152","volume":"317","author":[{"suffix":"III","given":"Bruns A.","family":"Watts","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, University of Texas Medical Branch, Galveston, Texas"}]},{"given":"Esther","family":"Tamayo","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Texas Medical Branch, Galveston, Texas"}]},{"given":"Edward R.","family":"Sherwood","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology, Vanderbilt University Medical Center, Nashville, Tennessee"}]},{"given":"David W.","family":"Good","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Texas Medical Branch, Galveston, Texas"},{"name":"Department of Neuroscience and Cell Biology, University of Texas Medical Branch, Galveston, Texas"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/j.immuni.2009.06.024"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1097\/00024382-199410000-00007"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1097\/00003246-199501000-00006"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1001\/archsurg.1991.01410250027003"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.03681106"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007040395"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1097\/CCM.0B013E318162ED7B"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1016\/j.it.2009.07.009"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/j.biocel.2007.04.021"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1097\/SHK.0000000000000042"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.167.2.987"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1038\/35014038"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.20.12203"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/j.micinf.2011.08.018"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1007\/s00018-008-8228-6"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0037584"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1186\/cc5055"},{"key":"B18","doi-asserted-by":"crossref","first-page":"711","DOI":"10.1128\/IAI.53.3.711-712.1986","volume":"53","author":"Chase JJ","year":"1986","journal-title":"Infect Immun"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1007\/s00109-012-0969-x"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfq589"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1172\/JCI39421"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2015.01.009"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1179\/096805104225003997"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.1602106"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1016\/j.bcp.2010.06.020"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/S1471-4906(03)00139-X"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2010.091279"},{"key":"B28","first-page":"225","volume":"13","author":"Good DW","year":"1993","journal-title":"Semin Nephrol"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.2000.279.5.C1443"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M803019200"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00335.2009"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M111.336255"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00378.x"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M203298200"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1097\/00075198-200312000-00002"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1186\/cc3987"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1016\/B978-0-12-381462-3.00055-0"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.04680514"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1189\/jlb.1A0216-072R"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.3389\/fimmu.2014.00553"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1016\/S1097-2765(03)00053-4"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2006.03.047"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1016\/S1074-7613(00)80086-2"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1038\/ni.1863"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1016\/j.ccc.2005.01.002"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(02)00827-9"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M309251200"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1053\/ajkd.2001.27688"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0810169106"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1189\/jlb.69.4.522"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1136\/emj.2007.055558"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2011.261"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M001950200"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1016\/j.molimm.2004.03.009"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1038\/nri1630"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010111210"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1126\/science.1138963"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.164.11.5564"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.169.9.5209"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1016\/S1097-2765(00)80136-7"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1189\/jlb.0507290"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1097\/CCM.0b013e3181a59165"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfp011"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1038\/nri2957"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.1800062"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1189\/jlb.0309189"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2015030261"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0029893"},{"key":"B69","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.00022-11"},{"key":"B70","doi-asserted-by":"publisher","DOI":"10.1038\/icb.2014.55"},{"key":"B71","doi-asserted-by":"crossref","first-page":"3569","DOI":"10.1128\/IAI.66.8.3569-3578.1998","volume":"66","author":"Salkowski CA","year":"1998","journal-title":"Infect Immun"},{"key":"B72","doi-asserted-by":"crossref","first-page":"3239","DOI":"10.1128\/IAI.65.8.3239-3247.1997","volume":"65","author":"Salkowski CA","year":"1997","journal-title":"Infect Immun"},{"key":"B73","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00258.2006"},{"key":"B74","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006050454"},{"key":"B75","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.1103541"},{"key":"B76","doi-asserted-by":"publisher","DOI":"10.1042\/CS20150592"},{"key":"B77","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0164858"},{"key":"B78","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.164.8.4301"},{"key":"B79","doi-asserted-by":"publisher","DOI":"10.1001\/jama.294.7.813"},{"key":"B80","doi-asserted-by":"publisher","DOI":"10.1016\/j.bmcl.2015.10.060"},{"key":"B81","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M410719200"},{"key":"B82","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00507.2005"},{"key":"B83","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00102.2013"},{"key":"B84","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00237.2011"},{"key":"B85","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00608.2012"},{"key":"B86","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00064.2017"},{"key":"B87","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00033.2018"},{"key":"B88","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00133.2001"},{"key":"B89","doi-asserted-by":"publisher","DOI":"10.1016\/S1074-7613(00)80402-1"},{"key":"B90","doi-asserted-by":"publisher","DOI":"10.1097\/00003246-200201001-00009"},{"key":"B91","doi-asserted-by":"publisher","DOI":"10.1097\/01.shk.0000209542.76305.55"},{"key":"B92","doi-asserted-by":"publisher","DOI":"10.1172\/JCI31008"},{"key":"B93","doi-asserted-by":"publisher","DOI":"10.1097\/MCC.0000000000000153"},{"key":"B94","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007090982"},{"key":"B95","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.12.7611"},{"key":"B96","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M109537200"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00170.2019","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,1,8]],"date-time":"2021-01-08T02:27:33Z","timestamp":1610072853000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00170.2019"}},"issued":{"date-parts":[[2019,9,1]]},"references-count":96,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2019,9,1]]}},"alternative-id":["10.1152\/ajprenal.00170.2019"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00170.2019","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2019,9,1]]}},{"indexed":{"date-parts":[[2026,1,20]],"date-time":"2026-01-20T11:51:35Z","timestamp":1768909895910,"version":"3.49.0"},"reference-count":37,"publisher":"American Physiological Society","issue":"4","funder":[{"name":"Scientific Commission of Italian Federation of Sport Medicine"},{"name":"Association of EV-K2-CNR"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2019,10,1]]},"abstract":"<jats:p> Exposure to high altitude is one of the most widely used models to study the adaptive response to hypoxia in humans. However, little is known about the related effects on micturition. The present study addresses the adaptive urinary responses in four healthy adult lowlanders, comparing urodynamic indexes at Kathmandu [1,450 m above sea level (a.s.l.); K<jats:sup>1450<\/jats:sup>] and during a sojourn in Namche Bazar (3,500 m a.s.l.; NB<jats:sup>3500<\/jats:sup>). The urodynamic testing consisted of cistomanometry and bladder pressure\/flow measurements. Anthropometrics, electrocardiographic, and peripheral capillary oxygen saturation data were also collected. The main findings consisted of significant reductions in bladder power at maximum urine flow by ~30%, bladder contractility index by 13%, and infused volume both at first (by 57%) and urgency sensation (by 14%) to urinate, indicating a reduced cystometric capacity, at NB<jats:sup>3500<\/jats:sup>. In addition to the urinary changes, we found that oxygen saturation, body mass index, body surface area, and median RR time were all significantly reduced at altitude. We submit that the hypoxia-related parasympathetic inhibition could be the underlying mechanism of both urodynamic and heart rate adaptive responses to high-altitude exposure. Moreover, increased diuresis and faster bladder filling at altitude may trigger the anticipation of being able to void, a common cause of urgency. We believe that the present pilot study represents an original approach to the study of urinary physiology at altitude. <\/jats:p>","DOI":"10.1152\/ajprenal.00333.2019","type":"journal-article","created":{"date-parts":[[2019,8,28]],"date-time":"2019-08-28T12:50:59Z","timestamp":1566996659000},"page":"F1081-F1086","source":"Crossref","is-referenced-by-count":8,"title":["Urinary physiology and hypoxia: a pilot study of moderate-altitude trekking effects on urodynamic indexes"],"prefix":"10.1152","volume":"317","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8343-9024","authenticated-orcid":false,"given":"Vittore","family":"Verratti","sequence":"first","affiliation":[{"name":"Department of Psychological Sciences, Health, and Territory, University \u201cG. d\u2019Annunzio\u201d of Chieti-Pescara, Chieti, Italy"},{"name":"Laboratory of Clinical and Hypoxic Physiology, University \u201cG. d\u2019Annunzio\u201d of Chieti-Pescara, Chieti, Italy"}]},{"given":"Simona","family":"Mrakic-Sposta","sequence":"additional","affiliation":[{"name":"Institute of Bioimaging and Molecular Physiology, National Research Council of Italy, Segrate, Italy"}]},{"given":"Manuela","family":"Moriggi","sequence":"additional","affiliation":[{"name":"Institute of Bioimaging and Molecular Physiology, National Research Council of Italy, Segrate, Italy"}]},{"given":"Alessandro","family":"Tonacci","sequence":"additional","affiliation":[{"name":"Institute of Clinical Physiology, National Research Council of Italy, Pisa, Italy"}]},{"given":"Suwas","family":"Bhandari","sequence":"additional","affiliation":[{"name":"Wenzhou Medical University, Wenzhou, Zhejiang Province, China"}]},{"given":"Danilo","family":"Migliorelli","sequence":"additional","affiliation":[{"name":"COMPUMED Europe, Rome, Italy"}]},{"given":"Ashok","family":"Bajracharya","sequence":"additional","affiliation":[{"name":"Capital Hospital, Putalisadak-Kathmandu, Nepal"}]},{"given":"Danilo","family":"Bondi","sequence":"additional","affiliation":[{"name":"Department of Neuroscience, Imaging, and Clinical Sciences, University \u201cG. d\u2019Annunzio\u201d of Chieti-Pescara, Chieti, Italy"}]},{"given":"Enrico Finazzi","family":"Agr\u00f2","sequence":"additional","affiliation":[{"name":"Department of Surgical Sciences, University of Rome \u201cTor Vergata\u201d and Unit of Urology Policlinic, Tor Vergata University Hospital, Rome, Italy"}]},{"given":"Paolo","family":"Cerretelli","sequence":"additional","affiliation":[{"name":"Institute of Bioimaging and Molecular Physiology, National Research Council of Italy, Segrate, Italy"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1109\/IEMBS.2007.4353892"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1109\/10.212067"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.2174\/1874609810902020095"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1007\/s00421-010-1399-5"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1097\/MAJ.0b013e3181629a32"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1159\/000279255"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.00239.2004"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.01439.2010"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/jappl.2000.88.2.599"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.04520413"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1111\/j.1442-2042.2009.02326.x"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00180.2016"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1580\/1080-6032(2001)012[0008:AIANCO]2.0.CO;2"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/S0165-1838(96)00117-8"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1974.tb05621.x"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00336.2003"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.7759\/cureus.c10"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00004.2005"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1089\/ham.2009.1097"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1109\/10.43621"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1097-0185(19990301)254:3<375:AID-AR8>3.0.CO;2-R"},{"key":"B22","first-page":"15","volume":"184","author":"Morrison JF","year":"1997","journal-title":"Scand J Urol Nephrol Suppl"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1016\/j.ucl.2014.04.007"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.3389\/fphys.2017.00360"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1002\/nau.23124"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/j.juro.2011.04.111"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1113\/JP273726"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1159\/000495519"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1109\/EMBC.2018.8513047"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/0165-1838(92)90059-P"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1111\/and.12515"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1111\/j.1743-6109.2011.02320.x"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00284.2016"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1016\/j.juro.2014.11.055"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1002\/nau.22517"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00074.2014"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1113\/JP276973"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00333.2019","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,10,9]],"date-time":"2019-10-09T08:13:56Z","timestamp":1570608836000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00333.2019"}},"issued":{"date-parts":[[2019,10,1]]},"references-count":37,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2019,10,1]]}},"alternative-id":["10.1152\/ajprenal.00333.2019"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00333.2019","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2019,10,1]]}},{"indexed":{"date-parts":[[2026,1,21]],"date-time":"2026-01-21T10:21:36Z","timestamp":1768990896130,"version":"3.49.0"},"reference-count":30,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2007,2]]},"abstract":"<jats:p>Leptospirosis is a public health problem worldwide. Severe leptospirosis manifests as pulmonary edema leading to acute respiratory distress syndrome and polyuric acute renal failure (ARF). The etiology of leptospirosis-induced pulmonary edema is unclear. Lung edema clearance is largely affected by active sodium transport out of the alveoli rather than by reversal of the Starling forces. The objective of this study was to profile leptospirosis-induced ARF and pulmonary edema. We inoculated hamsters with leptospires and collected 24-h urine samples on postinoculation day 4. On day 5, the animals were killed, whole blood was collected, and the kidneys and lungs were removed. Immunoblotting was used to determine expression and abundance of water and sodium transporters. Leptospirosis-induced ARF resulted in natriuresis, lower creatinine clearance, and impaired urinary concentrating ability. Renal expression of the sodium\/hydrogen exchanger isoform 3 and of aquaporin 2 was lower in infected animals, whereas that of the Na-K-2Cl cotransporter NKCC2 was higher. Leptospirosis-induced lesions, predominantly in the proximal tubule, were responsible for the polyuria and natriuresis observed. The polyuria might also be attributed to reduced aquaporin 2 expression and the attendant urinary concentrating defect. In the lungs, expression of the epithelial sodium channel was lower, and NKCC1 expression was upregulated. We found that leptospirosis profoundly influences the sodium transport capacity of alveolar epithelial cells and that impaired pulmonary fluid handling can impair pulmonary function, increasing the chance of lung injury. Greater knowledge regarding sodium transporter dysregulation in the lungs and kidneys can provide new perspectives on leptospirosis treatment.<\/jats:p>","DOI":"10.1152\/ajprenal.00102.2006","type":"journal-article","created":{"date-parts":[[2006,8,30]],"date-time":"2006-08-30T08:32:02Z","timestamp":1156926722000},"page":"F586-F592","source":"Crossref","is-referenced-by-count":58,"title":["Leptospirosis leads to dysregulation of sodium transporters in the kidney and lung"],"prefix":"10.1152","volume":"292","author":[{"given":"L\u00facia","family":"Andrade","sequence":"first","affiliation":[]},{"suffix":"Jr.","given":"Ad\u00edlson C.","family":"Rodrigues","sequence":"additional","affiliation":[]},{"given":"Talita R. C.","family":"Sanches","sequence":"additional","affiliation":[]},{"given":"Rodrigo B.","family":"Souza","sequence":"additional","affiliation":[]},{"given":"Antonio Carlos","family":"Seguro","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.243"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.01201.2001"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1016\/S1473-3099(03)00830-2"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.01171.2001"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1159\/000078877"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1001\/jama.289.16.2104"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(99)80012-9"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.6.F925"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1159\/000187069"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1086\/313501"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1152\/ajplung.1996.270.4.L487"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1378\/chest.122.6_suppl.340S"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00003.2002"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1097\/01.qco.0000178824.05715.2c"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00227.2002"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00029.2002"},{"key":"R18","doi-asserted-by":"crossref","unstructured":"Nally JE, Chantranuwat C, Wu XY, Silva JJP, Blanco DR, Lovett MA.Alveolar septal deposition of immunoglobulin and complement parallels pulmonary hemorrhage in a guinea pig model of severe pulmonary leptospirosis.Am J Pathol163: 1115\u20131127, 2004.","DOI":"10.1016\/S0002-9440(10)63198-7"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.4269\/ajtmh.1997.56.181"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1999.276.5.C995"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1001\/jama.282.1.54"},{"key":"R22","unstructured":"Reeves WB, Winters CJ, Zimniak L, Andreoli TE.Medullary thick limbs: renal concentrating segments.Kidney Int50,Suppl57: S154\u2013S164, 1996."},{"key":"R23","unstructured":"Sands JM, Kokko J.Current concepts of the countercurrent multiplication system.Kidney Int50,Suppl57: S93\u2013S99, 1996."},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1183\/09031936.02.00401602"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1159\/000185943"},{"key":"R26","unstructured":"Sitprija V, Kearkiak P.Nephropathy in Leptospirosis.J Postgrad Med51: 184\u2013188, 2005."},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1378\/chest.108.3.874"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199605303342207"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1152\/ajplung.2000.279.6.L1110"},{"key":"R30","doi-asserted-by":"crossref","unstructured":"Yang CW, Wu MS, Yu Pan MJ, Hong JJ, Yu CC, Vandewalle A, Huang CC.Leptospira outer membrane protein activates NF-\u03baB and downstream genes expressed in medullary thick ascending limb cells.J Am Soc Nephrol11: 2017\u20132026, 2000.","DOI":"10.1681\/ASN.V11112017"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.1997.tb52350.x"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00102.2006","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,8,1]],"date-time":"2021-08-01T00:19:47Z","timestamp":1627777187000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00102.2006"}},"issued":{"date-parts":[[2007,2]]},"references-count":30,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2007,2]]}},"alternative-id":["10.1152\/ajprenal.00102.2006"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00102.2006","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2007,2]]}},{"indexed":{"date-parts":[[2026,1,19]],"date-time":"2026-01-19T07:18:27Z","timestamp":1768807107867,"version":"3.49.0"},"reference-count":57,"publisher":"American Physiological Society","issue":"1","funder":[{"DOI":"10.13039\/100008272","name":"Novartis Pharmaceuticals Corporation","doi-asserted-by":"crossref","award":["CRLX030AUSNC08T"],"award-info":[{"award-number":["CRLX030AUSNC08T"]}],"id":[{"id":"10.13039\/100008272","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2018,1,1]]},"abstract":"<jats:p>Serelaxin is a novel recombinant human relaxin-2 that has been investigated for the treatment of acute heart failure. However, its effects on renal function, especially on the renal microcirculation, remain incompletely characterized. Our immunoexpression studies localized RXFP1 receptors on vascular smooth muscle cells and endothelial cells of afferent arterioles and on principal cells of collecting ducts. Clearance experiments were performed in male and female normotensive rats and Ang II-infused male rats. Serelaxin increased mean arterial pressure slightly and significantly increased renal blood flow, urine flow, and sodium excretion rate. Group analysis of all serelaxin infusion experiments showed significant increases in GFR. During infusion with subthreshold levels of Ang II, serelaxin did not alter mean arterial pressure, renal blood flow, GFR, urine flow, or sodium excretion rate. Heart rates were elevated during serelaxin infusion alone (37\u2009\u00b1\u20095%) and in Ang II-infused rats (14\u2009\u00b1\u20092%). In studies using the in vitro isolated juxtamedullary nephron preparation, superfusion with serelaxin alone (40 ng\/ml) significantly dilated afferent arterioles (10.8\u2009\u00b1\u20091.2 vs. 13.5\u2009\u00b1\u20091.1 \u00b5m) and efferent arterioles (9.9\u2009\u00b1\u20090.9 vs. 11.9\u2009\u00b1\u20091.0 \u00b5m). During Ang II superfusion, serelaxin did not alter afferent or efferent arteriolar diameters. During NO synthase inhibition (l-NNA), afferent arterioles also did not show any vasodilation during serelaxin infusion. In conclusion, serelaxin increased overall renal blood flow, urine flow, GFR, and sodium excretion and dilated the afferent and efferent arterioles in control conditions, but these effects were attenuated or prevented in the presence of exogenous Ang II and NO synthase inhibitors.<\/jats:p>","DOI":"10.1152\/ajprenal.00201.2017","type":"journal-article","created":{"date-parts":[[2017,10,5]],"date-time":"2017-10-05T00:20:13Z","timestamp":1507162813000},"page":"F70-F80","source":"Crossref","is-referenced-by-count":10,"title":["Effects of serelaxin on renal microcirculation in rats under control and high-angiotensin environments"],"prefix":"10.1152","volume":"314","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5371-0618","authenticated-orcid":false,"given":"Weijian","family":"Shao","sequence":"first","affiliation":[{"name":"Department of Physiology, Tulane Hypertension and Renal Center of Excellence, Tulane University School of Medicine, New Orleans, Louisiana"}]},{"given":"Carla B.","family":"Rosales","sequence":"additional","affiliation":[{"name":"Department of Physiology, Tulane Hypertension and Renal Center of Excellence, Tulane University School of Medicine, New Orleans, Louisiana"}]},{"given":"Camila","family":"Gonzalez","sequence":"additional","affiliation":[{"name":"Department of Physiology, Tulane Hypertension and Renal Center of Excellence, Tulane University School of Medicine, New Orleans, Louisiana"}]},{"given":"Minolfa C.","family":"Prieto","sequence":"additional","affiliation":[{"name":"Department of Physiology, Tulane Hypertension and Renal Center of Excellence, Tulane University School of Medicine, New Orleans, Louisiana"}]},{"given":"L. Gabriel","family":"Navar","sequence":"additional","affiliation":[{"name":"Department of Physiology, Tulane Hypertension and Renal Center of Excellence, Tulane University School of Medicine, New Orleans, Louisiana"}]}],"member":"24","reference":[{"key":"B1","first-page":"337","volume":"3","author":"Bani G","year":"1988","journal-title":"Histol Histopathol"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00001.2012"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.2008.03797.x"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00509.2004"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1210\/endo.136.11.7588212"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2010.10.003"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00156.2011"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1984.129"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.109.133926"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1210\/en.2003-1612"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.00545.2003"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.2000.279.4.R1298"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1172\/JCI5630"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.01083.2004"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000184230.52059.33"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1196\/annals.1282.023"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1210\/en.2006-0567"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1007\/s40256-014-0069-0"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1253\/circj.CJ-14-0014"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00233.2012"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0004845"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.2001.280.1.R1"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1097\/CRD.0b013e3181f493e3"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1097\/MAJ.0b013e31820fa8da"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1096\/fj.13-233429"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.265.5.F670"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/j.mce.2010.02.003"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1161\/JAHA.113.000493"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1126\/science.2463673"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.2009.03829.x"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1016\/j.jacc.2012.11.005"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00786.2014"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1172\/JCI11975"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1096\/fj.06-6263com"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00635.2001"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1677\/joe.0.1530033"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.2.F326"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1016\/S0735-1097(00)01064-0"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1210\/en.2004-0209"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1111\/bph.12964"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00407.2014"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.110.164392"},{"key":"B43","first-page":"861","volume-title":"The Physiology of Reproduction","author":"Sherwood OD","year":"1994"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1210\/er.2003-0013"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1210\/endo-107-3-691"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1210\/endo.140.11.7091"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005090950"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1016\/j.fertnstert.2005.11.070"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.82.5.1730"},{"key":"B50","doi-asserted-by":"crossref","first-page":"1046","DOI":"10.1681\/ASN.V441046","volume":"4","author":"Takenaka T","year":"1993","journal-title":"J Am Soc Nephrol"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(12)61855-8"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1007\/s10741-008-9129-3"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1007\/s11897-010-0010-z"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.264.4.F690"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1096\/fj.12-210567"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1677\/joe.0.1370505"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1989.257.6.C1101"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00201.2017","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,3]],"date-time":"2022-08-03T23:46:58Z","timestamp":1659570418000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00201.2017"}},"issued":{"date-parts":[[2018,1,1]]},"references-count":57,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2018,1,1]]}},"alternative-id":["10.1152\/ajprenal.00201.2017"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00201.2017","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2018,1,1]]}},{"indexed":{"date-parts":[[2026,2,11]],"date-time":"2026-02-11T14:38:35Z","timestamp":1770820715119,"version":"3.50.1"},"reference-count":44,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2012,7,1]]},"abstract":"<jats:p>Laminin-\u03b22 (LAMB2) is a critical component of the glomerular basement membrane as content of LAMB2 in part determines glomerular barrier permeability. Previously, we reported that high concentrations of glucose reduce expression of this laminin subunit at the translational level. The present studies were undertaken to further define systems that control Lamb2 translation and the effect of high glucose on those systems. Complementary studies were performed using in vitro differentiation of cultured podocytes and mesangial cells exposed to normal and elevated concentrations of glucose, and tissues from control and diabetic rats. Together, these studies provide evidence for regulation of Lamb2 translation by IMP2, an RNA binding protein that targets Lamb2 mRNA to the actin cytoskeleton. Expression of Imp2 itself is regulated by the transcription factor HMGA2, which in turn is regulated by the microRNA let-7b. Elevated concentrations of glucose increase let-7b, which reduces HMGA2 expression, in turn reducing IMP2 and LAMB2. Correlative changes in kidney tissues from control and streptozotocin-induced diabetic rats suggest these control mechanisms are operative in vivo and may contribute to proteinuria in diabetic nephropathy. To our knowledge, this is the first time that translation of Lamb2 mRNA has been linked to the actin cytoskeleton, as well as to specific RNA-binding proteins. These translational control points may provide new targets for therapy in proteinuric disorders such as diabetic nephropathy where LAMB2 levels are reduced.<\/jats:p>","DOI":"10.1152\/ajprenal.00185.2012","type":"journal-article","created":{"date-parts":[[2012,4,19]],"date-time":"2012-04-19T04:28:58Z","timestamp":1334809738000},"page":"F75-F82","source":"Crossref","is-referenced-by-count":47,"title":["RNA-binding protein IGF2BP2\/IMP2 is required for laminin-\u03b22 mRNA translation and is modulated by glucose concentration"],"prefix":"10.1152","volume":"303","author":[{"given":"Valerie","family":"Schaeffer","sequence":"first","affiliation":[{"name":"Primary and Specialty Care Medicine, Department of Veterans Affairs Puget Sound Health Care System, Seattle, Washington;"},{"name":"Division of Gerontology and Geriatric Medicine, Department of Medicine, University of Washington School of Medicine,"},{"name":"Allergy and Inflammation Program, University of Washington Medicine, South Lake Union, Seattle, Washington; and"}]},{"given":"Kim M.","family":"Hansen","sequence":"additional","affiliation":[{"name":"Primary and Specialty Care Medicine, Department of Veterans Affairs Puget Sound Health Care System, Seattle, Washington;"},{"name":"Division of Gerontology and Geriatric Medicine, Department of Medicine, University of Washington School of Medicine,"},{"name":"Allergy and Inflammation Program, University of Washington Medicine, South Lake Union, Seattle, Washington; and"}]},{"given":"David R.","family":"Morris","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, University of Washington School of Medicine,"}]},{"given":"Ren\u00e9e C.","family":"LeBoeuf","sequence":"additional","affiliation":[{"name":"Division of Metabolism, Endocrinology and Nutrition, Department of Medicine, University of Washington School of Medicine, Seattle, Washington"}]},{"given":"Christine K.","family":"Abrass","sequence":"additional","affiliation":[{"name":"Primary and Specialty Care Medicine, Department of Veterans Affairs Puget Sound Health Care System, Seattle, Washington;"},{"name":"Division of Gerontology and Geriatric Medicine, Department of Medicine, University of Washington School of Medicine,"},{"name":"Allergy and Inflammation Program, University of Washington Medicine, South Lake Union, Seattle, Washington; and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5001706"},{"key":"B2","first-page":"1131","volume":"151","author":"Abrass CK","year":"1997","journal-title":"Am J Pathol"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.3"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.313"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1186\/1465-9921-6-110"},{"key":"B6","first-page":"1339","volume":"136","author":"Ayo SH","year":"1990","journal-title":"Am J Pathol"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.260.2.F185"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00623.2005"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/gkm995"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1158\/0008-5472.CAN-08-0264"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1016\/j.febslet.2004.05.075"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.05263-11"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010060632"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1677\/JME-09-0016"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1158\/1541-7786.MCR-06-0331"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1007\/s00441-009-0838-2"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1046\/j.1432-1327.2001.02292.x"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1038\/nature06783"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1186\/bcr1011"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1038\/mt.2009.313"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/30.11.2270"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1172\/JCI28414"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M111284200"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1038\/nrm2818"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1983.40"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1101\/gad.1540407"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1002\/humu.21304"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.4161\/org.7.2.15275"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1242\/dev.02270"},{"key":"B31","doi-asserted-by":"crossref","first-page":"2087","DOI":"10.1242\/jcs.00103","volume":"115","author":"Nielsen FC","year":"2002","journal-title":"J Cell Sci"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1038\/374258a0"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1038\/ng0895-400"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1016\/S0960-9822(03)00044-7"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1007\/s00018-009-0012-8"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.2337\/diab.43.3.478"},{"key":"B37","doi-asserted-by":"crossref","first-page":"630","DOI":"10.1681\/ASN.V133630","volume":"13","author":"Saleem MA","year":"2002","journal-title":"J Am Soc Nephrol"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1016\/j.trsl.2011.05.004"},{"key":"B39","first-page":"F314","volume":"297","author":"Schaeffer V","year":"2009","journal-title":"Am J Physiol Renal Physiol"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1007\/s00109-007-0182-5"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000138953.21377.80"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1016\/j.semcancer.2008.01.004"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1108269108"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1006\/dbio.1998.8962"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/ddh284"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00185.2012","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,1,13]],"date-time":"2022-01-13T07:45:10Z","timestamp":1642059910000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00185.2012"}},"issued":{"date-parts":[[2012,7,1]]},"references-count":44,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2012,7,1]]}},"alternative-id":["10.1152\/ajprenal.00185.2012"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00185.2012","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2012,7,1]]}},{"indexed":{"date-parts":[[2026,2,10]],"date-time":"2026-02-10T16:22:41Z","timestamp":1770740561023,"version":"3.49.0"},"reference-count":43,"publisher":"American Physiological Society","issue":"6","funder":[{"DOI":"10.13039\/100000050","name":"HHS | NIH | National Heart, Lung, and Blood Institute (NHBLI)","doi-asserted-by":"publisher","award":["P01HL0289982"],"award-info":[{"award-number":["P01HL0289982"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2016,12,1]]},"abstract":"<jats:p> Connecting tubule glomerular feedback (CTGF) is a mechanism where an increase in sodium (Na) concentration in the connecting tubule (CNT) causes the afferent arteriole (Af-Art) to dilate. We recently reported that aldosterone within the CNT lumen enhances CTGF via a nongenomic effect involving GPR30 receptors and sodium\/hydrogen exchanger (NHE), but the signaling pathways of this mechanism are unknown. We hypothesize that aldosterone enhances CTGF via cAMP\/protein kinase A (PKA) pathway that activates protein kinase C (PKC) and stimulates superoxide (O<jats:sub>2<\/jats:sub><jats:sup>\u2212<\/jats:sup>) production. Rabbit Af-Arts and their adherent CNTs were microdissected and simultaneously perfused. Two consecutive CTGF curves were elicited by increasing the CNT luminal NaCl. We found that the main effect of aldosterone was to sensitize CTGF and we analyzed data by comparing NaCl concentration in the CNT perfusate needed to achieve half of the maximal response (EC<jats:sub>50<\/jats:sub>). During the control period, the NaCl concentration that elicited a half-maximal response (EC<jats:sub>50<\/jats:sub>) was 37.0 \u00b1 2.0 mmol\/l; addition of aldosterone (10<jats:sup>\u22128<\/jats:sup> mol\/l) to the CNT lumen decreased EC<jats:sub>50<\/jats:sub> to 19.3 \u00b1 1.3 mmol\/l ( P \u2264 0.001 vs. Control). The specific adenylyl cyclase inhibitor 2\u2032,3\u2032-dideoxyadenosine (ddA; 2 \u00d7 10<jats:sup>\u22124<\/jats:sup> mol\/l) and the PKA inhibitor H-89 dihydrochloride hydrate (H-89; 2 \u00d7 10<jats:sup>\u22126<\/jats:sup> mol\/l) prevented the aldosterone effect. The selective PKC inhibitor GF109203X (10<jats:sup>\u22128<\/jats:sup> mol\/l) also prevented EC<jats:sub>50<\/jats:sub> reduction caused by aldosterone. CNT intraluminal addition of O<jats:sub>2<\/jats:sub><jats:sup>\u2212<\/jats:sup> scavenger tempol (10<jats:sup>\u22124<\/jats:sup> mol\/l) blocked the aldosterone effect. We conclude that aldosterone inside the CNT lumen enhances CTGF via a cAMP\/PKA\/PKC pathway and stimulates O<jats:sub>2<\/jats:sub><jats:sup>\u2212<\/jats:sup> generation and this process may contribute to renal damage by increasing glomerular capillary pressure. <\/jats:p>","DOI":"10.1152\/ajprenal.00076.2016","type":"journal-article","created":{"date-parts":[[2016,7,14]],"date-time":"2016-07-14T02:37:07Z","timestamp":1468463827000},"page":"F1182-F1188","source":"Crossref","is-referenced-by-count":9,"title":["Mechanisms of connecting tubule glomerular feedback enhancement by aldosterone"],"prefix":"10.1152","volume":"311","author":[{"given":"YiLin","family":"Ren","sequence":"first","affiliation":[{"name":"Hypertension and Vascular Research Division, Department of Internal Medicine, Henry Ford Hospital, Detroit, Michigan; and"}]},{"given":"Branislava","family":"Janic","sequence":"additional","affiliation":[{"name":"Hypertension and Vascular Research Division, Department of Internal Medicine, Henry Ford Hospital, Detroit, Michigan; and"}]},{"given":"Kristopher","family":"Kutskill","sequence":"additional","affiliation":[{"name":"Hypertension and Vascular Research Division, Department of Internal Medicine, Henry Ford Hospital, Detroit, Michigan; and"}]},{"given":"Edward L.","family":"Peterson","sequence":"additional","affiliation":[{"name":"Department of Public Health Sciences, Henry Ford Hospital, Detroit, Michigan"}]},{"given":"Oscar A.","family":"Carretero","sequence":"additional","affiliation":[{"name":"Hypertension and Vascular Research Division, Department of Internal Medicine, Henry Ford Hospital, Detroit, Michigan; and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1986.94"},{"key":"B2","first-page":"321","volume":"45","author":"Burg MB","year":"1972","journal-title":"Yale J Biol Med"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.99.11.1485"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1995.2106"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.15.8763"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1996.271.6.C1935"},{"key":"B7","first-page":"761","volume":"67","author":"Dorup J","year":"1992","journal-title":"Lab Invest"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00328.2010"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.3858\/emm.2009.41.4.058"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(01)80115-3"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1021\/bi011953s"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.111.173195"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1007\/s004240000507"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.93.19.10500"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1997.273.5.C1673"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1979.236.2.F192"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00981.x"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.33.1.408"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000077407.90309.65"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1210\/en.2007-0864"},{"key":"B21","doi-asserted-by":"crossref","first-page":"1249","DOI":"10.1152\/ajplegacy.1975.228.4.1249","volume":"228","author":"Khuri RN","year":"1975","journal-title":"Am J Physiol"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-199612000-00013"},{"key":"B23","first-page":"1145","volume":"15","author":"Le Moellic C","year":"2004","journal-title":"J Am Soc Nephrol"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00048.2008"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1159\/000081796"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1210\/en.2004-1130"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000226054.53527.bb"},{"key":"B28","first-page":"66","volume":"591","author":"Navar LG","year":"1990","journal-title":"Acta Physiol Scand [Suppl]"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.84.5.1464"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1038\/253357a0"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00072.2014"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.108.124545"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00689.2011"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-008-0852-8"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002190"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004100878"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000236646.83354.51"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.2001.0267k.x"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1996.0866"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.76.6.973"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00648.2008"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M007631200"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00596.2010"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00076.2016","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T17:23:54Z","timestamp":1567963434000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00076.2016"}},"issued":{"date-parts":[[2016,12,1]]},"references-count":43,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2016,12,1]]}},"alternative-id":["10.1152\/ajprenal.00076.2016"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00076.2016","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2016,12,1]]}},{"indexed":{"date-parts":[[2026,2,10]],"date-time":"2026-02-10T06:09:16Z","timestamp":1770703756937,"version":"3.49.0"},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1991,4,1]]},"abstract":"<jats:p> Sublethal heat exposure induces the production of heat stress protein (HSP) 72 kDa, a reported cytoprotectant, in several tissues including the rat kidney. However, the localization and time course of HSP 72 accumulation in the kidney in response to heat or other cell stresses such as transient ischemia have not been described. In anesthetized rats exposed to either 42 +\/- 0.5 degrees C (heat stress) or 37 degrees C (sham) for 15 min, accumulation of HSP 72 in kidney homogenates, detected by immunoblot analysis using a specific monoclonal anti-HSP 72 antibody, peaked 4-6 h after heat stress and persisted for 10 days. HSP 72 appeared rapidly in renal papilla within 1 h and in medulla and cortex within 4 h after heat stress. No HSP 72 was detected in tissues from sham heat stress. HSP 72 was also detected within 3 h of at least 15 min of renal ischemia in situ. Accumulation was maximal after 60 min of ischemia and persisted for 5 days, whereas no HSP 72 was detected after 90 min of ischemia or in the contralateral nonischemic kidney at any time point. This study demonstrates that transient ischemia, like heat stress, results in the rapid cytosolic accumulation of HSP 72, a known cytoprotectant that may be important in mediating cell repair or increasing resistance to subsequent injury. <\/jats:p>","DOI":"10.1152\/ajprenal.1991.260.4.f479","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T23:43:00Z","timestamp":1513986180000},"page":"F479-F485","source":"Crossref","is-referenced-by-count":13,"title":["Transient ischemia or heat stress induces a cytoprotectant protein in rat kidney"],"prefix":"10.1152","volume":"260","author":[{"given":"A.","family":"Emami","sequence":"first","affiliation":[{"name":"Department of Medicine, Boston City Hospital, Boston University Schoolof Medicine, Massachusetts 02118."}]},{"given":"J. H.","family":"Schwartz","sequence":"additional","affiliation":[{"name":"Department of Medicine, Boston City Hospital, Boston University Schoolof Medicine, Massachusetts 02118."}]},{"given":"S. C.","family":"Borkan","sequence":"additional","affiliation":[{"name":"Department of Medicine, Boston City Hospital, Boston University Schoolof Medicine, Massachusetts 02118."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1991.260.4.F479","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:26:29Z","timestamp":1567970789000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1991.260.4.F479"}},"issued":{"date-parts":[[1991,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1991,4,1]]}},"alternative-id":["10.1152\/ajprenal.1991.260.4.F479"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1991.260.4.f479","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1991,4,1]]}},{"indexed":{"date-parts":[[2026,2,10]],"date-time":"2026-02-10T16:27:48Z","timestamp":1770740868759,"version":"3.49.0"},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1995,6,1]]},"abstract":"<jats:p> Cells almost universally respond to the stress of long-term hyperosmolality by accumulating compatible organic osmolytes. This allows them to maintain normal cell volume without a deleterious increase in intracellular inorganic ion concentration. Cells in the renal inner medulla are exposed to variable concentrations of salt and urea that may reach molal levels. The organic osmolytes that they accumulate include sorbitol, betaine, inositol, taurine, and glycerophosphocholine (GPC). This review considers recent advances in understanding osmotic regulation of these substances. Sorbitol is synthesized from glucose catalyzed by aldose reductase. Hypertonicity elevates the abundance of this enzyme by increasing transcription of its gene. Betaine is taken up via a specialized transporter. Hypertonicity raises the number of transporters by increasing their transcription. Current studies demonstrate that the 5' regions flanking the aldose reductase and betaine transporter genes contain osmotic response elements that increase transcription in response to hypertonicity. Osmotic regulation of inositol and taurine uptake also involves increased expression of specific transporter genes. GPC is unique in that its level rises in response to high urea, as well as hypertonicity. GPC accumulation is mainly regulated by changes in its degradation to choline, catalyzed by GPC:choline phosphodiesterase. Numerous other genes, including those for heat shock proteins, are also induced by hypertonicity. Their regulation and their role in osmotic regulation are the subject of considerable ongoing research. <\/jats:p>","DOI":"10.1152\/ajprenal.1995.268.6.f983","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T05:34:24Z","timestamp":1514007264000},"page":"F983-F996","source":"Crossref","is-referenced-by-count":67,"title":["Molecular basis of osmotic regulation"],"prefix":"10.1152","volume":"268","author":[{"given":"M. B.","family":"Burg","sequence":"first","affiliation":[{"name":"National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892\u20131598, USA."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1995.268.6.F983","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:00:51Z","timestamp":1567972851000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1995.268.6.F983"}},"issued":{"date-parts":[[1995,6,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1995,6,1]]}},"alternative-id":["10.1152\/ajprenal.1995.268.6.F983"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1995.268.6.f983","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1995,6,1]]}},{"indexed":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T09:14:08Z","timestamp":1773306848313,"version":"3.50.1"},"reference-count":38,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2007,11]]},"abstract":"<jats:p>Oxygen radicals play an important role in signal transduction and have been shown to influence epithelial sodium channel (ENaC) activity. We show that aldosterone, the principal hormone regulating renal ENaC activity, increases superoxide (O<jats:sub>2<\/jats:sub><jats:sup>\u2212<\/jats:sup>) production in A6 distal nephron cells. Aldosterone (50 nM to 1.5 \u03bcM) induced increases in dihydroethidium fluorescence in a dose-dependent manner in confluent A6 epithelial cells. Using single-channel measurements, we showed that sequestering endogenous O<jats:sub>2<\/jats:sub><jats:sup>\u2212<\/jats:sup>(with the O<jats:sub>2<\/jats:sub><jats:sup>\u2212<\/jats:sup>scavenger 2,2,6,6-tetramethylpiperidine 1-oxyl) significantly decreased ENaC open probability from 0.10 \u00b1 0.03 to 0.03 \u00b1 0.01. We also found that increasing endogenous O<jats:sub>2<\/jats:sub><jats:sup>\u2212<\/jats:sup>in A6 cells, by applying a superoxide dismutase inhibitor, prevented nitric oxide (NO) inhibition of ENaC activity. ENaC open probability values did not significantly change from control values (0.23 \u00b1 0.05) after superoxide dismutase and 1.5 \u03bcM NO coincubation (0.21 \u00b1 0.04). We report that xanthine oxidase and hypoxanthine compounds increase local concentrations of O<jats:sub>2<\/jats:sub><jats:sup>\u2212<\/jats:sup>by \u223c30%; with this mix, an increase in ENaC number of channels times the open probability (from 0.1 to 0.3) can be achieved in a cell-attached patch. Our data also suggest that O<jats:sub>2<\/jats:sub><jats:sup>\u2212<\/jats:sup>alters NO activity in a cGMP-independent mechanism, since pretreating A6 cells with ODQ compound (a selective inhibitor of NO-sensitive guanylyl cyclase) failed to block 2,2,6,6-tetramethylpiperidine 1-oxyl inhibition of ENaC activity.<\/jats:p>","DOI":"10.1152\/ajprenal.00444.2006","type":"journal-article","created":{"date-parts":[[2007,9,6]],"date-time":"2007-09-06T01:01:32Z","timestamp":1189040492000},"page":"F1666-F1677","source":"Crossref","is-referenced-by-count":59,"title":["Aldosterone-induced increases in superoxide production counters nitric oxide inhibition of epithelial Na channel activity in A6 distal nephron cells"],"prefix":"10.1152","volume":"293","author":[{"given":"Ling","family":"Yu","sequence":"first","affiliation":[]},{"given":"Hui-Fang","family":"Bao","sequence":"additional","affiliation":[]},{"given":"Julie L.","family":"Self","sequence":"additional","affiliation":[]},{"given":"Douglas C.","family":"Eaton","sequence":"additional","affiliation":[]},{"given":"My N.","family":"Helms","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1530\/jrf.0.0970441"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.2001.0105g.x"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1996.271.5.C1424"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1016\/S0039-128X(00)00183-5"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1055\/s-2004-814339"},{"key":"R6","doi-asserted-by":"crossref","unstructured":"Beltowski J, Marciniak A, Jamroz-Wisniewska A, Borkowska E.Nitric oxide\u2014superoxide cooperation in the regulation of renal Na+,K+-ATPase.Acta Biochim Pol51: 933\u2013942, 2004.","DOI":"10.18388\/abp.2004_3560"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1161\/hy1101.093423"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.37.2.781"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1998.274.1.C39"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000258594.87211.6b"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1998.274.5.C1417"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1542\/neo.7-2-e88"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00028.2004"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1165\/rcmb.2003-0325OC"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00006.2005"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1038\/ng0396-325"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1152\/ajplung.1998.274.4.L475"},{"key":"R18","doi-asserted-by":"crossref","unstructured":"Jain L, Chen XJ, Ramosevac S, Brown LA, Eaton DC.Expression of highly selective sodium channels in alveolar type II cells is determined by culture conditions.Am J Physiol Lung Cell Mol Physiol280: L646\u2013L658, 2001.","DOI":"10.1152\/ajplung.2001.280.4.L646"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.042689399"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1007\/s004410000244"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1021\/tx00030a017"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1203\/01.PDR.0000134256.30519.9B"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1991.260.5.C1071"},{"key":"R24","doi-asserted-by":"crossref","unstructured":"McCord JM, Fridovich I.Superoxide dismutase. An enzymic function for erythrocuprein (hemocuprein).J Biol Chem244: 6049\u20136055, 1969.","DOI":"10.1016\/S0021-9258(18)63504-5"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005040390"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1161\/01.ATV.0000034022.11764.EC"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.259.4.F672"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1152\/jappl.1990.68.4.1758"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1165\/ajrcmb.17.4.2680"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1515\/BC.2006.167"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1152\/ajplung.1998.275.4.L764"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1993.264.4.C875"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1016\/S1471-4892(02)00133-9"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00605.2001"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1016\/0034-5687(92)90043-V"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1152\/ajplung.00218.2002"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.275.12.8600"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.18.8418"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00444.2006","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,8,22]],"date-time":"2021-08-22T21:32:39Z","timestamp":1629667959000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00444.2006"}},"issued":{"date-parts":[[2007,11]]},"references-count":38,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2007,11]]}},"alternative-id":["10.1152\/ajprenal.00444.2006"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00444.2006","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2007,11]]}},{"indexed":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T09:16:27Z","timestamp":1773306987505,"version":"3.50.1"},"reference-count":76,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2005,4]]},"abstract":"<jats:p>Mouse proximal tubular cells (BUMPT), when cultured in the absence of growth factors, activate a default apoptotic pathway. Although Wnt signaling antagonizes the effect of proapoptotic triggers, its role in regulating the default pathway of apoptosis is less well defined. The present study examines the hypothesis that lithium (Li<jats:sup>+<\/jats:sup>) and (2\u2032Z,3\u2032E)-6-bromoindirubin-3\u2032-oxime (BIO), two glycogen synthase kinase-3\u03b2 (GSK3\u03b2) inhibitors, promote survival of growth factor-deprived renal epithelial cells by activating the Wnt pathway. These studies demonstrate that Li<jats:sup>+<\/jats:sup>and BIO activate Wnt signaling as indicated by the following changes: phosphorylation (inhibition) of GSK3\u03b2; decreased phosphorylation of \u03b2-catenin (a GSK3\u03b2 substrate); nuclear translocation of \u03b2-catenin; specific transcriptional activation of Tcf\/catenin-responsive pTopflash constructs; and an increase in the expression of cyclin D1 (indicative of a promitogenic cell response). In addition, Li<jats:sup>+<\/jats:sup>or BIO significantly increases the phosphorylation (activation) of Akt, an anti-apoptotic protein, and inhibits apoptosis (decreases both annexin-V staining and caspase-3 activation), during serum deprivation. Inhibition of phosphatidylinositol 3-kinase (responsible for Akt activation) either by wortmanin or LY-294002 prevented Li<jats:sup>+<\/jats:sup>- or BIO-induced Akt phosphorylation and reduces cell survival without altering the phosphorylation state of GSK3\u03b2. Li<jats:sup>+<\/jats:sup>or BIO also increases the expression of insulin-like growth factor-II (IGF-II), a potent proliferative signaling protein. Li<jats:sup>+<\/jats:sup>or BIO-free conditioned medium harvested from Li<jats:sup>+<\/jats:sup>- or BIO-exposed cells also induced Akt phosphorylation, mimicking the protective effect of the two GSK3\u03b2 inhibitors on serum-starved cells. Furthermore, the effect of conditioned medium on Akt phosphorylation could be inhibited by either LY-294002 or IGF-binding protein. BIO, a specific GSK3\u03b2 inhibitor, replicated the protective effect of Li<jats:sup>+<\/jats:sup>on cell viability, suggesting that GSK3\u03b2 activation is important for initiating the apoptotic pathway. Taken together, these data suggest that Li<jats:sup>+<\/jats:sup>or BIO promotes renal epithelial cell survival by inhibiting apoptosis through GSK3\u03b2-dependent activation of the Wnt pathway and subsequent release of IGF-II. Extracellular IGF-II serves as an autocrine survival factor that is responsible, in part, for activating the anti-apoptotic phosphatidylinositol-3-kinase-Akt pathway during serum deprivation.<\/jats:p>","DOI":"10.1152\/ajprenal.00189.2004","type":"journal-article","created":{"date-parts":[[2004,12,1]],"date-time":"2004-12-01T01:24:17Z","timestamp":1101864257000},"page":"F703-F713","source":"Crossref","is-referenced-by-count":105,"title":["Lithium activates the Wnt and phosphatidylinositol 3-kinase Akt signaling pathways to promote cell survival in the absence of soluble survival factors"],"prefix":"10.1152","volume":"288","author":[{"given":"Diviya","family":"Sinha","sequence":"first","affiliation":[]},{"given":"Zhiyong","family":"Wang","sequence":"additional","affiliation":[]},{"given":"Kathleen L.","family":"Ruchalski","sequence":"additional","affiliation":[]},{"given":"Jerrold S.","family":"Levine","sequence":"additional","affiliation":[]},{"given":"Selvi","family":"Krishnan","sequence":"additional","affiliation":[]},{"given":"Wilfred","family":"Lieberthal","sequence":"additional","affiliation":[]},{"given":"John H.","family":"Schwartz","sequence":"additional","affiliation":[]},{"given":"Steven C.","family":"Borkan","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1097-4644(19960616)61:4<514::AID-JCB4>3.0.CO;2-R"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1016\/S0959-437X(98)80062-2"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200205000-00006"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1002\/1097-4547(20000701)61:1<21::AID-JNR3>3.0.CO;2-7"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1016\/S0968-0004(01)01958-2"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1101\/gad.11.24.3286"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M204861200"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.15.8745"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.10.6039"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.152.1.87"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1038\/378785a0"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1046\/j.1471-4159.2001.t01-1-00251.x"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1101\/gad.13.22.2905"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)80405-5"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.00384"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1016\/S0955-0674(98)80149-X"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1126\/science.281.5381.1317"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(92)90123-T"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1006\/dbio.2000.9816"},{"key":"R20","doi-asserted-by":"crossref","unstructured":"Florini JR, Magri KA, Ewton DZ, James PL, Grindstaff K, and Rotwein PS.\u201cSpontaneous\u201d differentiation of skeletal myoblasts is dependent upon autocrine secretion of insulin-like growth factor-II.J Biol Chem266: 15917\u201315923, 1991.","DOI":"10.1016\/S0021-9258(18)98496-6"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1042\/bj3590001"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.C000880200"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1210\/endo.142.1.7902"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.cb.08.110192.001515"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1046\/j.1471-4159.2002.00957.x"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1016\/S0301-0082(01)00011-9"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1006\/mcne.2002.1117"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1016\/S0306-4522(02)00577-8"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1016\/0929-7855(96)00534-2"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)81664-5"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1126\/science.281.5382.1509"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1016\/S0955-0674(97)80079-8"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.5.F711"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1016\/S0960-9822(99)80235-8"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00209.2003"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.93.16.8455"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.19.8.5696"},{"key":"R38","unstructured":"Kronfeld-Kinar Y, Vilchik S, Hyman T, Leibkowicz F, and Salzberg S.Involvement of PKR in the regulation of myogenesis.Cell Growth Differ10: 201\u2013212, 1999."},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.3.F477"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.2.F315"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.275.5.F691"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M206405200"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M206402200"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ijo.0800626"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.47.12.1948"},{"key":"R46","doi-asserted-by":"publisher","DOI":"10.1002\/med.10011"},{"key":"R47","doi-asserted-by":"publisher","DOI":"10.1046\/j.1471-4159.2001.00410.x"},{"key":"R48","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1204660"},{"key":"R49","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.93.15.7950"},{"key":"R50","doi-asserted-by":"publisher","DOI":"10.1677\/joe.0.1670165"},{"key":"R51","doi-asserted-by":"publisher","DOI":"10.1097\/00001756-199806220-00031"},{"key":"R52","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.5.2642"},{"key":"R53","unstructured":"Nonaka S, Katsube N, and Chuang DM.Lithium protects rat cerebellar granule cells against apoptosis induced by anticonvulsants, phenytoin and carbamazepine.J Pharmacol Exp Ther286: 539\u2013547, 1998."},{"key":"R54","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.neuro.22.1.123"},{"key":"R55","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M101287200"},{"key":"R56","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.210394297"},{"key":"R57","doi-asserted-by":"publisher","DOI":"10.1038\/356397a0"},{"key":"R58","doi-asserted-by":"publisher","DOI":"10.1023\/A:1009680229931"},{"key":"R59","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M309325200"},{"key":"R60","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000108521.39082.E1"},{"key":"R61","doi-asserted-by":"publisher","DOI":"10.1038\/nm979"},{"key":"R62","unstructured":"Satyamoorthy K, Li G, Vaidya B, Patel D, and Herlyn M.Insulin-like growth factor-1 induces survival and growth of biologically early melanoma cells through both the mitogen-activated protein kinase and \u03b2-catenin pathways.Cancer Res61: 7318\u20137324, 2001."},{"key":"R63","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M201919200"},{"key":"R64","doi-asserted-by":"publisher","DOI":"10.1042\/bj3170385"},{"key":"R65","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M312048200"},{"key":"R66","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00172.2002"},{"key":"R67","doi-asserted-by":"publisher","DOI":"10.1023\/A:1006369223282"},{"key":"R68","doi-asserted-by":"publisher","DOI":"10.1182\/blood.V98.5.1374"},{"key":"R69","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1203126"},{"key":"R70","doi-asserted-by":"publisher","DOI":"10.1038\/18884"},{"key":"R71","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.21.17.5899-5912.2001"},{"key":"R72","doi-asserted-by":"publisher","DOI":"10.1023\/A:1006321324190"},{"key":"R73","doi-asserted-by":"publisher","DOI":"10.1038\/417292a"},{"key":"R74","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.9.5089"},{"key":"R75","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000103696.60047.55"},{"key":"R76","doi-asserted-by":"publisher","DOI":"10.1007\/s00109-003-0517-9"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00189.2004","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,6,30]],"date-time":"2021-06-30T04:04:23Z","timestamp":1625025863000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00189.2004"}},"issued":{"date-parts":[[2005,4]]},"references-count":76,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2005,4]]}},"alternative-id":["10.1152\/ajprenal.00189.2004"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00189.2004","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2005,4]]}},{"indexed":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T06:36:27Z","timestamp":1773297387931,"version":"3.50.1"},"reference-count":42,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2003,5,1]]},"abstract":"<jats:p>Hypothyroidism is associated with significant abnormalities in the renal handling of salt and water. To address the involvement of tubular transport proteins in these abnormalities, rats were rendered pharmacologically hypothyroid and the abundance of major tubular transport proteins was assessed by immunoblot and immunohistochemistry. Hypothyroidism resulted in a marked reduction in kidney size and creatinine clearance along with decreased or unchanged total kidney abundance of the transport proteins. Whereas the proximal tubular type 3 Na\/H exchanger (NHE3) and type 2 Na-phosphate cotransporter (NaPi2) stood out by their disproportionately reduced abundance, the bumetanide-sensitive type 2 Na-K-2Cl cotransporter (NKCC2) and aquaporin-2 (AQP2) were unaltered in their total kidney abundance despite a markedly lower kidney mass. The latter proteins in fact showed enhanced immunostaining. Decreased NHE3 and NaPi2 expression was most likely due to a combination of triiodo-l-thyronine (T<jats:sub>3<\/jats:sub>) deficiency along with a reduced glomerular filtration rate. The increased abundance of NKCC2 and AQP2 may have been caused by an increased action of vasopressin since urinary excretion of this hormone was elevated. On the other hand, the thiazide-sensitive Na-Cl cotransporter; the \u03b1-, \u03b2-, and \u03b3-subunits of the amiloride-sensitive epithelial Na channel; and the \u03b1<jats:sub>1<\/jats:sub>-subunit of Na-K-ATPase showed a moderate decrease in total kidney abundance that was largely proportional to the smaller kidney mass. Although the observed expression of transporters was associated with a balanced renal sodium handling, altered transporter abundance may become functionally relevant if the hypothyroid kidney is challenged by an additional destabilization of the milieu interieur that has previously been shown to result in an inadequate natriuresis and clinical symptoms.<\/jats:p>","DOI":"10.1152\/ajprenal.00368.2002","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:38:06Z","timestamp":1425415086000},"page":"F1097-F1104","source":"Crossref","is-referenced-by-count":61,"title":["Renal expression of sodium transporters and aquaporin-2 in hypothyroid rats"],"prefix":"10.1152","volume":"284","author":[{"given":"Roland","family":"Schmitt","sequence":"first","affiliation":[{"name":"Institut f\u00fcr Anatomie, Charit\u00e9, Humboldt Universit\u00e4t, 10115 Berlin;"}]},{"given":"Enno","family":"Klussmann","sequence":"additional","affiliation":[{"name":"Forschungsinstitut f\u00fcr Molekulare Pharmakologie, Campus Berlin-Buch, 13125 Berlin, Germany; and"}]},{"given":"Thomas","family":"Kahl","sequence":"additional","affiliation":[{"name":"Institut f\u00fcr Anatomie, Charit\u00e9, Humboldt Universit\u00e4t, 10115 Berlin;"}]},{"given":"David H.","family":"Ellison","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Hypertension, and Clinical Pharmacology, Oregon Health Sciences University, Portland, Oregon 97201"}]},{"given":"Sebastian","family":"Bachmann","sequence":"additional","affiliation":[{"name":"Institut f\u00fcr Anatomie, Charit\u00e9, Humboldt Universit\u00e4t, 10115 Berlin;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1210\/endo.140.4.6658"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/S0008-6363(01)00328-5"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1172\/JCI112858"},{"key":"B4","doi-asserted-by":"crossref","first-page":"1347","DOI":"10.1681\/ASN.V981347","volume":"9","author":"Bostanjoglo M","year":"1998","journal-title":"J Am Soc Nephrol"},{"key":"B5","first-page":"344","volume":"85","author":"Bradley SE","year":"1972","journal-title":"Trans Assoc Am Physicians"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/0024-3205(82)90279-X"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1974.119"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.2001.0359k.x"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1999.276.1.C102"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1987.231"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1007\/BF00583693"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2265.2001.01270.x"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1006\/exnr.2001.7775"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.3.F619"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1172\/JCI107833"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1210\/endo-71-5-693"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.253.1.F170"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.6.F1093"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1210\/endo-102-5-1475"},{"key":"B20","first-page":"82","volume":"59","author":"Hierholzer K","year":"1997","journal-title":"Kidney Int Suppl"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1172\/JCI106336"},{"key":"B22","doi-asserted-by":"crossref","first-page":"14308","DOI":"10.1016\/S0021-9258(18)77301-8","volume":"265","author":"Horowitz B","year":"1990","journal-title":"J Biol Chem"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(12)80837-7"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1210\/jcem-70-2-534"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1159\/000180514"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.253.1.F104"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1007\/BFb0119577"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M010270200"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.2.F257"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(91)80522-5"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1172\/JCI106936"},{"key":"B32","doi-asserted-by":"crossref","first-page":"699","DOI":"10.1152\/ajplegacy.1976.230.3.699","volume":"230","author":"Michael UF","year":"1976","journal-title":"Am J Physiol"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1161\/hy1001.092641"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00024.2001"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1016\/S0016-5085(96)70017-3"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.262.1.F47"},{"key":"B38","first-page":"174","volume":"161","author":"Reville P","year":"1967","journal-title":"C R Seances Soc Biol Fil"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.3.F367"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1016\/0026-0495(79)90078-7"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1007\/BF00410200"},{"key":"B42","first-page":"332","volume":"153","author":"St\u00e9phan F","year":"1959","journal-title":"C R Soc Biol"},{"key":"B43","doi-asserted-by":"crossref","first-page":"1926","DOI":"10.1681\/ASN.V11101926","volume":"11","author":"Vogel M","year":"2000","journal-title":"J Am Soc Nephrol"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00368.2002","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,5,1]],"date-time":"2022-05-01T09:37:13Z","timestamp":1651397833000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00368.2002"}},"issued":{"date-parts":[[2003,5,1]]},"references-count":42,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2003,5,1]]}},"alternative-id":["10.1152\/ajprenal.00368.2002"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00368.2002","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2003,5,1]]}},{"indexed":{"date-parts":[[2026,2,26]],"date-time":"2026-02-26T15:07:05Z","timestamp":1772118425564,"version":"3.50.1"},"reference-count":38,"publisher":"American Physiological Society","issue":"2","funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81670623"],"award-info":[{"award-number":["81670623"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81830021"],"award-info":[{"award-number":["81830021"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"name":"National Key Grants of the Ministry of Science and Technology","award":["2018YFA0108802"],"award-info":[{"award-number":["2018YFA0108802"]}]},{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health","doi-asserted-by":"publisher","award":["1R01DK113256-01A1"],"award-info":[{"award-number":["1R01DK113256-01A1"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2020,2,1]]},"abstract":"<jats:p> Protein arginine methyltransferase 1 (PRMT1), which primarily causes asymmetric arginine methylation of histone and nonhistone proteins, has been found to activate gene expression and mediate multiple pathological processes. Its role in renal fibrosis, however, remains unclear. In the present study, we observed that PRMT1 and its specific epigenetic marker, asymmetric di-methylated histone 4 arginine 3 (H4R3Me2a), were highly expressed in cultured renal interstitial fibroblasts. Treatment of PRMT1 with AMI-1, a selective inhibitor of PRMT1, or silencing PRMT1 with siRNA inhibited serum-induced and transforming growth factor (TGF)-\u03b2<jats:sub>1<\/jats:sub>-induced expression of \u03b1-smooth muscle actin (\u03b1-SMA) and collagen type I, two hallmarks of renal fibroblast activation, in a dose-dependent and time-dependent manner. In a murine model of renal fibrosis induced by unilateral ureteral obstruction, PRMT1 expression and H4R3Me2a were also upregulated, which was coincident with increased expression of \u03b1-SMA, collagen type I, and fibronectin. Administration of AMI-1 reduced PRMT1 and H4R3Me2a expression, attenuated extracellular matrix protein deposition, and inhibited renal fibroblast activation and proliferation. Moreover, AMI-1 treatment inhibited Smad3 phosphorylation and TGF-\u03b2 receptor I expression but prevented Smad7 downregulation both in the kidney after unilateral ureteral obstruction injury and in cultured renal interstitial fibroblasts exposed to TGF-\u03b2<jats:sub>1<\/jats:sub>. Collectively, these results demonstrate that PRMT1 may mediate renal fibroblast activation and renal fibrosis development through activation of the TGF-\u03b2\/Smad3 signaling pathway. They also suggest that PRMT1 inhibition may be a potential therapeutic approach for the treatment of fibrotic kidney disease. <\/jats:p>","DOI":"10.1152\/ajprenal.00487.2019","type":"journal-article","created":{"date-parts":[[2019,12,9]],"date-time":"2019-12-09T04:30:31Z","timestamp":1575865831000},"page":"F375-F387","source":"Crossref","is-referenced-by-count":31,"title":["Protein arginine methyltransferase 1 mediates renal fibroblast activation and fibrogenesis through activation of Smad3 signaling"],"prefix":"10.1152","volume":"318","author":[{"given":"Yu","family":"Zhu","sequence":"first","affiliation":[{"name":"Department of Nephrology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China"}]},{"given":"Chao","family":"Yu","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China"}]},{"given":"Shougang","family":"Zhuang","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China"},{"name":"Department of Medicine, Rhode Island Hospital and Alpert Medical School, Brown University Providence, Rhode Island"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M114.636050"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.2174\/1568026611313020007"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.14348\/molcells.2015.0113"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/j.exer.2009.09.004"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/j.celrep.2016.05.051"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1038\/srep19874"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2009.74"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/nm.3901"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2443.2008.01266.x"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/j.febslet.2006.11.008"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1016\/j.lfs.2009.05.007"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.RA118.002027"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1016\/j.pharmthera.2006.06.007"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2012.04.002"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000054"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1155\/2016\/8319283"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2016.48"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00282.2009"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.20.13.4859-4869.2000"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2011.31"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.207761"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.1402465"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00365.2015"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.3109\/15376516.2015.1061082"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00548.2005"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/j.cyto.2016.08.019"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2015010006"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00141.2017"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.4161\/cc.27353"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1007\/s00018-017-2515-z"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.2741\/1802"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1016\/j.molcel.2013.05.004"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1101\/cshperspect.a022087"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1038\/nrc3409"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbadis.2015.09.008"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.3390\/ijms131012383"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2015040457"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1038\/kisup.2014.13"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00487.2019","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2020,1,29]],"date-time":"2020-01-29T08:57:52Z","timestamp":1580288272000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00487.2019"}},"issued":{"date-parts":[[2020,2,1]]},"references-count":38,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2020,2,1]]}},"alternative-id":["10.1152\/ajprenal.00487.2019"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00487.2019","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2020,2,1]]}},{"indexed":{"date-parts":[[2026,2,26]],"date-time":"2026-02-26T14:03:45Z","timestamp":1772114625124,"version":"3.50.1"},"reference-count":98,"publisher":"American Physiological Society","issue":"3","funder":[{"DOI":"10.13039\/100000968","name":"American Heart Association","doi-asserted-by":"publisher","award":["23PRE1025798"],"award-info":[{"award-number":["23PRE1025798"]}],"id":[{"id":"10.13039\/100000968","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"HHS | NIH | National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["R01HL151407"],"award-info":[{"award-number":["R01HL151407"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["R01DK109133"],"award-info":[{"award-number":["R01DK109133"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000049","name":"HHS | NIH | National Institute on Aging","doi-asserted-by":"publisher","award":["R01AG057842"],"award-info":[{"award-number":["R01AG057842"]}],"id":[{"id":"10.13039\/100000049","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health","doi-asserted-by":"publisher","award":["P20GM103476"],"award-info":[{"award-number":["P20GM103476"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health","doi-asserted-by":"publisher","award":["P20GM104357"],"award-info":[{"award-number":["P20GM104357"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health","doi-asserted-by":"publisher","award":["P20GM121334"],"award-info":[{"award-number":["P20GM121334"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2023,9,1]]},"abstract":"<jats:p> Childhood\/prepubertal obesity is a public health concern that is associated with early signs of proteinuria. Insulin resistance has been described in obese children. However, studies investigating the role of insulin resistance during childhood obesity-associated renal injury are limited. This study provides evidence of an early relationship between insulin resistance and renal injury in a rat model of prepubertal obesity. These data also suggest that reducing insulin resistance with metformin may be renoprotective in obese children. <\/jats:p>","DOI":"10.1152\/ajprenal.00078.2023","type":"journal-article","created":{"date-parts":[[2023,7,27]],"date-time":"2023-07-27T15:17:50Z","timestamp":1690471070000},"page":"F363-F376","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":6,"title":["Metformin reduces insulin resistance and attenuates progressive renal injury in prepubertal obese Dahl salt-sensitive rats"],"prefix":"10.1152","volume":"325","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9962-5371","authenticated-orcid":false,"given":"Ubong S.","family":"Ekperikpe","sequence":"first","affiliation":[{"name":"Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4694-2269","authenticated-orcid":false,"given":"Sautan","family":"Mandal","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi, United States"}]},{"ORCID":"https:\/\/orcid.org\/0009-0001-8745-9345","authenticated-orcid":false,"given":"Stephen J.","family":"Holt","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi, United States"}]},{"given":"Jacori K.","family":"Daniels","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi, United States"}]},{"given":"Tyler D.","family":"Johnson","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi, United States"}]},{"given":"Jonita S.","family":"Cooper","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi, United States"}]},{"given":"Sarah M.","family":"Safir","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6730-6499","authenticated-orcid":false,"given":"Denise C.","family":"Cornelius","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7078-9567","authenticated-orcid":false,"given":"Jan M.","family":"Williams","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi, United States"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/S2213-8587(21)00089-9"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/j.circen.2016.08.013"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1542\/peds.2021-053708"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000127130.82333.C9"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa1014296"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1038\/s41576-021-00414-z"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1002\/oby.23116"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1017\/S1368980007000626"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1126\/sciadv.abe4841"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-006-0027-4"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005111241"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00324.2007"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(05)67483-1"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1093\/qjmed\/hcy200.138"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1159\/000492826"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1053\/j.ackd.2006.07.016"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.4081\/pr.2011.e27"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1038\/nrendo.2017.90"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.4093\/dmj.2013.37.3.165"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1159\/000308161"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00438.2019"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00100.2020"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00179.2021"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.2337\/dc19-1651"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1038\/srep46962"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1161\/01.hyp.28.1.127"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00497.2016"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1007\/s00125-013-2857-5"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.3390\/ijms21113798"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00590.2015"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.122.001298"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1053\/meta.2001.28078"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.2337\/diacare.25.1.89"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1542\/peds.107.4.e55"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1176\/appi.ajp.159.4.655"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.103.064964"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1016\/s0006-291x(02)02565-2"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1093\/gerona\/gls199"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00182.2018"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1186\/1471-2458-10-318"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1210\/jc.2010-1047"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1111\/pedi.12562"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1186\/1758-5996-6-100"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1542\/peds.2016-4285"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.2337\/db10-1185"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1111\/j.1559-4564.2007.05734.x"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfq817"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00340.2016"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1172\/JCI110067"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.3389\/fphys.2021.765305"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1038\/nutd.2017.31"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1016\/j.atherosclerosis.2010.02.029"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1007\/s00125-013-2869-1"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1038\/nm.4350"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1194\/jlr.M300368-JLR200"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2012.10.019"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1007\/s00125-015-3676-7"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1016\/j.molmet.2017.05.002"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.116.07991"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1210\/jc.2004-0276"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.105.563213"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2362.1991.tb01391.x"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1016\/0026-0495(89)90207-2"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1161\/01.hyp.33.5.1135"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-017-11430-7"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1161\/01.hyp.0000022880.45113.c9"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1186\/1475-2840-7-19"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.3389\/fphys.2017.00227"},{"key":"B69","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1994.267.4.H1250"},{"key":"B70","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00195.2018"},{"key":"B71","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2796.1997.00236.x"},{"key":"B72","doi-asserted-by":"publisher","DOI":"10.1007\/s12020-018-1722-1"},{"key":"B73","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.2000.278.5.G682"},{"key":"B74","doi-asserted-by":"publisher","DOI":"10.1590\/s0100-879x2006000400009"},{"key":"B75","doi-asserted-by":"publisher","DOI":"10.1016\/j.ijcard.2012.01.013"},{"key":"B76","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00400.2017"},{"key":"B77","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfi201"},{"key":"B78","first-page":"7","volume":"242","author":"Brenner BM","year":"1981","journal-title":"Acta Endocrinol Suppl (Copenh)"},{"key":"B79","doi-asserted-by":"publisher","DOI":"10.1007\/s00125-018-4669-0"},{"key":"B80","doi-asserted-by":"publisher","DOI":"10.1038\/s41366-021-01001-2"},{"key":"B81","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-021-86109-1"},{"key":"B82","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2018.01.027"},{"key":"B83","doi-asserted-by":"publisher","DOI":"10.1186\/s12882-022-02794-8"},{"key":"B84","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.5.F817"},{"key":"B85","doi-asserted-by":"publisher","DOI":"10.1159\/000499486"},{"key":"B86","doi-asserted-by":"publisher","DOI":"10.14814\/phy2.14141"},{"key":"B87","doi-asserted-by":"publisher","DOI":"10.1038\/srep35952"},{"key":"B88","doi-asserted-by":"publisher","DOI":"10.1210\/en.2015-1572"},{"key":"B89","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2022.08.026"},{"key":"B90","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00149.2018"},{"key":"B91","doi-asserted-by":"publisher","DOI":"10.1038\/nri3523"},{"key":"B92","doi-asserted-by":"publisher","DOI":"10.1038\/s41581-020-0272-y"},{"key":"B93","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007111233"},{"key":"B94","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010050548"},{"key":"B95","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009070741"},{"key":"B96","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0178352"},{"key":"B97","doi-asserted-by":"publisher","DOI":"10.1089\/chi.2019.0040"},{"key":"B98","first-page":"A42","author":"Ekperikpe US","year":"2021","journal-title":"Hypertension 78 (Suppl_1)"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00078.2023","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,8,22]],"date-time":"2023-08-22T04:11:17Z","timestamp":1692677477000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00078.2023"}},"issued":{"date-parts":[[2023,9,1]]},"references-count":98,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2023,9,1]]}},"alternative-id":["10.1152\/ajprenal.00078.2023"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00078.2023","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2023,9,1]]},"assertion":[{"value":"2023-04-06","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2023-07-12","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2023-07-24","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2023-08-21","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,2,25]],"date-time":"2026-02-25T09:39:25Z","timestamp":1772012365144,"version":"3.50.1"},"reference-count":26,"publisher":"American Physiological Society","issue":"2","funder":[{"name":"Research Institute, Children's Hospital Colorado","award":["RSA Soranno"],"award-info":[{"award-number":["RSA Soranno"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2016,8,1]]},"abstract":"<jats:p> Injectable hydrogels can be used to deliver drugs in situ over a sustained period of time. We hypothesized that sustained delivery of interleukin-10 (IL-10) following acute kidney injury (AKI) would mitigate the local and systemic proinflammatory cascade induced by AKI and reduce subsequent fibrosis. Wild-type C57BL\/6 mice underwent ischemia-reperfusion AKI with avertin anesthesia. Three days later, mice were treated with either hyaluronic acid injectable hydrogel with or without IL-10, or IL-10 suspended in saline, injected under the capsule of the left kidney, or hydrogel with IL-10 injected subcutaneously. Untreated AKI served as controls. Serial in vivo optical imaging tracked the location and degradation of the hydrogel over time. Kidney function was assessed serially. Animals were killed 28 days following AKI and the following were evaluated: serum IL-6, lung inflammation, urine neutrophil gelatinase-associated lipocalin, and renal histology for fibroblast activity, collagen type III deposition and fibrosis via Picrosirius Red staining and second harmonic imaging. Our model shows persistent systemic inflammation, and renal inflammation and fibrosis 28 days following AKI. The hydrogels are biocompatible and reduced serum IL-6 and renal collagen type III 28 days following AKI even when delivered without IL-10. Treatment with IL-10 reduced renal and systemic inflammation, regardless of whether the IL-10 was delivered in a sustained manner via the injectable hydrogel under the left kidney capsule, as a bolus injection via saline under the left kidney capsule, or via the injectable hydrogel subcutaneously. Injectable hydrogels are suitable for local drug delivery following renal injury, are biocompatible, and help mitigate local and systemic inflammation. <\/jats:p>","DOI":"10.1152\/ajprenal.00579.2015","type":"journal-article","created":{"date-parts":[[2016,3,10]],"date-time":"2016-03-10T03:49:12Z","timestamp":1457581752000},"page":"F362-F372","source":"Crossref","is-referenced-by-count":65,"title":["Delivery of interleukin-10 via injectable hydrogels improves renal outcomes and reduces systemic inflammation following ischemic acute kidney injury in mice"],"prefix":"10.1152","volume":"311","author":[{"given":"Danielle E.","family":"Soranno","sequence":"first","affiliation":[{"name":"Departments of Pediatrics and Bioengineering, University of Colorado, Aurora, Colorado;"}]},{"given":"Christopher B.","family":"Rodell","sequence":"additional","affiliation":[{"name":"Department of Bioengineering, University of Pennsylvania, Philadelphia, Pennsylvania; and"}]},{"given":"Christopher","family":"Altmann","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Colorado, Aurora, Colorado"}]},{"given":"Jane","family":"Duplantis","sequence":"additional","affiliation":[{"name":"Departments of Pediatrics and Bioengineering, University of Colorado, Aurora, Colorado;"}]},{"given":"Ana","family":"Andres-Hernando","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Colorado, Aurora, Colorado"}]},{"given":"Jason A.","family":"Burdick","sequence":"additional","affiliation":[{"name":"Department of Bioengineering, University of Pennsylvania, Philadelphia, Pennsylvania; and"}]},{"given":"Sarah","family":"Faubel","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Colorado, Aurora, Colorado"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1089\/ten.tea.2011.0391"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00025.2012"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.14814\/phy2.12084"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1002\/adma.201003963"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1159\/000329396"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2011.42"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra1214243"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2012.208"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1038\/srep05814"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00043.x"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1007\/s10157-008-0119-5"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/j.jtcvs.2015.07.035"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1016\/j.biomaterials.2012.01.061"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1039\/C1SM06513K"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.2144\/000112729"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2014.06.001"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1097\/01.mnh.0000437332.31418.e0"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1038\/ncb2904"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.med.59.061506.154239"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(13)60647-9"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.4103\/1673-5374.139460"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(15)60126-X"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1002\/adfm.201403550"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1016\/j.jconrel.2015.03.025"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1002\/jbm.a.34902"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.3892\/etm.2014.2004"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00579.2015","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T00:43:58Z","timestamp":1567989838000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00579.2015"}},"issued":{"date-parts":[[2016,8,1]]},"references-count":26,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2016,8,1]]}},"alternative-id":["10.1152\/ajprenal.00579.2015"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00579.2015","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2016,8,1]]}},{"indexed":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T07:06:58Z","timestamp":1773299218714,"version":"3.50.1"},"reference-count":29,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2002,1,1]]},"abstract":"<jats:p>The accumulation of extracellular matrix in the glomerular mesangium reflects the net balance between the synthesis and degradation of matrix components. We have shown that estradiol suppresses the synthesis of types I and IV collagen by cultured mesangial cells (Kwan G, Neugarten J, Sherman M, Ding Q, Fotadar U, Lei J, and Silbiger S. Kidney Int 50: 1173\u20131179, 1996; Neugarten J, Acharya A, Lei J, and Silbiger S. Am J Physiol Renal Physiol 279: F309\u2013F318, 2000; Neugarten J, Medve I, Lei J, and Silbiger SR. Am J Physiol Renal Physiol 277: F1\u2013F8, 1999; Neugarten J and Silbiger S. Am J Kidney Dis 26: 147\u2013151, 1995; Silbiger S, Lei J, and Neugarten J. Kidney Int 55: 1268\u20131276, 1998; Silbiger S, Lei J, Ziyadeh FN, and Neugarten J. Am J Physiol Renal Physiol 274: F1113\u2013F1118, 1998). In the present study, we evaluated the effects of sex hormones on the activity of matrix metalloproteinase-2 (MMP-2) in murine mesangial cells, the synthesis of which is regulated by the transcription factor activator protein-2 (AP-2). Estradiol stimulated MMP-2 activity by increasing MMP-2 protein levels in a dose-dependent manner. These effects occurred at physiological concentrations of estradiol and were receptor mediated. Estradiol also increased AP-2 protein levels and increased binding of mesangial cell nuclear extracts to an AP-2 consensus binding sequence oligonucleotide. The ability of estradiol to increase AP-2 protein expression, AP-2\/DNA binding activity, MMP-2 protein expression, and metalloproteinase activity was reversed by PD-98059, a selective inhibitor of the extracellular signal-regulated kinase\/mitogen-activated protein kinase (ERK\/MAPK) signaling cascade. We conclude that estradiol upregulates the MAPK cascade, which in turn stimulates the synthesis of AP-2 protein. The resultant increased AP-2\/DNA binding activity leads to increased synthesis of MMP-2 and increased metalloproteinase activity. Stimulation of metalloproteinase activity by estradiol may contribute to the protective effect of female gender on renal disease progression.<\/jats:p>","DOI":"10.1152\/ajprenal.0318.2000","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:33:25Z","timestamp":1425414805000},"page":"F164-F169","source":"Crossref","is-referenced-by-count":66,"title":["Estradiol upregulates mesangial cell MMP-2 activity via the transcription factor AP-2"],"prefix":"10.1152","volume":"282","author":[{"given":"Michael","family":"Guccione","sequence":"first","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Montefiore Medical Center, and the Albert Einstein College of Medicine, Bronx, New York 10467"}]},{"given":"Sharon","family":"Silbiger","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Montefiore Medical Center, and the Albert Einstein College of Medicine, Bronx, New York 10467"}]},{"given":"Jun","family":"Lei","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Montefiore Medical Center, and the Albert Einstein College of Medicine, Bronx, New York 10467"}]},{"given":"Joel","family":"Neugarten","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Montefiore Medical Center, and the Albert Einstein College of Medicine, Bronx, New York 10467"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1991.196"},{"key":"B2","first-page":"327","volume":"11","author":"Baricos WH","year":"1991","journal-title":"Semin Nephrol"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1992.103"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.86.21.8207"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.16.6.2913"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.45"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1991.310"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.425"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.2.F252"},{"key":"B11","doi-asserted-by":"crossref","first-page":"574","DOI":"10.1681\/ASN.V113574","volume":"11","author":"Lenz O","year":"2000","journal-title":"J Am Soc Nephrol"},{"key":"B12","doi-asserted-by":"crossref","first-page":"2480","DOI":"10.1681\/ASN.V10122480","volume":"10","author":"Mertens PR","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.36.22905"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.29.18165"},{"key":"B15","first-page":"151","volume":"378","author":"Nagase H.","year":"1997","journal-title":"Biol Chem"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.2.F309"},{"key":"B17","doi-asserted-by":"crossref","first-page":"319","DOI":"10.1681\/ASN.V112319","volume":"11","author":"Neugarten J","year":"2000","journal-title":"J Am Soc Nephrol"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.6.F875"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/0272-6386(95)90168-X"},{"key":"B20","first-page":"S61","volume":"49","author":"Norman JT","year":"1996","journal-title":"Kidney Int"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1203303"},{"key":"B22","doi-asserted-by":"crossref","first-page":"241","DOI":"10.1681\/ASN.V122241","volume":"12","author":"Potier M","year":"2001","journal-title":"J Am Soc Nephrol"},{"key":"B23","first-page":"460A","volume":"10","author":"Potier M","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B24","first-page":"460A","volume":"10","author":"Potier M","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B25","doi-asserted-by":"crossref","first-page":"1835","DOI":"10.1681\/ASN.V3111835","volume":"3","author":"Reckelhoff JF","year":"1993","journal-title":"J Am Soc Nephrol"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00376.x"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.6.F1113"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1016\/0272-6386(95)90119-1"},{"key":"B29","doi-asserted-by":"crossref","first-page":"17374","DOI":"10.1016\/S0021-9258(18)71503-2","volume":"264","author":"Stetler-Stevenson WG","year":"1989","journal-title":"J Biol Chem"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/S0925-4439(97)00097-5"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.0318.2000","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,5,1]],"date-time":"2022-05-01T09:33:31Z","timestamp":1651397611000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.0318.2000"}},"issued":{"date-parts":[[2002,1,1]]},"references-count":29,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2002,1,1]]}},"alternative-id":["10.1152\/ajprenal.0318.2000"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.0318.2000","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2002,1,1]]}},{"indexed":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T05:00:15Z","timestamp":1773291615083,"version":"3.50.1"},"reference-count":26,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1998,4,1]]},"abstract":"<jats:p>Confluent monolayers of immunodissected rabbit connecting tubule and cortical collecting duct cells, cultured on permeable supports, were used to study the effect of adenosine on net apical-to-basolateral Ca<jats:sup>2+<\/jats:sup>transport. Apical, but not basolateral, adenosine increased this transport dose dependently from 48 \u00b1 3 to 110 \u00b1 4 nmol \u22c5 h<jats:sup>\u22121<\/jats:sup>\u22c5 cm<jats:sup>\u22122<\/jats:sup>. Although a concomitant increase in cAMP formation suggested the involvement of an A<jats:sub>2<\/jats:sub>receptor, the A<jats:sub>2<\/jats:sub>agonist CGS-21680 did not stimulate Ca<jats:sup>2+<\/jats:sup>transport, while readily increasing cAMP. By contrast, the A<jats:sub>1<\/jats:sub>agonist N<jats:sup>6<\/jats:sup>-cyclopentyladenosine (CPA) maximally stimulated Ca<jats:sup>2+<\/jats:sup>transport without significantly affecting cAMP. Adenosine-stimulated transport was effectively inhibited by the A<jats:sub>1<\/jats:sub>antagonist 1,3-dipropyl-8-cyclopenthylxanthine but not the A<jats:sub>2<\/jats:sub>antagonist 3,7-dimethyl-1-propargylxanthine, providing additional evidence for the involvement of an A<jats:sub>1<\/jats:sub>receptor. Both abolishment of the adenosine-induced transient increase in intracellular Ca<jats:sup>2+<\/jats:sup>concentration by 1,2-bis(2-aminophenoxy)ethane- N, N, N\u2032, N\u2032-tetraacetic acid and downregulation of protein kinase C (PKC) by prolonged phorbol ester treatment were without effect on adenosine-stimulated Ca<jats:sup>2+<\/jats:sup>transport. The data presented suggest that adenosine interacts with an apical A<jats:sub>1<\/jats:sub>receptor to stimulate Ca<jats:sup>2+<\/jats:sup>transport via a hitherto unknown pathway that does not involve cAMP formation, PKC activation, and\/or Ca<jats:sup>2+<\/jats:sup>mobilization.<\/jats:p>","DOI":"10.1152\/ajprenal.1998.274.4.f736","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T15:43:32Z","timestamp":1514043812000},"page":"F736-F743","source":"Crossref","is-referenced-by-count":13,"title":["Adenosine-stimulated Ca<sup>2+<\/sup>reabsorption is mediated by apical A<sub>1<\/sub>receptors in rabbit cortical collecting system"],"prefix":"10.1152","volume":"274","author":[{"given":"Joost G. J.","family":"Hoenderop","sequence":"first","affiliation":[{"name":"Departments of Biochemistry and"},{"name":"Cell Physiology, Institute of Cellular Signalling, University of Nijmegen, 6500 HB Nijmegen, The Netherlands"}]},{"given":"Anita","family":"Hartog","sequence":"additional","affiliation":[{"name":"Cell Physiology, Institute of Cellular Signalling, University of Nijmegen, 6500 HB Nijmegen, The Netherlands"}]},{"given":"Peter H. G. M.","family":"Willems","sequence":"additional","affiliation":[{"name":"Departments of Biochemistry and"}]},{"given":"Ren\u00e9 J. M.","family":"Bindels","sequence":"additional","affiliation":[{"name":"Cell Physiology, Institute of Cellular Signalling, University of Nijmegen, 6500 HB Nijmegen, The Netherlands"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1988.255.5.C581"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI112875"},{"issue":"30","key":"B3","first-page":"F799","volume":"261","author":"Bindels R. J. M.","year":"1991","journal-title":"Am. J. Physiol."},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.1990.tb37674.x"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1991.260.1.C143"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1021\/jm00345a001"},{"key":"B8","first-page":"122","volume":"10","author":"Fredholm B. B.","year":"1995","journal-title":"News Physiol. Sci."},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.221"},{"issue":"39","key":"B10","first-page":"F53","volume":"270","author":"Koster H. P. G.","year":"1996","journal-title":"Am. J. Physiol."},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1993.117"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1985.249.3.C330"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1096\/fasebj.5.12.1916091"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/0165-6147(94)90011-6"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.77.5.2551"},{"key":"B16","doi-asserted-by":"crossref","first-page":"17067","DOI":"10.1016\/S0021-9258(19)47340-7","volume":"266","author":"Lytton J.","year":"1991","journal-title":"J. Biol. Chem."},{"key":"B17","first-page":"31","volume":"13","author":"McCoy D. E.","year":"1993","journal-title":"Semin. Nephrol."},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1990.259.4.C675"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.1992.tb12748.x"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115662"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.17.2.117"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1992.263.2.C502"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1996.sp021763"},{"key":"B24","first-page":"1808","volume":"7","author":"Van Baal J.","year":"1996","journal-title":"J. Am. Soc. Nephrol."},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1007\/s004240050255"},{"issue":"32","key":"B26","first-page":"F268","volume":"263","author":"Yagil Y.","year":"1992","journal-title":"Am. J. Physiol."},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1007\/BF00374528"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1998.274.4.F736","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:49:20Z","timestamp":1660189760000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1998.274.4.F736"}},"issued":{"date-parts":[[1998,4,1]]},"references-count":26,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1998,4,1]]}},"alternative-id":["10.1152\/ajprenal.1998.274.4.F736"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1998.274.4.f736","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1998,4,1]]}},{"indexed":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T01:43:40Z","timestamp":1773279820471,"version":"3.50.1"},"reference-count":35,"publisher":"American Physiological Society","issue":"1","funder":[{"DOI":"10.13039\/100002028","name":"The Collins Medical Trust","doi-asserted-by":"publisher","award":["20CDA35320169"],"award-info":[{"award-number":["20CDA35320169"]}],"id":[{"id":"10.13039\/100002028","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000968","name":"American Heart Association","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000968","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"HHS | NIH | National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["R01 HL142672"],"award-info":[{"award-number":["R01 HL142672"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"HHS | NIH | National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["P01 HL129941"],"award-info":[{"award-number":["P01 HL129941"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000060","name":"HHS | NIH | National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["R01 AI143599"],"award-info":[{"award-number":["R01 AI143599"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["R01 DK098382"],"award-info":[{"award-number":["R01 DK098382"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["R01 DK083785"],"award-info":[{"award-number":["R01 DK083785"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["K01 DK121737"],"award-info":[{"award-number":["K01 DK121737"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2021,7,1]]},"abstract":"<jats:p> Our study defines a novel role for proximal tubule angiotensin receptors in regulating the abundance of Na<jats:sup>+<\/jats:sup> transporters throughout the nephron, thereby contributing to the integrated control of fluid balance in vivo. <\/jats:p>","DOI":"10.1152\/ajprenal.00014.2021","type":"journal-article","created":{"date-parts":[[2021,5,31]],"date-time":"2021-05-31T10:54:17Z","timestamp":1622458457000},"page":"F69-F81","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":6,"title":["Local and downstream actions of proximal tubule angiotensin II signaling on Na<sup>+<\/sup> transporters in the mouse nephron"],"prefix":"10.1152","volume":"321","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1456-9399","authenticated-orcid":true,"given":"Jonathan W.","family":"Nelson","sequence":"first","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Medicine, Oregon Health and Science University, Portland, Oregon"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0459-469X","authenticated-orcid":true,"given":"Alicia A.","family":"McDonough","sequence":"additional","affiliation":[{"name":"Department of Physiology and Neuroscience, Keck School of Medicine, University of Southern California, Los Angeles, California"}]},{"given":"Zhidan","family":"Xiang","sequence":"additional","affiliation":[{"name":"Wake Forest University, Winston-Salem, North Carolina"}]},{"given":"Donna L.","family":"Ralph","sequence":"additional","affiliation":[{"name":"Department of Physiology and Neuroscience, Keck School of Medicine, University of Southern California, Los Angeles, California"}]},{"given":"Joshua A.","family":"Robertson","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Medicine, Oregon Health and Science University, Portland, Oregon"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0481-6595","authenticated-orcid":true,"given":"Jorge F.","family":"Giani","sequence":"additional","affiliation":[{"name":"Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, California"}]},{"given":"Kenneth E.","family":"Bernstein","sequence":"additional","affiliation":[{"name":"Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, California"}]},{"given":"Susan B.","family":"Gurley","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Medicine, Oregon Health and Science University, Portland, Oregon"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.08860813"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.12391213"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90235.2008"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1113\/jp274927"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00011.2014"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.115.04593"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-148-1-200801010-00189"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1002\/cphy.c130040"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2011.03.001"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014080816"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010101095"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00015.2014"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00400.2014"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.114.04147"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00485.2017"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2018030323"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00317.2006"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.114.04975"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1161\/hy02t2.102959"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.14814\/phy2.12496"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00183.2013"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1111\/apha.13448"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00072.2015"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00353.2005"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-008-0580-8"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1155\/2020\/8492467"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M117.779520"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1710964114"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2018.11.028"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014111067"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00550.2020"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00055.2017"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00608.2007"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.108.120246"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00335.2019"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00014.2021","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,7,6]],"date-time":"2021-07-06T17:09:53Z","timestamp":1625591393000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00014.2021"}},"issued":{"date-parts":[[2021,7,1]]},"references-count":35,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2021,7,1]]}},"alternative-id":["10.1152\/ajprenal.00014.2021"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00014.2021","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2021,7,1]]},"assertion":[{"value":"2021-01-12","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2021-05-23","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2021-06-30","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,3,11]],"date-time":"2026-03-11T18:44:30Z","timestamp":1773254670023,"version":"3.50.1"},"reference-count":38,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2006,11]]},"abstract":"<jats:p> Aberrant sodium absorption has been linked to the development of hypertension in both renal disease and diabetes. Efficient absorption depends on coordination of cellular activity across the entire epithelium via cell-to-cell coupling. In the current study we have utilized a model human collecting duct cell line (HCD) to assess the role of connexin43 (Cx43)-mediated gap junctions in the transfer of intracellular Ca<jats:sup>2+<\/jats:sup> transients within coupled cell clusters. HCD cells express Cx43 mRNA and protein, as well as that for the mechanosensitive transient receptor potential receptor (TRPV4). Mechanical stimulation of individual cells within a cluster evoked a transient rise in cytosolic Ca<jats:sup>2+<\/jats:sup> concentration ([Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>) that propagated between cells via a heptanol-sensitive mechanism. The rise in [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub> was dependent on both store release and Ca<jats:sup>2+<\/jats:sup>-influx pathways. Lucifer yellow dye transfer and Cx43 knockdown experiments confirmed direct cell-to-cell communication. Application of the Ca<jats:sup>2+<\/jats:sup> ionophore ionomycin, or an increase in glucose (5 to 25 mM), produced a time-dependent (48 h) increase in Cx43 protein expression. The transmission rate of touch-evoked Ca<jats:sup>2+<\/jats:sup> transients between coupled cells was accelerated after exposure to high glucose, providing a functional correlate to increased Cx43 expression. These data suggest a pivotal role for Cx43-mediated gap junctions in the synchronization of activity between HCD cells in response to stimuli that mimic osmotic and physical changes. Cx43 expression and cell-to-cell communication increased in response to high glucose and may protect the collecting duct from renal damage associated with more established diabetic nephropathy. <\/jats:p>","DOI":"10.1152\/ajprenal.00344.2005","type":"journal-article","created":{"date-parts":[[2006,5,9]],"date-time":"2006-05-09T23:36:35Z","timestamp":1147217795000},"page":"F1045-F1051","source":"Crossref","is-referenced-by-count":26,"title":["Glucose-evoked alterations in connexin43-mediated cell-to-cell communication in human collecting duct: a possible role in diabetic nephropathy"],"prefix":"10.1152","volume":"291","author":[{"given":"Claire E.","family":"Hills","sequence":"first","affiliation":[]},{"given":"Rosemary","family":"Bland","sequence":"additional","affiliation":[]},{"given":"Dianne C.","family":"Wheelans","sequence":"additional","affiliation":[]},{"given":"Jeanette","family":"Bennett","sequence":"additional","affiliation":[]},{"given":"Pierre M.","family":"Ronco","sequence":"additional","affiliation":[]},{"given":"Paul E.","family":"Squires","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1210\/endo.140.5.6683"},{"key":"R2","doi-asserted-by":"crossref","unstructured":"Chomczynski P and Sacchi N. Single-step method of RNA isolation by acid guanidinium thiocyanate-phenol-chloroform extraction. Anal Biochem 162: 156\u2013159, 1987.","DOI":"10.1016\/0003-2697(87)90021-2"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00030.2002"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1038\/nature02196"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1007\/s00249-004-0409-0"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M400446200"},{"key":"R7","doi-asserted-by":"crossref","unstructured":"Gomes P, Malfait M, Himpens B, and Vereecke J. Intercellular Ca2+-transient propagation in normal and high glucose solutions in rat retinal epithelial (RPE-J) cells during mechanical stimulation. Cell Calcium 32: 185\u2013192, 2003.","DOI":"10.1016\/S0143-4160(03)00083-6"},{"key":"R8","doi-asserted-by":"crossref","unstructured":"Gomez P, Vereecke J, and Himpens B. Intra- and intercellular Ca2+-transient propagation in normal and high glucose solutions in ROS cells during mechanical stimulation. Cell Calcium 29: 137\u2013148, 2000.","DOI":"10.1054\/ceca.2000.0173"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1998.275.2.R439"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00786.x"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1016\/j.cardiores.2003.11.015"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1016\/S0303-7207(02)00051-5"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1096-9896(199708)182:4<373::AID-PATH858>3.0.CO;2-B"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000129115.69395.65"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1995.1365"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1007\/s007950170002"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.47.6.931"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1016\/S0090-4295(02)01837-X"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1167\/iovs.03-0360"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00067.2003"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1007\/s0023200100082"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1980.238.3.C114"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.260.3.F402"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(90)80493-3"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00365.2003"},{"key":"R26","unstructured":"Oku H, Kodama T, Sakagami K, and Puro DG. Diabetes-induced disruption of gap-junction pathways within the retinal microvasculature. Invest Ophthalmol Vis Sci 42: 1915\u20131920, 2001."},{"key":"R27","doi-asserted-by":"crossref","unstructured":"Praetorius HA and Spring KR. The renal cell primary cilium functions as a flow sensor. Curr Opin Nephrol Hypertens 12: 129\u2013137, 2003.","DOI":"10.1097\/00041552-200309000-00006"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.51.5.1565"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1007\/s002239900120"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1007\/s004670100611"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.267.1.F130"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1159\/000016375"},{"key":"R33","unstructured":"Tonon R and D\u2019Andrea P. The functional expression of connexin 43 in articular chondrocytes is increased by interleukin 1\u03b2: evidence for a Ca2+-dependent mechanism. Biorheology 39: 153\u2013160, 2002."},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1007\/s002329900495"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1007\/s00232-003-0636-9"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.398"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000023436.71816.56"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)64438-0"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00344.2005","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:21:18Z","timestamp":1567970478000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00344.2005"}},"issued":{"date-parts":[[2006,11]]},"references-count":38,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2006,11]]}},"alternative-id":["10.1152\/ajprenal.00344.2005"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00344.2005","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2006,11]]}},{"indexed":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T07:23:47Z","timestamp":1773300227407,"version":"3.50.1"},"reference-count":39,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2010,7]]},"abstract":"<jats:p>The transient receptor potential channel TRPC3 is exclusively expressed in the apical membrane of principal cells of the collecting duct (CD) both in vivo and in the mouse CD cell line IMCD-3. Previous studies revealed that ATP-induced apical-to-basolateral transepithelial Ca<jats:sup>2+<\/jats:sup>flux across IMCD-3 monolayers is increased by overexpression of TRPC3 and attenuated by a dominant negative TRPC3 construct, suggesting that Ca<jats:sup>2+<\/jats:sup>entry across the apical membrane occurs via TRPC3 channels. To test this hypothesis, we selectively measured the Ca<jats:sup>2+<\/jats:sup>permeability of the apical membrane of fura-2-loaded IMCD-3 cells using the Mn<jats:sup>2+<\/jats:sup>quench technique. Mn<jats:sup>2+<\/jats:sup>influx across the apical membrane was increased 12- to 16-fold by apical ATP and was blocked by the pyrazole derivative BTP2, a known inhibitor of TRPC3 channels, with an IC<jats:sub>50<\/jats:sub>value &lt;100 nM. In contrast, Mn<jats:sup>2+<\/jats:sup>influx was only increased \u223c2-fold by basolateral ATP. Mn<jats:sup>2+<\/jats:sup>influx was also activated by apical, but not basolateral, 1-stearoyl-2-acetyl- sn-glycerol (SAG), a known activator of TRPC3 channels. Apical ATP- and SAG-induced Mn<jats:sup>2+<\/jats:sup>influx was increased by overexpression of TRPC3 and completely blocked by expression of the dominant negative TRPC3 construct. Mn<jats:sup>2+<\/jats:sup>influx was also stimulated \u223c2-fold by thapsigargin applied to either the apical or basolateral side. Thapsigargin-induced flux was blocked by BTP2 but was unaffected by overexpression of TRPC3 or by dominant negative TRPC3. Apical ATP, but not basolateral ATP, increased transepithelial<jats:sup>45<\/jats:sup>Ca<jats:sup>2+<\/jats:sup>flux. These results demonstrate that the apical membrane of IMCD-3 cells has two distinct Ca<jats:sup>2+<\/jats:sup>influx pathways: 1) a store-operated channel activated by thapsigargin and basolateral ATP and 2) TRPC3 channels activated by apical ATP. Only activation of TRPC3 leads to net transepithelial apical-to-basolateral Ca<jats:sup>2+<\/jats:sup>flux. Furthermore, these results demonstrate that native TRPC3 is not a store-operated channel in IMCD-3 cells.<\/jats:p>","DOI":"10.1152\/ajprenal.00670.2009","type":"journal-article","created":{"date-parts":[[2010,4,22]],"date-time":"2010-04-22T01:47:44Z","timestamp":1271900864000},"page":"F225-F233","source":"Crossref","is-referenced-by-count":25,"title":["Role of TRPC3 channels in ATP-induced Ca<sup>2+<\/sup>signaling in principal cells of the inner medullary collecting duct"],"prefix":"10.1152","volume":"299","author":[{"given":"Monu","family":"Goel","sequence":"first","affiliation":[{"name":"Rammelkamp Center for Education and Research, MetroHealth Medical Center, and Department of Physiology and Biophysics, Case Western Reserve University School of Medicine, Cleveland, Ohio"}]},{"given":"William P.","family":"Schilling","sequence":"additional","affiliation":[{"name":"Rammelkamp Center for Education and Research, MetroHealth Medical Center, and Department of Physiology and Biophysics, Case Western Reserve University School of Medicine, Cleveland, Ohio"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1007\/s11302-009-9149-z"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/j.ceca.2009.03.013"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/j.ymeth.2008.09.009"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.3158-06.2006"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2009.170431"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M402320200"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00376.2005"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00186.2007"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M411797200"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1038\/16711"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1007\/s11302-007-9072-0"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1007\/s11302-008-9102-6"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.88.3.325"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.1.F43"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0808793106"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000169"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M406073200"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00217.2002"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.0085.2001"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.4.F552"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)81857-7"},{"key":"B22","doi-asserted-by":"crossref","first-page":"re3","DOI":"10.1126\/stke.2722005re3","volume":"2005","author":"Montell C","year":"2005","journal-title":"Sci STKE"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.39.27359"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00057.2003"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.70.113006.100618"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/j.ceca.2007.05.012"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-065X.2009.00810.x"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1046\/j.1440-1681.2001.03451.x"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1007\/s11302-009-9152-4"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00252.2009"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M510541200"},{"key":"B32","first-page":"237","volume":"18","author":"Unwin RJ","year":"2003","journal-title":"News Physiol Sci"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M302751200"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00316.2001"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1016\/j.ceca.2007.03.004"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1016\/j.ceca.2007.03.003"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00281.2003"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90542.2008"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M309297200"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00670.2009","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,3,25]],"date-time":"2024-03-25T23:30:53Z","timestamp":1711409453000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00670.2009"}},"issued":{"date-parts":[[2010,7]]},"references-count":39,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2010,7]]}},"alternative-id":["10.1152\/ajprenal.00670.2009"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00670.2009","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2010,7]]}},{"indexed":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T16:25:14Z","timestamp":1773419114798,"version":"3.50.1"},"reference-count":49,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2009,10]]},"abstract":"<jats:p> Studies have shown that the length-tension ( L-T) relationships in airway and vascular smooth muscles are dynamic and can adapt to length changes over a period of time. Our prior studies have shown that the passive L-T relationship in rabbit detrusor smooth muscle (DSM) is also dynamic and that DSM exhibits adjustable passive stiffness (APS) characterized by a passive L-T curve that can shift along the length axis as a function of strain history and activation history. The present study demonstrates that the active L-T curve for DSM is also dynamic and that the peak active tension produced at a particular muscle length is a function of both strain and activation history. More specifically, this study reveals that the active L-T relationship, or curve, does not have a unique peak tension value with a single ascending and descending limb, but instead reveals that multiple ascending and descending limbs can be exhibited in the same DSM strip. This study also demonstrates that for DSM strips not stretched far enough to reveal a descending limb, the peak active tension produced by a maximal KCl-induced contraction at a short, passively slack muscle length of 3 mm was reduced by 58.6 \u00b1 4.1% ( n = 1 5) following stretches to and contractions at threefold the original muscle length, 9 mm. Moreover, five subsequent contractions at the short muscle length displayed increasingly greater tension; active tension produced by the sixth contraction was 91.5 \u00b1 9.1% of that produced by the prestretch contraction at that length. Together, these findings indicate for the first time that DSM exhibits length adaptation, similar to vascular and airway smooth muscles. In addition, our findings demonstrate that preconditioning, APS and adaptation of the active L-T curve can each impact the maximum total tension observed at a particular DSM length. <\/jats:p>","DOI":"10.1152\/ajprenal.00298.2009","type":"journal-article","created":{"date-parts":[[2009,8,13]],"date-time":"2009-08-13T01:55:32Z","timestamp":1250128532000},"page":"F1119-F1128","source":"Crossref","is-referenced-by-count":33,"title":["Adaptation of the length-active tension relationship in rabbit detrusor"],"prefix":"10.1152","volume":"297","author":[{"given":"John E.","family":"Speich","sequence":"first","affiliation":[{"name":"Departments of 1Mechanical Engineering,"}]},{"given":"Atheer M.","family":"Almasri","sequence":"additional","affiliation":[{"name":"Departments of 1Mechanical Engineering,"}]},{"given":"Hersch","family":"Bhatia","sequence":"additional","affiliation":[{"name":"Biomedical Engineering,"}]},{"given":"Adam P.","family":"Klausner","sequence":"additional","affiliation":[{"name":"Division of Urology, Department of Surgery, Virginia Commonwealth University, Richmond, Virginia"}]},{"given":"Paul H.","family":"Ratz","sequence":"additional","affiliation":[{"name":"Biochemistry and Molecular Biology and Pediatrics, and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/S0090-4295(99)00523-3"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.00216.2007"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1139\/y05-052"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.00884.2004"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1513\/pats.200705-056VS"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/S0090-4295(97)00587-6"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1385\/CRIAI:24:1:73"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1115\/1.2796067"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/S1569-9048(03)00141-1"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1103\/PhysRevLett.87.148102"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1139\/y05-089"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.00130.2007"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1139\/y94-190"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-4757-2257-4"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1966.sp007909"},{"key":"B16","doi-asserted-by":"crossref","first-page":"1243","DOI":"10.1152\/ajplegacy.1971.221.5.1243","volume":"221","author":"Gordon AR","year":"1971","journal-title":"Am J Physiol"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1114\/1.109"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1995.268.5.C1267"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/S1569-9048(03)00144-7"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/jappl.2001.90.2.741"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00253.2008"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.33.3.275"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.02368"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0704241"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00095.2003"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.00736.2003"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/0300-9629(90)90069-5"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1007\/s002400000168"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.01180.2002"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1001\/archneur.1960.03840110001001"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.105.1.73"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.72.6.1308"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00596.2002"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00329.2005"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/jappl.2000.89.5.2065"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1139\/Y07-052"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1152\/jappl.2000.89.3.869"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(01)64077-1"},{"key":"B39","doi-asserted-by":"crossref","first-page":"1501","DOI":"10.1152\/ajplegacy.1976.231.5.1501","volume":"231","author":"Siegman MJ","year":"1976","journal-title":"Am J Physiol"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.00159.2005"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1139\/y05-092"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1960.sp006561"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00418.2004"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.00548.2006"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.00396.2006"},{"key":"B46","first-page":"S7","volume":"4","author":"Steers WD","year":"2002","journal-title":"Rev Urol"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1976.tb10230.x"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1016\/S1056-8719(01)00132-0"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1152\/jappl.2001.90.2.734"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00298.2009","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T00:12:27Z","timestamp":1567987947000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00298.2009"}},"issued":{"date-parts":[[2009,10]]},"references-count":49,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2009,10]]}},"alternative-id":["10.1152\/ajprenal.00298.2009"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00298.2009","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2009,10]]}},{"indexed":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T17:15:01Z","timestamp":1773422101164,"version":"3.50.1"},"reference-count":34,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2004,8]]},"abstract":"<jats:p>Endothelin-1 (ET-1) acutely inhibits NaCl reabsorption by the thick ascending limb (THAL) by activating the ET<jats:sub>B<\/jats:sub>receptor, stimulating endothelial nitric oxide synthase (eNOS), and releasing nitric oxide (NO). In nonrenal tissue, chronic exposure to ET-1 stimulates eNOS expression via the ET<jats:sub>B<\/jats:sub>receptor and activation of phosphatidylinositol 3-kinase (PI3K). We hypothesized that ET-1 increases eNOS expression in the THAL by binding to ET<jats:sub>B<\/jats:sub>receptors and stimulating PI3K. In primary cultures of medullary THALs treated for 24 h, eNOS expression increased by 36 \u00b1 18% with 0.01 nM ET-1, 123 \u00b1 30% with 0.1 nM ( P &lt; 0.05; n = 5), and 71 \u00b1 30% with 1 nM, whereas 10 nM had no effect. BQ-788, a selective ET<jats:sub>B<\/jats:sub>receptor antagonist, completely blocked stimulation of eNOS expression caused by 0.1 nM ET-1 (12 \u00b1 25 vs. 120 \u00b1 40% for ET-1 alone; P &lt; 0.05; n = 5). BQ-123, a selective ET<jats:sub>A<\/jats:sub>receptor antagonist, did not affect the increase in eNOS caused by 0.1 nM ET-1. Sarafotoxin c (S6c; 0.1 \u03bcM), a selective ET<jats:sub>B<\/jats:sub>receptor agonist, increased eNOS expression by 77 \u00b1 30% ( P &lt; 0.05; n = 6). Wortmannin (0.01 \u03bcM), a PI3K inhibitor, completely blocked the stimulatory effect of 0.1 \u03bcM S6c (77 \u00b1 30 vs. \u221228 \u00b1 9%; P &lt; 0.05; n = 6). To test whether the increase in eNOS expression heightens activity, we measured NO release in response to simultaneous treatment with l-arginine, ionomycin, and clonidine using a NO-sensitive electrode. NO release by control cells was 337 \u00b1 61 and 690 \u00b1 126 pA in ET-1-treated cells ( P &lt; 0.05; n = 5). Taken together, these data suggest that ET-1 stimulates THAL eNOS, activating ET<jats:sub>B<\/jats:sub>receptors and PI3K and thereby increasing NO production.<\/jats:p>","DOI":"10.1152\/ajprenal.00413.2003","type":"journal-article","created":{"date-parts":[[2004,5,4]],"date-time":"2004-05-04T00:19:03Z","timestamp":1083629943000},"page":"F231-F235","source":"Crossref","is-referenced-by-count":43,"title":["Endothelin stimulates endothelial nitric oxide synthase expression in the thick ascending limb"],"prefix":"10.1152","volume":"287","author":[{"given":"Marcela","family":"Herrera","sequence":"first","affiliation":[]},{"given":"Jeffrey L.","family":"Garvin","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"crossref","unstructured":"Abassi ZA, Ellahham S, Winaver J, and Hoffman A.The intrarenal endothelin system and hypertension.News Physiol Sci16: 152\u2013156, 2001.","DOI":"10.1152\/physiologyonline.2001.16.4.152"},{"key":"R2","unstructured":"Baldi Eand Dunn MJ.Endothelin binding and receptor downregulation in rat glomerular mesangial cells.J Pharmacol Exp Ther256: 581\u2013586, 1991."},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00054.2002"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M005305200"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.2000.279.5.C1443"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00249.2003"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-199816080-00001"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.72"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1126\/science.292.5518.929"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1016\/0006-291X(89)91603-3"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000014782.37591.C7"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.261.2.F221"},{"key":"R13","doi-asserted-by":"crossref","unstructured":"Kohan DE, Hughes AK, and Perkins SL.Characterization of endothelin receptors in the inner medullary collecting duct of the rat.J Biol Chem267: 12336\u201312340, 1992.","DOI":"10.1016\/S0021-9258(19)49844-X"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199508103330607"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1007\/s004249900079"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1046\/j.1440-1681.1999.03013.x"},{"key":"R17","doi-asserted-by":"crossref","unstructured":"Okada T, Sakuma L, Fukui Y, Hazeki O, and Ui M.Blockage of chemotactic peptide-induced stimulation of neutrophils by wortmannin as a result of selective inhibition of phosphatidylinositol 3-kinase.J Biol Chem269: 3563\u20133567, 1994.","DOI":"10.1016\/S0021-9258(17)41900-4"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000047872.07864.20"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.3346\/jkms.2002.17.2.161"},{"key":"R20","doi-asserted-by":"crossref","unstructured":"Plato CFand Garvin JL.\u03b12-Adrenergic-mediated tubular NO production inhibits thick ascending limb chloride absorption.Am J Physiol Renal Physiol281: F679\u2013F686, 2001.","DOI":"10.1152\/ajprenal.2001.281.4.F679"},{"key":"R21","doi-asserted-by":"crossref","unstructured":"Plato CF, Pollock DM, and Garvin JL.Endothelin inhibits thick ascending limb chloride flux via ETBreceptor-mediated NO release.Am J Physiol Renal Physiol279: F326\u2013F333, 2000.","DOI":"10.1152\/ajprenal.2000.279.2.F326"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.35.1.319"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200003000-00010"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.281.1.F144"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1016\/S0735-1097(03)00481-9"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1999.276.2.H699"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.46.33057"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1097\/00005344-198301000-00015"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1093\/jn\/125.suppl_7.2028S"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1054\/jcaf.2002.129282"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115822"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.1997.273.5.G1036"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000047204.72286.34"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.1999.277.5.G944"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00413.2003","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,6,17]],"date-time":"2021-06-17T07:53:11Z","timestamp":1623916391000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00413.2003"}},"issued":{"date-parts":[[2004,8]]},"references-count":34,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2004,8]]}},"alternative-id":["10.1152\/ajprenal.00413.2003"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00413.2003","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2004,8]]}},{"indexed":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T17:15:38Z","timestamp":1773422138049,"version":"3.50.1"},"reference-count":37,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1998,9,1]]},"abstract":"<jats:p>Cl<jats:sup>\u2212<\/jats:sup>\/[Formula: see text]exchange was measured in luminal (LMV) and basolateral (BLMV) membrane vesicles purified from rat medullary thick ascending limb (MTAL). Cl<jats:sup>\u2212<\/jats:sup>\/[Formula: see text]exchange in BLMV and LMV was inhibited by DIDS, with respective IC<jats:sub>50<\/jats:sub>values of 3.2 \u00b1 0.9 and 15.2 \u00b1 5.2 \u03bcM, whereas Cl<jats:sup>\u2212<\/jats:sup>conductances were DIDS insensitive. At constant external pH, BLMV<jats:sup>36<\/jats:sup>Cl<jats:sup>\u2212<\/jats:sup>\/[Formula: see text]and<jats:sup>36<\/jats:sup>Cl<jats:sup>\u2212<\/jats:sup>\/Cl<jats:sup>\u2212<\/jats:sup>exchanges exhibited a sigmoidal pattern of activation as internal pH (pH<jats:sub>i<\/jats:sub>) increased from 6.1 to 8.0, whereas LMV<jats:sup>36<\/jats:sup>Cl<jats:sup>\u2212<\/jats:sup>\/Cl<jats:sup>\u2212<\/jats:sup>exchange was unchanged between pH<jats:sub>i<\/jats:sub>6.7 and 7.8. The 165-kDa AE2 polypeptide and \u223c115-kDa AE1-related polypeptide were present only in BLMV. In contrast, AE1-related polypeptides of \u223c90 and 95 kDa were present not only in BLMV but also (in variable abundance) in LMV. We conclude that rat MTAL BLMV and LMV express distinct anion exchange activities and distinct sets of AE polypeptides. AE2 (and perhaps AE1) in BLMV likely contribute to[Formula: see text] absorption. In contrast, LMV exchangers may contribute to NaCl absorption via parallel coupling with the luminal Na<jats:sup>+<\/jats:sup>\/H<jats:sup>+<\/jats:sup>antiporters and\/or may provide negative feedback regulation of[Formula: see text] absorption.<\/jats:p>","DOI":"10.1152\/ajprenal.1998.275.3.f334","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T17:18:08Z","timestamp":1514049488000},"page":"F334-F342","source":"Crossref","is-referenced-by-count":24,"title":["Functional and molecular characterization of luminal and basolateral Cl<sup>\u2212<\/sup>\/ HCO 3 \u2212 exchangers of rat thick limbs"],"prefix":"10.1152","volume":"275","author":[{"given":"Dominique","family":"Eladari","sequence":"first","affiliation":[{"name":"Laboratoire de Physiologie et Endocrinologie Cellulaire R\u00e9nale, Facult\u00e9 de M\u00e9decine Broussais-H\u00f4tel Dieu, Institut National de la Sant\u00e9 et de la Recherche M\u00e9dicale, Unit\u00e9 356, Paris, France; and the"}]},{"given":"Anne","family":"Blanchard","sequence":"additional","affiliation":[{"name":"Laboratoire de Physiologie et Endocrinologie Cellulaire R\u00e9nale, Facult\u00e9 de M\u00e9decine Broussais-H\u00f4tel Dieu, Institut National de la Sant\u00e9 et de la Recherche M\u00e9dicale, Unit\u00e9 356, Paris, France; and the"}]},{"given":"Fran\u00e7oise","family":"Leviel","sequence":"additional","affiliation":[{"name":"Laboratoire de Physiologie et Endocrinologie Cellulaire R\u00e9nale, Facult\u00e9 de M\u00e9decine Broussais-H\u00f4tel Dieu, Institut National de la Sant\u00e9 et de la Recherche M\u00e9dicale, Unit\u00e9 356, Paris, France; and the"}]},{"given":"Michel","family":"Paillard","sequence":"additional","affiliation":[{"name":"Laboratoire de Physiologie et Endocrinologie Cellulaire R\u00e9nale, Facult\u00e9 de M\u00e9decine Broussais-H\u00f4tel Dieu, Institut National de la Sant\u00e9 et de la Recherche M\u00e9dicale, Unit\u00e9 356, Paris, France; and the"}]},{"given":"Alan K.","family":"Stuart-Tilley","sequence":"additional","affiliation":[{"name":"Departments of Cell Biology and Medicine, Harvard Medical School, and the Molecular Medicine and Renal Units, Beth Israel Hospital, Boston, Massachusetts 02215"}]},{"given":"Seth L.","family":"Alper","sequence":"additional","affiliation":[{"name":"Departments of Cell Biology and Medicine, Harvard Medical School, and the Molecular Medicine and Renal Units, Beth Israel Hospital, Boston, Massachusetts 02215"}]},{"given":"Ren\u00e9-Alexandre","family":"Podevin","sequence":"additional","affiliation":[{"name":"Laboratoire de Physiologie et Endocrinologie Cellulaire R\u00e9nale, Facult\u00e9 de M\u00e9decine Broussais-H\u00f4tel Dieu, Institut National de la Sant\u00e9 et de la Recherche M\u00e9dicale, Unit\u00e9 356, Paris, France; and the"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1996.270.6.C1571"},{"issue":"42","key":"B2","first-page":"F601","volume":"273","author":"Alper S. L.","year":"1997","journal-title":"Am. J. Physiol."},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.404"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.408"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.1998.689bv.x"},{"issue":"38","key":"B6","first-page":"F461","volume":"269","author":"Brosius F. C. I.","year":"1995","journal-title":"Am. J. Physiol."},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1172\/JCI113833"},{"issue":"44","key":"B8","first-page":"F379","volume":"275","author":"Chambrey R.","year":"1998","journal-title":"Am. J. Physiol."},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/S0005-2736(97)00090-4"},{"issue":"12","key":"B10","first-page":"F311","volume":"243","author":"Dobyan D. C.","year":"1982","journal-title":"Am. J. Physiol."},{"key":"B11","doi-asserted-by":"crossref","first-page":"26717","DOI":"10.1016\/S0021-9258(18)47078-0","volume":"269","author":"Fejes-Toth G.","year":"1994","journal-title":"J. Biol. Chem."},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.80.5.683"},{"key":"B13","first-page":"225","volume":"13","author":"Good D. W.","year":"1993","journal-title":"Semin. Nephrol."},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.26.12525"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1986.250.6.C920"},{"issue":"10","key":"B16","first-page":"F412","volume":"241","author":"Hebert S. C.","year":"1981","journal-title":"Am. J. Physiol."},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1997.272.4.C1232"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1994.267.5.C1295"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1995.268.1.C201"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.11.6380"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1997.272.1.C191"},{"key":"B22","doi-asserted-by":"crossref","first-page":"23544","DOI":"10.1016\/S0021-9258(17)31550-8","volume":"269","author":"Kapus A.","year":"1994","journal-title":"J. Biol. Chem."},{"issue":"27","key":"B23","first-page":"F445","volume":"258","author":"Kikeri D.","year":"1990","journal-title":"Am. J. Physiol."},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115962"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1989.256.2.C428"},{"issue":"22","key":"B26","first-page":"G666","volume":"259","author":"Mugharbil A.","year":"1990","journal-title":"Am. J. Physiol."},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1994.sp020467"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1007\/BF00583592"},{"issue":"43","key":"B29","first-page":"F453","volume":"274","author":"Rivers R.","year":"1998","journal-title":"Am. J. Physiol."},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.16"},{"key":"B31","first-page":"1261","volume":"7","author":"Sato S.","year":"1996","journal-title":"J. Am. Soc. Nephrol."},{"key":"B32","doi-asserted-by":"crossref","first-page":"946","DOI":"10.1681\/ASN.V96946","volume":"9","author":"Stuart-Tilley A. K.","year":"1998","journal-title":"J. Am. Soc. Nephrol."},{"key":"B33","first-page":"316","volume":"6","author":"Sun A. M.","year":"1995","journal-title":"J. Am. Soc. Nephrol."},{"key":"B34","first-page":"1261","volume":"7","author":"Sun A. M.","year":"1996","journal-title":"J. Am. Soc. Nephrol."},{"key":"B35","doi-asserted-by":"crossref","first-page":"20250","DOI":"10.1016\/S0021-9258(17)31983-X","volume":"269","author":"Watts B. A.","year":"1994","journal-title":"J. Biol. Chem."},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.10.5741"},{"issue":"34","key":"B37","first-page":"G311","volume":"271","author":"Zolotarev A. S.","year":"1996","journal-title":"Am. J. Physiol."}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1998.275.3.F334","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:52:45Z","timestamp":1660189965000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1998.275.3.F334"}},"issued":{"date-parts":[[1998,9,1]]},"references-count":37,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1998,9,1]]}},"alternative-id":["10.1152\/ajprenal.1998.275.3.F334"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1998.275.3.f334","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1998,9,1]]}},{"indexed":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T16:12:06Z","timestamp":1773418326990,"version":"3.50.1"},"reference-count":31,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2009,4]]},"abstract":"<jats:p> Secondary hyperparathyroidism is characterized by increased parathyroid hormone (PTH) mRNA stability that leads to increased PTH mRNA and serum PTH levels. PTH gene expression is reduced by the calcimimetic R568 and the oral phosphorus binder lanthanum carbonate (La). Changes in PTH mRNA stability are regulated by the binding of trans-acting stabilizing and destabilizing factors to a defined cis element in the PTH mRNA 3\u2032-untranslated region (UTR). Adenosine-uridine (AU)-binding factor 1 (AUF1) is a PTH mRNA-stabilizing protein, and K-homology splicing regulatory protein (KSRP) is a destabilizing protein that targets mRNAs, including PTH mRNA, to degradation by the ribonuclease complex exosome. We now show that KSRP-PTH mRNA binding is decreased in parathyroids from rats with adenine-induced chronic kidney disease (CKD) where PTH mRNA is more stable. KSRP-PTH mRNA binding is increased by treatment with both R568 and La, correlating with decreased PTH gene expression. In vitro degradation assays using transcripts for PTH mRNA and rat parathyroid extracts reproduce the differences in mRNA stability in vivo. Accordingly, PTH mRNA is destabilized in vitro by parathyroid extracts from CKD rats treated with R568 or La compared with parathyroid extracts from untreated CKD rats. This destabilizing effect of R568 and La is dependent on KSRP and the PTH mRNA 3\u2032-UTR. Therefore, the calcimimetic R568 and correction of serum phosphorus by La determine PTH mRNA stability through KSRP-mediated recruitment of a degradation complex to the PTH mRNA, thereby decreasing PTH expression. <\/jats:p>","DOI":"10.1152\/ajprenal.90625.2008","type":"journal-article","created":{"date-parts":[[2009,1,8]],"date-time":"2009-01-08T01:34:25Z","timestamp":1231378465000},"page":"F795-F800","source":"Crossref","is-referenced-by-count":37,"title":["Regulation of PTH mRNA stability by the calcimimetic R568 and the phosphorus binder lanthanum carbonate in CKD"],"prefix":"10.1152","volume":"296","author":[{"given":"Morris","family":"Nechama","sequence":"first","affiliation":[]},{"given":"Iddo Z.","family":"Ben-Dov","sequence":"additional","affiliation":[]},{"given":"Justin","family":"Silver","sequence":"additional","affiliation":[]},{"given":"Tally","family":"Naveh-Many","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1097\/01.mnh.0000133973.86816.e9"},{"key":"R2","doi-asserted-by":"crossref","unstructured":"Ben Dov IZ, Pappo O, Sklair-Levy M, Galitzer H, Ilan Y, Naveh-Many T, Silver J. Lanthanum carbonate decreases PTH gene expression with no hepatotoxicity in uraemic rats. Nephrol Dial Transplant 22: 362\u2013368, 2007.","DOI":"10.1093\/ndt\/gfl623"},{"key":"R3","doi-asserted-by":"crossref","unstructured":"Ben Dov IZ, Galitzer H, Lavi-Moshayoff V, Goetz R, Kuro-o M, Mohammadi M, Sirkis R, Naveh-Many T, Silver J. The parathyroid is a target organ for FGF23 in rats. J Clin Invest 117: 4003\u20134008, 2007.","DOI":"10.1172\/JCI32409"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa031633"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(01)00578-5"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.26.10.3695-3706.2006"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.67103.x"},{"key":"R8","doi-asserted-by":"crossref","unstructured":"D'Haese PC, Spasovski GB, Sikole A, Hutchison A, Freemont TJ, Sulkova S, Swanepoel C, Pejanovic S, Djukanovic L, Balducci A, Coen G, Sulowicz W, Ferreira A, Torres A, Curic S, Popovic M, Dimkovic N, De Broe ME. A multicenter study on the effects of lanthanum carbonate (Fosrenol) and calcium carbonate on renal bone disease in dialysis patients. Kidney Int Suppl S73\u2013S78, 2003.","DOI":"10.1046\/j.1523-1755.63.s85.18.x"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.21.12179"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1210\/me.2005-0333"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1126\/stke.2000.18.pe1"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1016\/j.molcel.2004.05.002"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(03)00554-7"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118038"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M005471200"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.17.8.4870"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1111\/j.1525-139X.2007.00248.x"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005070679"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1111\/j.1525-139X.2006.00161.x"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.9.5253"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.67139.x"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfh966"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0b013e3281c55ede"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1096\/fj.08-107250"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.3.F611"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00014.2004"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00262.2006"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.275.10.7424"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1172\/JCI112714"},{"key":"R31","unstructured":"Yalcindag C, Silver J, Naveh-Many T. Mechanism of increased parathyroid hormone mRNA in experimental uremia: roles of protein RNA binding and RNA degradation. J Am Soc Nephrol 10: 2562\u20132568, 1999."},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1159\/000183992"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.90625.2008","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T22:54:27Z","timestamp":1567983267000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.90625.2008"}},"issued":{"date-parts":[[2009,4]]},"references-count":31,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2009,4]]}},"alternative-id":["10.1152\/ajprenal.90625.2008"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.90625.2008","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2009,4]]}},{"indexed":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T17:52:38Z","timestamp":1773424358971,"version":"3.50.1"},"reference-count":43,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,8,15]]},"abstract":"<jats:p> In the distal nephron, the large-conductance Ca-activated K (BK) channel, comprised of a pore-forming-\u03b1 (BK-\u03b1) and the BK-\u03b24 subunit, promotes K excretion when mice are maintained on a high-K alkaline diet (HK-alk). We examined whether BK-\u03b24 and the acid-base status regulate apical membrane expression of BK-\u03b1 in the cortical (CCD) and medullary collecting ducts (MCD) using immunohistochemical analysis (IHC) and Western blot. With the use of IHC, BK-\u03b1 of mice on acontrol diet localized mostly cytoplasmically in intercalated cells (IC) of the CCD and in the perinuclear region of both principle cells (PC) and IC of the MCD. HK-alk wild-type mice (WT), but not BK-\u03b24 knockout mice (\u03b24KO), exhibited increased apical BK-\u03b1 in both the CCD and MCD. When given a high-K acidic diet (HK-Cl), BK-\u03b1 expression increased but remained cytoplasmic in the CCD and perinuclear in the MCD of both WT and \u03b24KO. Western blot confirmed that total BK-\u03b1 expression was enhanced by either HK-alk or HK-Cl but only increased in the plasma membrane with HK-alk. Compared with controls, mice drinking NaHCO<jats:sub>3<\/jats:sub> water exhibited more apical BK-\u03b1 and total cellular BK-\u03b24. Spironolactone given to mice on HK-alk significantly reduced K secretion and decreased total cellular BK-\u03b1 but did not affect cellular BK-\u03b24 and apical BK-\u03b1. Experiments with MDCK-C11 cells indicated that BK-\u03b24 stabilizes surface BK-\u03b1 by inhibiting degradation through a lysosomal pathway. These data suggest that aldosterone mediates a high-K-induced increase in BK-\u03b1 and urinary alkalinization increases BK-\u03b24 expression, which promotes the apical localization of BK-\u03b1. <\/jats:p>","DOI":"10.1152\/ajprenal.00171.2013","type":"journal-article","created":{"date-parts":[[2013,6,13]],"date-time":"2013-06-13T03:14:41Z","timestamp":1371093281000},"page":"F463-F476","source":"Crossref","is-referenced-by-count":49,"title":["Regulation of BK-\u03b1 expression in the distal nephron by aldosterone and urine pH"],"prefix":"10.1152","volume":"305","author":[{"given":"Donghai","family":"Wen","sequence":"first","affiliation":[{"name":"Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska"}]},{"given":"Ryan J.","family":"Cornelius","sequence":"additional","affiliation":[{"name":"Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska"}]},{"given":"Yang","family":"Yuan","sequence":"additional","affiliation":[{"name":"Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska"}]},{"given":"Steven C.","family":"Sansom","sequence":"additional","affiliation":[{"name":"Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00437.2010"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-3495(03)70023-X"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1007\/BF00492456"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00449.2010"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajplegacy.1976.230.1.239"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00490.2012"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00002.2008"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2011.214247"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1172\/JCI111598"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00018.2007"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00191.2009"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0904635106"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1006128107"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1988.254.5.F697"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00112.2011"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009080817"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0b013e3283488889"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010050468"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2007.12.168"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1124\/mol.108.051912"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2006.116889"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00057.2007"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1136\/jcp.22.3.334"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1002\/cne.20931"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1172\/JCI114913"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00057.2005"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.261.4.F696"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00537.2007"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009121257"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.300"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00118.2006"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00340.2004"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.89.1.132"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1529\/biophysj.107.110122"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1038\/nn.2383"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0033429"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2008.156968"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1982.242.5.F514"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1172\/JCI113967"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1177\/39.3.1993828"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000088321.67254.B7"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.5.F786"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00518.2010"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00171.2013","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T23:47:35Z","timestamp":1567986455000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00171.2013"}},"issued":{"date-parts":[[2013,8,15]]},"references-count":43,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2013,8,15]]}},"alternative-id":["10.1152\/ajprenal.00171.2013"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00171.2013","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2013,8,15]]}},{"indexed":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T17:25:10Z","timestamp":1773422710715,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1986,2,1]]},"abstract":"<jats:p> 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) was tested as an inhibitor of the sulfate transport systems in rat renal brush border and basolateral membrane vesicles. Na+-driven sulfate uptake into brush border membrane vesicles was half-maximally inhibited at 350 microM DIDS. Proton gradient-driven sulfate uptake into basolateral membrane vesicles was competitively inhibited by DIDS with a Ki of 2.4 microM. The Km for delta pH-driven sulfate uptake was 5.4 microM. The different affinities of the sulfate transport systems for DIDS correlated with different substrate specificities. The luminal transport system accepted a smaller range of anions than the contraluminal system and did not operate as a Na+-independent anion exchanger. After treatment of basolateral membrane vesicles with 50 microM DIDS at pH 8.4 for 30 min, an irreversible inhibition of sulfate uptake was observed. With brush border membranes, only a small irreversible inhibition was obtained. Lack of inhibition after treatment of basolateral membranes with DIDS at pH 6.4 indicated that DIDS reacted with deprotonated amino groups of the transport protein. Sulfate was protected from the irreversible inhibition by DIDS. Sodium-driven uptake of L-glutamate and methylsuccinate into basolateral membrane vesicles was not irreversibly inhibited by DIDS, indicating a specific action of DIDS on the contraluminal sulfate transport system. Irreversible and substrate-protectable inhibition of sulfate transport render DIDS suitable for future affinity labeling studies on the sulfate transport system in basolateral membranes. <\/jats:p>","DOI":"10.1152\/ajprenal.1986.250.2.f226","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T20:43:52Z","timestamp":1513975432000},"page":"F226-F234","source":"Crossref","is-referenced-by-count":7,"title":["Sensitivity of rat renal luminal and contraluminal sulfate transport systems to DIDS"],"prefix":"10.1152","volume":"250","author":[{"given":"C.","family":"Bastlein","sequence":"first","affiliation":[]},{"given":"G.","family":"Burckhardt","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1986.250.2.F226","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:38:09Z","timestamp":1567957089000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1986.250.2.F226"}},"issued":{"date-parts":[[1986,2,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1986,2,1]]}},"alternative-id":["10.1152\/ajprenal.1986.250.2.F226"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1986.250.2.f226","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1986,2,1]]}},{"indexed":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T18:56:41Z","timestamp":1773428201632,"version":"3.50.1"},"reference-count":90,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2007,7]]},"abstract":"<jats:p>The proximal tubule (PT) is major site for the reabsorption of filtered HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup>. Previous work on the rabbit PT showed that 1) increases in basolateral (BL) CO<jats:sub>2<\/jats:sub>concentration ([CO<jats:sub>2<\/jats:sub>]<jats:sub>BL<\/jats:sub>) raise the HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup>reabsorption rate ( J<jats:sub>HCO<jats:sub>3<\/jats:sub><\/jats:sub>), and 2) the increase that luminal angiotensin II (ANG II) produces in J<jats:sub>HCO<jats:sub>3<\/jats:sub><\/jats:sub>is greatest at 0% [CO<jats:sub>2<\/jats:sub>]<jats:sub>BL<\/jats:sub>and falls to nearly zero at 20%. Here, we investigate the role of angiotensin receptors in the [CO<jats:sub>2<\/jats:sub>]<jats:sub>BL<\/jats:sub>dependence of J<jats:sub>HCO<jats:sub>3<\/jats:sub><\/jats:sub>in isolated perfused PTs. We found that, in rabbit S2 PT segments, luminal 10<jats:sup>\u22128<\/jats:sup>M saralasin (peptide antagonist of ANG II receptors), lowers baseline J<jats:sub>HCO<jats:sub>3<\/jats:sub><\/jats:sub>(5% CO<jats:sub>2<\/jats:sub>) to the value normally seen at 0% in the absence of inhibitors and eliminates the J<jats:sub>HCO<jats:sub>3<\/jats:sub><\/jats:sub>response to changes in [CO<jats:sub>2<\/jats:sub>]<jats:sub>BL<\/jats:sub>. However, basolateral 10<jats:sup>\u22128<\/jats:sup>M saralasin has no effect. As with saralasin, luminal 10<jats:sup>\u22128<\/jats:sup>M candesartan (AT<jats:sub>1<\/jats:sub>antagonist) reduces baseline J<jats:sub>HCO<jats:sub>3<\/jats:sub><\/jats:sub>and eliminates the [CO<jats:sub>2<\/jats:sub>]<jats:sub>BL<\/jats:sub>dependence of J<jats:sub>HCO<jats:sub>3<\/jats:sub><\/jats:sub>. Luminal 10<jats:sup>\u22127<\/jats:sup>M PD 123319 (AT<jats:sub>2<\/jats:sub>antagonist) has no effect. Finally, we compared PTs from wild-type and AT<jats:sub>1A<\/jats:sub>-null mice of the same genetic background. Knocking out AT<jats:sub>1A<\/jats:sub>modestly lowers baseline J<jats:sub>HCO<jats:sub>3<\/jats:sub><\/jats:sub>and, like luminal saralasin or candesartan in rabbits, eliminates the J<jats:sub>HCO<jats:sub>3<\/jats:sub><\/jats:sub>response to changes in [CO<jats:sub>2<\/jats:sub>]<jats:sub>BL<\/jats:sub>. Our accumulated evidence suggests that ANG II endogenous to the PT binds to the apical AT<jats:sub>1A<\/jats:sub>receptor and that this interaction is critical for both baseline J<jats:sub>HCO<jats:sub>3<\/jats:sub><\/jats:sub>and its response to changes in [CO<jats:sub>2<\/jats:sub>]<jats:sub>BL<\/jats:sub>. Neither apical AT<jats:sub>2<\/jats:sub>receptors nor basolateral ANG II receptors are involved in these processes.<\/jats:p>","DOI":"10.1152\/ajprenal.00516.2006","type":"journal-article","created":{"date-parts":[[2007,3,14]],"date-time":"2007-03-14T00:50:23Z","timestamp":1173833423000},"page":"F110-F120","source":"Crossref","is-referenced-by-count":18,"title":["Role of the AT<sub>1A<\/sub>receptor in the CO<sub>2<\/sub>-induced stimulation of HCO<sub>3<\/sub><sup>\u2212<\/sup>reabsorption by renal proximal tubules"],"prefix":"10.1152","volume":"293","author":[{"given":"Yuehan","family":"Zhou","sequence":"first","affiliation":[]},{"given":"Patrice","family":"Bouyer","sequence":"additional","affiliation":[]},{"given":"Walter F.","family":"Boron","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1038\/289507a0"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1983.245.6.F647"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1016\/S0167-0115(99)00075-0"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.273.4.F595"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1980.238.6.F445"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1983.244.2.F165"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.81.1.29"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.81.1.53"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.264.5.F891"},{"key":"R10","doi-asserted-by":"crossref","unstructured":"Brazeau P, Gilman A.Effect of plasma CO2tension on renal tubular reabsorption of bicarbonate.Am J Physiol175: 33\u201338, 1953.","DOI":"10.1152\/ajplegacy.1953.175.1.33"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.87.19.7457"},{"key":"R12","doi-asserted-by":"crossref","unstructured":"Burg M, Grantham J, Abramow M, Orloff J.Preparation and study of fragments of single rabbit nephrons.Am J Physiol210: 1293\u20131298, 1966.","DOI":"10.1152\/ajplegacy.1966.210.6.1293"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1172\/JCI105888"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.103.6.904"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.1.F66"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.78.6.3897"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.33.1.102"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.260.3.F340"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1984.247.3.F387"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1042\/cs1000481"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1172\/JCI102874"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00261.2002"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.8.6.544"},{"key":"R24","unstructured":"Dzau VJ, Re RN.Evidence for the existence of renin in the heart.Circulation75: I134\u2013I136, 1987."},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1016\/0006-291X(92)90700-U"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1016\/S0895-7061(00)00286-7"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1126\/science.6879184"},{"key":"R28","doi-asserted-by":"crossref","unstructured":"Garvin JL.Angiotensin stimulates bicarbonate transport and Na+\/K+ATPase in rat proximal straight tubules.J Am Soc Nephrol1: 1146\u20131152, 1991.","DOI":"10.1681\/ASN.V1101146"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.ph.58.030196.002235"},{"key":"R30","doi-asserted-by":"crossref","unstructured":"Gunther S.Characterization of angiotensin II receptor subtypes in rat liver.J Biol Chem259: 7622\u20137629, 1984.","DOI":"10.1016\/S0021-9258(17)42836-5"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1007\/BF00581370"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000036449.70110.DE"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1172\/JCI114454"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.8.3521"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(92)80071-N"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-199208000-00013"},{"key":"R37","doi-asserted-by":"crossref","unstructured":"Kambayashi Y, Bardhan S, Takahashi K, Tsuzuki S, Inui H, Hamakubo T, Inagami T.Molecular cloning of a novel angiotensin II receptor isoform involved in phosphotyrosine phosphatase inhibition.J Biol Chem268: 24543\u201324546, 1993.","DOI":"10.1016\/S0021-9258(19)74499-8"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.430"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.21.4.446"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1007\/s002329900219"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1016\/S0167-4889(97)00015-3"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1677\/jme.0.0300263"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1172\/JCI113638"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1987.61"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1979.236.3.F232"},{"key":"R46","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1977.72"},{"key":"R47","doi-asserted-by":"publisher","DOI":"10.1172\/JCI116296"},{"key":"R48","doi-asserted-by":"crossref","unstructured":"Mukoyama M, Nakajima M, Horiuchi M, Sasamura H, Pratt RE, Dzau VJ.Expression cloning of type 2 angiotensin II receptor reveals a unique class of seven-transmembrane receptors.J Biol Chem268: 24539\u201324542, 1993.","DOI":"10.1016\/S0021-9258(19)74498-6"},{"key":"R49","doi-asserted-by":"publisher","DOI":"10.1042\/bj1540597"},{"key":"R50","doi-asserted-by":"publisher","DOI":"10.1038\/351233a0"},{"key":"R51","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1986.250.1.H144"},{"key":"R52","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.92.3.369"},{"key":"R53","doi-asserted-by":"crossref","unstructured":"Navar LG, Lewis L, Hymel A, Braam B, Mitchell KD.Tubular fluid concentrations and kidney contents of angiotensins I and II in anesthetized rats.J Am Soc Nephrol5: 1153\u20131158, 1994.","DOI":"10.1681\/ASN.V541153"},{"key":"R54","doi-asserted-by":"crossref","unstructured":"Orlowski J, Kandasamy RA, Shull GE.Molecular cloning of putative members of the Na\/H exchanger gene family. cDNA cloning, deduced amino acid sequence, and mRNA tissue expression of the rat Na\/H exchanger NHE-1 and two structurally related proteins.J Biol Chem267: 9331\u20139339, 1992.","DOI":"10.1016\/S0021-9258(19)50428-8"},{"key":"R55","doi-asserted-by":"publisher","DOI":"10.1016\/0006-291X(84)90590-4"},{"key":"R56","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.1996.271.3.E439"},{"key":"R57","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.56.2.212"},{"key":"R58","doi-asserted-by":"publisher","DOI":"10.1007\/s00232-002-1055-z"},{"key":"R59","doi-asserted-by":"publisher","DOI":"10.1007\/s00232-002-1042-4"},{"key":"R60","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.67.040403.101353"},{"key":"R61","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118745"},{"key":"R62","doi-asserted-by":"publisher","DOI":"10.1172\/JCI102823"},{"key":"R63","doi-asserted-by":"publisher","DOI":"10.1007\/BF00238309"},{"key":"R64","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-003-1180-2"},{"key":"R65","doi-asserted-by":"publisher","DOI":"10.1038\/387409a0"},{"key":"R66","doi-asserted-by":"publisher","DOI":"10.1038\/351230a0"},{"key":"R67","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-291X(05)80983-0"},{"key":"R68","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.16.9660"},{"key":"R69","doi-asserted-by":"publisher","DOI":"10.1038\/969"},{"key":"R70","doi-asserted-by":"publisher","DOI":"10.1172\/JCI111237"},{"key":"R71","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1981.241.4.F380"},{"key":"R72","unstructured":"Schwartz GJ.Physiology and molecular biology of renal carbonic anhydrase.J Nephrol15: S61\u2013S74, 2002."},{"key":"R73","doi-asserted-by":"publisher","DOI":"10.1172\/JCI114846"},{"key":"R74","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.bi.64.070195.002111"},{"key":"R75","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1974.82"},{"key":"R76","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.32.18719"},{"key":"R77","doi-asserted-by":"crossref","unstructured":"Tse CM, Brant SR, Walker MS, Pouyss\u00e9gur J, Donowitz M.Cloning and sequencing of a rabbit cDNA encoding an intestinal and kidney-specific Na+\/H+exchanger isoform (NHE-3).J Biol Chem267: 9340\u20139346, 1992.","DOI":"10.1016\/S0021-9258(19)50429-X"},{"key":"R78","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.2000.278.4.H1030"},{"key":"R79","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00759.x"},{"key":"R80","unstructured":"Wang T, Chan YL.Mechanism of angiotensin II action on proximal tubular transport.J Pharmacol Exp Ther252: 689\u2013695, 1990."},{"key":"R81","doi-asserted-by":"publisher","DOI":"10.1172\/JCI112325"},{"key":"R82","doi-asserted-by":"publisher","DOI":"10.1677\/joe.0.1250457"},{"key":"R83","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1991.117"},{"key":"R84","doi-asserted-by":"publisher","DOI":"10.1038\/374636a0"},{"key":"R85","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00013.2003"},{"key":"R86","doi-asserted-by":"publisher","DOI":"10.1677\/joe.0.1490217"},{"key":"R87","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000064700.58048.C1"},{"key":"R88","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00287.2005"},{"key":"R89","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00520.2005"},{"key":"R90","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0500423102"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00516.2006","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,5,11]],"date-time":"2023-05-11T00:15:20Z","timestamp":1683764120000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00516.2006"}},"issued":{"date-parts":[[2007,7]]},"references-count":90,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2007,7]]}},"alternative-id":["10.1152\/ajprenal.00516.2006"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00516.2006","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2007,7]]}},{"indexed":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T19:05:23Z","timestamp":1773428723034,"version":"3.50.1"},"reference-count":39,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2005,5]]},"abstract":"<jats:p>Caspase-1-deficient (\u2212\/\u2212) mice are protected against sepsis-induced hypotension and mortality. We investigated the role of caspase-1 and its associated cytokines in a nonhypotensive model of endotoxemic acute renal failure (ARF). Mice were injected intraperitoneally with 2.5 mg of LPS that induces endotoxemic ARF. On immunoblot analysis of whole kidney, there was an increase in caspase-1 protein in LPS-treated mice compared with vehicle-treated controls. In LPS-treated mice, the glomerular filtration rate (GFR) was significantly higher in caspase-1 \u2212\/\u2212 vs. wild-type mice at 16 and 36 h after LPS. To determine the mechanism of this protection, the caspase-1-activated cytokines IL-1\u03b2 and IL-18 were investigated. IL-1\u03b2 and IL-18 protein were significantly increased in the kidneys of LPS- vs. vehicle-treated mice. To determine the role of these cytokines, mice were treated with recombinant IL-1 receptor antagonist (IL-1Ra) or IL-18-neutralizing antiserum. In LPS-treated mice, GFR was not different in IL-1Ra-treated or IL-18-neutralizing antiserum-treated or combination therapy (IL-1Ra plus IL-18-neutralizing antiserum-treated) compared with control mice. In addition, tubular cell apoptosis, neutrophil infiltration, myeloperoxidase activity, caspase-3 activity, and calpain activity were not different between wild-type and caspase-1 \u2212\/\u2212 mice with endotoxemic ARF. In LPS- vs. vehicle-treated wild-type mice, renal IL-1\u03b1 was significantly increased. In both LPS- and vehicle-treated caspase-1 \u2212\/\u2212 mice, renal IL-1\u03b1 was very low. In summary, caspase-1 \u2212\/\u2212 mice are functionally protected against endotoxemic ARF. Neutralization of IL-1\u03b2 and IL-18 is not functionally protective. The role of the intracellular proinflammatory cytokine IL-1\u03b1 in endotoxemic ARF merits further study.<\/jats:p>","DOI":"10.1152\/ajprenal.00130.2004","type":"journal-article","created":{"date-parts":[[2005,1,12]],"date-time":"2005-01-12T03:14:02Z","timestamp":1105499642000},"page":"F997-F1004","source":"Crossref","is-referenced-by-count":83,"title":["Endotoxemic acute renal failure is attenuated in caspase-1-deficient mice"],"prefix":"10.1152","volume":"288","author":[{"given":"Wei","family":"Wang","sequence":"first","affiliation":[]},{"given":"Sarah","family":"Faubel","sequence":"additional","affiliation":[]},{"given":"Danica","family":"Ljubanovic","sequence":"additional","affiliation":[]},{"given":"Amit","family":"Mitra","sequence":"additional","affiliation":[]},{"given":"Sandor A.","family":"Falk","sequence":"additional","affiliation":[]},{"given":"Jun","family":"Kim","sequence":"additional","affiliation":[]},{"given":"Yunxia","family":"Tao","sequence":"additional","affiliation":[]},{"given":"Andrei","family":"Soloviev","sequence":"additional","affiliation":[]},{"given":"Leonid L.","family":"Reznikov","sequence":"additional","affiliation":[]},{"given":"Charles A.","family":"Dinarello","sequence":"additional","affiliation":[]},{"given":"Robert W.","family":"Schrier","sequence":"additional","affiliation":[]},{"given":"Charles L.","family":"Edelstein","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"crossref","unstructured":"AiuraK, Gelfand JA, Burke JF, Thompson RC, and Dinarello CA.Interleukin-1 (IL-1) receptor antagonist preventsStaphylococcusepidermidis-induced hypotension and reduces circulating levels of tumor necrosis factor and IL-1\u03b2 in rabbits.Infect Immun61: 3342\u20133350, 1993.","DOI":"10.1128\/IAI.61.8.3342-3350.1993"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1097\/00003246-199602000-00003"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000055652.37763.F7"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1999.277.3.R922"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.452"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.17.7662"},{"key":"R7","doi-asserted-by":"crossref","unstructured":"FantuzziG, Puren AJ, Harding MW, Livingston DJ, and Dinarello CA.Interleukin-18 regulation of interferon \u03b3 production and cell proliferation as shown in interleukin-1\u03b2-converting enzyme (caspase-1)-deficient mice.Blood91: 2118\u20132125, 1998.","DOI":"10.1182\/blood.V91.6.2118.2118_2118_2125"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1172\/JCI7501"},{"key":"R9","doi-asserted-by":"crossref","unstructured":"FantuzziG, Zheng H, Faggioni R, Benigni F, Ghezzi P, Sipe JD, Shaw AR, and Dinarello CA.Effect of endotoxin in IL-1\u03b2-deficient mice.J Immunol157: 291\u2013296, 1996.","DOI":"10.4049\/jimmunol.157.1.291"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.66010.x"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1038\/386619a0"},{"key":"R12","doi-asserted-by":"crossref","unstructured":"GobeG, Zhang XJ, Willgoss DA, Schoch E, Hogg NA, and Endre ZH.Relationship between expression of Bcl-2 genes and growth factors in ischemic acute renal failure in the rat.J Am Soc Nephrol11: 454\u2013467, 2000.","DOI":"10.1681\/ASN.V113454"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1126\/science.275.5297.206"},{"key":"R14","doi-asserted-by":"crossref","unstructured":"HaqM, Norman J, Saba SR, Ramirez G, and Rabb H.Role of IL-1 in renal ischemic reperfusion injury.J Am Soc Nephrol9: 614\u2013619, 1998.","DOI":"10.1681\/ASN.V94614"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1159\/000070996"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1016\/0160-5402(90)90013-B"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1182\/blood.V98.1.235"},{"key":"R18","doi-asserted-by":"crossref","unstructured":"KaplanskiG, Farnarier C, Kaplanski S, Porat R, Shapiro L, Bongrand P, and Dinarello CA.Interleukin-1 induces interleukin-8 secretion from endothelial cells by a juxtacrine mechanism.Blood84: 4242\u20134248, 1994.","DOI":"10.1182\/blood.V84.12.4242.bloodjournal84124242"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00740.x"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1126\/science.7535475"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1001\/jama.1996.03530430033035"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(95)90490-5"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1097-4644(199701)64:1<27::AID-JCB5>3.0.CO;2-1"},{"key":"R24","unstructured":"LianoF, Junco E, Pascual J, Madero R, and Verde E.The spectrum of acute renal failure in the intensive care unit compared with that seen in other settings. The Madrid Acute Renal Failure Study Group.Kidney Int Suppl66: S16\u2013S24, 1998."},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.1.F172"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1172\/JCI12089"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1172\/JCI0215623"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.164.5.2644"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1093\/oxfordjournals.ndt.a027256"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1001\/jama.1995.03520260039030"},{"key":"R31","unstructured":"RoncoC, Ricci Z, and Bellomo R.Importance of increased ultrafiltration volume and impact on mortality: sepsis and cytokine story and the role for CVVH.EDTNA ERCA J2: 13\u201318, 2002."},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1046\/j.1525-1594.2003.07289.x"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra032401"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.3.F509"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.29.17907"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1097\/00075198-200312000-00006"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00270.2001"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00323.2002"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0308705101"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00130.2004","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,5,1]],"date-time":"2023-05-01T13:53:29Z","timestamp":1682949209000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00130.2004"}},"issued":{"date-parts":[[2005,5]]},"references-count":39,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2005,5]]}},"alternative-id":["10.1152\/ajprenal.00130.2004"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00130.2004","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2005,5]]}},{"indexed":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T19:34:46Z","timestamp":1773430486282,"version":"3.50.1"},"reference-count":29,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2008,10]]},"abstract":"<jats:p> Extracellular ATP is an autocrine\/paracrine factor that regulates renal function. Transient receptor potential vanilloid (TRPV) 4 is a cation channel that mediates release of autocrine\/paracrine factors by acting as an osmosensor. The renal medulla, and therefore the thick ascending limb, is exposed to osmotic stress. We hypothesize that reduced osmolality stimulates ATP release from the thick ascending limb via transient receptor potential vanilloid (TRPV) 4 activation. We measured ATP release by medullary thick ascending limb suspensions after reducing bath osmolality from 350 to 323 mosmol\/kgH<jats:sub>2<\/jats:sub>O, using the luciferin-luciferase assay. Decreasing osmolality stimulated ATP release compared with control (38.9 \u00b1 7.2 vs. 2.4 \u00b1 1.0 pmol\/mg protein; n = 6, P &lt; 0.01). To examine the role of TRPV4, we used 1) Ca-free solutions, 2) a TRPV4 inhibitor, 3) small interfering (si) RNA against TRPV4, and 4) a TRPV4 activator. Removal of Ca completely blocked osmolality-induced ATP release (42.2 \u00b1 5.9 vs. 2.6 \u00b1 1.5 pmol\/mg protein; n = 6, P &lt; 0.01). In the presence of the TRPV4-selective inhibitor ruthenium red, osmolality-induced ATP release was blocked by 73% (56.4 \u00b1 19.9 vs. 8.8 \u00b1 2.3 pmol\/mg protein; n = 6; P &lt; 0.03). In vivo treatment of thick ascending limbs with siRNA against TRPV4 decreased osmolality-induced ATP release by 62% (31.5 \u00b1 3.4 vs. 12.4 \u00b1 1.1 pmol\/mg protein; n = 6; P &lt; 0.01), while reducing TRPV4 expression by 74% compared with the nontreated kidney. Treatment with scrambled siRNA did not affect TRPV4 expression and\/or osmolality-induced ATP release. Finally, in the absence of changes in osmolality, the specific TRPV4 agonist 4\u03b1-PDD increased ATP release (3.6 \u00b1 0.9 vs. 25.4 \u00b1 7.4 pmol\/mg protein; n = 6; P &lt; 0.04). We concluded that decreases in osmolality stimulate ATP release by thick ascending limbs and this effect is mediated by TRPV4 activation. <\/jats:p>","DOI":"10.1152\/ajprenal.90365.2008","type":"journal-article","created":{"date-parts":[[2008,8,6]],"date-time":"2008-08-06T20:55:10Z","timestamp":1218056110000},"page":"F1090-F1095","source":"Crossref","is-referenced-by-count":51,"title":["TRPV4 mediates hypotonicity-induced ATP release by the thick ascending limb"],"prefix":"10.1152","volume":"295","author":[{"given":"Guillermo B.","family":"Silva","sequence":"first","affiliation":[]},{"given":"Jeffrey L.","family":"Garvin","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M409708200"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.ph.38.030176.000345"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1016\/j.exer.2007.02.007"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000035243.66189.92"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.267.6.F998"},{"key":"R6","doi-asserted-by":"crossref","unstructured":"Edwards A, Delong MJ, Pallone TL. Interstitial water and solute recovery by inner medullary vasa recta. Am J Physiol Renal Physiol 278: F257\u2013F269, 2000.","DOI":"10.1152\/ajprenal.2000.278.2.F257"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.252.1.F1"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.24.14906"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1007\/s002329900483"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1172\/JCI31766"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0705964104"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1988.255.5.F962"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00209.2004"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00465.2005"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.6.F927"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00336.2003"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00075.2002"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00559.2002"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.37.2.753"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1291\/hypres.27.791"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00827.x"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M700290200"},{"key":"R24","unstructured":"Plant TD, Strotmann R. TRPV4. In: Handbook of Experimental Pharmacology. Berlin: Springer-Verlag, 2007, p. 189\u2013205."},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1983.244.5.F472"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000197954.93874.ef"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000236646.83354.51"},{"key":"R28","doi-asserted-by":"crossref","unstructured":"Taouil K, Hannaert P. Evidence for the involvement of K+ channels and K+-Cl- cotransport in the regulatory volume decrease of newborn rat cardiomyocytes. Pfl\u00fcgers Arch 439: 56\u201366, 1999.","DOI":"10.1007\/s004249900117"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M200062200"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00462.2006"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.90365.2008","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:02:04Z","timestamp":1567969324000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.90365.2008"}},"issued":{"date-parts":[[2008,10]]},"references-count":29,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2008,10]]}},"alternative-id":["10.1152\/ajprenal.90365.2008"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.90365.2008","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2008,10]]}},{"indexed":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T19:28:32Z","timestamp":1773430112555,"version":"3.50.1"},"reference-count":40,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2011,5]]},"abstract":"<jats:p>\n                    The present study tested the hypothesis that intrarenal adenoviral transfer of an intracellular cyan fluorescent fusion of angiotensin II (ECFP\/ANG II) selectively in proximal tubules of the kidney increases blood pressure by activating AT\n                    <jats:sub>1<\/jats:sub>\n                    (AT\n                    <jats:sub>1a<\/jats:sub>\n                    ) receptors. Intrarenal transfer of ECFP\/ANG II was induced in the superficial cortex of rat and mouse kidneys, and the sodium and glucose cotransporter 2 (sglt2) promoter was used to drive ECFP\/ANG II expression selectively in proximal tubules. Intrarenal transfer of ECFP\/ANG II induced a time-dependent, proximal tubule-selective expression of ECFP\/ANG II in the cortex, which peaked at 2 wk and was sustained for 4 wk. ECFP\/ANG II expression was low in the glomeruli and the entire medulla and was absent in the contralateral kidney or extrarenal tissues. At its peak of expression in proximal tubules at day 14, ANG II was increased by twofold in the kidney ( P &lt; 0.01) and more than threefold in proximal tubules ( P &lt; 0.01), but remained unchanged in plasma or urine. Systolic blood pressure was increased in ECFP\/ANG II-transferred rats by 28 \u00b1 6 mmHg ( P &lt; 0.01), whereas fractional sodium excretion was decreased by 20% ( P &lt; 0.01) and fractional lithium excretion was reduced by 24% ( P &lt; 0.01). These effects were blocked by losartan and prevented in AT\n                    <jats:sub>1a<\/jats:sub>\n                    knockout mice. Transfer of a scrambled ECFP\/ANG IIc had no effects on blood pressure, kidney, and proximal tubule ANG II, or sodium excretion. These results provide evidence that proximal tubule-selective transfer of an intracellular ANG II fusion protein increases blood pressure by activating AT\n                    <jats:sub>1a<\/jats:sub>\n                    receptors and increasing sodium reabsorption in proximal tubules.\n                  <\/jats:p>","DOI":"10.1152\/ajprenal.00329.2010","type":"journal-article","created":{"date-parts":[[2011,2,9]],"date-time":"2011-02-09T21:10:40Z","timestamp":1297285840000},"page":"F1076-F1088","source":"Crossref","is-referenced-by-count":46,"title":["Intrarenal transfer of an intracellular fluorescent fusion of angiotensin II selectively in proximal tubules increases blood pressure in rats and mice"],"prefix":"10.1152","volume":"300","author":[{"given":"Xiao C.","family":"Li","sequence":"first","affiliation":[{"name":"Laboratory of Receptor and Signal Transduction, Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi;"}]},{"given":"Julia L.","family":"Cook","sequence":"additional","affiliation":[{"name":"Ochsner Clinic Foundation, New Orleans, Louisiana;"}]},{"given":"Isabelle","family":"Rubera","sequence":"additional","affiliation":[{"name":"UMR-CNRS 6548, University of Nice-Sophia Antipolis, Parc Valrose, Nice, France; and"}]},{"given":"Michel","family":"Tauc","sequence":"additional","affiliation":[{"name":"UMR-CNRS 6548, University of Nice-Sophia Antipolis, Parc Valrose, Nice, France; and"}]},{"given":"Fan","family":"Zhang","sequence":"additional","affiliation":[{"name":"Division of Hypertension and Vascular Research, Department of Internal Medicine, Henry Ford Hospital, Detroit, Michigan"}]},{"given":"Jia L.","family":"Zhuo","sequence":"additional","affiliation":[{"name":"Laboratory of Receptor and Signal Transduction, Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi;"},{"name":"Division of Hypertension and Vascular Research, Department of Internal Medicine, Henry Ford Hospital, Detroit, Michigan"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/j.regpep.2004.04.004"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00238.2006"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/j.yjmcc.2005.11.014"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/j.yjmcc.2003.09.021"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1161\/hh2401.101270"},{"key":"B6","doi-asserted-by":"crossref","first-page":"415","DOI":"10.1016\/S0031-6997(24)01458-3","volume":"52","author":"deGasparo M","year":"2000","journal-title":"Pharmacol Rev"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.44.28142"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90766.2008"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.109.141622"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.79.4.765"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00727.2009"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/j.tem.2007.05.001"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/physiolgenomics.00120.2003"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90734.2008"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00489.2006"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2009.134"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00463.2006"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00398.2007"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00432.2007"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00374.2004"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00287.2006"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.162"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00827.x"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00504.2006"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00317.2005"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2009.04.126"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.35.6.1189"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00027.2010"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000133023.89251.01"},{"key":"B30","doi-asserted-by":"crossref","first-page":"205","DOI":"10.1016\/S0031-6997(25)00446-6","volume":"45","author":"Timmermans PB","year":"1993","journal-title":"Pharmacol Rev"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1093\/cvr\/cvq004"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M106132200"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1981.241.4.F403"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00379.2007"},{"key":"B35","first-page":"1739","volume-title":"Hypertension: Pathology, Diagnosis & Management","author":"Zhuo JL","year":"1995","edition":"2"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1992.sp019214"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.14.6.666"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1161\/hy0102.100780"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.3317\/jraas.2007.003"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00269.2005"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00329.2010","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,3,2]],"date-time":"2025-03-02T08:37:40Z","timestamp":1740904660000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00329.2010"}},"issued":{"date-parts":[[2011,5]]},"references-count":40,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2011,5]]}},"alternative-id":["10.1152\/ajprenal.00329.2010"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00329.2010","relation":{"has-review":[{"id-type":"doi","id":"10.3410\/f.11937957.13059055","asserted-by":"object"},{"id-type":"doi","id":"10.3410\/f.11937957.13536055","asserted-by":"object"}]},"ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2011,5]]}},{"indexed":{"date-parts":[[2026,3,11]],"date-time":"2026-03-11T23:31:55Z","timestamp":1773271915850,"version":"3.50.1"},"reference-count":51,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2003,5,1]]},"abstract":"<jats:p>Nucleoside transporters are important in the disposition of nucleosides and nucleoside analogs in the kidney. Two human equilibrative nucleoside transporters have been cloned and characterized, hENT1 and hENT2. The primary goal of this study was to localize these transporters in polarized renal epithelia. hENT1 and hENT2 were tagged with green fluorescence protein, stably expressed in renal epithelial cells, and localized by immunofluorescence and functional analysis. Our data demonstrated that both transporters are expressed on the basolateral membrane. hENT1 is also present on the apical membrane. Additionally, we examined the importance to basolateral targeting of two COOH-terminal targeting motifs: a RXXV motif for hENT1 and a dileucine repeat for hENT2. Neither motif appeared to affect targeting, but the dileucine repeat was implicated in surface expression of hENT2. In addition, a splice variant of hENT2 was identified that is predicted to result in a 156-residue COOH-terminal truncation. This variant had a tissue distribution similar to wild-type hENT2 but was retained intracellularly. These data suggest that hENT1 and hENT2 on the basolateral membrane function with concentrative nucleoside transporters on the apical membrane to mediate active reabsorption of nucleosides within the kidney.<\/jats:p>","DOI":"10.1152\/ajprenal.00215.2002","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:38:06Z","timestamp":1425415086000},"page":"F902-F910","source":"Crossref","is-referenced-by-count":66,"title":["Localization of human equilibrative nucleoside transporters, hENT1 and hENT2, in renal epithelial cells"],"prefix":"10.1152","volume":"284","author":[{"given":"Lara M.","family":"Mangravite","sequence":"first","affiliation":[{"name":"Department of Biopharmaceutical Sciences, University of California, San Francisco, San Francisco, California 94143-0446"}]},{"given":"Guangqing","family":"Xiao","sequence":"additional","affiliation":[{"name":"Department of Biopharmaceutical Sciences, University of California, San Francisco, San Francisco, California 94143-0446"}]},{"given":"Kathleen M.","family":"Giacomini","sequence":"additional","affiliation":[{"name":"Department of Biopharmaceutical Sciences, University of California, San Francisco, San Francisco, California 94143-0446"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/S0304-4157(98)00005-7"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1042\/bj2320681"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.1990.259.3.G504"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.268.3.F391"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-2952(97)00170-6"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2736(94)90236-4"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.9.5288"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.1.186"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2736(90)90350-W"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1023\/A:1007510801253"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2736(92)90010-J"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1038\/nm0197-89"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1042\/bj3280739"},{"key":"B14","first-page":"25","volume":"25","author":"Hamilton SR","year":"2001","journal-title":"J Biol Chem"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1016\/S0378-1119(00)00555-2"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1521-1878(199907)21:7<558::AID-BIES4>3.0.CO;2-R"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.17-01-00032.1997"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/S0028-3908(00)00207-0"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1042\/bj3520363"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.16.10731"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1046\/j.1471-4159.2000.740621.x"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M204986200"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2736(88)90283-0"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.258.5.F1203"},{"key":"B25","first-page":"154","volume":"13","author":"Le Hir M.","year":"1990","journal-title":"Renal Physiol Biochem"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2362.1985.tb00154.x"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.5.F879"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-5793(97)00314-1"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-5793(99)01221-1"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/S0955-0674(00)00120-4"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.1998.274.2.G261"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.2000.4205"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M007746200"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1997.272.2.C707"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1996.1419"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.2.995"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.3168\/jds.S0022-0302(01)74515-8"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.6.F864"},{"key":"B39","doi-asserted-by":"crossref","first-page":"19419","DOI":"10.1016\/S0021-9258(19)77649-2","volume":"263","author":"Vijayalakshmi D","year":"1988","journal-title":"J Biol Chem"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.273.6.F1058"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1210\/mend-5-11-1707"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.275.12.8375"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1016\/S0005-2736(99)00045-0"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.23.13733"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1042\/bj2640223"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1042\/bj2740027"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1124\/mol.59.2.339"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.45.28423"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M200966200"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1999.79.1.73"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1042\/bj3360257"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00215.2002","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,5,1]],"date-time":"2022-05-01T09:37:40Z","timestamp":1651397860000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00215.2002"}},"issued":{"date-parts":[[2003,5,1]]},"references-count":51,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2003,5,1]]}},"alternative-id":["10.1152\/ajprenal.00215.2002"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00215.2002","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2003,5,1]]}},{"indexed":{"date-parts":[[2026,3,14]],"date-time":"2026-03-14T03:45:38Z","timestamp":1773459938517,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1990,9,1]]},"abstract":"<jats:p> The terminal part of the inner medullary collecting duct (terminal IMCD) is unique among collecting duct segments in part because its permeability to urea is regulated by vasopressin. The urea permeability can rise to extremely high levels (greater than 100 x 10(-5) cm\/s) in response to vasopressin. Recent studies in isolated perfused IMCD segments have established that the rapid movement of urea across the tubule epithelium occurs via a specialized urea transporter, presumably an intrinsic membrane protein, present in both the apical and basolateral membranes. This urea transporter has properties similar to those of the urea transporters in mammalian erythrocytes and in toad urinary bladder, namely, inhibition by phloretin, inhibition by urea analogues, saturation kinetics in equilibrium-exchange experiments, and regulation by vasopressin. The urea transport pathway is distinct from and independent of the vasopressin-regulated water channel. The increase in transepithelial urea transport in response to vasopressin is mediated by adenosine 3',5'-cyclic monophosphate and is associated with an increase in the urea permeability of the apical membrane. However, little is known about the physical events associated with the activation or insertion of urea transporters in the apical membrane. Because of the importance of this transporter to the urinary concentrating mechanism, efforts toward understanding its molecular structure and the molecular basis of its regulation appear to be justified. <\/jats:p>","DOI":"10.1152\/ajprenal.1990.259.3.f393","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T22:21:18Z","timestamp":1513981278000},"page":"F393-F401","source":"Crossref","is-referenced-by-count":20,"title":["The vasopressin-regulated urea transporter in renal inner medullary collecting duct"],"prefix":"10.1152","volume":"259","author":[{"given":"M. A.","family":"Knepper","sequence":"first","affiliation":[{"name":"Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung,and Blood Institute, National Institutes of Health, Bethesda, Maryland20892."}]},{"given":"R. A.","family":"Star","sequence":"additional","affiliation":[{"name":"Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung,and Blood Institute, National Institutes of Health, Bethesda, Maryland20892."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1990.259.3.F393","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:16:52Z","timestamp":1567970212000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1990.259.3.F393"}},"issued":{"date-parts":[[1990,9,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1990,9,1]]}},"alternative-id":["10.1152\/ajprenal.1990.259.3.F393"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1990.259.3.f393","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1990,9,1]]}},{"indexed":{"date-parts":[[2026,3,14]],"date-time":"2026-03-14T03:13:56Z","timestamp":1773458036581,"version":"3.50.1"},"reference-count":61,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2009,12]]},"abstract":"<jats:p>Cyclooxygenase-2 activity is required for the development of lithium-induced polyuria. However, the involvement of a specific, terminal prostaglandin (PG) isomerase has not been evaluated. The present study was undertaken to assess lithium-induced polyuria in mice deficient in microsomal prostaglandin E synthase-1 (mPGES-1). A 2-wk administration of LiCl (4 mmol\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7day<jats:sup>\u22121<\/jats:sup>ip) in mPGES-1 +\/+ mice led to a marked polyuria with hyposmotic urine. This was associated with elevated renal mPGES-1 protein expression and increased urine PGE<jats:sub>2<\/jats:sub>excretion. In contrast, mPGES-1 \u2212\/\u2212 mice were largely resistant to lithium-induced polyuria and a urine concentrating defect, accompanied by nearly complete blockade of high urine PGE<jats:sub>2<\/jats:sub>and cAMP output. Immunoblotting, immunohistochemistry, and quantitative (q) RT-PCR consistently detected a significant decrease in aquaporin-2 (AQP2) protein expression in both the renal cortex and medulla of lithium-treated +\/+ mice. This decrease was significantly attenuated in the \u2212\/\u2212 mice. qRT-PCR detected similar patterns of changes in AQP2 mRNA in the medulla but not in the cortex. Similarly, the total protein abundance of the Na-K-2Cl cotransporter (NKCC2) in the medulla but not in the cortex of the +\/+ mice was significantly reduced by lithium treatment. In contrast, the dowregulation of renal medullary NKCC2 expression was significantly attenuated in the \u2212\/\u2212 mice. We conclude that mPGES-1-derived PGE<jats:sub>2<\/jats:sub>mediates lithium-induced polyuria likely via inhibition of AQP2 and NKCC2 expression.<\/jats:p>","DOI":"10.1152\/ajprenal.00117.2009","type":"journal-article","created":{"date-parts":[[2009,8,20]],"date-time":"2009-08-20T00:59:07Z","timestamp":1250729947000},"page":"F1689-F1696","source":"Crossref","is-referenced-by-count":34,"title":["Mice lacking mPGES-1 are resistant to lithium-induced polyuria"],"prefix":"10.1152","volume":"297","author":[{"given":"Zhanjun","family":"Jia","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, University of Utah, and Veterans Affairs Medical Center, Salt Lake City, Utah"}]},{"given":"Haiping","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Utah, and Veterans Affairs Medical Center, Salt Lake City, Utah"}]},{"given":"Tianxin","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Utah, and Veterans Affairs Medical Center, Salt Lake City, Utah"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1976.99"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000089566.28106.F6"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.2165\/00002018-199921060-00002"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(87)80098-7"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.1.F12"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1097\/01.ju.0000143882.52960.ee"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00383.2005"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00266.2003"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1172\/JCI111901"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1172\/JCI112465"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1984.247.5.F784"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1172\/JCI105804"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.259.2.F318"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115227"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.265.5.F643"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2760(95)00194-8"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/j.prostaglandins.2008.10.003"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/j.prostaglandins.2008.10.003"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.449"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.108.111229"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000251306.40546.08"},{"key":"B22","doi-asserted-by":"crossref","first-page":"939","DOI":"10.1152\/ajplegacy.1967.213.4.939","volume":"213","author":"Johnston HH","year":"1967","journal-title":"Am J Physiol"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2006.03.004"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00366.2007"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00176.2003"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00210.x"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00114.2004"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.3.F552"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.3109\/08860229709026274"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005080884"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.02314-06"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117863"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1097\/00007611-199308000-00027"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.2174\/138161206776055912"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000139689.94776.7A"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2007.07.180"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.46.6.739"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00291.2004"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0800001105"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2008.03.002"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.4.1013"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.90.24.11663"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00061.2005"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00287.2003"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00304.2002"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M309325200"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00287.2004"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00305.2004"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00493.x"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.52.33157"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90478.2008"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00132.2007"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1172\/JCI109487"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1172\/JCI108733"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1988.254.6.R863"},{"key":"B56","doi-asserted-by":"crossref","first-page":"666","DOI":"10.1681\/ASN.V103666","volume":"10","author":"Timmer RT","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1332766100"},{"key":"B58","first-page":"S93","volume":"42","author":"Walker RG","year":"1993","journal-title":"Kidney Int Suppl"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.108.138776"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002326"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.3.F388"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00117.2009","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,10,9]],"date-time":"2021-10-09T21:09:28Z","timestamp":1633813768000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00117.2009"}},"issued":{"date-parts":[[2009,12]]},"references-count":61,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2009,12]]}},"alternative-id":["10.1152\/ajprenal.00117.2009"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00117.2009","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2009,12]]}},{"indexed":{"date-parts":[[2026,3,14]],"date-time":"2026-03-14T03:14:08Z","timestamp":1773458048124,"version":"3.50.1"},"reference-count":61,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2003,3,1]]},"abstract":"<jats:p>A TP receptor (TP-R) mimetic causes salt-sensitive hypertension and renal afferent arteriolar vasoconstriction. TP-Rs mediate effects of ANG II on renal vascular resistance and drinking. Therefore, we investigated the hypothesis that thromboxane A<jats:sub>2<\/jats:sub>synthase (TxA<jats:sub>2<\/jats:sub>-S) and\/or TP-R expression is regulated by salt and\/or ANG II. Rats ( n= 6) received high-salt (HS) or low-salt (LS) diets. Additional HS-diet rats received ANG II while other HS- and LS-diet rats received the AT<jats:sub>1<\/jats:sub>receptor (AT<jats:sub>1<\/jats:sub>-R) antagonist losartan. Excretion of thromboxane B<jats:sub>2<\/jats:sub>by conscious rats was increased with the HS diet compared with the LS diet (126 \u00b1 10 vs. 48 \u00b1 5 pmol\/24 h, respectively; P &lt; 0.01). The mRNA abundance for TP-Rs (relative to \u03b2-actin) in the kidney cortex was enhanced 30% by the HS diet ( P&lt; 0.001) and was reduced 50% by the addition of ANG II ( P &lt; 0.001). However, during losartan administration, the effects of salt were reversed; mRNA more than doubled during the LS diet ( P &lt; 0.001). Similarly, the mRNA abundance for TP-Rs in the brain stem was reduced by 50% with the addition of ANG II ( P &lt; 0.001) and during losartan administration was almost doubled by the LS diet ( P &lt; 0.001). The mRNA abundance for TxA<jats:sub>2<\/jats:sub>-S in the kidney cortex also was increased many times with the HS diet ( P &lt; 0.001). In contrast, the mRNA for TxA<jats:sub>2<\/jats:sub>-S in the brain was unaffected by salt. ANG II did not affect TxA<jats:sub>2<\/jats:sub>-S at either site. During losartan administration, TxA<jats:sub>2<\/jats:sub>-S increased modestly in the brain stem with the LS diet. mRNA abundance for TP-Rs in the kidney cortex and brain stem is suppressed by ANG II acting on AT<jats:sub>1<\/jats:sub>-Rs. In the absence of AT<jats:sub>1<\/jats:sub>-Rs, expression of TP-Rs at both sites is enhanced by LS intake. In contrast, ANG II does not affect the mRNA abundance for TxA<jats:sub>2<\/jats:sub>-S. Expression of TxA<jats:sub>2<\/jats:sub>-S is enhanced by HS intake in the kidney cortex but by LS intake in the brain stem only during losartan administration. Thus TP-Rs are strongly dependent on ANG II acting on AT<jats:sub>1<\/jats:sub>-Rs, whereas TxA<jats:sub>2<\/jats:sub>-S is regulated differentially in the kidney cortex and brain stem by salt intake.<\/jats:p>","DOI":"10.1152\/ajprenal.00256.2002","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:37:13Z","timestamp":1425415033000},"page":"F525-F531","source":"Crossref","is-referenced-by-count":15,"title":["Thromboxane synthase and TP receptor mRNA in rat kidney and brain: effects of salt intake and ANG II"],"prefix":"10.1152","volume":"284","author":[{"given":"Christopher S.","family":"Wilcox","sequence":"first","affiliation":[{"name":"Division of Nephrology and Hypertension and Center for Hypertension and Renal Disease Research, Georgetown University Medical Center, Washington, DC 20007"}]},{"given":"William J.","family":"Welch","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension and Center for Hypertension and Renal Disease Research, Georgetown University Medical Center, Washington, DC 20007"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118108"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.253.3.F377"},{"key":"B3","doi-asserted-by":"crossref","first-page":"6109","DOI":"10.1016\/S0021-9258(17)37576-2","volume":"269","author":"Borg C","year":"1994","journal-title":"J Biol Chem"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.174"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.256.1.F152"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.67.3.674"},{"key":"B7","first-page":"715","volume":"51","author":"Chlopicki S","year":"2000","journal-title":"J Physiol Pharmacol"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1002\/jnr.490200116"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.27.5.1173"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/0922-4106(92)90144-K"},{"key":"B11","doi-asserted-by":"crossref","first-page":"669","DOI":"10.1016\/S0022-3565(25)20430-X","volume":"258","author":"Folger WH","year":"1991","journal-title":"J Pharmacol Exp Ther"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1997.272.5.R1493"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1997.273.2.H734"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/0929-7855(95)00023-J"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.281.1.F1"},{"key":"B16","doi-asserted-by":"crossref","first-page":"25","DOI":"10.1681\/ASN.V8125","volume":"8","author":"Hayashi K","year":"1997","journal-title":"J Am Soc Nephrol"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/0167-4889(94)00225-4"},{"key":"B19","first-page":"R865","volume":"10","author":"Kitiyakara C","year":"2002","journal-title":"Am J Physiol"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/S0952-3278(98)90152-1"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1097\/00005344-199808000-00005"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.74.2.197"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.17.4.517"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.18.2.158"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1986.250.4.F619"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.14.4.396"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.6.F1131"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1986.251.6.F1029"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1989.69.4.1347"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/S0304-4165(98)00109-3"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-199001000-00012"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.11.6.758"},{"key":"B33","doi-asserted-by":"crossref","first-page":"90","DOI":"10.1016\/S0022-3565(25)12486-5","volume":"253","author":"Mistry M","year":"1990","journal-title":"J Pharmacol Exp Ther"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-8993(10)80013-7"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1016\/0014-2999(89)90331-2"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1111\/j.1432-1033.1993.tb17671.x"},{"key":"B37","first-page":"175","volume":"3","author":"N\u00fcsing R","year":"1990","journal-title":"Eicosanoids"},{"key":"B38","first-page":"159","volume":"13","author":"Osanai T","year":"1991","journal-title":"Clin Exp Hypertens"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1097\/00007890-199502270-00008"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.35.1.476"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.34.4.943"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.2.F302"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(87)91361-8"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1016\/0006-2952(84)90099-6"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1161\/01.STR.13.4.494"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1989.256.3.R616"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1210\/endo.137.11.8895394"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1159\/000134513"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2000.00380.x"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1536\/ihj.36.389"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1016\/S0090-6980(97)00059-2"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1016\/0090-6980(87)90038-4"},{"key":"B55","first-page":"277","volume":"2","author":"Welch WJ","year":"1992","journal-title":"Eur J Int Med"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.273.6.F976"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1172\/JCI113529"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115790"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1996.271.4.R891"},{"key":"B60","first-page":"124","volume":"6","author":"Wilcox CS","year":"1993","journal-title":"J Nephrol"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1985.116"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1991.319"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1988.12"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1016\/0006-291X(91)91060-P"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00256.2002","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,5,20]],"date-time":"2025-05-20T17:51:37Z","timestamp":1747763497000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00256.2002"}},"issued":{"date-parts":[[2003,3,1]]},"references-count":61,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2003,3,1]]}},"alternative-id":["10.1152\/ajprenal.00256.2002"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00256.2002","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2003,3,1]]}},{"indexed":{"date-parts":[[2026,3,14]],"date-time":"2026-03-14T03:38:10Z","timestamp":1773459490150,"version":"3.50.1"},"reference-count":68,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2007,9]]},"abstract":"<jats:p>Arginine vasopressin (AVP) is essential for maintaining body fluid homeostasis. The antidiuretic effects of AVP are initialized by binding of AVP to the type-2 vasopressin receptor (V2R) in the kidney collecting duct (CD), resulting in the exocytic insertion of aquaporin-2 (AQP-2) water channels into the apical plasma membrane. In this study, we describe the generation and characterization of a polyclonal antibody targeted against the NH<jats:sub>2<\/jats:sub>terminus of the rat V2R. HEK-293 cells overexpressing the rat, mouse, or human V2R showed strong intracellular immunolabeling. Additionally, immunostaining of M-1 kidney cells expressing a V2R-green fluorescent protein (GFP) fusion construct showed colocalization between GFP and antibody-specific V2R labeling. Immunoblots of rat kidney showed 43- and 47-kDa proteins in all zones that were both reduced to 34-kDa by N-glycosidase F. Protein solubilization with nonionic detergents or the use of homobifunctional cross-linkers demonstrated that the rat V2R exists as a protein complex in native kidney. Immunohistochemistry of rat and mouse kidney revealed abundant labeling of the CD. Double-labeling confocal immunofluorescence microscopy [using distal convoluted tubule\/connecting tubule (CNT)-specific marker calbindin and CNT\/CD-specific marker AQP-2] showed V2R labeling in both CD and CNT. There was a complete absence of labeling in vascular structures and other renal tubules, including the thick ascending limb (TAL), although RT-PCR of microdissected tubules showed expression of V2R mRNA in TAL. Confocal microscopy demonstrated that at the subcellular level, V2R labeling was predominantly intracellular in normal kidneys, although some staining was apparent in basolateral membrane domains. Confocal microscopy of isolated inner medullary collecting duct tubules showed that the V2R is expressed both intracellularly and in basolateral membrane domains.<\/jats:p>","DOI":"10.1152\/ajprenal.00316.2006","type":"journal-article","created":{"date-parts":[[2007,6,7]],"date-time":"2007-06-07T00:54:51Z","timestamp":1181177691000},"page":"F748-F760","source":"Crossref","is-referenced-by-count":90,"title":["Cellular and subcellular distribution of the type-2 vasopressin receptor in the kidney"],"prefix":"10.1152","volume":"293","author":[{"given":"Robert A.","family":"Fenton","sequence":"first","affiliation":[]},{"given":"Lone","family":"Br\u00f8nd","sequence":"additional","affiliation":[]},{"given":"S\u00f8ren","family":"Nielsen","sequence":"additional","affiliation":[]},{"given":"Jeppe","family":"Praetorius","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1007\/BF00370519"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1038\/357333a0"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1042\/BC20040054"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00353.2004"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00278.2003"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00387.2002"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00049.2006"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M408565200"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.1.F78"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00234.2002"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.5.F874"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1111\/j.0953-8194.2004.01188.x"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.91.19.8984"},{"key":"R14","doi-asserted-by":"crossref","unstructured":"Earm JH, Christensen BM, Frokiaer J, Marples D, Han JS, Knepper MA, Nielsen S.Decreased aquaporin-2 expression and apical plasma membrane delivery in kidney collecting ducts of polyuric hypercalcemic rats.J Am Soc Nephrol9: 2181\u20132193, 1998.","DOI":"10.1681\/ASN.V9122181"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00048.x"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.270.4.F657"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.6.F926"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1053\/gast.2003.50143"},{"key":"R19","doi-asserted-by":"crossref","unstructured":"Gheorghiade M.The clinical effects of vasopressin receptor antagonists in heart failure.Cleve Clin J Med73, Suppl2: S24\u2013S33, 2006.","DOI":"10.3949\/ccjm.73.Suppl_2.S24"},{"key":"R20","unstructured":"Gottschalk CW, Mylle M.Micropuncture study of the mammalian urinary concentrating mechanism: evidence for the countercurrent hypothesis.Am J Physiol196: 927\u2013936, 1959."},{"key":"R21","unstructured":"Hill SJ.G-protein-coupled receptors: past, present and future.Br J Pharmacol147, Suppl1: S27\u2013S37, 2006."},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1979.46"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1210\/endo-102-4-1254"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1007\/BF00585973"},{"key":"R25","doi-asserted-by":"crossref","unstructured":"Jonassen TE, Nielsen S, Christensen S, Petersen JS.Decreased vasopressin-mediated renal water reabsorption in rats with compensated liver cirrhosis.Am J Physiol Renal Physiol275: F216\u2013F225, 1998.","DOI":"10.1152\/ajprenal.1998.275.2.F216"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118731"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1016\/j.jsb.2007.01.006"},{"key":"R28","doi-asserted-by":"crossref","unstructured":"Knepper MA, Kim GH, Fernandez-Llama P, Ecelbarger CA.Regulation of thick ascending limb transport by vasopressin.J Am Soc Nephrol10: 628\u2013634, 1999.","DOI":"10.1681\/ASN.V103628"},{"key":"R29","doi-asserted-by":"crossref","unstructured":"Krause G, Hermosilla R, Oksche A, Rutz C, Rosenthal W, Schulein R.Molecular and conformational features of a transport-relevant domain in the C-terminal tail of the vasopressin V(2) receptor.Mol Pharmacol57: 232\u2013242, 2000.","DOI":"10.1016\/S0026-895X(24)23194-1"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1999.277.1.H413"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.275.5.F724"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1038\/357336a0"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117863"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118628"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1981.240.3.F159"},{"key":"R36","unstructured":"Morel F, Chabardes D, Imbert-Teboul M, Le Bouffant F, Hus-Citharel A, Montegut M.Multiple hormonal control of adenylate cyclase in distal segments of the rat kidney.Kidney Int Suppl11: S55\u2013S62, 1982."},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1986.66.2.377"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1987.30"},{"key":"R39","doi-asserted-by":"crossref","unstructured":"Nielsen J, Kwon TH, Praetorius J, Kim YH, Frokiaer J, Knepper MA, Nielsen S.Segment-specific ENaC downregulation in kidney of rats with lithium-induced NDI.Am J Physiol Renal Physiol285: F1198\u2013F1209, 2003.","DOI":"10.1152\/ajprenal.00118.2003"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00024.2001"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.94.10.5450"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118222"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1210\/mend.16.4.0796"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1210\/endo.131.1.1535312"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1210\/endo.133.4.8404628"},{"key":"R46","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.5.F906"},{"key":"R47","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1997.273.1.R243"},{"key":"R48","doi-asserted-by":"publisher","DOI":"10.1124\/pr.57.3.1"},{"key":"R49","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2006.02.003"},{"key":"R50","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00491.2005"},{"key":"R51","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00404.2004"},{"key":"R52","doi-asserted-by":"publisher","DOI":"10.1093\/glycob\/9.7.731"},{"key":"R53","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-4615-4871-3_43"},{"key":"R54","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00426.x"},{"key":"R55","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000211"},{"key":"R56","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.275.4.2381"},{"key":"R57","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00132.2001"},{"key":"R58","doi-asserted-by":"publisher","DOI":"10.1172\/JCI116838"},{"key":"R59","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0305322101"},{"key":"R60","doi-asserted-by":"publisher","DOI":"10.1038\/sj.embor.7400052"},{"key":"R61","doi-asserted-by":"publisher","DOI":"10.1210\/me.2002-0222"},{"key":"R62","doi-asserted-by":"publisher","DOI":"10.1007\/BF00581564"},{"key":"R63","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1981.189"},{"key":"R64","doi-asserted-by":"publisher","DOI":"10.1016\/S1521-690X(03)00049-6"},{"key":"R65","doi-asserted-by":"publisher","DOI":"10.1159\/000094539"},{"key":"R66","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2001.012606"},{"key":"R67","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00411.2005"},{"key":"R68","doi-asserted-by":"publisher","DOI":"10.1021\/bi981162z"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00316.2006","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,1,17]],"date-time":"2025-01-17T01:13:10Z","timestamp":1737076390000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00316.2006"}},"issued":{"date-parts":[[2007,9]]},"references-count":68,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2007,9]]}},"alternative-id":["10.1152\/ajprenal.00316.2006"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00316.2006","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2007,9]]}},{"indexed":{"date-parts":[[2026,3,14]],"date-time":"2026-03-14T03:11:53Z","timestamp":1773457913350,"version":"3.50.1"},"reference-count":33,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2009,4]]},"abstract":"<jats:p> Uptake of substrate and electric charge was measured simultaneously in voltage-clamped Xenopus laevis oocytes expressing rat organic cation transporter 2 (rOCT2). At 0 mV, saturating substrate concentrations induced uptake of more positive elementary charges than monovalent organic cations, with charge-to-substrate ratios of 1.5 for guanidinium<jats:sup>+<\/jats:sup>, 3.5 for tetraethylammonium<jats:sup>+<\/jats:sup>, and 4.0 for 1-methyl-4-phenylpyridinium<jats:sup>+<\/jats:sup>. At negative holding potentials, the charge-to-substrate ratios decreased toward unity. At 0 mV, charge-to-substrate ratios higher than unity were observed at different extracellular pH and after replacement of extracellular Na<jats:sup>+<\/jats:sup>, K<jats:sup>+<\/jats:sup>, Ca<jats:sup>2+<\/jats:sup>, Mg<jats:sup>2+<\/jats:sup>, and\/or Cl<jats:sup>\u2212<\/jats:sup>. Charge-to-substrate ratios were not influenced by intracellular succinate<jats:sup>2\u2212<\/jats:sup> or glutarate<jats:sup>2\u2212<\/jats:sup>. The effects of membrane potential and ion substitution strongly suggest that the surplus of transported positive charge is not generated by passive ion permeabilities. Rather, we hypothetize that small cations are taken up together with organic cation substrates whereas the outward reorientation of the empty transporter is electroneutral. Nonselective cotransport of small cations was supported by the three-dimensional structures of rOCT2 in its inward-facing and outward-facing conformations, which we determined by homology modeling based on known corresponding structures of H<jats:sup>+<\/jats:sup>-lactose permease of E. coli, and by functional analysis of OCT mutants. In our model, the innermost cavity of the outward-open binding cleft is negatively charged by Glu448 and Asp475, whereas the inward-open innermost cavity is electroneutral, containing Asp379, Asp475, Lys215, and Arg440. Substitution of Glu448 by glutamine reduced the charge-to-TEA<jats:sup>+<\/jats:sup> ratio at 0 mV to unity. The observed charge excess associated with organic cation uptake into depolarized cells may contribute to tubular damage in renal failure. <\/jats:p>","DOI":"10.1152\/ajprenal.90323.2008","type":"journal-article","created":{"date-parts":[[2009,2,12]],"date-time":"2009-02-12T02:08:58Z","timestamp":1234404538000},"page":"F709-F722","source":"Crossref","is-referenced-by-count":19,"title":["Charge-to-substrate ratio during organic cation uptake by rat OCT2 is voltage dependent and altered by exchange of glutamate 448 with glutamine"],"prefix":"10.1152","volume":"296","author":[{"given":"Bernhard M.","family":"Schmitt","sequence":"first","affiliation":[]},{"given":"Dmitry","family":"Gorbunov","sequence":"additional","affiliation":[]},{"given":"Peter","family":"Schlachtbauer","sequence":"additional","affiliation":[]},{"given":"Brigitte","family":"Egenberger","sequence":"additional","affiliation":[]},{"given":"Valentin","family":"Gorboulev","sequence":"additional","affiliation":[]},{"given":"Erhard","family":"Wischmeyer","sequence":"additional","affiliation":[]},{"given":"Thomas","family":"M\u00fcller","sequence":"additional","affiliation":[]},{"given":"Hermann","family":"Koepsell","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1126\/science.1088196"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.281.3.F454"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M004645200"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1124\/mol.54.2.342"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(96)01030-7"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.51.32599"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-2952(00)00334-8"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1021\/bi052631h"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1124\/mol.104.008821"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1124\/mol.56.6.1254"},{"key":"R11","doi-asserted-by":"crossref","unstructured":"Gorbunov D, Gorboulev V, Shatskaya N, Mueller T, Bamberg E, Friedrich T, Koepsell H. High-affinity cation binding to organic cation transporter 1 induces movement of helix 11 and blocks transport after mutations in a modeled interaction domain between two helices. Mol Pharmacol 73: 50\u201361, 2008.","DOI":"10.1124\/mol.107.040170"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1038\/372549a0"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1016\/j.str.2007.06.004"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1126\/science.1087619"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0609968104"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1016\/j.neulet.2005.03.014"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1007\/s11095-007-9254-z"},{"key":"R18","doi-asserted-by":"crossref","unstructured":"Koepsell H, Schmitt BM, Gorboulev V. Organic cation transporters. Rev Physiol Biochem Pharmacol 150: 36\u201390, 2003.","DOI":"10.1007\/s10254-003-0017-x"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0700969104"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.20-01-00156.2000"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1124\/mol.104.008839"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1998.9978"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1007\/s11095-006-9181-4"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M414550200"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.30.18526"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0708258104"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1021\/bi061632m"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.6.F890"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.48.30088"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.5147-03.2004"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1124\/mol.64.5.1037"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1007\/BF01869212"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2001.014530"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.90323.2008","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T22:54:07Z","timestamp":1567983247000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.90323.2008"}},"issued":{"date-parts":[[2009,4]]},"references-count":33,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2009,4]]}},"alternative-id":["10.1152\/ajprenal.90323.2008"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.90323.2008","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2009,4]]}},{"indexed":{"date-parts":[[2026,3,10]],"date-time":"2026-03-10T13:47:55Z","timestamp":1773150475531,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1994,1,1]]},"abstract":"<jats:p> In this study we defined some of the important elements in the acidification process of rat inner medullary collecting duct (IMCD) cells in culture. After cell acidification, i.e., cell pH (pHi) = 6.51 +\/- 0.02, pHi increased 0.046 +\/- 0.003 units\/min. N-ethylmaleimide, N,N'-cyclohexylcarbodiimide, and bafilomycin reduced this rate by over 85%. In contrast, omeprazole and Sch-28080 had no effect. 1,2-Bis(2-aminophenoxy)ethane-N,N,N,N'-tetraacetic acid, which prevents a rise in cell Ca2<jats:sup>+<\/jats:sup> concentration ([Ca2<jats:sup>+<\/jats:sup>]i) reduced the rate of pHi recovery to 0.013 +\/- 0.002 units\/min. Calmodulin inhibitors or disruption of cytoskeletal elements with cytochalasin B and colchicine also reduced pHi recovery significantly. In addition, these cells contain acidic vesicles and undergo pHi-regulated endocytosis and exocytosis, which are inhibited by disrupting the cytoskeleton. We conclude that, in our cultured line of rat IMCD cells, proton secretion is mediated by an H(<jats:sup>+<\/jats:sup>)-adenosinetriphosphatase. Changes in pHi produce alterations in acid secretion through a signal cascade that requires changes in [Ca2<jats:sup>+<\/jats:sup>]i, activation of calmodulin, an intact cytoskeleton, and alteration in the rate of exocytosis and endocytosis. <\/jats:p>","DOI":"10.1152\/ajprenal.1994.266.1.f94","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T05:59:45Z","timestamp":1514008785000},"page":"F94-F101","source":"Crossref","is-referenced-by-count":7,"title":["Intracellular modulation of acid secretion in rat inner medullary collecting duct cells"],"prefix":"10.1152","volume":"266","author":[{"given":"J. H.","family":"Schwartz","sequence":"first","affiliation":[{"name":"Thorndike Memorial Laboratory, Boston City Hospital, Massachusetts."}]},{"given":"S. A.","family":"Masino","sequence":"additional","affiliation":[{"name":"Thorndike Memorial Laboratory, Boston City Hospital, Massachusetts."}]},{"given":"R. D.","family":"Nichols","sequence":"additional","affiliation":[{"name":"Thorndike Memorial Laboratory, Boston City Hospital, Massachusetts."}]},{"given":"E. A.","family":"Alexander","sequence":"additional","affiliation":[{"name":"Thorndike Memorial Laboratory, Boston City Hospital, Massachusetts."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1994.266.1.F94","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:31:44Z","timestamp":1567960304000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1994.266.1.F94"}},"issued":{"date-parts":[[1994,1,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1994,1,1]]}},"alternative-id":["10.1152\/ajprenal.1994.266.1.F94"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1994.266.1.f94","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1994,1,1]]}},{"indexed":{"date-parts":[[2026,3,11]],"date-time":"2026-03-11T13:32:09Z","timestamp":1773235929376,"version":"3.50.1"},"reference-count":26,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2004,11]]},"abstract":"<jats:p>This essay looks at the historical significance of four APS classic papers that are freely available online:<\/jats:p><jats:p>Jolliffe N, Shannon JA, and Smith HW. The excretion of urine in the dog. III. The use of non-metabolized sugars in the measurement of the glomerular filtrate. Am J Physiol 100: 301\u2014312, 1932 ( http:\/\/ajplegacy.physiology.org\/cgi\/reprint\/100\/2\/301 ).<\/jats:p><jats:p>Shannon JA. The excretion of inulin by the dog. Am J Physiol 112: 405\u2014413, 1935 ( http:\/\/ajplegacy.physiology.org\/cgi\/reprint\/112\/3\/405 ).<\/jats:p><jats:p>Shannon JA and Fisher S. The renal tubular reabsorption of glucose in the normal dog. Am J Physiol 122: 765\u2014774, 1938 ( http:\/\/ajplegacy.physiology.org\/cgi\/reprint\/122\/3\/765 ).<\/jats:p><jats:p>Shannon JA, Farber S, and Troast L. The measurement of glucose Tm in the normal dog. Am J Physiol 133: 752\u2014761, 1941 ( http:\/\/ajplegacy.physiology.org\/cgi\/reprint\/133\/3\/752 ).<\/jats:p>","DOI":"10.1152\/classicessays.00020.2004","type":"journal-article","created":{"date-parts":[[2004,10,9]],"date-time":"2004-10-09T02:52:57Z","timestamp":1097290377000},"page":"F861-F863","source":"Crossref","is-referenced-by-count":1,"title":["Experimental validation of the countercurrent model of urinary concentration"],"prefix":"10.1152","volume":"287","author":[{"given":"James A.","family":"Schafer","sequence":"first","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"crossref","unstructured":"Berliner RW.Formation of concentrated urine. In:Renal Physiology: People and Ideas, edited by Gottschalk CW, Berliner RW, and Giebisch GH. Bethesda, MD: Am. Physiol. Soc. 1987, p. 247\u2013276.","DOI":"10.1007\/978-1-4614-7545-3_8"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1016\/0002-9343(58)90377-2"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1126\/science.121.3139.302"},{"key":"R4","unstructured":"Burgess WW, Harvey AM, and Marshall EKJ.The site of the antidiuretic action of pituitary extract.J Pharmacol Exp Ther49: 237\u2013249, 1933."},{"key":"R5","doi-asserted-by":"crossref","unstructured":"Crane MR.Observation on the function of the frog's kidney.Am J Physiol81: 232\u2013243, 1927.","DOI":"10.1152\/ajplegacy.1927.81.1.232"},{"key":"R6","unstructured":"Gottschalk CW.Fifth Bowditch lecture. Micropuncture studies of tubular function in the mammalian kidney.Physiologist4: 35\u201355, 1961."},{"key":"R7","unstructured":"Gottschalk CW.Renal tubular function: lessons from micropuncture. In:The Harvey Lectures (Ser. 58).New York: Academic, 1962, p. 99\u2013124."},{"key":"R8","doi-asserted-by":"crossref","unstructured":"Gottschalk CW, Lassiter WE, Mylle M, Ullrich KJ, Schmidt-Nielsen B, O'Dell R, and Pehling G.Micropuncture study of composition of loop of Henle fluid in desert rodents.Am J Physiol204: 532\u2013535, 1963.","DOI":"10.1152\/ajplegacy.1963.204.4.532"},{"key":"R9","unstructured":"Gottschalk CWand Mylle M.Micropuncture study of the mammalian urinary concentrating mechanism: evidence for the countercurrent hypothesis.Am J Physiol196: 927\u2013936, 1959."},{"key":"R10","doi-asserted-by":"crossref","unstructured":"Hargitay Band Kuhn W.Das Multiplikationsprinzip als Grundlage der Harnkonzentrierung in der Niere.Z Elektrochem55: 539\u2013558, 1951.","DOI":"10.1002\/bbpc.19510550617"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1007\/BF00362426"},{"key":"R12","unstructured":"Hirokawa W.\u00dcber den osmotischen Druck des Nierenparanchyms.Hofmeisters Beitr Physiol Pathol11: 458\u2013478, 1908."},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1515\/bchm2.1942.276.4-6.145"},{"key":"R14","doi-asserted-by":"crossref","unstructured":"Lassiter WE, Gottschalk CW, and Mylle M.Micropuncture study of net transtubular movement of water and urea in nondiuretic mammalian kidney.Am J Physiol200: 1139\u20131147, 1961.","DOI":"10.1152\/ajplegacy.1961.200.6.1139"},{"key":"R15","unstructured":"Peter K.Untersuchungen \u00fcber Bau und Entwicklung der Nierre(monograph). Jena, Germany: Fischer, 1909."},{"key":"R16","unstructured":"Schmidt-Nielsen B.The resourcefulness of nature in physiological adaptation to the environment.Physiologist1: 4\u201320, 1958."},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1958.38.2.139"},{"key":"R18","unstructured":"Smith HW.The Kidney. Structure and Function in Health and Disease.New York: Oxford Univ. Press, 1951."},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1007\/BF00363541"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1007\/BF00362116"},{"key":"R21","doi-asserted-by":"crossref","unstructured":"Ullrich KJ, Schmidt-Nielsen B, O'Dell R, Pehling G, Gottschalk CW, Lassiter WE, and Mylle M.Micropuncture study of composition of proximal and distal tubular fluid in rat kidney.Am J Physiol204: 527\u2013531, 1963.","DOI":"10.1152\/ajplegacy.1963.204.4.527"},{"key":"R22","doi-asserted-by":"crossref","unstructured":"Walker AM, Bott PA, Oliver J, and MacDowell MC.The collection and analysis of fluid from single nephrons of the mammalian kidney.Am J Physiol134: 580\u2013595, 1941.","DOI":"10.1152\/ajplegacy.1941.134.3.580"},{"key":"R23","unstructured":"Windhager EE.Micropuncture and microperfusion. In:Renal Physiology: People and Ideas, edited by Gottschalk CW, Berliner RW, and Giebisch GH. Bethesda, MD:Am. Physiol. Soc., 1987, p. 101\u2013129."},{"key":"R24","unstructured":"Wirz H.Der osmotische Druck des Blutes in der Nierenpapille.Helv Physiol Pharm Acta11: 20\u201329, 1953."},{"key":"R25","unstructured":"Wirz H.Der osmotische Druck in den corticalen Tubuli der Rattenniere.Helv Physiol Pharm Acta14: 353\u2013362, 1953."},{"key":"R26","unstructured":"Wirz H, Hargitay B, and Kuhn W.Lokalization des Konzentrierungsprozesses in der Niere durch direkte Kryoscopie.Helv Physiol Pharmacol9: 196\u2013207, 1951."}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/classicessays.00020.2004","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,1,14]],"date-time":"2024-01-14T15:30:13Z","timestamp":1705246213000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/classicessays.00020.2004"}},"issued":{"date-parts":[[2004,11]]},"references-count":26,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2004,11]]}},"alternative-id":["10.1152\/classicessays.00020.2004"],"URL":"https:\/\/doi.org\/10.1152\/classicessays.00020.2004","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2004,11]]}},{"indexed":{"date-parts":[[2026,3,11]],"date-time":"2026-03-11T15:23:44Z","timestamp":1773242624984,"version":"3.50.1"},"reference-count":48,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1997,12,1]]},"abstract":"<jats:p>Peroxisome proliferator-activated receptors (PPARs, \u03b1, \u03b2\/\u03b4, and \u03b3) are members of the nuclear receptor superfamily of ligand-activated transcription factors. PPARs regulate the expression of genes involved in lipid metabolism. 8( S)-hydroxyeicosatetraenoic acid (8- S-HETE), leukotriene B<jats:sub>4<\/jats:sub>(LTB<jats:sub>4<\/jats:sub>), and hypolipidemic fibrates activate PPAR\u03b1, whereas PPAR\u03b3 is activated by prostaglandin metabolites. The present studies examined the intrarenal and tissue distribution of rabbit and human PPAR\u03b1, -\u03b2\/\u03b4, and -\u03b3 mRNAs. Nuclease protection showed PPAR\u03b1 predominated in liver, heart, and kidney, whereas PPAR\u03b3, a putative adipose-specific transcription factor, was in white adipose tissue, bladder, and ileum, followed by kidney and spleen. Lower expression levels of PPAR\u03b2\/\u03b4 were observed in several tissues. In situ hybridization of kidney showed PPAR\u03b1 mRNA predominated in proximal tubules and medullary thick ascending limbs of both rabbit and human. PPAR\u03b3 was exclusively expressed in medullary collecting duct and papillary urothelium. Immunoblot confirmed the expression of PPAR\u03b3 protein in freshly isolated inner medullary collecting ducts. mRNAs for all the PPARs were expressed in the ureter and bladder in both rabbit and human, but PPAR\u03b3 expression was greatest. This distinct distribution of PPAR isoforms has important implications for lipid-activated gene transcription in urinary epithelia.<\/jats:p>","DOI":"10.1152\/ajprenal.1997.273.6.f1013","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T14:32:50Z","timestamp":1514039570000},"page":"F1013-F1022","source":"Crossref","is-referenced-by-count":60,"title":["Expression of peroxisome proliferator-activated receptors in urinary tract of rabbits and humans"],"prefix":"10.1152","volume":"273","author":[{"given":"Youfei","family":"Guan","sequence":"first","affiliation":[{"name":"Division of Nephrology,"}]},{"given":"Yahua","family":"Zhang","sequence":"additional","affiliation":[{"name":"Division of Nephrology,"}]},{"given":"Linda","family":"Davis","sequence":"additional","affiliation":[{"name":"Division of Nephrology,"}]},{"given":"Matthew D.","family":"Breyer","sequence":"additional","affiliation":[{"name":"Division of Nephrology,"},{"name":"Departments of Medicine and Molecular Physiology and Biophysics,"},{"name":"Veterans Affairs Medical Center, and Vanderbilt University School of Medicine, Nashville, Tennessee 37212"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1210\/endo.137.1.8536636"},{"key":"B2","first-page":"451","volume":"4","author":"Breyer M.","year":"1993","journal-title":"J. Am. Soc. Nephrol."},{"issue":"39","key":"B3","first-page":"F485","volume":"270","author":"Breyer M.","year":"1996","journal-title":"Am. J. Physiol."},{"key":"B4","doi-asserted-by":"crossref","first-page":"8","DOI":"10.1681\/ASN.V718","volume":"7","author":"Breyer M.","year":"1996","journal-title":"J. Am. Soc. Nephrol."},{"issue":"39","key":"B5","first-page":"F912","volume":"270","author":"Breyer M. D.","year":"1996","journal-title":"Am. J. Physiol."},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117978"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1038\/384039a0"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(92)90031-7"},{"issue":"2","key":"B9","first-page":"F169","volume":"233","author":"Dunn M. J.","year":"1977","journal-title":"Am. J. Physiol."},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.40.24698"},{"issue":"21","key":"B11","first-page":"F53","volume":"252","author":"Farman N.","year":"1987","journal-title":"Am. J. Physiol."},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(95)90193-0"},{"key":"B13","first-page":"189","volume":"3","author":"Fukushima M.","year":"1990","journal-title":"Eicosanoids"},{"key":"B14","first-page":"281","volume":"4","author":"Greene M. E.","year":"1995","journal-title":"Gene Expr."},{"issue":"42","key":"B15","first-page":"F18","volume":"273","author":"Guan Y.-F.","year":"1997","journal-title":"Am. J. Physiol."},{"key":"B16","doi-asserted-by":"crossref","first-page":"16619","DOI":"10.1016\/S0021-9258(18)37435-0","volume":"263","author":"Hirata Y.","year":"1988","journal-title":"J. Biol. Chem."},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.16.9376"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1038\/347645a0"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1111\/j.1432-1033.1995.219_1.x"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.8.3836"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.95"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(93)80110-G"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(95)90194-9"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.91.15.7355"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1038\/358771a0"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1996.5906"},{"key":"B27","doi-asserted-by":"crossref","first-page":"19051","DOI":"10.1016\/S0021-9258(18)41738-3","volume":"267","author":"Muerhoff A. S.","year":"1992","journal-title":"J. Biol. Chem."},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1016\/0960-0760(94)90089-2"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199411033311803"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.27.16114"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1984.136"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1093\/carcin\/17.7.1435"},{"key":"B33","doi-asserted-by":"crossref","first-page":"18767","DOI":"10.1016\/S0021-9258(17)32234-2","volume":"269","author":"Rodriguez J. C.","year":"1994","journal-title":"J. Biol. Chem."},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118609"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.33.19269"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1021\/bi00072a015"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1016\/0090-6980(77)90217-9"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)81359-8"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(95)00129-W"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.15.1.351"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1016\/0959-437X(95)80025-5"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1101\/gad.8.10.1224"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1002\/j.1460-2075.1992.tb05072.x"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.4.2147"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.41.23975"},{"issue":"21","key":"B46","first-page":"F551","volume":"252","author":"Zeidel M. L.","year":"1987","journal-title":"Am. J. Physiol."},{"key":"B47","first-page":"1457","volume":"10","author":"Zhang B.","year":"1996","journal-title":"Mol. Endocrinol."},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.89.16.7541"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1997.273.6.F1013","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:47:06Z","timestamp":1660189626000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1997.273.6.F1013"}},"issued":{"date-parts":[[1997,12,1]]},"references-count":48,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1997,12,1]]}},"alternative-id":["10.1152\/ajprenal.1997.273.6.F1013"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1997.273.6.f1013","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1997,12,1]]}},{"indexed":{"date-parts":[[2026,3,8]],"date-time":"2026-03-08T23:37:51Z","timestamp":1773013071638,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1988,12,1]]},"abstract":"<jats:p> Current evidence suggests guanosine 3',5'-cyclic monophosphate (cGMP) serves as the second messenger for atrial natriuretic factor (ANF) in the kidney in vivo. We examined whether extracellular cGMP accumulation quantitatively reflected the concentration of cGMP within renal cells and whether urinary excretion of cGMP correlated with the physiological action of ANF. cGMP egression was examined in renal epithelial LLC-PK1 cells. ANF augmented intracellular cGMP concentration and extracellular cGMP appearance. Extracellular cGMP was an excellent function of the time-integrated intracellular cGMP concentration. In clearance studies in awake rats, urinary cGMP was primarily of renal cellular origin and correlated with the natriuresis induced by ANF in a time-dependent and concentration-dependent fashion. Urinary cGMP excretion may be useful as a biological marker for the renal activity of ANF in vivo. <\/jats:p>","DOI":"10.1152\/ajprenal.1988.255.6.f1220","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T16:10:56Z","timestamp":1513959056000},"page":"F1220-F1224","source":"Crossref","is-referenced-by-count":15,"title":["Urinary cGMP as biological marker of the renal activity of atrial natriuretic factor"],"prefix":"10.1152","volume":"255","author":[{"given":"K. R.","family":"Wong","sequence":"first","affiliation":[{"name":"Department of Medicine, University of California, San Francisco94143."}]},{"given":"M. H.","family":"Xie","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of California, San Francisco94143."}]},{"given":"L. B.","family":"Shi","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of California, San Francisco94143."}]},{"given":"F. Y.","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of California, San Francisco94143."}]},{"given":"C. L.","family":"Huang","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of California, San Francisco94143."}]},{"given":"D. G.","family":"Gardner","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of California, San Francisco94143."}]},{"given":"M. G.","family":"Cogan","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of California, San Francisco94143."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1988.255.6.F1220","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:09:08Z","timestamp":1567955348000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1988.255.6.F1220"}},"issued":{"date-parts":[[1988,12,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1988,12,1]]}},"alternative-id":["10.1152\/ajprenal.1988.255.6.F1220"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1988.255.6.f1220","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1988,12,1]]}},{"indexed":{"date-parts":[[2026,3,7]],"date-time":"2026-03-07T15:01:46Z","timestamp":1772895706344,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1997,1,1]]},"abstract":"<jats:p> When cultured in type I collagen gels, two kidney-derived cell lines, Madin-Darby canine kidney (MDCK) cells and murine inner medullary collecting duct (mIMCD3) cells, from branching tubular structures in the presence of Swiss 3T3 conditioned medium, in which hepatocyte growth factor (HGF) is the major branching tubule inducing factor. However, upon incubation with transforming growth factor-beta (TGF-beta) in the presence of 3T3 conditioned medium, MDCK tubulogenesis and branching was markedly inhibited. In contrast, mIMCD3 cells, which are much less susceptible to growth and tubulogenesis inhibition by TGF-beta, formed long straight tubulelike structures in presence of TGF-beta, suggesting a dissociation between tubulogenesis and branching morphogenesis. Interestingly, those long tubules that did branch often superficially resembled the early branching ureteric bud in embryonic kidneys. Quantitation of branching events revealed a selective branch-inhibiting effect of TGF-beta on mIMCD3 cells at concentrations between 0.02 and 2 ng\/ml. There was no qualitative or quantitative difference among TGF-beta 1, -beta 2, and -beta 3 on inhibition of branching events, suggesting existence of potentially redundant mechanisms for modulating branching morphogenesis. Concentrations of TGF-beta that resulted in long nonbranching tubules also altered the profile of extracellular matrix-degrading proteases and their inhibitors expressed by developing tubules. Ratios of urokinase type plasminogen activator (u-PA) to plasminogen activator inhibitor (PAI-l) and matrix metalloprotease (MMP)-1 to tissue inhibitor of metalloprotease (TIMP)-1 were both markedly decreased. In addition, apart from a direct effect on epithelial cell branching morphogenesis, TGF-beta downregulated the expression of HGF mRNA in Swiss 3T3 cells. Thus TGF-beta exerts at least three distinct effects relevant to tubulogenesis and branching morphogenesis inhibition of branching morphogenesis alone (mIMCD3 cells), inhibition of both tubulogenesis and branching morphogenesis (MDCK cells), and inhibition of the expression of growth factor which induce tubulogenesis and branching morphogenesis (3T3 cells). In the context of epithelial tissue development, which requires tightly regulated branching tubulogenesis of epithelial cells, the data suggest a model where branching patterns are regulated by a precise temporal and spatial balance between branching morphogens such as HGF and inhibitory morphogens such as members of the TGF-beta superfamily [e.g., TGF-beta isoforms, certain bone morphogenetic proteins]. <\/jats:p>","DOI":"10.1152\/ajprenal.1997.272.1.f139","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T08:32:04Z","timestamp":1514017924000},"page":"F139-F146","source":"Crossref","is-referenced-by-count":22,"title":["Transforming growth factor-beta selectively inhibits branching morphogenesis but not tubulogenesis"],"prefix":"10.1152","volume":"272","author":[{"given":"H.","family":"Sakurai","sequence":"first","affiliation":[{"name":"Department of Medicine, Brigham and Women's Hospital, Boston,Massachusetts, USA."}]},{"given":"S. K.","family":"Nigam","sequence":"additional","affiliation":[{"name":"Department of Medicine, Brigham and Women's Hospital, Boston,Massachusetts, USA."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1997.272.1.F139","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:15:44Z","timestamp":1567973744000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1997.272.1.F139"}},"issued":{"date-parts":[[1997,1,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1997,1,1]]}},"alternative-id":["10.1152\/ajprenal.1997.272.1.F139"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1997.272.1.f139","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1997,1,1]]}},{"indexed":{"date-parts":[[2026,3,7]],"date-time":"2026-03-07T15:07:13Z","timestamp":1772896033676,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1993,9,1]]},"abstract":"<jats:p> We recently reported a novel intracellular mechanism of Na-K-adenosinetriphosphatase (Na-K-ATPase) regulation in the cortical collecting duct (CCD) by agents that increase cell adenosine 3',5'-cyclic monophosphate (cAMP), which involves stimulation of protein kinase A (PKA) and phospholipase A2 (PLA2). We now determined whether this mechanism also operates in other nephron segments. In the medullary thick ascending limb (MTAL) dopamine, the DA1 agonist fenoldopam, forskolin, or dibutyryl-cAMP inhibited Na-K-ATPase activity, similar to results in CCD. In both segments this effect was blocked by 20-residue inhibitory peptide (IP20), a peptide inhibitor of PKA, but not by staurosporine, a protein kinase C (PKC) inhibitor. PKC activators phorbol 12-myristate 13-acetate, phorbol 12,13-dibutyrate, and 1,2-myristate 13-acetate, phorbol 12,13-dibutyrate, and 1,2-dioctanoylglycerol had no effect on Na-K pump activity in either CCD or MTAL. In contrast, all three PKC activators inhibited pump activity in the proximal convoluted tubule (PCT), an effect reproduced only by dopamine or by parathyroid hormone [PTH-(1-34)]. In PCT the pump inhibition by dopamine or PTH-(1-34) was abolished by staurosporine but not by IP20. The PLA2 inhibitor mepacrine prevented the effect of all agents, and arachidonic acid produced a dose-dependent pump inhibition in each of the three segments studied. We conclude that intracellular mechanisms of Na-K-ATPase regulation differ along the nephron, as they involve activation of PKA in CCD and MTAL and of PKC in PCT. These two pathways probably share a common mechanism in stimulating PLA2, arachidonic acid release, and production of eicosanoids in both the proximal and distal nephron. <\/jats:p>","DOI":"10.1152\/ajprenal.1993.265.3.f399","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T05:17:13Z","timestamp":1514006233000},"page":"F399-F405","source":"Crossref","is-referenced-by-count":24,"title":["Different mechanisms of renal Na-K-ATPase regulation by protein kinases in proximal and distal nephron"],"prefix":"10.1152","volume":"265","author":[{"given":"T.","family":"Satoh","sequence":"first","affiliation":[{"name":"Department of Medicine, University of Chicago Pritzker School ofMedicine, Illinois 60637."}]},{"given":"H. T.","family":"Cohen","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Chicago Pritzker School ofMedicine, Illinois 60637."}]},{"given":"A. I.","family":"Katz","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Chicago Pritzker School ofMedicine, Illinois 60637."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1993.265.3.F399","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:27:21Z","timestamp":1567960041000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1993.265.3.F399"}},"issued":{"date-parts":[[1993,9,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1993,9,1]]}},"alternative-id":["10.1152\/ajprenal.1993.265.3.F399"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1993.265.3.f399","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1993,9,1]]}},{"indexed":{"date-parts":[[2026,3,9]],"date-time":"2026-03-09T03:40:47Z","timestamp":1773027647992,"version":"3.50.1"},"reference-count":44,"publisher":"American Physiological Society","issue":"3","funder":[{"DOI":"10.13039\/100000050","name":"HHS | NIH | National Heart, Lung, and Blood Institute (NHBLI)","doi-asserted-by":"publisher","award":["HL 128053"],"award-info":[{"award-number":["HL 128053"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)","doi-asserted-by":"publisher","award":["DK 07470"],"award-info":[{"award-number":["DK 07470"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2019,3,1]]},"abstract":"<jats:p>Fructose consumption has increased because of widespread use of high-fructose corn syrup by the food industry. Renal proximal tubules are thought to reabsorb fructose. However, fructose reabsorption (J<jats:sub>fructose<\/jats:sub>) by proximal tubules has not yet been directly demonstrated, nor the effects of dietary fructose on J<jats:sub>fructose<\/jats:sub>. This segment expresses Na<jats:sup>+<\/jats:sup>- and glucose-linked transporters (SGLTs) 1, 2, 4, and 5 and glucose transporters (GLUTs) 2 and 5. SGLT4 and -5 transport fructose, but SGLT1 and -2 do not. Knocking out SGLT5 increases urinary fructose excretion. We hypothesize that J<jats:sub>fructose<\/jats:sub>in the S2 portion of the proximal tubule is mediated by luminal entry via SGLT4\/5 and basolateral exit by GLUT2 and that it is enhanced by a fructose-enriched diet. We measured J<jats:sub>fructose<\/jats:sub>by proximal straight tubules from rats consuming either tap water (Controls) or 20% fructose (FRU). Basal J<jats:sub>fructose<\/jats:sub>in Controls was 14.1\u2009\u00b1\u20091.5 pmol\u00b7mm<jats:sup>\u22121<\/jats:sup>\u00b7min<jats:sup>\u22121<\/jats:sup>. SGLT inhibition with phlorizin reduced J<jats:sub>fructose<\/jats:sub>to 4.9\u2009\u00b1\u20091.4 pmol\u00b7mm<jats:sup>\u22121<\/jats:sup>\u00b7min<jats:sup>\u22121<\/jats:sup>( P &lt; 0.008), whereas removal of Na<jats:sup>+<\/jats:sup>diminished J<jats:sub>fructose<\/jats:sub>by 86\u2009\u00b1\u20095% ( P &lt; 0.0001). A fructose-enriched diet increased J<jats:sub>fructose<\/jats:sub>from 12.8\u2009\u00b1\u20092.5 to 19.3\u2009\u00b1\u20090.5 pmol\u00b7mm<jats:sup>\u22121<\/jats:sup>\u00b7min<jats:sup>\u22121<\/jats:sup>, a 51% increase ( P &lt; 0.03). Using immunofluorescence, we detected luminal SGLT4 and SGLT5 and basolateral GLUT2; GLUT5 was undetectable. The expression of apical transporters SGLT4 and SGLT5 was higher in FRU than in Controls [137\u2009\u00b1\u200910% ( P &lt; 0.01) and 38\u2009\u00b1\u200914% ( P &lt; 0.04), respectively]. GLUT2 was also elevated by 88\u2009\u00b1\u200927% ( P &lt; 0.02) in FRU. We conclude that J<jats:sub>fructose<\/jats:sub>by proximal tubules occurs primarily via Na<jats:sup>+<\/jats:sup>-linked cotransport processes, and a fructose-enriched diet enhances reabsorption. Transport across luminal and basolateral membranes is likely mediated by SGLT4\/5 and GLUT2, respectively.<\/jats:p>","DOI":"10.1152\/ajprenal.00247.2018","type":"journal-article","created":{"date-parts":[[2018,12,19]],"date-time":"2018-12-19T16:21:57Z","timestamp":1545236517000},"page":"F473-F480","source":"Crossref","is-referenced-by-count":34,"title":["Fructose reabsorption by rat proximal tubules: role of Na<sup>+<\/sup>-linked cotransporters and the effect of dietary fructose"],"prefix":"10.1152","volume":"316","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3682-0815","authenticated-orcid":false,"given":"Agustin","family":"Gonzalez-Vicente","sequence":"first","affiliation":[{"name":"Department of Physiology and Biophysics, School of Medicine, Case Western Reserve University, Cleveland, Ohio"},{"name":"Facultad de Farmacia y Bioqu\u00edmica, Universidad de Buenos Aires, Ciudad Aut\u00f3noma de Buenos Aires, Argentina"}]},{"given":"Pablo D.","family":"Cabral","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, School of Medicine, Case Western Reserve University, Cleveland, Ohio"},{"name":"Facultad de Medicina, Departamento de Ciencias Fisiol\u00f3gicas, Universidad de Buenos Aires, Ciudad Aut\u00f3noma de Buenos Aires, Argentina"}]},{"given":"Nancy J.","family":"Hong","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, School of Medicine, Case Western Reserve University, Cleveland, Ohio"}]},{"given":"Jessica","family":"Asirwatham","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, School of Medicine, Case Western Reserve University, Cleveland, Ohio"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2171-9490","authenticated-orcid":false,"given":"Fara","family":"Saez","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, School of Medicine, Case Western Reserve University, Cleveland, Ohio"}]},{"given":"Jeffrey L.","family":"Garvin","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, School of Medicine, Case Western Reserve University, Cleveland, Ohio"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00180.2008"},{"key":"B2","doi-asserted-by":"crossref","first-page":"260.6","DOI":"10.1096\/fasebj.29.1_supplement.960.6","volume":"29","author":"Beierwaltes W","year":"2015","journal-title":"FASEB J"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.2337\/diab.31.6.516"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00512.2017"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.1994.267.1.G71"},{"key":"B6","doi-asserted-by":"crossref","first-page":"14523","DOI":"10.1016\/S0021-9258(18)42067-4","volume":"267","author":"Burant CF","year":"1992","journal-title":"J Biol Chem"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.113.02564"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1016\/0016-5085(93)90948-C"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008060576"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/S0005-2736(03)00129-9"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1369\/jhc.2009.953190"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.90245.2008"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0056681"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00239.x"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.3390\/nu9080885"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0201293"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.3390\/nu10091244"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.14814\/phy2.13162"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2003.049247"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.257.4.F658"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/j.febslet.2011.12.027"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.10.5.512"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1172\/JCI116972"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.3390\/nu6083117"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfh612"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/physiol.00011.2007"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2003.046268"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1080\/10408391003626223"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1042\/bj2950211"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1093\/jn\/137.6.1447"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00433.2009"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1038\/ctg.2015.50"},{"issue":"71","key":"B33","first-page":"1","author":"Ogden CL","year":"2011","journal-title":"NCHS Data Brief"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00270.2005"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.ph.52.030190.003425"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.112.193045"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.21853"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1038\/ejcn.2014.267"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00635.x"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1177\/39.3.1993828"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1016\/j.lfs.2004.10.016"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1990.259.2.C286"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010030246"},{"key":"B44","first-page":"160","volume":"10","author":"Vos MB","year":"2008","journal-title":"Medscape J Med"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00247.2018","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,9,8]],"date-time":"2022-09-08T20:20:03Z","timestamp":1662668403000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00247.2018"}},"issued":{"date-parts":[[2019,3,1]]},"references-count":44,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2019,3,1]]}},"alternative-id":["10.1152\/ajprenal.00247.2018"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00247.2018","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2019,3,1]]}},{"indexed":{"date-parts":[[2026,3,9]],"date-time":"2026-03-09T03:01:38Z","timestamp":1773025298606,"version":"3.50.1"},"reference-count":44,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1999,5,1]]},"abstract":"<jats:p>Urea treatment (100\u2013300 mM) increased expression of the oxidative stress-responsive transcription factor, Gadd153\/CHOP, at the mRNA and protein levels (at \u22654 h) in renal medullary mIMCD3 cells in culture, whereas other solutes did not. Expression of the related protein, CCAAT\/enhancer-binding protein (C\/EBP-\u03b2), was not affected, nor was expression of the sensor of endoplasmic reticulum stress, grp78. Urea modestly increased Gadd153 transcription by reporter gene analysis but failed to influence Gadd153 mRNA stability. Importantly, upregulation of Gadd153 mRNA and protein expression by urea was antioxidant sensitive. Accordingly, urea treatment was associated with oxidative stress, as quantitated by intracellular reduced glutathione content in mIMCD3 cells. In addition, antioxidant treatment partially inhibited the ability of urea to activate transcription of an Egr-1 luciferase reporter gene. Therefore oxidative stress represents a novel solute-signaling pathway in the kidney medulla and, potentially, in other tissues.<\/jats:p>","DOI":"10.1152\/ajprenal.1999.276.5.f786","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T17:50:46Z","timestamp":1514051446000},"page":"F786-F793","source":"Crossref","is-referenced-by-count":37,"title":["Urea-associated oxidative stress and Gadd153\/CHOP induction"],"prefix":"10.1152","volume":"276","author":[{"given":"Zheng","family":"Zhang","sequence":"first","affiliation":[{"name":"Division of Nephrology, Hypertension, and Clinical Pharmacology and Division of Molecular Medicine, Department of Medicine, Oregon Health Sciences University and the Portland Veterans Affairs Medical Center, Portland, Oregon 97201"}]},{"given":"Xiao-Yan","family":"Yang","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Hypertension, and Clinical Pharmacology and Division of Molecular Medicine, Department of Medicine, Oregon Health Sciences University and the Portland Veterans Affairs Medical Center, Portland, Oregon 97201"}]},{"given":"David M.","family":"Cohen","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Hypertension, and Clinical Pharmacology and Division of Molecular Medicine, Department of Medicine, Oregon Health Sciences University and the Portland Veterans Affairs Medical Center, Portland, Oregon 97201"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.1.217"},{"key":"B2","doi-asserted-by":"crossref","first-page":"475","DOI":"10.1681\/ASN.V83475","volume":"8","author":"Becker B. N.","year":"1997","journal-title":"J. Am. Soc. Nephrol."},{"issue":"41","key":"B3","first-page":"F305","volume":"272","author":"Berl T.","year":"1997","journal-title":"Am. J. Physiol."},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/16.23.7207"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.93.20.11242"},{"key":"B6","doi-asserted-by":"crossref","first-page":"25865","DOI":"10.1016\/S0021-9258(18)47326-7","volume":"269","author":"Cohen D. M.","year":"1994","journal-title":"J. Biol. Chem."},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118619"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.22.12903"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)81360-4"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199708073370607"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1042\/bj0420628"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.24.14285"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.85.23.8800"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.9.10.4196"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(94)01335-X"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.34.20588"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1038\/bjc.1996.4"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1042\/bj3140547"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(95)90403-4"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1126\/science.275.5306.1649"},{"key":"B22","first-page":"5656","volume":"54","author":"Jackman J.","year":"1994","journal-title":"Cancer Res."},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1002\/j.1460-2075.1996.tb00916.x"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1248\/bpb1978.13.254"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.22.13645"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM197403282901301"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1007\/BF00207507"},{"key":"B28","first-page":"5","volume":"52","author":"Luethy J. D.","year":"1992","journal-title":"Cancer Res."},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1006\/abio.1993.1226"},{"key":"B30","doi-asserted-by":"crossref","first-page":"482","DOI":"10.1093\/clinchem\/42.3.482","volume":"42","author":"Nilsson L.","year":"1996","journal-title":"Clin. Chem."},{"key":"B31","first-page":"454","volume":"6","author":"Nordeen S. K.","year":"1988","journal-title":"Biotechniques"},{"issue":"34","key":"B32","first-page":"F416","volume":"265","author":"Rauchman M. I.","year":"1993","journal-title":"Am. J. Physiol."},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1101\/gad.6.3.439"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.37.23086"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1126\/science.270.5234.296"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)81619-0"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(97)90280-8"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/16.18.8835"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.16.4.1479"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1126\/science.272.5266.1347"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/17.13.3619"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.16.8.4273"},{"issue":"42","key":"B43","first-page":"F837","volume":"273","author":"Zhang Z.","year":"1997","journal-title":"Am. J. Physiol."},{"issue":"40","key":"B44","first-page":"F1234","volume":"271","author":"Zhang Z.","year":"1996","journal-title":"Am. J. Physiol."},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1101\/gad.12.7.982"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1999.276.5.F786","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:54:00Z","timestamp":1660190040000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1999.276.5.F786"}},"issued":{"date-parts":[[1999,5,1]]},"references-count":44,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1999,5,1]]}},"alternative-id":["10.1152\/ajprenal.1999.276.5.F786"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1999.276.5.f786","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1999,5,1]]}},{"indexed":{"date-parts":[[2026,3,9]],"date-time":"2026-03-09T04:26:46Z","timestamp":1773030406806,"version":"3.50.1"},"reference-count":34,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2008,10]]},"abstract":"<jats:p>It is known that renal tissue plays a role in normal iron homeostasis. The current study examines kidney function in iron metabolism under hemolytic anemia studying renal expression of Prohepcidin, Ferroportin (MTP1), and divalent metal transporter 1 (DMT1). The relationship between these proteins and iron pigments was also investigated. Immunohistochemical procedures to study renal expression of Prohepcidin, MTP1, and DMT1 were performed in healthy and anemic mice. Renal tissue iron was determined by Prussian blue iron staining. To assess anemia evolution and erythropoietic recovery, we used conventional tests. In healthy mice, Prohepcidin expression was marked in proximal tubules and inner medulla and absent in outer medulla. Cortical tissue of healthy mice also showed MTP1 immunostaining, mainly in the S2 segment of proximal tubules. Medullar tissue showed MTP1 expression in the inner zone. In addition, S2 segments showed intense DMT1 immunoreactivity with homogeneous DMT1 distribution throughout renal medulla. The main cortical findings in hemolytic anemia were in S2 segments of proximal tubules where we found that decreased Prohepcidin expression coincided with an increment in Ferroportin and DMT1 expression. This expression pattern was concomitant with increased iron in the same tubular zone. However, in medullar tissue both Prohepcidin and MTP1 decreased and DMT1 was detected mainly in larger diameter tubules. Our findings clearly demonstrate that in hemolytic anemia, renal Prohepcidin acts in coordination with renal Ferroportin and DMT1, indicating the key involvement of kidney in iron homeostasis when iron demand is high. Further research is required to learn more about these regulatory mechanisms.<\/jats:p>","DOI":"10.1152\/ajprenal.90216.2008","type":"journal-article","created":{"date-parts":[[2008,7,24]],"date-time":"2008-07-24T00:46:38Z","timestamp":1216860398000},"page":"F1213-F1221","source":"Crossref","is-referenced-by-count":42,"title":["Role of the kidney in iron homeostasis: renal expression of Prohepcidin, Ferroportin, and DMT1 in anemic mice"],"prefix":"10.1152","volume":"295","author":[{"given":"Tania","family":"Veuthey","sequence":"first","affiliation":[]},{"given":"Mar\u00eda Cecilia","family":"D'Anna","sequence":"additional","affiliation":[]},{"given":"Marta Elena","family":"Roque","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M000713200"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1042\/bst0300724"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1172\/JCI113833"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00405.x"},{"key":"R5","doi-asserted-by":"crossref","unstructured":"Canonne-Hergaux F, Gruenheid S, Ponka P, Gros P.Cellular and subcellular localization of the Nramp2 iron transporter in the intestinal brush border and regulation by dietary iron.Blood93: 4406\u20134417, 1999.","DOI":"10.1182\/blood.V93.12.4406"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1099-1263(200001\/02)20:1<25::AID-JAT624>3.0.CO;2-7"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2005-07-2854"},{"key":"R8","doi-asserted-by":"crossref","unstructured":"Donovan A, Brownlie A, Zhou Y, Shepard J, Pratt SJ, Moynihan J, Paw BH, Drejer A, Barut B, Zapata A, Law TC, Brugnara C, Lux SE, Pinkus GS, Pinkus JL, Kingsley PD, Palis J, Fleming MD, Andrews NC, Zon LI.Positional cloning of zebrafish Ferroportin 1 identifies a conserved vertebrate iron exporter.Nature403: 778\u2013781, 2000.","DOI":"10.1038\/35001596"},{"key":"R9","unstructured":"Dworkin LD, Brenner BM.The kidney. In:The Renal Circulations, edited by Brenner BM. Philadelphia: Saunders, 1996."},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.5.F803"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1053\/gast.2002.35353"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbamcr.2006.03.014"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1038\/41343"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1002\/ajh.2830010410"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1016\/S0025-7125(16)31175-0"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1677\/joe.1.05729"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1172\/JCI113363"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbadis.2004.06.011"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1159\/000098522"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-003-1102-3"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1016\/S1097-2765(00)80425-6"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1126\/science.1104742"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.151179498"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1172\/JCI0215686"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1006\/bcmd.2002.0573"},{"key":"R26","doi-asserted-by":"crossref","unstructured":"Oates PS, Jeffrey GP, Basclain KA, Thomas C, Morgan EH.Iron excretion in iron-overloaded rats following the change from an iron-loaded to an iron-deficient diet.Hepatology15: 665\u2013674, 2000.","DOI":"10.1046\/j.1440-1746.2000.02210.x"},{"key":"R27","unstructured":"Oates PS, Thomas C.Ferroportin is expressed on the mucous granule membrane of a subpopulation of goblet cells in the duodenum of the rat.Histol Histopathol20: 681\u2013687, 2005."},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1136\/gut.53.1.44"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M008923200"},{"key":"R30","doi-asserted-by":"crossref","unstructured":"Ponka P.Cellular iron metabolism.Kidney Int55: S2\u2013S11, 1990.","DOI":"10.1046\/j.1523-1755.1999.055Suppl.69002.x"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2257.2001.00413.x"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1136\/gut.46.2.270"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00064.2003"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.2000.00581.x"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.90216.2008","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2020,5,7]],"date-time":"2020-05-07T06:36:26Z","timestamp":1588833386000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.90216.2008"}},"issued":{"date-parts":[[2008,10]]},"references-count":34,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2008,10]]}},"alternative-id":["10.1152\/ajprenal.90216.2008"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.90216.2008","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2008,10]]}},{"indexed":{"date-parts":[[2026,3,8]],"date-time":"2026-03-08T11:24:26Z","timestamp":1772969066009,"version":"3.50.1"},"reference-count":40,"publisher":"American Physiological Society","issue":"5","funder":[{"DOI":"10.13039\/100006098","name":"Radiological Society of North America (RSNA)","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100006098","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100001259","name":"National Kidney Foundation (NKF)","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100001259","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health (NIH)","doi-asserted-by":"publisher","award":["R01 DK109349"],"award-info":[{"award-number":["R01 DK109349"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2018,5,1]]},"abstract":"<jats:p> Glomerular fibrosis occurs in the early stages of multiple renal diseases, including hypertensive and diabetic nephropathy. Conventional assessment of glomerular fibrosis relies on kidney biopsy, which is invasive and does not reflect physiological aspects such as blood perfusion. In this study, we sought to assess potential changes of cortical perfusion and microstructure at different degrees of glomerular fibrosis using magnetic resonance imaging (MRI). A rat model of glomerular fibrosis was induced by injecting anti-Thy-1 monoclonal antibody OX-7 to promote mesangial extracellular matrix proliferation. For six rats on day 5 and five rats on day 12 after the induction, we measured renal cortical perfusion and spin-spin relaxation time (T<jats:sub>2<\/jats:sub>) in a 3-Tesla MRI scanner. T<jats:sub>2<\/jats:sub> reflects tissue microstructural changes. Glomerular fibrosis severity was evaluated by histological analysis and proteinuria. Four rats without fibrosis were included as controls. In the control rats, the periodic acid-Schiff (PAS)-positive area was 22\u2009\u00b1\u20091% of total glomerular tuft, which increased significantly to 56\u2009\u00b1\u200912% and 45\u2009\u00b1\u200910% in the day 5 and day 12 fibrotic groups, respectively ( P &lt; 0.01). For the three groups (control, day 5, and day 12 after OX-7 injection), cortical perfusion was 7.27\u2009\u00b1\u20092.54, 3.78\u2009\u00b1\u20092.17, and 3.32\u2009\u00b1\u20092.62 ml\u00b7min<jats:sup>\u22121<\/jats:sup>\u00b7g<jats:sup>\u22121<\/jats:sup>, respectively, decreasing with fibrosis severity ( P &lt; 0.01), and cortical T<jats:sub>2<\/jats:sub> was 75.2\u2009\u00b1\u20094.6, 84.1\u2009\u00b1\u20093.0, and 87.9\u2009\u00b1\u20095.6 ms, respectively ( P &lt; 0.01). In conclusion, extracellular matrix proliferation in glomerular mesangial cells severely diminished blood flow through the glomeruli and also altered cortical microstructure to increase cortical T<jats:sub>2<\/jats:sub>. The MRI-measured parameters are proven to be sensitive markers for characterizing glomerular fibrosis. <\/jats:p>","DOI":"10.1152\/ajprenal.00529.2017","type":"journal-article","created":{"date-parts":[[2018,1,4]],"date-time":"2018-01-04T12:01:41Z","timestamp":1515067301000},"page":"F747-F752","source":"Crossref","is-referenced-by-count":10,"title":["Quantitative characterization of glomerular fibrosis with magnetic resonance imaging: a feasibility study in a rat glomerulonephritis model"],"prefix":"10.1152","volume":"314","author":[{"given":"Christopher C.","family":"Conlin","sequence":"first","affiliation":[{"name":"Department of Radiology and Imaging Sciences, University of Utah, Salt Lake City, Utah"},{"name":"Department of Bioengineering, University of Utah, Salt Lake City, Utah"}]},{"given":"Yufeng","family":"Huang","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Internal Medicine, University of Utah, Salt Lake City, Utah"}]},{"given":"Brian Adam Jamison","family":"Gordon","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Internal Medicine, University of Utah, Salt Lake City, Utah"}]},{"given":"Jeff L.","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Radiology and Imaging Sciences, University of Utah, Salt Lake City, Utah"},{"name":"Department of Bioengineering, University of Utah, Salt Lake City, Utah"}]}],"member":"24","reference":[{"key":"B1","first-page":"680","volume":"55","author":"Bagchus WM","year":"1986","journal-title":"Lab Invest"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfm393"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1118\/1.595535"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1007\/s11154-008-9100-6"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1002\/mrm.1910400308"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1111\/j.0959-9673.2004.00376.x"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/j.mri.2016.11.010"},{"key":"B8","first-page":"1","volume":"4","author":"Ghayur MN","year":"2008","journal-title":"Med Hypotheses Res"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/1056-8727(95)80015-7"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1177\/1470320312466127"},{"key":"B11","first-page":"637","volume-title":"Magnetic Resonance Imaging: Physical Principles and Sequence Design","author":"Haacke EM","year":"1999"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/14.12.2873"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1016\/j.mri.2015.07.012"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1053\/ajkd.2002.31399"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1097\/RLI.0b013e31829d0414"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/j.mri.2012.08.004"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1053\/ajkd.2001.27693"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1002\/mrm.1910340303"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1097\/00004424-198601000-00002"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000054"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/j.pharmthera.2010.05.006"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1002\/mrm.10709"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1159\/000044975"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1006\/mvre.1995.1043"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00114.2005"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.94.12.3271"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.2337\/db08-0061"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199811123392007"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004110970"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1096\/fasebj.1.4.3308611"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1998.78.3.723"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00357.2005"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1038\/modpathol.3800239"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00945.x"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1016\/j.ddmod.2010.08.002"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.07121.x"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00901.x"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00271.2011"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2013.361"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1002\/mrm.21489"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00529.2017","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,23]],"date-time":"2019-09-23T00:42:58Z","timestamp":1569199378000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00529.2017"}},"issued":{"date-parts":[[2018,5,1]]},"references-count":40,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2018,5,1]]}},"alternative-id":["10.1152\/ajprenal.00529.2017"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00529.2017","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2018,5,1]]}},{"indexed":{"date-parts":[[2026,3,7]],"date-time":"2026-03-07T02:26:12Z","timestamp":1772850372382,"version":"3.50.1"},"reference-count":133,"publisher":"American Physiological Society","issue":"5","funder":[{"DOI":"10.13039\/100000738","name":"Department of Veterans Affairs","doi-asserted-by":"crossref","id":[{"id":"10.13039\/100000738","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000050","name":"HHS | NIH | National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["R01HL135183"],"award-info":[{"award-number":["R01HL135183"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"HHS | NIH | National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["F32HL147547"],"award-info":[{"award-number":["F32HL147547"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health","doi-asserted-by":"publisher","award":["R61AT010457"],"award-info":[{"award-number":["R61AT010457"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2020,11,1]]},"abstract":"<jats:p>Patients with chronic kidney disease (CKD) and end-stage kidney disease (ESKD) experience an increased risk of cerebrovascular disease and cognitive dysfunction. Hemodialysis (HD), a major modality of renal replacement therapy in ESKD, can cause rapid changes in blood pressure, osmolality, and acid-base balance that collectively present a unique stress to the cerebral vasculature. This review presents an update regarding cerebral blood flow (CBF) regulation in CKD and ESKD and how the maintenance of cerebral oxygenation may be compromised during HD. Patients with ESKD exhibit decreased cerebral oxygen delivery due to anemia, despite cerebral hyperperfusion at rest. Cerebral oxygenation further declines during HD due to reductions in CBF, and this may induce cerebral ischemia or \u201cstunning.\u201d Intradialytic reductions in CBF are driven by decreases in cerebral perfusion pressure that may be partially opposed by bicarbonate shifts during dialysis. Intradialytic reductions in CBF have been related to several variables that are routinely measured in clinical practice including ultrafiltration rate and blood pressure. However, the role of compensatory cerebrovascular regulatory mechanisms during HD remains relatively unexplored. In particular, cerebral autoregulation can oppose reductions in CBF driven by reductions in systemic blood pressure, while cerebrovascular reactivity to CO<jats:sub>2<\/jats:sub>may attenuate intradialytic reductions in CBF through promoting cerebral vasodilation. However, whether these mechanisms are effective in ESKD and during HD remain relatively unexplored. Important areas for future work include investigating potential alterations in cerebrovascular regulation in CKD and ESKD and how key regulatory mechanisms are engaged and integrated during HD to modulate intradialytic declines in CBF.<\/jats:p>","DOI":"10.1152\/ajprenal.00438.2020","type":"journal-article","created":{"date-parts":[[2020,9,28]],"date-time":"2020-09-28T10:41:45Z","timestamp":1601289705000},"page":"F782-F791","source":"Crossref","is-referenced-by-count":40,"title":["Cerebral blood flow regulation in end-stage kidney disease"],"prefix":"10.1152","volume":"319","author":[{"given":"Justin D.","family":"Sprick","sequence":"first","affiliation":[{"name":"Division of Renal Medicine, Department of Medicine, Emory University Department of Medicine, Atlanta, Georgia"},{"name":"Department of Veterans Affairs Health Care System, Decatur, Georgia"}]},{"given":"Joe R.","family":"Nocera","sequence":"additional","affiliation":[{"name":"Department of Veterans Affairs Health Care System, Decatur, Georgia"},{"name":"Center for Visual and Neurocognitive Rehabilitation, Department of Veterans Affairs Health Care System, Decatur, Georgia"},{"name":"Departments of Neurology and Rehabilitation Medicine, Emory University Department of Medicine, Atlanta, Georgia"}]},{"given":"Ihab","family":"Hajjar","sequence":"additional","affiliation":[{"name":"Department of Neurology, Emory University Department of Medicine, Atlanta, Georgia"}]},{"given":"W. Charles","family":"O\u2019Neill","sequence":"additional","affiliation":[{"name":"Division of Renal Medicine, Department of Medicine, Emory University Department of Medicine, Atlanta, Georgia"}]},{"given":"James","family":"Bailey","sequence":"additional","affiliation":[{"name":"Division of Renal Medicine, Department of Medicine, Emory University Department of Medicine, Atlanta, Georgia"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5799-9172","authenticated-orcid":false,"given":"Jeanie","family":"Park","sequence":"additional","affiliation":[{"name":"Division of Renal Medicine, Department of Medicine, Emory University Department of Medicine, Atlanta, Georgia"},{"name":"Department of Veterans Affairs Health Care System, Decatur, Georgia"},{"name":"Center for Visual and Neurocognitive Rehabilitation, Department of Veterans Affairs Health Care System, Decatur, Georgia"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1161\/01.STR.20.1.45"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.91008.2008"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1161\/01.STR.0000113737.58014.B4"},{"key":"B4","first-page":"315","volume":"41","author":"Alfakir M","year":"2011","journal-title":"Ann Clin Lab Sci"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.84"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1973.100"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/j.ekir.2019.01.001"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1001\/archinte.162.12.1401"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.2337\/dc11-s239"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2011111078"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1038\/jcbfm.1982.35"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2016.01.010"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1183\/09031936.06.00075405"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1007\/BF01692550"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.82.3.723"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.01237.2010"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2012050536"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1097\/00003246-199403000-00010"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.03900808"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.3389\/fneur.2017.00113"},{"key":"B21","volume-title":"National Chronic Kidney Disease Fact Sheet, 2017","author":"Centers for Disease Control and Prevention","year":"2017"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00411.x"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1177\/0271678X19866733"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0036332"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1007\/s00330-018-5675-9"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfx037"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.3346\/jkms.2016.31.8.1239"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1172\/JCI116037"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.4103\/ijn.IJN_124_18"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfn501"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1161\/STROKEAHA.110.605618"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2011.05.028"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2012.08.035"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfh1097"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1111\/hdi.12754"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.2174\/187153012800493477"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1186\/cc11877"},{"key":"B38","first-page":"559","volume":"37","author":"Esposito G","year":"1996","journal-title":"J Nucl Med"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00474.2018"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1016\/0022-510X(95)00226-7"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2018050462"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014020222"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1038\/jcbfm.1987.119"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.110.164780"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1136\/jnnp.28.5.449"},{"key":"B46","first-page":"52","volume":"151","author":"Harris CP","year":"1989","journal-title":"West J Med"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1161\/01.STR.25.2.408"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1038\/hr.2012.138"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.262.5.F737"},{"key":"B50","first-page":"126","volume":"18","author":"Holzer H","year":"1981","journal-title":"Proc Eur Dial Transplant Assoc"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1159\/000186471"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1159\/000358432"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2008.03.010"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/17.suppl_5.38"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1161\/STROKEAHA.107.493494"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2009.08.013"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1007\/s00540-017-2422-3"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0117474"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1007\/s11011-016-9829-7"},{"key":"B60","first-page":"2137","volume":"10","author":"Jing W","year":"2018","journal-title":"Am J Transl Res"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.39.4.555"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1159\/000013551"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1136\/jnnp-2019-320526"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1161\/01.STR.0000231640.32543.11"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000098687.01005.A5"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00142.x"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1152\/jappl.1961.16.3.473"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.1007\/s12975-016-0499-x"},{"key":"B69","doi-asserted-by":"publisher","DOI":"10.1136\/bmj.c4249"},{"key":"B70","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2125.1981.tb01231.x"},{"key":"B71","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.24.3.287"},{"key":"B72","doi-asserted-by":"publisher","DOI":"10.1016\/j.neurad.2018.03.002"},{"key":"B73","doi-asserted-by":"crossref","first-page":"493","DOI":"10.1111\/aas.13298","volume":"63","author":"Lund A","year":"2019","journal-title":"Acta Anaesthesiol Scand"},{"key":"B74","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2016060704"},{"key":"B75","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.00327.2013"},{"key":"B76","doi-asserted-by":"publisher","DOI":"10.5301\/jva.5000630"},{"key":"B77","doi-asserted-by":"publisher","DOI":"10.1249\/JES.0000000000000065"},{"key":"B78","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfv009"},{"key":"B79","doi-asserted-by":"publisher","DOI":"10.1186\/s40981-017-0084-7"},{"key":"B80","doi-asserted-by":"publisher","DOI":"10.1097\/00000542-199909000-00019"},{"key":"B81","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2015.03.028"},{"key":"B82","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1984.36"},{"key":"B83","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.03170707"},{"key":"B84","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2015.62"},{"key":"B85","doi-asserted-by":"crossref","first-page":"854","DOI":"10.1681\/ASN.V104854","volume":"10","author":"Metry G","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B86","doi-asserted-by":"publisher","DOI":"10.2147\/IJNRD.S165925"},{"key":"B87","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2141.1971.tb02707.x"},{"key":"B88","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.357"},{"key":"B89","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1797.2012.01596.x"},{"key":"B90","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000256530.39695.a3"},{"key":"B91","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00644.2002"},{"key":"B92","doi-asserted-by":"crossref","first-page":"1437","DOI":"10.1213\/00000539-199912000-00021","volume":"89","author":"Nishiyama T","year":"1999","journal-title":"Anesth Analg"},{"key":"B93","doi-asserted-by":"publisher","DOI":"10.3109\/0886022X.2013.794675"},{"key":"B94","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.90849.2008"},{"key":"B95","doi-asserted-by":"publisher","DOI":"10.1016\/j.ekir.2018.07.025"},{"key":"B96","doi-asserted-by":"publisher","DOI":"10.14814\/phy2.12059"},{"key":"B97","doi-asserted-by":"publisher","DOI":"10.1378\/chest.96.5.1136"},{"key":"B98","doi-asserted-by":"publisher","DOI":"10.1177\/0271678X18818652"},{"key":"B99","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2017101088"},{"key":"B100","doi-asserted-by":"publisher","DOI":"10.1161\/01.STR.22.12.1508"},{"key":"B101","doi-asserted-by":"publisher","DOI":"10.1159\/000356086"},{"key":"B102","doi-asserted-by":"publisher","DOI":"10.1038\/sj.jcbfm.9600478"},{"key":"B103","doi-asserted-by":"publisher","DOI":"10.1111\/sdi.12659"},{"key":"B104","doi-asserted-by":"publisher","DOI":"10.1007\/s11682-019-00235-z"},{"key":"B105","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfs182"},{"key":"B106","doi-asserted-by":"publisher","DOI":"10.1016\/j.jash.2015.07.007"},{"key":"B107","doi-asserted-by":"publisher","DOI":"10.1038\/jcbfm.1988.133"},{"key":"B108","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.7.4.514"},{"key":"B109","doi-asserted-by":"publisher","DOI":"10.1111\/hdi.12138"},{"key":"B110","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2019.09.003"},{"key":"B111","doi-asserted-by":"publisher","DOI":"10.1007\/s12630-013-9912-z"},{"key":"B112","doi-asserted-by":"crossref","first-page":"1600","DOI":"10.1681\/ASN.V661600","volume":"6","author":"Silver SM","year":"1995","journal-title":"J Am Soc Nephrol"},{"key":"B113","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1992.273"},{"key":"B114","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa065485"},{"key":"B115","doi-asserted-by":"publisher","DOI":"10.1097\/00002480-196204000-00061"},{"key":"B116","doi-asserted-by":"publisher","DOI":"10.1093\/bja\/aei016"},{"key":"B117","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0084943"},{"key":"B118","doi-asserted-by":"publisher","DOI":"10.5414\/CNP64129"},{"key":"B119","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-158-11-201306040-00007"},{"key":"B120","doi-asserted-by":"publisher","DOI":"10.3390\/toxins6061742"},{"key":"B121","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.53.4.720"},{"key":"B122","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.91088.2008"},{"key":"B123","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1992.162"},{"key":"B124","doi-asserted-by":"publisher","DOI":"10.1007\/s004670050060"},{"key":"B125","doi-asserted-by":"publisher","DOI":"10.1212\/WNL.0000000000002527"},{"key":"B126","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2013.03.035"},{"key":"B127","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.01390.2009"},{"key":"B128","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.91077.2008"},{"key":"B129","doi-asserted-by":"publisher","DOI":"10.1038\/jcbfm.1992.105"},{"key":"B130","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2011.03.031"},{"key":"B131","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2013.268953"},{"key":"B132","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0208127"},{"key":"B133","doi-asserted-by":"publisher","DOI":"10.1038\/srep22346"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00438.2020","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,10,8]],"date-time":"2023-10-08T12:39:17Z","timestamp":1696768757000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00438.2020"}},"issued":{"date-parts":[[2020,11,1]]},"references-count":133,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2020,11,1]]}},"alternative-id":["10.1152\/ajprenal.00438.2020"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00438.2020","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2020,11,1]]}},{"indexed":{"date-parts":[[2026,2,13]],"date-time":"2026-02-13T21:42:26Z","timestamp":1771018946075,"version":"3.50.1"},"reference-count":184,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2006,1]]},"abstract":"<jats:p>The epithelial tight junction (TJ) has three major functions. As a \u201cgate,\u201d it serves as a regulatory barrier separating and maintaining biological fluid compartments of different composition. As a \u201cfence,\u201d it generates and maintains the apicobasal polarity of cells that form the confluent epithelium. Finally, the TJ proteins form a trafficking and signaling platform that regulates cell growth, proliferation, differentiation, and dedifferentiation. Six examples are selected that illustrate the emerging link between TJ dysfunction and kidney disease. First, the glomerular slit diaphragm (GSD) is evolved, in part, from the TJ and, on maturation, exhibits all three functions of the TJ. GSD dysfunction leads to proteinuria and, in some instances, podocyte dedifferentiation and proliferation. Second, accumulating evidence supports epithelial-mesenchymal transformation (EMT) as a major player in renal fibrosis, the final common pathway that leads to end-stage renal failure. EMT is characterized by a loss of cell-cell contact and apicobasal polarity, which are hallmarks of TJ dysfunction. Third, in autosomal dominant polycystic kidney disease, mutations of the polycystins may disrupt their known interactions with the apical junction complex, of which the TJ is a major component. This can lead to disturbances in epithelial polarity regulation with consequent abnormal tubulogenesis and cyst formation. Fourth, evidence for epithelial barrier and polarity dysregulation in the pathogenesis of ischemic acute renal failure will be summarized. Fifth, the association between mutations of paracellin-1, the first TJ channel identified, and clinical disorders of magnesium and calcium wasting and bovine renal fibrosis will be used to highlight an integral TJ protein that can serve multiple TJ functions. Finally, the role of WNK4 protein kinase in shunting chloride across the TJ of the distal nephron will be addressed.<\/jats:p>","DOI":"10.1152\/ajprenal.00052.2005","type":"journal-article","created":{"date-parts":[[2005,12,9]],"date-time":"2005-12-09T21:51:00Z","timestamp":1134165060000},"page":"F20-F34","source":"Crossref","is-referenced-by-count":150,"title":["Tight junction biology and kidney dysfunction"],"prefix":"10.1152","volume":"290","author":[{"given":"David B. N.","family":"Lee","sequence":"first","affiliation":[]},{"given":"Edmund","family":"Huang","sequence":"additional","affiliation":[]},{"given":"Harry J.","family":"Ward","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1205351"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117732"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.1995.269.4.G467"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1097-4652(199905)179:2<115::AID-JCP1>3.0.CO;2-T"},{"key":"R5","unstructured":"Bacallao R, Garfinkel A, Monke S, Zampighi G, and Mandel LJ.ATP depletion: a novel method to study junctional properties in epithelial tissues. I. Rearrangement of the actin cytoskeleton.J Cell Sci107: 3301\u20133313, 1994."},{"key":"R6","unstructured":"Barisoni L, Kriz W, Mundel P, and D'Agati V.The dysregulated podocyte phenotype: a novel concept in the pathogenesis of collapsing idiopathic focal segmental glomerulosclerosis and HIV-associated nephropathy.J Am Soc Nephrol10: 51\u201361, 1999."},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1126\/science.1105776"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(01)00231-8"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1038\/35000034"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00035.2003"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000130167.30769.55"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1101\/gad.1211604"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1038\/ng1203-302"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1038\/labinvest.3700129"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1016\/S0962-8924(03)00169-7"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1016\/S1097-2765(00)00123-4"},{"key":"R17","unstructured":"Bracke ME, Depypere H, Labit C, Van Marck V, Vennekens K, Vermeulen SJ, Maelfait I, Philippe J, Serreyn R, and Mareel MM.Functional downregulation of the E-cadherin\/catenin complex leads to loss of contact inhibition of motility and of mitochondrial activity, but not of growth in confluent epithelial cell cultures.Eur J Cell Biol74: 342\u2013349, 1997."},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1997.273.2.H1003"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/11.8.923"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1172\/JCI10968"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.5.F847"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.261.6.F1038"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1038\/35000025"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.129"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00001.2004"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.149.1.111"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00009.2002"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1111\/1523-1747.ep12345525"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.261452898"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2004.07.007"},{"key":"R31","unstructured":"Diamond JM.Twenty-first Bowditch lecture. The epithelial junction: bridge, gate, and fence.Physiologist20: 10\u201318, 1977."},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1978.31"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1159\/000147752"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00406.2003"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.17.2.375"},{"key":"R36","unstructured":"Farquhar MG, Wissig SL, and Palade GE.Glomerular permeability I. Ferritin transfer across the normal glomerular capillary wall.J Am Soc Nephrol10: 2645\u20132662, 1999."},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1038\/35103068"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1016\/S0955-0674(03)00097-8"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00411.2004"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1016\/j.ceb.2003.10.008"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1006\/scdb.2000.0178"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1016\/S0079-6107(02)00037-8"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1998.275.3.C798"},{"key":"R44","doi-asserted-by":"crossref","unstructured":"Goto S, Yaoita E, Matsunami H, Kondo D, Yamamoto T, Kawasaki K, Arakawa M, and Kihara I.Involvement of R-cadherin in the early stage of glomerulogenesis.J Am Soc Nephrol9: 1234\u20131241, 1998.","DOI":"10.1681\/ASN.V971234"},{"key":"R45","unstructured":"Graber M, Lane B, Lamia R, and Pastoriza-Munoz E.Bubble cells: renal tubular cells in the urinary sediment with characteristics of viability.J Am Soc Nephrol1: 999\u20131004, 1991."},{"key":"R46","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.00091"},{"key":"R47","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.107.4.1575"},{"key":"R48","doi-asserted-by":"publisher","DOI":"10.1126\/science.279.5350.509"},{"key":"R49","doi-asserted-by":"publisher","DOI":"10.1159\/000147748"},{"key":"R50","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2052.2002.00844.x"},{"key":"R51","doi-asserted-by":"publisher","DOI":"10.1101\/gr.10.5.659"},{"key":"R52","doi-asserted-by":"publisher","DOI":"10.1172\/JCI5111"},{"key":"R53","doi-asserted-by":"publisher","DOI":"10.1016\/S0166-2236(00)02004-X"},{"key":"R54","doi-asserted-by":"publisher","DOI":"10.1002\/bies.10286"},{"key":"R55","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.R100065200"},{"key":"R56","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/9.11.1641"},{"key":"R57","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M406331200"},{"key":"R58","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.00389"},{"key":"R59","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.439"},{"key":"R60","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.0590031003.x"},{"key":"R61","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.121.3.491"},{"key":"R62","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200405000-00003"},{"key":"R63","doi-asserted-by":"publisher","DOI":"10.1172\/JCI0215518"},{"key":"R64","doi-asserted-by":"publisher","DOI":"10.1016\/0163-7258(94)90013-2"},{"key":"R65","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200405023"},{"key":"R66","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0406172101"},{"key":"R67","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200409000-00012"},{"key":"R68","doi-asserted-by":"publisher","DOI":"10.1016\/j.tem.2005.02.012"},{"key":"R69","doi-asserted-by":"crossref","unstructured":"Kari JA, Farouq M, and Alshaya HO.Familial hypomagnesemia with hypercalciuria and nephrocalcinosis.Pediatr Nephrol18: 506\u2013510, 2003.","DOI":"10.1007\/s00467-003-1139-8"},{"key":"R70","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1992.366"},{"key":"R71","doi-asserted-by":"publisher","DOI":"10.1172\/JCI200114629"},{"key":"R72","doi-asserted-by":"publisher","DOI":"10.1080\/09687680210137219"},{"key":"R73","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2052.2000.00589.x"},{"key":"R74","unstructured":"Kokko JP.Membrane characteristics governing salt and water transport in the loop of Henle.Federation Proc33: 25\u201330, 1974."},{"key":"R75","doi-asserted-by":"publisher","DOI":"10.1111\/1523-1747.ep12363000"},{"key":"R76","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000054887.42550.14"},{"key":"R77","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.055003963.x"},{"key":"R78","doi-asserted-by":"publisher","DOI":"10.1172\/JCI772"},{"key":"R79","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.6.F925"},{"key":"R80","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000139478.03463.D9"},{"key":"R81","doi-asserted-by":"publisher","DOI":"10.1159\/000066656"},{"key":"R82","doi-asserted-by":"publisher","DOI":"10.1093\/carcin\/bgh248"},{"key":"R83","unstructured":"Le Hir M, Keller C, Eschmann V, Hahnel B, Hosser H, and Kriz W.Podocyte bridges between the tuft and Bowman's capsule: an early event in experimental crescentic glomerulonephritis.J Am Soc Nephrol12: 2060\u20132071, 2001."},{"key":"R84","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.148.4.791"},{"key":"R85","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-2836(02)01333-5"},{"key":"R86","doi-asserted-by":"crossref","unstructured":"Lieberthal W, McKenney JB, Kiefer CR, Snyder LM, Kroshian VM, and Sjaastad MD.\u03b21 Integrin-mediated adhesion between renal tubular cells after anoxic injury.J Am Soc Nephrol8: 175\u2013183, 1997.","DOI":"10.1681\/ASN.V82175"},{"key":"R87","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.2000.278.6.Ha1"},{"key":"R88","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.11.12.4259"},{"key":"R89","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000106015.29070.E7"},{"key":"R90","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(02)01283-7"},{"key":"R91","doi-asserted-by":"publisher","DOI":"10.1038\/361552a0"},{"key":"R92","unstructured":"Mandel LJ, Doctor RB, and Bacallao R.ATP depletion: a novel method to study junctional properties in epithelial tissues. II. Internalization of Na+,K+-ATPase and E-cadherin.J Cell Sci107: 3315\u20133324, 1994."},{"key":"R93","doi-asserted-by":"publisher","DOI":"10.1007\/BF00581689"},{"key":"R94","doi-asserted-by":"publisher","DOI":"10.1038\/nrm1055"},{"key":"R95","doi-asserted-by":"publisher","DOI":"10.1210\/jcem.87.7.8449"},{"key":"R96","unstructured":"Michl P, Barth C, Buchholz M, Lerch MM, Rolke M, Holzmann KH, Menke A, Fensterer H, Giehl K, Lohr M, Leder G, Iwamura T, Adler G, and Gress TM.Claudin-4 expression decreases invasiveness and metastatic potential of pancreatic cancer.Cancer Res63: 6265\u20136271, 2003."},{"key":"R97","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00818.x"},{"key":"R98","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.263.3.F488"},{"key":"R99","doi-asserted-by":"publisher","DOI":"10.1172\/JCI114302"},{"key":"R100","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9343(99)00061-3"},{"key":"R101","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(91)90115-F"},{"key":"R102","doi-asserted-by":"publisher","DOI":"10.1172\/JCI112122"},{"key":"R103","doi-asserted-by":"publisher","DOI":"10.1086\/380418"},{"key":"R104","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000039661.06947.FD"},{"key":"R105","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1979.237.4.F319"},{"key":"R106","doi-asserted-by":"publisher","DOI":"10.1016\/S0955-0674(00)00257-X"},{"key":"R107","doi-asserted-by":"publisher","DOI":"10.1016\/S0968-0004(06)80023-X"},{"key":"R108","doi-asserted-by":"publisher","DOI":"10.1038\/ng1076"},{"key":"R109","doi-asserted-by":"publisher","DOI":"10.1038\/nrm757"},{"key":"R110","doi-asserted-by":"publisher","DOI":"10.1006\/geno.2000.6298"},{"key":"R111","doi-asserted-by":"publisher","DOI":"10.1136\/vr.149.4.115"},{"key":"R112","doi-asserted-by":"publisher","DOI":"10.1136\/vr.151.13.384"},{"key":"R113","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.01004"},{"key":"R114","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.273.4.F563"},{"key":"R115","doi-asserted-by":"publisher","DOI":"10.1007\/BF00710559"},{"key":"R116","doi-asserted-by":"publisher","DOI":"10.1126\/science.1105718"},{"key":"R117","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00020.2002"},{"key":"R118","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(03)00108-9"},{"key":"R119","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1995.269.6.C1433"},{"key":"R120","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.199"},{"key":"R121","unstructured":"Pricam C, Humbert F, Perrelet A, Amherdt M, and Orci L.Intercellular junctions in podocytes of the nephrotic glomerulus as seen with freeze-fracture.Lab Invest33: 209\u2013218, 1975."},{"key":"R122","doi-asserted-by":"publisher","DOI":"10.2741\/A544"},{"key":"R123","unstructured":"Racusen LC, Fivush BA, Li YL, Slatnik I, and Solez K.Dissociation of tubular cell detachment and tubular cell death in clinical and experimental \u201cacute tubular necrosis.\u201dLab Invest64: 546\u2013556, 1991."},{"key":"R124","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00439.2002"},{"key":"R125","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00355.2002"},{"key":"R126","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.12.12.3717"},{"key":"R127","unstructured":"Rangel LB, Agarwal R, D'Souza T, Pizer ES, Alo PL, Lancaster WD, Gregoire L, Schwartz DR, Cho KR, and Morin PJ.Tight junction proteins claudin-3 and claudin-4 are frequently overexpressed in ovarian cancer but not in ovarian cystadenomas.Clin Cancer Res9: 2567\u20132575, 2003."},{"key":"R128","unstructured":"Reeves W, Caulfield JP, and Farquhar MG.Differentiation of epithelial foot processes and filtration slits: sequential appearance of occluding junctions, epithelial polyanion, and slit membranes in developing glomeruli.Lab Invest39: 90\u2013100, 1978."},{"key":"R129","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.275.13.9492"},{"key":"R130","doi-asserted-by":"crossref","unstructured":"Reiser J, Kriz W, Kretzler M, and Mundel P.The glomerular slit diaphragm is a modified adherens junction.J Am Soc Nephrol11: 1\u20138, 2000.","DOI":"10.1681\/ASN.V1111"},{"key":"R131","doi-asserted-by":"publisher","DOI":"10.1172\/JCI2071"},{"key":"R132","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.60.2.423"},{"key":"R133","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2004.04.165"},{"key":"R134","doi-asserted-by":"publisher","DOI":"10.1172\/JCI200318232"},{"key":"R135","doi-asserted-by":"publisher","DOI":"10.1016\/S0968-0004(96)30044-3"},{"key":"R136","doi-asserted-by":"publisher","DOI":"10.1136\/vr.150.20.628"},{"key":"R137","doi-asserted-by":"publisher","DOI":"10.1002\/bies.1132"},{"key":"R138","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1981.72"},{"key":"R139","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/9.18.2743"},{"key":"R140","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.111.3.1255"},{"key":"R141","unstructured":"Schnabel E, Dekan G, Miettinen A, and Farquhar MG.Biogenesis of podocalyxin\u2014the major glomerular sialoglycoprotein\u2014in the newborn rat kidney.Eur J Cell Biol48: 313\u2013326, 1989."},{"key":"R142","doi-asserted-by":"crossref","unstructured":"Schwartz EJ, Cara A, Snoeck H, Ross MD, Sunamoto M, Reiser J, Mundel P, and Klotman PE.Human immunodeficiency virus-1 induces loss of contact inhibition in podocytes.J Am Soc Nephrol12: 1677\u20131684, 2001.","DOI":"10.1681\/ASN.V1281677"},{"key":"R143","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.2000.279.6.G1129"},{"key":"R144","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200007000-00015"},{"key":"R145","doi-asserted-by":"publisher","DOI":"10.1126\/science.285.5424.103"},{"key":"R146","doi-asserted-by":"publisher","DOI":"10.1038\/74139"},{"key":"R147","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00042.2003"},{"key":"R148","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199102143240707"},{"key":"R149","doi-asserted-by":"crossref","unstructured":"Tanner GAand Sophasan S.Kidney pressures after temporary renal artery occlusion in the rat.Am J Physiol230: 1173\u20131181, 1976.","DOI":"10.1152\/ajplegacy.1976.230.4.1173"},{"key":"R150","unstructured":"Tassin MT, Beziau A, Gubler MC, and Boyer B.Spatiotemporal expression of molecules associated with junctional complexes during the in vivo maturation of renal podocytes.Int J Dev Biol38: 45\u201354, 1994."},{"key":"R151","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199605303342207"},{"key":"R152","doi-asserted-by":"publisher","DOI":"10.1016\/j.devcel.2005.03.002"},{"key":"R153","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200107000-00009"},{"key":"R154","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.26.16133"},{"key":"R155","doi-asserted-by":"publisher","DOI":"10.1038\/35067088"},{"key":"R156","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.01235"},{"key":"R157","doi-asserted-by":"publisher","DOI":"10.1006\/scdb.2000.0180"},{"key":"R158","doi-asserted-by":"publisher","DOI":"10.1007\/s00429-002-0298-x"},{"key":"R159","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)81559-7"},{"key":"R160","doi-asserted-by":"publisher","DOI":"10.1016\/j.cub.2004.08.048"},{"key":"R161","doi-asserted-by":"publisher","DOI":"10.1016\/j.ceb.2003.12.002"},{"key":"R162","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00024.2003"},{"key":"R163","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(02)00912-1"},{"key":"R164","doi-asserted-by":"crossref","unstructured":"Weber S, Schneider L, Peters M, Misselwitz J, Ronnefarth G, Boswald M, Bonzel KE, Seeman T, Sulakova T, Kuwertz-Broking E, Gregoric A, Palcoux JB, Tasic V, Manz F, Scharer K, Seyberth HW, and Konrad M.Novel paracellin-1 mutations in 25 families with familial hypomagnesemia with hypercalciuria and nephrocalcinosis.J Am Soc Nephrol12: 1872\u20131881, 2001.","DOI":"10.1681\/ASN.V1291872"},{"key":"R165","unstructured":"Whiteside C, Prutis K, Cameron R, and Thompson J.Glomerular epithelial detachment, not reduced charge density, correlates with proteinuria in adriamycin and puromycin nephrosis.Lab Invest61: 650\u2013660, 1989."},{"key":"R166","doi-asserted-by":"publisher","DOI":"10.1046\/j.1469-7580.2003.00238.x"},{"key":"R167","doi-asserted-by":"publisher","DOI":"10.1126\/science.1062844"},{"key":"R168","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.242735399"},{"key":"R169","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra022161"},{"key":"R170","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)64726-8"},{"key":"R171","doi-asserted-by":"publisher","DOI":"10.1007\/s004240050420"},{"key":"R172","doi-asserted-by":"publisher","DOI":"10.1016\/S0960-9822(00)00658-8"},{"key":"R173","doi-asserted-by":"publisher","DOI":"10.1126\/science.285.5424.62"},{"key":"R174","doi-asserted-by":"publisher","DOI":"10.1593\/neo.04241"},{"key":"R175","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0306924101"},{"key":"R176","doi-asserted-by":"publisher","DOI":"10.1172\/JCI17443"},{"key":"R177","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)62533-3"},{"key":"R178","doi-asserted-by":"publisher","DOI":"10.1007\/s004410100380"},{"key":"R179","doi-asserted-by":"crossref","unstructured":"Yeaman C, Grindstaff KK, and Nelson WJ.Mechanism of recruiting Sec6\/8 (exocyst) complex to the apical junctional complex during polarization of epithelial cells.J Cell Sci117: 559\u2013570, 2005.","DOI":"10.1242\/jcs.00893"},{"key":"R180","doi-asserted-by":"publisher","DOI":"10.1002\/path.1711360207"},{"key":"R181","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200309000-00004"},{"key":"R182","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.151.5.F31"},{"key":"R183","doi-asserted-by":"publisher","DOI":"10.1016\/S0962-8924(03)00036-9"},{"key":"R184","doi-asserted-by":"publisher","DOI":"10.1007\/s00109-003-0517-9"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00052.2005","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,7,21]],"date-time":"2021-07-21T06:08:19Z","timestamp":1626847699000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00052.2005"}},"issued":{"date-parts":[[2006,1]]},"references-count":184,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2006,1]]}},"alternative-id":["10.1152\/ajprenal.00052.2005"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00052.2005","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2006,1]]}},{"indexed":{"date-parts":[[2026,2,13]],"date-time":"2026-02-13T12:50:08Z","timestamp":1770987008038,"version":"3.50.1"},"reference-count":39,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2008,11]]},"abstract":"<jats:p> Visfatin is an adipocytokine that improves insulin resistance and has an antidiabetic effect. However, the role of visfatin in the kidney has not yet been reported. In this experiment, the synthesis and physiological action of visfatin in cultured mesangial cells (MCs) were studied to investigate the role of visfatin in diabetic nephropathy. Visfatin was found synthesized in MCs as well as adipocytes. Visfatin synthesis was markedly increased, not by angiotensin II, but by high glucose stimuli. In addition, visfatin treatment induced a rapid uptake of glucose, peaking at 20 min after visfatin treatment in a dose-dependent manner. A small inhibiting RNA against insulin receptor significantly blocked visfatin-mediated glucose uptake. Visfatin stimuli also enhanced intracellular NAD levels, and treatment with FK866, which is a specific inhibitor of nicotinamide phosphoribosyltransferase (Nampt), significantly inhibited visfatin-induced NAD synthesis and glucose uptake. Visfatin treatment increased glucose transporter-1 (GLUT-1) protein expression in isolated cellular membranes, and pretreatment with cytochalasin B completely inhibited visfatin-induced glucose uptake. Moreover, immunofluorescent microscopy showed the migration of cytosolic GLUT-1 into cellular membranes after visfatin treatment. In accordance with these results, the activation of protein kinase B was detected after visfatin treatment. Furthermore, visfatin treatment dramatically increased the synthesis of profibrotic molecules including transforming growth factor-\u03b21, plasminogen activator inhibitor-1, and type I collagen, and pretreatment with cytochalasin B completely inhibited visfatin-induced upregulation of profibrotic molecules. These results suggest that visfatin is produced in MCs, which are a novel target for visfatin, and play an important role in the pathogenesis of diabetic nephropathy. <\/jats:p>","DOI":"10.1152\/ajprenal.90231.2008","type":"journal-article","created":{"date-parts":[[2008,9,4]],"date-time":"2008-09-04T00:24:23Z","timestamp":1220487863000},"page":"F1485-F1494","source":"Crossref","is-referenced-by-count":86,"title":["Visfatin: a new player in mesangial cell physiology and diabetic nephropathy"],"prefix":"10.1152","volume":"295","author":[{"given":"Hye Kyoung","family":"Song","sequence":"first","affiliation":[]},{"given":"Mi Hwa","family":"Lee","sequence":"additional","affiliation":[]},{"given":"Bo Kyung","family":"Kim","sequence":"additional","affiliation":[]},{"given":"Yun Gyu","family":"Park","sequence":"additional","affiliation":[]},{"given":"Gang Jee","family":"Ko","sequence":"additional","affiliation":[]},{"given":"Young Sun","family":"Kang","sequence":"additional","affiliation":[]},{"given":"Jee Young","family":"Han","sequence":"additional","affiliation":[]},{"given":"Sang Youb","family":"Han","sequence":"additional","affiliation":[]},{"given":"Kum Hyun","family":"Han","sequence":"additional","affiliation":[]},{"given":"Hyoung Kyu","family":"Kim","sequence":"additional","affiliation":[]},{"given":"Dae Ryong","family":"Cha","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1016\/S1043-2760(00)00301-5"},{"key":"R2","unstructured":"Ayo S, Radnik R, Garoni J, Glass W, Kreisberg J. High glucose causes an increase in extracellular matrix proteins in cultured mesangial cells. Am J Pathol 136: 1339\u20131348, 1990."},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.261.4.F571"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.260.2.F185"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2006.11.021"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.54.10.2911"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1002\/art.22833"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1210\/jc.2005-1475"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1172\/JCI114066"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.106.665893"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199309303291401"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1126\/science.1097243"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1007\/s00125-006-0303-7"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1210\/jc.2005-2248"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1007\/BF00418276"},{"key":"R16","unstructured":"Hasmann M, Schemainda I. FK866, a highly specific noncompetitive inhibitor of nicotinamide phosphoribosyltransferase, represents a novel mechanism for induction of tumor cell apoptosis. Cancer Res 63: 7436\u20137442, 2003."},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118226"},{"key":"R18","unstructured":"Heilig C, Zaloga C, Lee M, Zhao X, Riser B, Brosius F, Cortes P. Immunogold localization of high affinity glucose transporter isoforms in normal rat kidney. Lab Invest 73: 674\u2013684, 1995."},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1126\/science.7678183"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00438.x"},{"key":"R21","unstructured":"Kikkwa R, Kajiwara N, Haneda M, Shigeta Y, Tsuda K, Yano H, Seino Y. GLUT1 is the main glucose transporter in rat mesangial cells (Abstract). J Am Soc Nephrol 3: 830, 1992."},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.2337\/diab.36.2.240"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2007.03.105"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2005.05.058"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.249"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2265.2007.02966.x"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1111\/j.1462-8902.2004.00334.x"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2007.09.003"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.14.2.1431"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1016\/j.metabol.2006.12.005"},{"key":"R31","unstructured":"Sochor M, Maquer NZ, Hothersall JS, Mclean P. Effect of experimental diabetes on the activity of hexokinase isoenzymes in tissues of the rat. Biochem Int 22: 467\u2013474, 1990."},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1210\/en.2004-0610"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.2337\/diab.42.1.118"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1016\/j.metabol.2006.12.001"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1210\/jc.2006-1303"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1007\/BF00400633"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1172\/JCI200319246"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.260.1.F138"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1992.330"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.90231.2008","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T23:03:43Z","timestamp":1567983823000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.90231.2008"}},"issued":{"date-parts":[[2008,11]]},"references-count":39,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2008,11]]}},"alternative-id":["10.1152\/ajprenal.90231.2008"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.90231.2008","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2008,11]]}},{"indexed":{"date-parts":[[2026,2,13]],"date-time":"2026-02-13T17:54:16Z","timestamp":1771005256170,"version":"3.50.1"},"reference-count":31,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2007,5]]},"abstract":"<jats:p> Hypertensive patients exhibit elevated cancer incidence, especially of cancers of the kidney. Elevated levels of ANG II, the active peptide of the renin-angiotensin system, regulating blood pressure and cardiovascular homeostasis, are known to cause hypertension and kidney diseases. There is evidence that ANG II is an activator of NAD(P)H oxidase, leading to the formation of free radicals, which are known to participate in the induction of DNA damage. This study was undertaken to characterize ANG II-induced DNA damage. DNA damage was measured by comet assay and micronucleus frequency test. Incubation of pig kidney cells (LLC-PK<jats:sub>1<\/jats:sub>) in vitro with ANG II concentrations between 85 and 340 nM led to a 6- to 15-fold increase of DNA damage compared with the control as revealed by comet assay analysis. Micronuclei were induced about fourfold compared with the control in pig and rat kidney cells (LLC-PK<jats:sub>1<\/jats:sub>, NRK) and in human promyelocytic cells (HL-60). ANG II-induced DNA damage could be prevented by coincubation with the ANG II type 1 receptor blocker candesartan and the antioxidants N-acetylcysteine and \u03b1-tocopherol. The ANG II type 2 receptor antagonist PD123319 could not reduce ANG II-induced DNA damage. Measurement of reactive oxygen species (ROS) by flow cytometry showed an enhanced formation after exposure to ANG II and a reduction of ROS after candesartan, N-acetylcysteine, and \u03b1-tocopherol. The present findings support our hypothesis that ANG II causes DNA damage via ANG II type 1 receptor binding and subsequent formation of oxidative stress. <\/jats:p>","DOI":"10.1152\/ajprenal.00458.2006","type":"journal-article","created":{"date-parts":[[2007,1,18]],"date-time":"2007-01-18T01:13:17Z","timestamp":1169082797000},"page":"F1427-F1434","source":"Crossref","is-referenced-by-count":47,"title":["Angiotensin II-induced genomic damage in renal cells can be prevented by angiotensin II type 1 receptor blockage or radical scavenging"],"prefix":"10.1152","volume":"292","author":[{"given":"Nicole","family":"Schupp","sequence":"first","affiliation":[]},{"given":"Ursula","family":"Schmid","sequence":"additional","affiliation":[]},{"given":"Przemyslaw","family":"Rutkowski","sequence":"additional","affiliation":[]},{"given":"Ursula","family":"Lakner","sequence":"additional","affiliation":[]},{"given":"Nilesh","family":"Kanase","sequence":"additional","affiliation":[]},{"given":"August","family":"Heidland","sequence":"additional","affiliation":[]},{"given":"Helga","family":"Stopper","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","unstructured":"Burlinson B, Tice RR, Speit G, Agurell E, Brendler-Schwaab SY, Collins AR, Escobar P, Honma M, Kumaravel TS, Nakajima M, Sasaki YF, Thybaud V, Uno Y, Vasquez M, Hartmann A. Fourth International Workgroup on Genotoxicity Testing: results of the in vivo comet assay workgroup. Mutat Res In press."},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1210\/er.2003-0001"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM200011023431804"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1016\/j.tem.2005.07.009"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1016\/j.mrfmmm.2006.05.028"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1002\/1097-0142(20011101)92:9<2462::AID-CNCR1596>3.0.CO;2-L"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.74.6.1141"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1016\/S0167-0115(00)00136-1"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9343(02)01049-5"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00212.x"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1126\/science.3287616"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1038\/sj.jhh.1001982"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1080\/08037050310001057"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.20.3.267"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1016\/j.febslet.2006.10.016"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1080\/02841860310022346"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.3317\/jraas.2002.043"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1177\/15353702-0322805-31"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1081\/CNV-200055962"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00562.x"},{"key":"R21","doi-asserted-by":"crossref","unstructured":"Rozen S, Skaletsky H. Primer3 on the WWW for general users and for biologist programmers. Methods Mol Biol 132: 365\u2013386, 2000.","DOI":"10.1385\/1-59259-192-2:365"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1196\/annals.1333.079"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1016\/0014-4827(88)90265-0"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.25.5.1021"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1186\/1476-9255-1-3"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1007\/s10147-005-0520-y"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.2174\/1568009054629663"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004060458"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1016\/j.cbi.2005.12.009"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-200302000-00027"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1097\/01.hjh.0000220402.53869.72"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00458.2006","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T23:26:24Z","timestamp":1567985184000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00458.2006"}},"issued":{"date-parts":[[2007,5]]},"references-count":31,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2007,5]]}},"alternative-id":["10.1152\/ajprenal.00458.2006"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00458.2006","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2007,5]]}},{"indexed":{"date-parts":[[2026,2,19]],"date-time":"2026-02-19T13:38:49Z","timestamp":1771508329577,"version":"3.50.1"},"reference-count":90,"publisher":"American Physiological Society","issue":"9","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,5,1]]},"abstract":"<jats:p>Meprin A, composed of \u03b1- and \u03b2-subunits, is a membrane-associated neutral metalloendoprotease that belongs to the astacin family of zinc endopeptidases. It was first discovered as an azocasein and benzoyl-l-tyrosyl- p-aminobenzoic acid hydrolase in the brush-border membranes of proximal tubules and intestines. Meprin isoforms are now found to be widely distributed in various organs (kidney, intestines, leukocytes, skin, bladder, and a variety of cancer cells) and are capable of hydrolyzing and processing a large number of substrates, including extracellular matrix proteins, cytokines, adherens junction proteins, hormones, bioactive peptides, and cell surface proteins. The ability of meprin A to cleave various substrates sheds new light on the functional properties of this enzyme, including matrix remodeling, inflammation, and cell-cell and cell-matrix processes. Following ischemia-reperfusion (IR)- and cisplatin-induced acute kidney injury (AKI), meprin A is redistributed toward the basolateral plasma membrane, and the cleaved form of meprin A is excreted in the urine. These studies suggest that altered localization and shedding of meprin A in places other than the apical membranes may be deleterious in vivo in acute tubular injury. These studies also provide new insight into the importance of a sheddase involved in the release of membrane-associated meprin A under pathological conditions. Meprin A is injurious to the kidney during AKI, as meprin A-knockout mice and meprin inhibition provide protective roles and improve renal function. Meprin A, therefore, plays an important role in AKI and potentially is a unique target for therapeutic intervention during AKI.<\/jats:p>","DOI":"10.1152\/ajprenal.00014.2013","type":"journal-article","created":{"date-parts":[[2013,2,21]],"date-time":"2013-02-21T06:41:33Z","timestamp":1361428893000},"page":"F1150-F1158","source":"Crossref","is-referenced-by-count":42,"title":["Meprin A metalloproteinase and its role in acute kidney injury"],"prefix":"10.1152","volume":"304","author":[{"given":"Gur P.","family":"Kaushal","sequence":"first","affiliation":[{"name":"Central Arkansas Veterans Healthcare System, Little Rock, Arkansas;"},{"name":"Department of Internal Medicine, University of Arkansas for Medical Sciences, Little Rock, Arkansas;"},{"name":"Department of Biochemistry, University of Arkansas for Medical Sciences, Little Rock, Arkansas; and"}]},{"given":"Randy S.","family":"Haun","sequence":"additional","affiliation":[{"name":"Central Arkansas Veterans Healthcare System, Little Rock, Arkansas;"},{"name":"Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences, Little Rock, Arkansas"}]},{"given":"Christian","family":"Herzog","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Arkansas for Medical Sciences, Little Rock, Arkansas;"}]},{"given":"Sudhir V.","family":"Shah","sequence":"additional","affiliation":[{"name":"Central Arkansas Veterans Healthcare System, Little Rock, Arkansas;"},{"name":"Department of Internal Medicine, University of Arkansas for Medical Sciences, Little Rock, Arkansas;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1038\/sj.emboj.7600974"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M802814200"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1042\/bj2640335"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1515\/BC.2003.092"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1038\/sj.jid.5700675"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/0968-0004(93)90049-S"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M208808200"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M011414200"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1042\/bj3150461"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1042\/bj1990591"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.81.17.5542"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/j.febslet.2005.03.045"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1016\/0888-7543(95)80142-9"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1042\/bj2410229"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00214.2007"},{"key":"B16","doi-asserted-by":"crossref","first-page":"1163","DOI":"10.1515\/BC.2007.156","volume":"388","author":"Bylander JE","year":"2007","journal-title":"J Biol Chem"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00209.x"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.47.30272"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1042\/bj2800057"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1177\/39.1.1701182"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1987.253.4.C535"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.172.7.4510"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1515\/BC.2008.075"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.4.2271"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1111\/j.1432-1033.1997.00920.x"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.4161\/chan.5.1.13759"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/j.febslet.2012.10.033"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(93)80422-Q"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1042\/bj3460083"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1111\/j.1432-1033.1997.00933.x"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M211169200"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1136\/jcp.2005.034223"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2008.12.161"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1016\/j.cyto.2005.06.012"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002189"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1093\/glycob\/cwr107"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.175.5.3177"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5001575"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0002153"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M102654200"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M414218200"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M602769200"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1007\/s00018-012-1106-2"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M111.252718"},{"key":"B45","first-page":"7682","volume":"269","author":"Johnson GD","year":"1994","journal-title":"J Biol Chem 1994"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M003521200"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.126.5.1319"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1042\/bj2450515"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-5793(99)01712-3"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1152\/physiolgenomics.00173.2011"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1038\/jid.2010.202"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1042\/bj20031163"},{"key":"B53","first-page":"106","volume":"1518","author":"Kumar JM","year":"2001","journal-title":"Biochem Biophys Acta"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.3181\/0703-MR-72"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M213021200"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1042\/bj20021398"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.44.29043"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1046\/j.1432-1327.1999.00071.x"},{"key":"B59","first-page":"1127","volume":"59","author":"Lottaz D","year":"1999","journal-title":"Cancer Res"},{"key":"B60","doi-asserted-by":"crossref","first-page":"15388","DOI":"10.1016\/S0021-9258(17)36618-8","volume":"269","author":"Marchand Pl Tang J","year":"1994","journal-title":"J Biol Chem"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1007\/s10585-005-0660-5"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1042\/bj3090683"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.272.4.F430"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1515\/bc.2010.023"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0002278"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00703.2010"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1515\/BC.2006.084"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M206203200"},{"key":"B69","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0008835"},{"key":"B70","doi-asserted-by":"publisher","DOI":"10.1515\/BC.2007.060"},{"key":"B71","doi-asserted-by":"publisher","DOI":"10.1515\/bc.2010.033"},{"key":"B72","doi-asserted-by":"crossref","first-page":"3213","DOI":"10.1242\/dev.120.11.3213","volume":"120","author":"Spencer-Dene B","year":"1994","journal-title":"Development"},{"key":"B73","doi-asserted-by":"publisher","DOI":"10.1042\/bj2550045"},{"key":"B74","doi-asserted-by":"publisher","DOI":"10.1042\/cs0620557"},{"key":"B75","doi-asserted-by":"publisher","DOI":"10.1016\/0003-9861(88)90377-3"},{"key":"B76","doi-asserted-by":"publisher","DOI":"10.1016\/j.mam.2008.08.002"},{"key":"B77","doi-asserted-by":"publisher","DOI":"10.1016\/0959-440X(95)80101-4"},{"key":"B78","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejphar.2007.11.044"},{"key":"B79","doi-asserted-by":"publisher","DOI":"10.1006\/abbi.1997.0453"},{"key":"B80","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1995.1366"},{"key":"B81","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.52.35260"},{"key":"B82","doi-asserted-by":"publisher","DOI":"10.1042\/bss0700053"},{"key":"B83","first-page":"339","volume":"70","author":"Walker PD","year":"1994","journal-title":"Lab Invest"},{"key":"B84","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00949.x"},{"key":"B85","doi-asserted-by":"publisher","DOI":"10.1097\/SHK.0b013e3181ec39cc"},{"key":"B86","doi-asserted-by":"publisher","DOI":"10.1021\/bi00098a029"},{"key":"B87","doi-asserted-by":"publisher","DOI":"10.1016\/0024-3205(94)00795-0"},{"key":"B88","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90524.2008"},{"key":"B89","doi-asserted-by":"publisher","DOI":"10.1016\/0955-0674(94)90093-0"},{"key":"B90","doi-asserted-by":"publisher","DOI":"10.1007\/978-0-387-70630-6_1"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00014.2013","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,6,29]],"date-time":"2023-06-29T17:55:28Z","timestamp":1688061328000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00014.2013"}},"issued":{"date-parts":[[2013,5,1]]},"references-count":90,"journal-issue":{"issue":"9","published-print":{"date-parts":[[2013,5,1]]}},"alternative-id":["10.1152\/ajprenal.00014.2013"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00014.2013","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2013,5,1]]}},{"indexed":{"date-parts":[[2026,2,18]],"date-time":"2026-02-18T23:43:22Z","timestamp":1771458202325,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1981,4,1]]},"abstract":"<jats:p> Normal potassium homeostasis is regulated by both renal and extrarenal mechanisms. Although chronic potassium balance is primarily regulated by the kidneys, acute potassium tolerance is largely determined by extrarenal tissues. During the first 4-6 h following an acute potassium load, only about 50% of the potassium is excreted by the kidneys. Of the remaining 50% that is retained, over 80% is translocated into cells, and this provides the primary defense against hyperkalemia. Potassium uptake by both liver and muscle and intestinal secretion of potassium are the most important mechanisms of extrarenal potassium disposal. Several hormones, including insulin and epinephrine, have been shown to play an important role in the maintenance of normal extrarenal potassium metabolism. These hormones function by enhancing potassium uptake by liver and muscle. There is also evidence that aldosterone is necessary in the maintenance of normal extrarenal potassium tolerance. Although the major extrarenal site of action of aldosterone has not yet been clearly defined, gastrointestinal potassium secretion and muscle transport of potassium are both affected by the hormone. Evidence exists that glucocorticoids may also have an effect on extrarenal potassium homeostasis. In addition to this hormonal regulation, cellular shifts of potassium are influenced by changes in acid-base balance. Extrarenal potassium tolerance is impaired in chronic renal insufficiency. These uremia-related changes are discussed in the context of our present understanding of normal extrarenal potassium metabolism. <\/jats:p>","DOI":"10.1152\/ajprenal.1981.240.4.f257","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T07:45:10Z","timestamp":1513928710000},"page":"F257-F268","source":"Crossref","is-referenced-by-count":30,"title":["Extrarenal potassium homeostasis"],"prefix":"10.1152","volume":"240","author":[{"given":"M. J.","family":"Bia","sequence":"first","affiliation":[]},{"given":"R. A.","family":"DeFronzo","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1981.240.4.F257","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T14:09:19Z","timestamp":1567951759000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1981.240.4.F257"}},"issued":{"date-parts":[[1981,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1981,4,1]]}},"alternative-id":["10.1152\/ajprenal.1981.240.4.F257"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1981.240.4.f257","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1981,4,1]]}},{"indexed":{"date-parts":[[2026,2,20]],"date-time":"2026-02-20T22:36:43Z","timestamp":1771627003942,"version":"3.50.1"},"reference-count":43,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2005,12]]},"abstract":"<jats:p> In a companion study (Layton AT and Layton HE. Am J Physiol Renal Physiol 289: F1346\u2013F1366, 2005), a region-based mathematical model was formulated for the urine concentrating mechanism (UCM) in the outer medulla (OM) of the rat kidney. In the present study, we quantified the sensitivity of that model to several structural assumptions, including the degree of regionalization and the degree of inclusion of short descending limbs (SDLs) in the vascular bundles of the inner stripe (IS). Also, we quantified model sensitivity to several parameters that have not been well characterized in the experimental literature, including boundary conditions, short vasa recta distribution, and ascending vasa recta (AVR) solute permeabilities. These studies indicate that regionalization elevates the osmolality of the fluid delivered into the inner medulla via the collecting ducts; that model predictions are not significantly sensitive to boundary conditions; and that short vasa recta distribution and AVR permeabilities significantly impact concentrating capability. Moreover, we investigated, in the context of the UCM, the functional significance of several aspects of tubular segmentation and heterogeneity: SDL segments in the IS that are likely to be impermeable to water but highly permeable to urea; a prebend segment of SDLs that may be functionally like thick ascending limb (TAL); differing IS and outer stripe Na<jats:sup>+<\/jats:sup> active transport rates in TAL; and potential active urea secretion into the proximal straight tubules. Model calculations predict that these aspects of tubular of segmentation and heterogeneity generally enhance solute cycling or promote effective UCM function. <\/jats:p>","DOI":"10.1152\/ajprenal.00347.2003","type":"journal-article","created":{"date-parts":[[2005,5,25]],"date-time":"2005-05-25T02:48:50Z","timestamp":1116989330000},"page":"F1367-F1381","source":"Crossref","is-referenced-by-count":44,"title":["A region-based mathematical model of the urine concentrating mechanism in the rat outer medulla. II. Parameter sensitivity and tubular inhomogeneity"],"prefix":"10.1152","volume":"289","author":[{"given":"Anita T.","family":"Layton","sequence":"first","affiliation":[]},{"given":"Harold E.","family":"Layton","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1007\/BF00592507"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1968.sp008568"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1007\/BF00216222"},{"key":"R4","unstructured":"Bankir L and Trinh-Trang-Tan MM. Urea and the kidney. In: The Kidney (6th ed.), edited by Brenner BM and Rector FC. Philadelphia, PA: Saunders, 2000, p. 637\u2013679."},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1996.271.1.R157"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1988.255.3.F500"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1007\/BF00582911"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1007\/BF00587241"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00045.2002"},{"key":"R10","unstructured":"Hoppensteadt FC and Peskin CS. Mathematics in Medicine and the Life Sciences (2d ed.). New York: Springer-Verlag, 2001."},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1007\/BF00583939"},{"key":"R12","unstructured":"Jamison RL and Kriz W. Urinary Concentrating Mechanism: Structure and Function. New York: Oxford University Press, 1982."},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1986.4"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1979.237.2.F114"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00246.2001"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1983.245.5.F634"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1977.118"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1007\/BF00337120"},{"key":"R19","unstructured":"Kriz W and Kaissling B. Structural organization of the mammalian kidney. In: The Kidney: Physiology and Pathophysiology (3rd ed.), edited by Seldin DW and Giebisch G. Philadelphia, PA: Lippincott Williams & Wilkins, 2000, p. 587\u2013654."},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1007\/BF00519771"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1007\/BF00520710"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8240(03)00045-4"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00346.2003"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-3495(86)83731-6"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1016\/0025-5564(93)90065-I"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.270.1.F9"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8240(03)00029-6"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.268.6.F1023"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1172\/JCI116948"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00304.2002"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1974.49"},{"key":"R32","doi-asserted-by":"crossref","unstructured":"Pfaller W. Structure Function Correlation on Rat Kidney: Quantitative Correlation of Structure and Function in the Normal and Injured Rat Kidney. New York: Springer-Verlag, 1982.","DOI":"10.1007\/978-3-642-68287-2"},{"key":"R33","unstructured":"Rasch R, Grann BL, and Andreasen A. 3D reconstruction of the bend of short loops from the loop of Henle (Abstract). J Am Soc Nephrol 13: SA\u2013P0017, 2002."},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.253.5.F823"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1972.75"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.268.4.F698"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.275.5.F671"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1998.274.5.H1662"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.1.F52"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.2.F413"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.1.F24"},{"key":"R42","doi-asserted-by":"crossref","unstructured":"Wesson LG and Anslow WP. Effect of osmotic and mercurial diuresis on simultaneous water diuresis. Am J Physiol 170: 255\u2013269, 1952.","DOI":"10.1152\/ajplegacy.1952.170.2.255"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.260.3.F368"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00347.2003","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T23:07:21Z","timestamp":1567984041000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00347.2003"}},"issued":{"date-parts":[[2005,12]]},"references-count":43,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2005,12]]}},"alternative-id":["10.1152\/ajprenal.00347.2003"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00347.2003","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2005,12]]}},{"indexed":{"date-parts":[[2026,2,20]],"date-time":"2026-02-20T22:36:56Z","timestamp":1771627016217,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1995,12,1]]},"abstract":"<jats:p> Nephron filtration rate (SNGFR) and proximal tubular reabsorption are coordinated by the processes of tubuloglomerular feedback (TGF) and glomerulotubular balance (GTB). We examined the role of nitric oxide (NO) in TGF and GTB, by delivering the NO synthase inhibitor, NG-monomethyl-L-arginine (L-NMMA) into late proximal nephrons by micropuncture in Inactin-anesthetized euvolemic rats. First, we determined the dependence of SNGFR on late proximal tubular flow rate (VLP) during orthograde microperfusion of Henle's loop downstream from an obstructing wax block (open-loop microperfusion). Second, we examined the homeostatic efficiency of the TGF-GTB system, (i.e., its ability to stabilize VLP) by perturbing VLP in free-flowing nephrons, while using a noninvasive optical technique to measure flow immediately upstream from the perturbation (closed-loop perturbation). Third, we tested whether L-NMMA could alter the afferent signal to TGF by changing the relationship between VLP and the flow rate (VED) or ionic content (CED) of early distal tubular fluid during open-loop microperfusion. During open-loop microperfusion, L-NMMA decreased SNGFR at VLP between 10 and 40 nl\/min but did not alter the relationship between VLP and VED or CED. During closed-loop perturbation, L-NMMA did not affect ambient VLP but increased the homeostatic efficiency of the TGF-GTB system. The combined effects on SNGFR and ambient VLP suggest that L-NMMA reduces proximal reabsorption. However, this could account for only a small fraction of the increase in homeostatic efficiency, the greater share of which must be mediated within the juxtaglomerular apparatus. It appears that juxtaglomerular NO exerts an upward pressure on SNGFR and reduces the efficiency of the TGF-GTB system in stabilizing VLP at ambient flow rates under euvolemic conditions. <\/jats:p>","DOI":"10.1152\/ajprenal.1995.269.6.f892","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T00:21:03Z","timestamp":1513988463000},"page":"F892-F899","source":"Crossref","is-referenced-by-count":17,"title":["Inhibition of local nitric oxide synthase increases homeostatic efficiency of tubuloglomerular feedback"],"prefix":"10.1152","volume":"269","author":[{"given":"V.","family":"Vallon","sequence":"first","affiliation":[{"name":"Department of Medicine, University of California San Diego, USA."}]},{"given":"S.","family":"Thomson","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of California San Diego, USA."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1995.269.6.F892","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:58:12Z","timestamp":1567958292000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1995.269.6.F892"}},"issued":{"date-parts":[[1995,12,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1995,12,1]]}},"alternative-id":["10.1152\/ajprenal.1995.269.6.F892"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1995.269.6.f892","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1995,12,1]]}},{"indexed":{"date-parts":[[2026,2,20]],"date-time":"2026-02-20T22:35:42Z","timestamp":1771626942005,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1995,3,1]]},"abstract":"<jats:p> Endothelin (ET) is a potent vasoconstrictor peptide of endothelial origin, which at low doses results in renal vasoconstriction and diuresis with variable actions on sodium excretion. The current study conducted in four groups of anesthetized dogs was designed to define the role of the ETA and ETB receptor subtypes in the renal actions of low-dose exogenous ET. Group 1 (n = 4) animals served as time controls. In group 2 (n = 6) a systemic ET-1 (5 ng.kg-1.min-1) infusion mediated renal vasoconstriction, antinatriuresis with increases in proximal fractional reabsorption of sodium, and diuresis with a decrease in urine osmolality. In group 3 (n = 6) intrarenal BQ-123 (4 micrograms.kg-1.min-1), a selective ETA antagonist, abolished the systemic ET-1-mediated changes in renal hemodynamics and unmasked a natriuretic action at the level of the proximal tubule. In contrast, the diuretic response of ET was not altered by BQ-123. In group 4 (n = 6) intrarenal sarafotoxin 6-c, a selective ETB receptor agonist, resulted in a diuretic response without a change in sodium excretion. These studies suggest that the ETA receptor contributes to the renal vasoconstriction, whereas the ETB receptor is largely responsible for the diuretic response during exogenous ET. This study also suggests that at low doses ET is natriuretic in vivo by decreasing proximal tubular reabsorption of sodium independent of ETA or ETB receptor activation. <\/jats:p>","DOI":"10.1152\/ajprenal.1995.268.3.f455","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T04:08:46Z","timestamp":1514002126000},"page":"F455-F460","source":"Crossref","is-referenced-by-count":34,"title":["Role of endothelin receptor subtypes in the in vivo regulation of renal function"],"prefix":"10.1152","volume":"268","author":[{"given":"A. L.","family":"Clavell","sequence":"first","affiliation":[{"name":"Department of Internal Medicine and Physiology, Mayo Clinic andFoundation, Rochester, Minnesota 55905."}]},{"given":"A. J.","family":"Stingo","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine and Physiology, Mayo Clinic andFoundation, Rochester, Minnesota 55905."}]},{"given":"K. B.","family":"Margulies","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine and Physiology, Mayo Clinic andFoundation, Rochester, Minnesota 55905."}]},{"given":"R. R.","family":"Brandt","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine and Physiology, Mayo Clinic andFoundation, Rochester, Minnesota 55905."}]},{"suffix":"Jr","given":"J. C.","family":"Burnett","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine and Physiology, Mayo Clinic andFoundation, Rochester, Minnesota 55905."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1995.268.3.F455","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:54:22Z","timestamp":1567972462000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1995.268.3.F455"}},"issued":{"date-parts":[[1995,3,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1995,3,1]]}},"alternative-id":["10.1152\/ajprenal.1995.268.3.F455"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1995.268.3.f455","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1995,3,1]]}},{"indexed":{"date-parts":[[2026,2,20]],"date-time":"2026-02-20T22:35:42Z","timestamp":1771626942008,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1994,11,1]]},"abstract":"<jats:p> The intervention of the L-arginine-NO pathway in renal vasodilation and renin secretion was studied in an isolated perfused rat kidney model. NG-nitro-L-arginine methyl ester (L-NAME, 1-25 microM), an inhibitor of nitric oxide (NO) synthesis, caused a dose-dependent increase in perfusion pressure (PP) and a dose-dependent decrease in renal perfusate flow. Renin was inhibited independently of the rise in PP, since the effect of L-NAME on renin release was the same when PP was maintained constant. Exposure of rats to low [salt depleted (SD)] or high [salt repleted (SR)] salt intake for 1 mo influenced the renal vascular response to L-NAME (3 microM). Isolated SR rat kidney vasculature vasoconstricted to a greater extent after inhibition of NO synthase than did that of SD kidneys. A similar fall in renin release was observed after L-NAME in both groups, despite a higher renin secretion rate in SD than in SR rats. These results suggest that NO-dependent vasodilation counteracts the renal vasoconstrictor effect of sodium loading. <\/jats:p>","DOI":"10.1152\/ajprenal.1994.267.5.f798","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T04:51:59Z","timestamp":1514004719000},"page":"F798-F804","source":"Crossref","is-referenced-by-count":4,"title":["Influence of sodium diet on L-NAME effects on renin release and renal vasoconstriction"],"prefix":"10.1152","volume":"267","author":[{"given":"J.","family":"Gardes","sequence":"first","affiliation":[{"name":"Institut National de la Sante et de la Recherche Medicale U367, Paris,France."}]},{"given":"M. F.","family":"Gonzalez","sequence":"additional","affiliation":[{"name":"Institut National de la Sante et de la Recherche Medicale U367, Paris,France."}]},{"given":"F.","family":"Alhenc-Gelas","sequence":"additional","affiliation":[{"name":"Institut National de la Sante et de la Recherche Medicale U367, Paris,France."}]},{"given":"J.","family":"Menard","sequence":"additional","affiliation":[{"name":"Institut National de la Sante et de la Recherche Medicale U367, Paris,France."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1994.267.5.F798","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:55:39Z","timestamp":1567972539000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1994.267.5.F798"}},"issued":{"date-parts":[[1994,11,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1994,11,1]]}},"alternative-id":["10.1152\/ajprenal.1994.267.5.F798"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1994.267.5.f798","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1994,11,1]]}},{"indexed":{"date-parts":[[2026,2,20]],"date-time":"2026-02-20T22:35:52Z","timestamp":1771626952042,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1994,11,1]]},"abstract":"<jats:p> We examined the renal effects of a specific adenosine A1-receptor antagonist, 1,3-dipropyl-8-cyclopentylxanthine (DPCPX, 10 micrograms.kg-1.min-1 iv). Since adenosine is a potent inhibitor of renin release, additional experiments were performed with an angiotensin AT1-receptor antagonist (losartan, 10 mg\/kg i.v.). DP CPX alone induced a significant (P &lt; 0.05) decrease in afferent arteriolar resistance (RA, 1.83 +\/- 0.18 to 1.43 +\/- 0.06 dyn.s.cm-5 x 10(10); P &lt; 0.05). This led to a rise in the transcapillary hydraulic pressure difference (delta P, 35 +\/- 1 to 43 +\/- 2 mmHg; P &lt; 0.05). Surprisingly, the glomerular capillary ultrafiltration coefficient (Kf) fell (0.101 +\/- 0.017 to 0.064 +\/- 0.009 nl.s-1.mmHg-1, P &lt; 0.05). Additionally, DPCPX infusion resulted in dramatic increases in both urine flow and sodium excretion. With losartan pretreatment, DPCPX did not cause significant changes in RA and delta P. Also, DPCPX increased Kf (0.057 +\/- 0.005 to 0.075 +\/- 0.008 nl.s-1.mmHg-1, P &lt; 0.05). Furthermore, the large DPCPX-induced increases in urine flow and sodium excretion were largely suppressed by pretreatment with losartan. These data indicate that endogenous adenosine plays a significant role in maintaining afferent arteriolar tone and that the renin-angiotensin system may mediate some of the wide ranging renal effects of adenosine. <\/jats:p>","DOI":"10.1152\/ajprenal.1994.267.5.f783","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T23:51:59Z","timestamp":1513986719000},"page":"F783-F790","source":"Crossref","is-referenced-by-count":16,"title":["Effects of selective A1 receptor blockade on glomerular hemodynamics: involvement of renin-angiotensin system"],"prefix":"10.1152","volume":"267","author":[{"given":"K. A.","family":"Munger","sequence":"first","affiliation":[{"name":"Department of Medicine, Emory University School of Medicine, Atlanta,Georgia 30022."}]},{"given":"E. K.","family":"Jackson","sequence":"additional","affiliation":[{"name":"Department of Medicine, Emory University School of Medicine, Atlanta,Georgia 30022."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1994.267.5.F783","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:55:37Z","timestamp":1567958137000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1994.267.5.F783"}},"issued":{"date-parts":[[1994,11,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1994,11,1]]}},"alternative-id":["10.1152\/ajprenal.1994.267.5.F783"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1994.267.5.f783","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1994,11,1]]}},{"indexed":{"date-parts":[[2026,2,20]],"date-time":"2026-02-20T22:36:02Z","timestamp":1771626962805,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1989,1,1]]},"abstract":"<jats:p> The purpose of this study was to investigate the hypothesis that changes in renal perfusion pressure may be transmitted to the renal interstitium and cause alterations in renal interstitial hydrostatic pressure and sodium excretion. A method that utilizes a chronically implanted polyethylene matrix that allows for direct continuous measurement of renal interstitial hydrostatic pressure, and agrees well with subcapsular measurement in rats, was developed. Renal interstitial hydrostatic pressure, fractional excretion of sodium, and urine flow rate were 3.0 +\/- 0.3 mmHg, 0.35 +\/- 0.13%, and 19.44 +\/- 3.00 microliter\/min, respectively, when renal perfusion pressure was 101 +\/- 0.8 mmHg. When renal perfusion pressure was increased to 123 +\/- 0.9 mmHg renal interstitial hydrostatic pressure, fractional excretion of sodium, and urine flow rate increased significantly to 5.8 +\/- 0.6 mmHg, 1.29 +\/- 0.29%, and 50.76 +\/- 8.83 microliter\/min, respectively, in anesthetized male Sprague-Dawley rats. These changes occur despite a well-autoregulated glomerular filtration rate and renal blood flow. In conclusion, increasing renal perfusion pressure caused a significant increase in renal interstitial hydrostatic pressure as measured directly by the implanted polyethylene matrix method and was associated with a significant increase in sodium excretion. <\/jats:p>","DOI":"10.1152\/ajprenal.1989.256.1.f165","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T21:05:54Z","timestamp":1513976754000},"page":"F165-F170","source":"Crossref","is-referenced-by-count":7,"title":["Effect of renal perfusion pressure on renal interstitial hydrostatic pressure in rats"],"prefix":"10.1152","volume":"256","author":[{"given":"A. A.","family":"Khraibi","sequence":"first","affiliation":[{"name":"Department of Physiology and Biophysics, Mayo Clinic and Foundation,Rochester, Minnesota 55905."}]},{"given":"J. A.","family":"Haas","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, Mayo Clinic and Foundation,Rochester, Minnesota 55905."}]},{"given":"F. G.","family":"Knox","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, Mayo Clinic and Foundation,Rochester, Minnesota 55905."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1989.256.1.F165","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:08:06Z","timestamp":1567969686000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1989.256.1.F165"}},"issued":{"date-parts":[[1989,1,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1989,1,1]]}},"alternative-id":["10.1152\/ajprenal.1989.256.1.F165"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1989.256.1.f165","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1989,1,1]]}},{"indexed":{"date-parts":[[2026,2,23]],"date-time":"2026-02-23T13:44:10Z","timestamp":1771854250541,"version":"3.50.1"},"reference-count":14,"publisher":"American Physiological Society","issue":"6","funder":[{"DOI":"10.13039\/100000052","name":"HHS | NIH | NIH Office of the Director (OD)","doi-asserted-by":"publisher","award":["U54OD020351"],"award-info":[{"award-number":["U54OD020351"]}],"id":[{"id":"10.13039\/100000052","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2018,12,1]]},"abstract":"<jats:p> Current methods of scoring histological kidney samples, specifically glomeruli, do not allow for collection of quantitative data in a high-throughput and consistent manner. Neither untrained individuals nor computers are presently capable of identifying glomerular features, so expert pathologists must do the identification and score using a categorical matrix, complicating statistical analysis. Critical information regarding overall health and physiology is encoded in these samples. Rapid comprehensive histological scoring could be used, in combination with other physiological measures, to significantly advance renal research. Therefore, we used machine learning to develop a high-throughput method to automatically identify and collect quantitative data from glomeruli. Our method requires minimal human interaction between steps and provides quantifiable data independent of user bias. The method uses free existing software and is usable without extensive image analysis training. Validation of the classifier and feature scores in mice is highlighted in this work and shows the power of applying this method in murine research. Preliminary results indicate that the method can be applied to data sets from different species after training on relevant data, allowing for fast glomerular identification and quantitative measurements of glomerular features. Validation of the classifier and feature scores are highlighted in this work and show the power of applying this method. The resulting data are free from user bias. Continuous data, such that statistical analysis can be performed, allows for more precise and comprehensive interrogation of samples. These data can then be combined with other physiological data to broaden our overall understanding of renal function. <\/jats:p>","DOI":"10.1152\/ajprenal.00629.2017","type":"journal-article","created":{"date-parts":[[2018,9,26]],"date-time":"2018-09-26T11:36:05Z","timestamp":1537961765000},"page":"F1644-F1651","source":"Crossref","is-referenced-by-count":31,"title":["Automatic glomerular identification and quantification of histological phenotypes using image analysis and machine learning"],"prefix":"10.1152","volume":"315","author":[{"given":"Susan M.","family":"Sheehan","sequence":"first","affiliation":[{"name":"The Jackson Laboratory, Bar Harbor, Maine"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2808-1610","authenticated-orcid":false,"given":"Ron","family":"Korstanje","sequence":"additional","affiliation":[{"name":"The Jackson Laboratory, Bar Harbor, Maine"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/physiolgenomics.00118.2017"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1145\/1143844.1143865"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1186\/1746-1596-8-92"},{"key":"B4","volume-title":"Diagnostic Atlas of Renal Pathology","author":"Fogo AB","year":"2016"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1186\/s12859-015-0739-1"},{"key":"B6","volume-title":"Atlas of Renal Pathology","author":"Kern WF","year":"1999"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00020.2017"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1016\/j.media.2017.07.005"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1109\/ISBI.2016.7493442"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2012080838"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1111\/acel.12008"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00002.2010"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1109\/ISBI.2011.5872394"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1109\/eScience.2016.7870897"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00629.2017","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,21]],"date-time":"2019-09-21T11:45:57Z","timestamp":1569066357000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00629.2017"}},"issued":{"date-parts":[[2018,12,1]]},"references-count":14,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2018,12,1]]}},"alternative-id":["10.1152\/ajprenal.00629.2017"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00629.2017","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2018,12,1]]}},{"indexed":{"date-parts":[[2026,2,20]],"date-time":"2026-02-20T07:04:33Z","timestamp":1771571073838,"version":"3.50.1"},"reference-count":51,"publisher":"American Physiological Society","issue":"7","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2012,4,1]]},"abstract":"<jats:p> Induction of hemeoxygenase-1 (HO-1) lowers blood pressure and reduces organ damage in hypertensive animal models; however, a potential protective role for HO-1 induction against diabetic-induced glomerular injury remains unclear. We hypothesize that HO-1 induction will protect against diabetes-induced glomerular injury by maintaining glomerular integrity and inhibiting renal apoptosis, inflammation, and oxidative stress. Diabetes was induced with streptozotocin in spontaneously hypertensive rats (SHR) as a model where the coexistence of hypertension and diabetes aggravates the progression of diabetic renal injury. Control and diabetic SHR were randomized to receive vehicle or the HO-1 inducer cobalt protoporphyrin (CoPP). Glomerular albumin permeability was significantly greater in diabetic SHR compared with control, consistent with an increase in apoptosis and decreased glomerular nephrin and \u03b1<jats:sub>3<\/jats:sub>\u03b2<jats:sub>1<\/jats:sub>-integrin protein expression in diabetic SHR. CoPP significantly reduced albumin permeability and apoptosis and restored nephrin and \u03b1<jats:sub>3<\/jats:sub>\u03b2<jats:sub>1<\/jats:sub>-integrin protein expression levels in diabetic SHR. Glomerular injury in diabetic SHR was also associated with increases in NF-\u03baB-induced inflammation and oxidative stress relative to vehicle-treated SHR, and CoPP significantly blunted diabetes-induced increases in glomerular inflammation and oxidative stress in diabetic SHR. These effects were specific to exogenous stimulation of HO-1, since incubation with the HO inhibitor stannous mesoporphyrin alone did not alter glomerular inflammatory markers or oxidative stress yet was able to prevent CoPP-mediated decreases in these parameters. These data suggest that induction of HO-1 reduces diabetic induced-glomerular injury and apoptosis and these effects are associated with decreased NF-\u03baB-induced inflammation and oxidative stress. <\/jats:p>","DOI":"10.1152\/ajprenal.00472.2011","type":"journal-article","created":{"date-parts":[[2011,12,29]],"date-time":"2011-12-29T02:58:29Z","timestamp":1325127509000},"page":"F791-F800","source":"Crossref","is-referenced-by-count":40,"title":["Induction of hemeoxygenase-1 reduces glomerular injury and apoptosis in diabetic spontaneously hypertensive rats"],"prefix":"10.1152","volume":"302","author":[{"given":"Ahmed A.","family":"Elmarakby","sequence":"first","affiliation":[{"name":"Departments of 1Oral Biology,"},{"name":"Pharmacology and Toxicology, and"}]},{"given":"Jessica","family":"Faulkner","sequence":"additional","affiliation":[{"name":"Departments of 1Oral Biology,"}]},{"given":"Babak","family":"Baban","sequence":"additional","affiliation":[{"name":"Departments of 1Oral Biology,"}]},{"given":"Mohamed A.","family":"Saleh","sequence":"additional","affiliation":[{"name":"Pharmacology and Toxicology, and"}]},{"given":"Jennifer C.","family":"Sullivan","sequence":"additional","affiliation":[{"name":"Medicine, Georgia Health Sciences University, Augusta, Georgia"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90449.2008"},{"key":"B2","first-page":"571","volume":"141","author":"Adler S","year":"1992","journal-title":"Am J Pathol"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.262.5.F697"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2003.12.028"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00546.2011"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.3390\/ijms9122388"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1007\/s00011-006-6190-z"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00367.x"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfh441"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000014"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00153.2010"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/j.phrs.2010.07.005"},{"key":"B12a","doi-asserted-by":"publisher","DOI":"10.1042\/CS20090395"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005080859"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1007\/s00125-006-0508-9"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004121082"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00510.2007"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2007.06.148"},{"key":"B18","first-page":"616","volume":"62","author":"Korhonen M","year":"1990","journal-title":"Lab Invest"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1080\/10715760310001604189"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/j.lfs.2008.12.014"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1007\/s00125-002-0946-y"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2009.286"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90649.2008"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.4161\/cc.6.5.3917"},{"key":"B25","doi-asserted-by":"crossref","first-page":"9","DOI":"10.1093\/ndt\/10.supp3.9","volume":"10","author":"Luft FC","year":"1995","journal-title":"Nephrol Dial Transplant"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5001830"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.91000.2008"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1210\/en.2008-1370"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.90241.2008"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1210\/en.2009-0471"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1797.2006.00576.x"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfm715"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.52.10.2586"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1159\/000098001"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1042\/CS20080394"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.2337\/diacare.28.9.2130"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1007\/s00125-010-2021-4"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.111.178988"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006030208"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1007\/s00125-008-0961-8"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.2337\/db06-0477"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1001\/archinternmed.2007.35"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00725.x"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.2337\/diab.46.12.2075"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.55.01.06.db05-0894"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2010.03.007"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006080894"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1042\/BJ20080476"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002531"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00311.x"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00472.2011","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T00:20:34Z","timestamp":1567988434000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00472.2011"}},"issued":{"date-parts":[[2012,4,1]]},"references-count":51,"journal-issue":{"issue":"7","published-print":{"date-parts":[[2012,4,1]]}},"alternative-id":["10.1152\/ajprenal.00472.2011"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00472.2011","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2012,4,1]]}},{"indexed":{"date-parts":[[2026,2,21]],"date-time":"2026-02-21T15:48:31Z","timestamp":1771688911223,"version":"3.50.1"},"reference-count":32,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2004,11]]},"abstract":"<jats:p>Because \u03b2<jats:sub>1<\/jats:sub>-integrin is involved in sensing of fluid flow rate in endothelial cells, a function that in Madin-Darby canine kidney (MDCK) cells is confined to the primary cilium, we hypothesized \u03b2<jats:sub>1<\/jats:sub>-integrin to be an important part of the primary ciliary mechanosensory apparatus in MDCK cells. We observed that \u03b2<jats:sub>1<\/jats:sub>-integrin, \u03b1<jats:sub>3<\/jats:sub>-integrin, and perhaps \u03b1<jats:sub>5<\/jats:sub>-integrin were localized to the primary cilium of MDCK cells by combining lectin and immunofluorescence confocal microscopy. \u03b2<jats:sub>1<\/jats:sub>-Integrin was also colocalized with tubulin to the primary cilia of the rat renal collecting ducts, as well as to the cilia of proximal tubules and thick ascending limbs. Immunogold-electron microscopy confirmed the presence of \u03b2<jats:sub>1<\/jats:sub>-integrin on primary cilia of MDCK cells and rat collecting ducts. Intracellular Ca<jats:sup>2+<\/jats:sup>levels, monitored by fluorescence microscopy on fluo 4-loaded MDCK cells, significantly increased on addition of fibronectin, a \u03b2<jats:sub>1<\/jats:sub>-integrin ligand, to mature MDCK cells with an IC<jats:sub>50<\/jats:sub>of 0.02 mg\/l. In immature, nonciliated cells or in deciliated mature cells, the IC<jats:sub>50<\/jats:sub>was 0.40 mg\/l. Blocking the fibronectin-binding sites of \u03b2<jats:sub>1<\/jats:sub>-integrin with RGD peptide prevented the Ca<jats:sup>2+<\/jats:sup>signal. Cross-linking of \u03b2<jats:sub>1<\/jats:sub>-integrins by Sambucus nigra agglutinin produced a Ca<jats:sup>2+<\/jats:sup>response similar to the addition of fibronectin. Furthermore, the fibronectin-induced response was not dependent on flow or a flow-induced Ca<jats:sup>2+<\/jats:sup>response. Finally, the flow-induced Ca<jats:sup>2+<\/jats:sup>response was not prevented by the fibronectin-induced signal. Although \u03b2<jats:sub>1<\/jats:sub>-integrin on the primary cilium greatly potentiates the fibronectin-induced Ca<jats:sup>2+<\/jats:sup>signaling in MDCK cells, the flow-dependent Ca<jats:sup>2+<\/jats:sup>signal is not mediated through activation of \u03b2<jats:sub>1<\/jats:sub>-integrin.<\/jats:p>","DOI":"10.1152\/ajprenal.00096.2004","type":"journal-article","created":{"date-parts":[[2004,6,30]],"date-time":"2004-06-30T00:53:53Z","timestamp":1088556833000},"page":"F969-F978","source":"Crossref","is-referenced-by-count":77,"title":["\u03b2<sub>1<\/sub>-Integrins in the primary cilium of MDCK cells potentiate fibronectin-induced Ca<sup>2+<\/sup>signaling"],"prefix":"10.1152","volume":"287","author":[{"given":"H. A.","family":"Praetorius","sequence":"first","affiliation":[]},{"given":"J.","family":"Praetorius","sequence":"additional","affiliation":[]},{"given":"S.","family":"Nielsen","sequence":"additional","affiliation":[]},{"given":"J.","family":"Frokiaer","sequence":"additional","affiliation":[]},{"given":"K. R.","family":"Spring","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1016\/0021-9290(95)00092-5"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.1041390209"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.133.6.1403"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1126\/science.7716514"},{"key":"R5","unstructured":"Eble JA.Integrins: a versatile and old family of cell adhesion molecules. In:Integrin-Ligand Interaction, edited by Eble JA and K\u00fchn K. New York, NY: Springer, 1997, p. 1\u201340."},{"key":"R6","doi-asserted-by":"crossref","unstructured":"Jaconi MEE, Rivest RW, Schlegel W, Wollheim Pitttet D CB, and Lew PD.Spontaneous and chemoattractant-induced oscillations of cytosolic free calcium in single adherent human neutrophils.J Biol Chem263: 10557\u201310560, 1988.","DOI":"10.1016\/S0021-9258(18)38006-2"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.0590051770.x"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.109.4.1807"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.110.3.803"},{"key":"R10","doi-asserted-by":"crossref","unstructured":"Littlewood Evans A, and Muller U.Stereocilia defects in sensory hair cells of the inner ear in mice deficient in integrin \u03b18\u03b21.Nature24: 424\u2013428, 2000.","DOI":"10.1038\/74286"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.113.5.981"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1038\/ng1076"},{"key":"R13","unstructured":"Pardi R, Bender JR, Dettori C, Giannazza E, and Engelman EG.Heterogeneous signaling properties of lymphocyte function-associated antigen (LFA-1) in human lymphocyte subsets.J Immunol266: C376\u2013C381, 1994."},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.3109\/15419069409004434"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1007\/s00232-001-0075-4"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1007\/s00232-002-1042-4"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200309000-00006"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1007\/s00232-001-0093-2"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1006\/excr.2002.5516"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1002\/path.1711670311"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1182\/blood.V97.9.2648"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1097\/00003086-200110001-00006"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1016\/0955-0674(93)90031-K"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1006\/jsbi.1994.1014"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1016\/S0955-0674(97)80125-1"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.7.7.1025"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(05)67095-4"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1126\/science.7684161"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1006\/abio.2002.5723"},{"key":"R30","unstructured":"Wilson PD, Geng L, Li X, and Burrows CR.The PKD1 gene product, \u201cpolycystin-1,\u201d is a tyrosine-phosphorylated protein that colocalizes with \u03b12\u03b21 integrin in focal clusters in adherent renal epithelia.Lab Invest79: 1311\u20131323, 1999."},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00273.2001"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1994.266.2.C376"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00096.2004","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,6,23]],"date-time":"2021-06-23T21:26:27Z","timestamp":1624483587000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00096.2004"}},"issued":{"date-parts":[[2004,11]]},"references-count":32,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2004,11]]}},"alternative-id":["10.1152\/ajprenal.00096.2004"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00096.2004","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2004,11]]}},{"indexed":{"date-parts":[[2026,2,21]],"date-time":"2026-02-21T13:25:15Z","timestamp":1771680315666,"version":"3.50.1"},"reference-count":60,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2004,1]]},"abstract":"<jats:p>We investigated the effects of pravastatin, a competitive inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, on interstitial inflammation and fibrosis, using an animal model of chronic cyclosporine A (CsA)-induced nephropathy. Sprague-Dawley rats were maintained on a low-salt diet (0.05% sodium) and treated daily for 1 or 4 wk with vehicle (olive oil; 1 ml\/kg sc), CsA (15 mg\/kg sc), or both CsA and pravastatin (5 or 20 mg\/kg in the drinking water). Anti-inflammatory and antifibrotic effects of pravastatin were studied by evaluating the concentrations of the inflammatory mediators osteopontin (OPN) and C-reactive protein (CRP), of fibrotic cytokine-transforming growth factor (TGF)-\u03b2<jats:sub>1<\/jats:sub>, and the presence of ED-1-positive cells (macrophages). In addition, renal function, serum lipid levels, histopathology (arteriolopathy and tubulointerstitial fibrosis), and the expression of the vasoactive factors endothelial nitric oxide synthase (eNOS) and renin protein were also compared for different treatment groups. Pravastatin induced dose-dependent decreases in the expression of OPN, intrarenal CRP, and TGF-\u03b2<jats:sub>1<\/jats:sub>, and in the numbers of ED-1-positive cells at 1 and 4 wk. These were accompanied by a significant attenuation of tubulointerstitial fibrosis at 4 wk. The downregulation of eNOS protein expression in CsA-treated rat kidney was markedly upregulated by pravastatin treatment, although intrarenal renin expression was unaffected. Renal dysfunction induced by CsA significantly improved with administration of pravastatin at a dose of 20 mg\/kg. Neither CsA nor pravastatin influenced serum lipid or high-sensitivity CRP levels in the treatment groups. Thus in chronic CsA nephropathy, pravastatin effectively abrogates the progression of tubulointerstitial inflammation and fibrosis. This may support the clinical use of pravastatin.<\/jats:p>","DOI":"10.1152\/ajprenal.00428.2002","type":"journal-article","created":{"date-parts":[[2004,1,31]],"date-time":"2004-01-31T00:56:49Z","timestamp":1075510609000},"page":"F46-F57","source":"Crossref","is-referenced-by-count":82,"title":["Pravastatin treatment attenuates interstitial inflammation and fibrosis in a rat model of chronic cyclosporine-induced nephropathy"],"prefix":"10.1152","volume":"286","author":[{"given":"Can","family":"Li","sequence":"first","affiliation":[]},{"given":"Chul Woo","family":"Yang","sequence":"additional","affiliation":[]},{"given":"Joo Hyun","family":"Park","sequence":"additional","affiliation":[]},{"given":"Sun Woo","family":"Lim","sequence":"additional","affiliation":[]},{"given":"Bo Kyung","family":"Sun","sequence":"additional","affiliation":[]},{"given":"Ju Young","family":"Jung","sequence":"additional","affiliation":[]},{"given":"Soon Bae","family":"Kim","sequence":"additional","affiliation":[]},{"given":"Yong Soo","family":"Kim","sequence":"additional","affiliation":[]},{"given":"Jin","family":"Kim","sequence":"additional","affiliation":[]},{"given":"Byung Kee","family":"Bang","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"REF1","doi-asserted-by":"publisher","DOI":"10.1097\/00007890-199711150-00002"},{"key":"REF2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2796.2002.01019.x"},{"key":"REF3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.4.F491"},{"key":"REF4","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.92.9.2419"},{"key":"REF5","doi-asserted-by":"publisher","DOI":"10.1053\/ajkd.2002.33393"},{"key":"REF6","doi-asserted-by":"publisher","DOI":"10.1016\/S0021-9150(01)00545-7"},{"key":"REF7","doi-asserted-by":"publisher","DOI":"10.1016\/S0167-5273(01)00423-5"},{"key":"REF8","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.34.4.987"},{"key":"REF9","doi-asserted-by":"publisher","DOI":"10.1097\/00005344-200208000-00002"},{"key":"REF10","doi-asserted-by":"publisher","DOI":"10.1053\/ajkd.1998.v32.pm9708608"},{"key":"REF11","doi-asserted-by":"publisher","DOI":"10.1016\/0006-291X(91)91870-I"},{"key":"REF12","unstructured":"Giachelli CM, Lombardi D, Johnson RJ, Murry CE, and Almeida M.Evidence for a role of osteopontin in macrophage infiltration in response to pathological stimuli in vivo.Am J Pathol152: 353-358, 1998."},{"key":"REF13","doi-asserted-by":"publisher","DOI":"10.1038\/343425a0"},{"key":"REF14","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.83.5.490"},{"key":"REF15","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(12)80587-7"},{"key":"REF16","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)64957-7"},{"key":"REF17","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9149(00)01516-2"},{"key":"REF18","doi-asserted-by":"publisher","DOI":"10.1002\/immu.200390018"},{"key":"REF19","doi-asserted-by":"publisher","DOI":"10.1097\/00007890-200209270-00016"},{"key":"REF20","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.1997.tb02724.x"},{"key":"REF21","doi-asserted-by":"publisher","DOI":"10.1006\/jsre.2001.6256"},{"key":"REF22","doi-asserted-by":"publisher","DOI":"10.1159\/000057375"},{"key":"REF23","unstructured":"Katznelson S, Wang XM, Chia D, Ozawa M, Zhong HP, Hirata M, Terasaki PI, and Kobashigawa JA.The inhibitory effects of pravastatin on natural killer cell activity in vivo and on cytotoxic T lymphocyte activity in vitro.J Heart Lung Transplant17: 335-340, 1998."},{"key":"REF24","doi-asserted-by":"publisher","DOI":"10.1097\/00007890-199605270-00010"},{"key":"REF25","doi-asserted-by":"crossref","unstructured":"Kim SI, Han DC, and Lee HB.Lovastatin inhibits transforming growth factor-\u03b21expression in diabetic rat glomeruli and cultured rat mesangial cells.J Am Soc Nephrol11: 80-87, 2000.","DOI":"10.1681\/ASN.V11180"},{"key":"REF26","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199509073331003"},{"key":"REF27","doi-asserted-by":"publisher","DOI":"10.1080\/00365519950185689"},{"key":"REF28","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.97.12.1129"},{"key":"REF29","unstructured":"Lee SK, Jin SY, Han DC, Hwang SD, and Lee HB.Effects of delayed treatment with enalapril and\/or lovastatin on the progression of glomerulosclerosis in \u215a nephrectomized rats.Nephrol Dial Transplant8: 1338-1343, 1993."},{"key":"REF30","doi-asserted-by":"crossref","unstructured":"Li C, Yang CW, Kim WY, Jung JY, Cha JH, Kim YS, Kim J, Bennett WM, and Bang BK.Reversibility of chronic cyclosporine nephropathy in rats after withdrawal of cyclosporine.Am J Physiol Renal Physiol284: F389-F398, 2003.","DOI":"10.1152\/ajprenal.00277.2002"},{"key":"REF31","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00751.x"},{"key":"REF32","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000042168.43665.9B"},{"key":"REF33","doi-asserted-by":"publisher","DOI":"10.1016\/S0021-9150(01)00469-5"},{"key":"REF34","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00408.x"},{"key":"REF35","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00724.x"},{"key":"REF36","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1988.38"},{"key":"REF37","doi-asserted-by":"publisher","DOI":"10.1161\/hh1701.096614"},{"key":"REF38","doi-asserted-by":"crossref","unstructured":"Nishimura M, Tanaka T, Yasuda T, Kurakata S, Kitagawa M, Yamada K, Saito Y, and Hirai A.Effect of pravastatin on type IV collagen secretion and mesangial cell proliferation.Kidney Int Suppl71: S97-S100, 1999.","DOI":"10.1046\/j.1523-1755.1999.07124.x"},{"key":"REF39","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1998.274.1.H43"},{"key":"REF40","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00580.x"},{"key":"REF41","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2567.2003.01681.x"},{"key":"REF42","unstructured":"Pichler RH, Franceschini N, Young BA, Hugo C, Andoh TF, Burdmann EA, Shankland SJ, Alpers CE, Bennett WM, and Couser WG.Pathogenesis of cyclosporine nephropathy: roles of angiotensin II and osteopontin.J Am Soc Nephrol6: 1186-1196, 1995."},{"key":"REF43","doi-asserted-by":"crossref","unstructured":"Rassouli M, Sambasivam H, Azadi P, Dell A, Morris HR, Nagpurkar A, Mookerjea S, and Murray RK.Derivation of the amino acid sequence of rat C-reactive protein from cDNA cloning with additional studies on the nature of its dimeric component.J Biol Chem267: 2947-2954, 1992.","DOI":"10.1016\/S0021-9258(19)50678-0"},{"key":"REF44","doi-asserted-by":"publisher","DOI":"10.1007\/s003950050158"},{"key":"atypb1","doi-asserted-by":"publisher","DOI":"10.1038\/labinvest.3780115"},{"key":"REF46","doi-asserted-by":"publisher","DOI":"10.1001\/jama.279.20.1643"},{"key":"REF47","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199511163332001"},{"key":"REF48","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(97)90567-9"},{"key":"REF49","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.165"},{"key":"REF50","doi-asserted-by":"publisher","DOI":"10.1016\/S0021-9150(00)00725-5"},{"key":"REF51","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00762.x"},{"key":"REF52","doi-asserted-by":"publisher","DOI":"10.1038\/89058"},{"key":"REF53","doi-asserted-by":"publisher","DOI":"10.2165\/00003088-200241050-00003"},{"key":"REF54","doi-asserted-by":"publisher","DOI":"10.1097\/01.TP.0000045034.48833.51"},{"key":"REF55","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.060003847.x"},{"key":"REF56","doi-asserted-by":"publisher","DOI":"10.1159\/000020504"},{"key":"REF57","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.07146.x"},{"key":"REF58","doi-asserted-by":"publisher","DOI":"10.1097\/00007890-199201000-00018"},{"key":"REF59","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.312"},{"key":"REF60","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00309.x"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00428.2002","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,6,14]],"date-time":"2021-06-14T05:31:29Z","timestamp":1623648689000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00428.2002"}},"issued":{"date-parts":[[2004,1]]},"references-count":60,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2004,1]]}},"alternative-id":["10.1152\/ajprenal.00428.2002"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00428.2002","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2004,1]]}},{"indexed":{"date-parts":[[2026,2,23]],"date-time":"2026-02-23T19:16:10Z","timestamp":1771874170249,"version":"3.50.1"},"reference-count":64,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2010,5]]},"abstract":"<jats:p> Nephrogenic dopamine is a potent natriuretic paracrine\/autocrine hormone that is central for mammalian sodium homeostasis. In the renal proximal tubule, dopamine induces natriuresis partly via inhibition of the sodium\/proton exchanger NHE3. The signal transduction pathways and mechanisms by which dopamine inhibits NHE3 are complex and incompletely understood. This manuscript describes the role of the serine\/threonine protein phosphatase 2A (PP2A) in the regulation of NHE3 by dopamine. The PP2A regulatory subunit B56\u03b4 (coded by the Ppp2r5d gene) directly associates with more than one region of the carboxy-terminal hydrophilic putative cytoplasmic domain of NHE3 (NHE3-cyto), as demonstrated by yeast-two-hybrid, coimmunoprecipitation, blot overlay, and in vitro pull-down assays. Phosphorylated NHE3-cyto is a substrate for purified PP2A in an in vitro dephosphorylation reaction. In cultured renal cells, inhibition of PP2A by either okadaic acid or by overexpression of the simian virus 40 (SV40) small T antigen blocks the ability of dopamine to inhibit NHE3 activity and to reduce surface NHE3 protein. Dopamine-induced NHE3 redistribution is also blocked by okadaic acid ex vivo in rat kidney cortical slices. These studies demonstrate that PP2A is an integral and critical participant in the signal transduction pathway between dopamine receptor activation and NHE3 inhibition. <\/jats:p>","DOI":"10.1152\/ajprenal.00708.2009","type":"journal-article","created":{"date-parts":[[2010,2,24]],"date-time":"2010-02-24T23:09:49Z","timestamp":1267052989000},"page":"F1205-F1213","source":"Crossref","is-referenced-by-count":28,"title":["Acute regulation of renal Na<sup>+<\/sup>\/H<sup>+<\/sup> exchanger NHE3 by dopamine: role of protein phosphatase 2A"],"prefix":"10.1152","volume":"298","author":[{"given":"I. Alexandru","family":"Bobulescu","sequence":"first","affiliation":[{"name":"Departments of 1Internal Medicine,"},{"name":"Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, Texas"}]},{"given":"Henry","family":"Qui\u00f1ones","sequence":"additional","affiliation":[{"name":"Departments of 1Internal Medicine,"}]},{"given":"Serge M.","family":"Gisler","sequence":"additional","affiliation":[{"name":"Departments of 1Internal Medicine,"}]},{"given":"Francesca","family":"Di Sole","sequence":"additional","affiliation":[{"name":"Departments of 1Internal Medicine,"},{"name":"Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, Texas"}]},{"given":"Ming-Chang","family":"Hu","sequence":"additional","affiliation":[{"name":"Departments of 1Internal Medicine,"},{"name":"Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, Texas"}]},{"given":"Mingjun","family":"Shi","sequence":"additional","affiliation":[{"name":"Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, Texas"}]},{"given":"Jianning","family":"Zhang","sequence":"additional","affiliation":[{"name":"Departments of 1Internal Medicine,"}]},{"given":"Daniel G.","family":"Fuster","sequence":"additional","affiliation":[{"name":"Departments of 1Internal Medicine,"}]},{"given":"Nancy","family":"Wright","sequence":"additional","affiliation":[{"name":"Pharmacology, and"}]},{"given":"Marc","family":"Mumby","sequence":"additional","affiliation":[{"name":"Pharmacology, and"}]},{"given":"Orson W.","family":"Moe","sequence":"additional","affiliation":[{"name":"Departments of 1Internal Medicine,"},{"name":"Physiology and"},{"name":"Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, Texas"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118670"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-2836(05)80360-2"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.404"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.252.1.F39"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.62.1.621"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1172\/JCI3685"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00308.x"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2125.1977.tb00681.x"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00156.x"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2005.05.012"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000198427.96225.36"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.259.6.F924"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1988.254.6.F795"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1042\/bj2560283"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00447.2004"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00447.2004"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1101\/SQB.1985.050.01.078"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.256.4.F672"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(92)90194-H"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.3181\/00379727-129-33286"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M306838200"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00030.2006"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.264.6.F1032"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.15.6.560"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M008745200"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejphar.2004.02.011"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.2170\/jjphysiol.40.351"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1991.30"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.13.6.828"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/0378-1119(87)90131-4"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.22-24-10801.2002"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.263.6.F1105"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M011338200"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1016\/0378-1119(90)90336-P"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1042\/bj3530417"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1016\/j.tibs.2007.12.004"},{"key":"B37","first-page":"915","volume-title":"The Kidney: Physiology and Pathophysiology","author":"Jose PA","year":"2000"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00042.2007"},{"key":"B39","first-page":"214","volume":"105","author":"Krishna GG","year":"1985","journal-title":"J Lab Clin Med"},{"key":"B40","first-page":"303","volume":"12","author":"Laradi A","year":"1986","journal-title":"Miner Electrolyte Metab"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-5793(00)02009-3"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.38.3.303"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00514.2006"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115487"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.21.6.767"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.29.1.115"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1983.245.2.F247"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00237.2003"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.257.3.F469"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.1994.tb13118.x"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.2.F243"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1016\/S0898-6568(00)00123-6"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1210\/endo-115-6-2085"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1016\/S0895-7061(03)01013-6"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1016\/S1535-6108(04)00027-3"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1016\/j.molcel.2009.02.015"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(93)90307-C"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.29.1.228"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00480.x"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1990.323"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1254\/jjp.46.193"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.36.6.1053"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1152\/physiolgenomics.00127.2004"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.7.3978"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00708.2009","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:06:50Z","timestamp":1567973210000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00708.2009"}},"issued":{"date-parts":[[2010,5]]},"references-count":64,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2010,5]]}},"alternative-id":["10.1152\/ajprenal.00708.2009"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00708.2009","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2010,5]]}},{"indexed":{"date-parts":[[2026,3,16]],"date-time":"2026-03-16T21:37:11Z","timestamp":1773697031232,"version":"3.50.1"},"reference-count":17,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2004,4]]},"abstract":"<jats:p>Clinical and animal studies show that treatment with angiotensin-converting enzyme (ACE) inhibitors or ANG II-receptor antagonists slows progression of nephropathy in diabetes, indicating ANG II plays an important role in its development. We previously reported that hyperglycemia augments both ANG II-induced growth and activation of Janus kinase (JAK)2 and signal transducers and activators of transcription (STAT) proteins in cultured rat mesangial cells. Furthermore, we demonstrated that the tyrosine kinase enzyme JAK2 plays a key role in both ANG II- and hyperglycemia-induced growth in these cells. We hypothesized that the ACE inhibitor captopril and the ANG II-receptor antagonist candesartan would hinder hyperglycemic-induced activation of JAK and STAT proteins in rat glomeruli, demonstrating that ANG II plays an important role in the activation of these proteins in vivo. Adult male Sprague-Dawley rats were given either streptozotocin (STZ; 60 mg\/kg iv) or vehicle, and glomeruli were isolated 2 wk later. Activation of JAK and STAT proteins was evaluated by Western blot analysis for specific tyrosine phosphorylation. Groups of rats were given captopril (75\u201385 mg\u00b7kg<jats:sup>-1<\/jats:sup>\u00b7day<jats:sup>-1<\/jats:sup>), candesartan (10 mg\u00b7 kg<jats:sup>-1<\/jats:sup>\u00b7day<jats:sup>-1<\/jats:sup>), or the JAK2 inhibitor AG-490 (5 mg\u00b7kg<jats:sup>-1<\/jats:sup>\u00b7day<jats:sup>-1<\/jats:sup>) for the study's duration. STZ stimulated glomerular phosphorylation of JAK2, STAT1, STAT3, and STAT5. Phosphorylation was reduced in rats treated with captopril, candesartan, and AG-490. Furthermore, both candesartan and AG-490 inhibited STZ-induced increases in urinary protein excretion. In conclusion, our studies demonstrate that hyperglycemia induces activation of JAK2 and the STATs in vivo via an ANG II-dependent mechanism and that these proteins may be involved in the early kidney damage associated with diabetes.<\/jats:p>","DOI":"10.1152\/ajprenal.00163.2003","type":"journal-article","created":{"date-parts":[[2004,3,4]],"date-time":"2004-03-04T19:24:57Z","timestamp":1078428297000},"page":"F653-F659","source":"Crossref","is-referenced-by-count":87,"title":["Angiotensin II blockade prevents hyperglycemia-induced activation of JAK and STAT proteins in diabetic rat kidney glomeruli"],"prefix":"10.1152","volume":"286","author":[{"given":"Amy K.","family":"Banes","sequence":"first","affiliation":[{"name":"Vascular Biology Center, Medical College of Georgia, Augusta, Georgia 30912-2500"}]},{"given":"S\u00e9an","family":"Shaw","sequence":"additional","affiliation":[{"name":"Vascular Biology Center, Medical College of Georgia, Augusta, Georgia 30912-2500"}]},{"given":"John","family":"Jenkins","sequence":"additional","affiliation":[{"name":"Vascular Biology Center, Medical College of Georgia, Augusta, Georgia 30912-2500"}]},{"given":"Heather","family":"Redd","sequence":"additional","affiliation":[{"name":"Vascular Biology Center, Medical College of Georgia, Augusta, Georgia 30912-2500"}]},{"given":"Farhad","family":"Amiri","sequence":"additional","affiliation":[{"name":"Vascular Biology Center, Medical College of Georgia, Augusta, Georgia 30912-2500"}]},{"given":"David M.","family":"Pollock","sequence":"additional","affiliation":[{"name":"Vascular Biology Center, Medical College of Georgia, Augusta, Georgia 30912-2500"}]},{"given":"Mario B.","family":"Marrero","sequence":"additional","affiliation":[{"name":"Vascular Biology Center, Medical College of Georgia, Augusta, Georgia 30912-2500"}]}],"member":"24","reference":[{"key":"REF1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1998.275.1.R245"},{"key":"REF2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.4.F603"},{"key":"REF3","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00311.x"},{"key":"REF4","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.45.32382"},{"key":"REF5","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2000.00386.x"},{"key":"REF6","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00880.x"},{"key":"REF7","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.C000318200"},{"key":"REF8","doi-asserted-by":"publisher","DOI":"10.1126\/science.277.5332.1630"},{"key":"REF9","unstructured":"De Gasparo M, Catt KJ, Inagami T, Wright JW, and Unger T.International Union of Pharmacology XXIII. The angiotensin II receptors.Pharmacol Rev52: 415-472, 2000."},{"key":"REF10","doi-asserted-by":"publisher","DOI":"10.1016\/S0008-6363(02)00614-4"},{"key":"REF11","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.39.24684"},{"key":"REF12","doi-asserted-by":"publisher","DOI":"10.1038\/375247a0"},{"key":"REF13","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1998.275.4.H1216"},{"key":"REF14","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1998.275.5.R1719"},{"key":"REF15","doi-asserted-by":"crossref","unstructured":"Ruff-Jamison S, Zhong Z, Wen Z, Chen K, Darnell JE Jr, and Cohen S.Epidermal growth factor and lipopolysaccharide activate STAT3 transcription factor in mouse liver.J Biol Chem269: 21933-21935, 1994.","DOI":"10.1016\/S0021-9258(17)31735-0"},{"key":"REF16","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.51.12.3505"},{"key":"REF17","doi-asserted-by":"publisher","DOI":"10.1006\/abio.1996.0171"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00163.2003","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,6,15]],"date-time":"2021-06-15T00:41:20Z","timestamp":1623717680000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00163.2003"}},"issued":{"date-parts":[[2004,4]]},"references-count":17,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2004,4]]}},"alternative-id":["10.1152\/ajprenal.00163.2003"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00163.2003","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2004,4]]}},{"indexed":{"date-parts":[[2026,3,16]],"date-time":"2026-03-16T10:28:46Z","timestamp":1773656926938,"version":"3.50.1"},"reference-count":22,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1999,10,1]]},"abstract":"<jats:p>This review focuses on the role of acute pH changes in the regulation of Gln\/Glu metabolism in the kidney, liver, and brain. Alterations of proton concentration ([H<jats:sup>+<\/jats:sup>]) profoundly affect flux through phosphate-dependent glutaminase (PDG) or glutamate dehydrogenase (GDH), the primary enzymes responsible for mitochondrial metabolism of glutamine and glutamate, respectively. In the kidney, acute acidosis stimulates Gln uptake and its metabolism via the PDG pathway. The Glu formed from Gln can be removed via 1) oxidative deamination through the GDH reaction, 2) transamination reactions, and 3) transport of Glu from intracellular to extracellular compartment, thereby diminishing the intramitochondrial pool of glutamate sufficiently to stimulate flux through the PDG pathway. Converse changes may occur with increased pH. In the liver, acidosis diminishes the rate of Gln and Glu metabolism via the PDG and GDH pathways, but stimulates glutamine synthesis (i.e., glutamine recycling). Alkalosis has little effect. Hepatic Gln metabolism via the PDG pathway has a central role in ureagenesis via 1) supplementation of nitrogen for the synthesis of carbamyl phosphate, and 2) providing glutamate for N-acetylglutamate synthesis. In the brain, Gln\/Glu metabolism links ammonia detoxification and energy metabolism via 1) detoxification of ammonia and excess glutamate by glutamine synthesis in astrocytes, 2) formation and export of glutamine to neurons where it is metabolized to glutamate and GABA, and 3) production of \u03b1-ketoglutarate and lactate from Glu and their transport to neurons. Changes in intracellular pH associated with changes in cellular [K<jats:sup>+<\/jats:sup>] may have a key role in the regulation of these processes of glial-neuronal metabolism of Gln\/Glu metabolism.<\/jats:p>","DOI":"10.1152\/ajprenal.1999.277.4.f493","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T12:29:22Z","timestamp":1514032162000},"page":"F493-F497","source":"Crossref","is-referenced-by-count":47,"title":["Newer aspects of glutamine\/glutamate metabolism: the role of acute pH changes"],"prefix":"10.1152","volume":"277","author":[{"given":"Itzhak","family":"Nissim","sequence":"first","affiliation":[{"name":"Division of Child Development and Rehabilitation, Department of Pediatrics, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104-4318"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1098-1136(199709)21:1<64::AID-GLIA7>3.0.CO;2-1"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.27.16199"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.nu.15.070195.001025"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.3109\/00365529609094733"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1046\/j.1471-4159.1996.67041584.x"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1042\/bj2840333"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1996.270.3.C920"},{"issue":"25","key":"B8","first-page":"F187","volume":"256","author":"Nissim I.","year":"1989","journal-title":"Am. J. Physiol."},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1159\/000420097"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/0003-9861(92)90008-K"},{"key":"B11","doi-asserted-by":"crossref","first-page":"1416","DOI":"10.1681\/ASN.V371416","volume":"3","author":"Nissim I.","year":"1993","journal-title":"J. Am. Soc. Nephrol."},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.137"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.11"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.49.31234"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1098-1136(199709)21:1<124::AID-GLIA14>3.0.CO;2-U"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1098-1136(199709)21:1<99::AID-GLIA11>3.0.CO;2-W"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1098-1136(199709)21:1<56::AID-GLIA6>3.0.CO;2-#"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.281"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1097\/00004647-199801000-00011"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1995.268.6.C1418"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-4159.1988.tb01820.x"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1016\/S0079-6123(08)61752-5"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1999.277.4.F493","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:39:10Z","timestamp":1660189150000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1999.277.4.F493"}},"issued":{"date-parts":[[1999,10,1]]},"references-count":22,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1999,10,1]]}},"alternative-id":["10.1152\/ajprenal.1999.277.4.F493"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1999.277.4.f493","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1999,10,1]]}},{"indexed":{"date-parts":[[2026,3,15]],"date-time":"2026-03-15T15:58:52Z","timestamp":1773590332046,"version":"3.50.1"},"reference-count":39,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2011,6]]},"abstract":"<jats:p> The tubuloglomerular feedback mechanism (TGF) plays an important role in regulating single-nephron glomerular filtration rate (GFR) by coupling distal tubular flow to arteriolar tone. It is not known whether TGF is active in the developing kidney or whether it can regulate renal vascular tone and thus GFR during intrauterine life. TGF characteristics were examined in late-gestation ovine fetuses and lambs under normovolemic and volume-expanded (VE) conditions. Lambs and pregnant ewes were anesthetized and the fetuses were delivered via a caesarean incision into a heated water bath, with the umbilical cord intact. Under normovolemic conditions, mean arterial pressure of the fetuses was lower than lambs (51 \u00b1 1 vs. 64 \u00b1 3 mmHg). The maximum TGF response (\u0394P<jats:sub>SFmax<\/jats:sub>) was found to be lower in fetuses than lambs when tubular perfusion was increased from 0 to 40 nl\/min (5.4 \u00b1 0.7 vs. 10.6 \u00b1 0.4 mmHg). Furthermore, the flow rate eliciting half-maximal response [turning point (TP)] was 15.7 \u00b1 0.9 nl\/min in fetuses compared with 19.3 \u00b1 1.0 nl\/min in lambs, indicating a greater TGF sensitivity of the prenatal kidney. VE decreased \u0394P<jats:sub>SFmax<\/jats:sub> (4.2 \u00b1 0.4 mmHg) and increased TP to 23.7 \u00b1 1.3 nl\/min in lambs. In fetuses, VE increased stop-flow pressure from 26.6 \u00b1 1.5 to 30.3 \u00b1 0.8 mmHg, and reset TGF sensitivity so that TP increased to 21.3 \u00b1 0.7 nl\/min, but it had no effect on \u0394P<jats:sub>SFmax<\/jats:sub>. This study provides direct evidence that the TGF mechanism is active during fetal life and responds to physiological stimuli. Moreover, reductions in TGF sensitivity may contribute to the increase in GFR at birth. <\/jats:p>","DOI":"10.1152\/ajprenal.00019.2011","type":"journal-article","created":{"date-parts":[[2011,3,31]],"date-time":"2011-03-31T00:54:44Z","timestamp":1301532884000},"page":"F1368-F1374","source":"Crossref","is-referenced-by-count":11,"title":["Tubuloglomerular feedback response in the prenatal and postnatal ovine kidney"],"prefix":"10.1152","volume":"300","author":[{"given":"Russell D.","family":"Brown","sequence":"first","affiliation":[{"name":"Department of Physiology, School of Medical Sciences, University of New South Wales, Sydney, Australia; and"},{"name":"Division of Integrative Physiology, Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden"}]},{"given":"Anita J.","family":"Turner","sequence":"additional","affiliation":[{"name":"Department of Physiology, School of Medical Sciences, University of New South Wales, Sydney, Australia; and"}]},{"given":"Mattias","family":"Carlstr\u00f6m","sequence":"additional","affiliation":[{"name":"Division of Integrative Physiology, Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden"}]},{"given":"A. Erik G.","family":"Persson","sequence":"additional","affiliation":[{"name":"Department of Physiology, School of Medical Sciences, University of New South Wales, Sydney, Australia; and"},{"name":"Division of Integrative Physiology, Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden"}]},{"given":"Karen J.","family":"Gibson","sequence":"additional","affiliation":[{"name":"Department of Physiology, School of Medical Sciences, University of New South Wales, Sydney, Australia; and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1975.tb05903.x"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1977.tb10379.x"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1111\/j.1651-2227.1983.tb09861.x"},{"key":"B4","doi-asserted-by":"crossref","first-page":"1319","DOI":"10.1152\/ajplegacy.1975.228.5.1319","volume":"228","author":"Aperia A","year":"1975","journal-title":"Am J Physiol"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1071\/RD9950491"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1992.tb09363.x"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.3.F409"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.2001.281.5.R1362"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00509.x"},{"key":"B10","first-page":"77","volume":"4","author":"Davies JA","year":"1996","journal-title":"Exp Nephrol"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1981.tb06786.x"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1983.245.3.F391"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1203\/00006450-199410000-00017"},{"key":"B14","first-page":"385","volume":"18","author":"Haeckel R","year":"1980","journal-title":"J Clin Chem Clin Biochem"},{"key":"B15","first-page":"149","volume":"10","author":"Hill KJ","year":"1988","journal-title":"J Dev Physiol"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1172\/JCI106549"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1973.sp010074"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1980.107"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1071\/RD9950415"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1139\/y88-111"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1992.262.5.R754"},{"key":"B22","first-page":"331","volume":"93","author":"Macdonald MS","year":"1959","journal-title":"J Anat"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1977.232.2.F178"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1172\/JCI107485"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00073.2007"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1984.247.6.F925"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1007\/BF00852576"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1203\/00006450-198109000-00005"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1998.274.2.R263"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.259.4.F565"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1998.274.1.R160"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1139\/y95-015"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1159\/000242933"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1990.259.5.R1050"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1995.tb09952.x"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00823.2007"},{"key":"B37","first-page":"3","volume-title":"Development and Function of the Fetal Kidney","author":"Wintour EM","year":"1998"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1111\/j.1651-2227.1983.tb09862.x"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1977.233.6.F519"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00019.2011","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T00:13:41Z","timestamp":1567988021000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00019.2011"}},"issued":{"date-parts":[[2011,6]]},"references-count":39,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2011,6]]}},"alternative-id":["10.1152\/ajprenal.00019.2011"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00019.2011","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2011,6]]}},{"indexed":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T03:50:38Z","timestamp":1772164238747,"version":"3.50.1"},"reference-count":37,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2005,8]]},"abstract":"<jats:p>Previously, we showed an increase in protein abundance of the renal thiazide-sensitive Na-Cl cotransporter (NCC) in young, prediabetic, obese Zucker rats relative to lean age mates (Bickel CA, Verbalis JF, Knepper MA, and Ecelbarger CA. Am J Physiol Renal Physiol 281: F639\u2013F648, 2001). To test whether this increase correlated with increased thiazide sensitivity (NCC activity) and blood pressure, and could be modified by insulin-sensitizing agents, we treated lean and obese Zucker rats (9 wk old) with either a control diet or this diet supplemented with 3 mg\/kg body wt rosiglitazone (RGZ), a peroxisomal proliferator-activated receptor subtype \u03b3 agonist and potent insulin-sensitizing agent, for 12 wk ( n = 9\/group). The rise in blood pressure, measured continuously by radiotelemetry, was significantly blunted in the RGZ-treated obese rats. Similarly, blood glucose and urinary albumin were markedly decreased in these rats. RGZ-treated rats whether lean or obese excreted a NaCl load faster but excreted less sodium in response to hydrochlorothiazide, applied as a novel in vivo measure of NCC activity. Obese rats had increased renal protein abundance and urinary excretion of NCC; however, this was not significantly reduced by RGZ (densitometry in cortex homogenate \u2212 %lean control): 100 \u00b1 9, 93 \u00b1 4, 124 \u00b1 9, and 141 \u00b1 14 for lean control, lean RGZ, obese control, and obese RGZ, respectively. Subcellular localization, as evaluated by confocal microscopy and immunoblotting following differential centrifugation, of NCC was not different between rat groups. Overall, RGZ reduced blood pressure and thiazide sensitivity; however, the mechanism(s) did not seem to involve a decrease in NCC protein abundance or cellular location. Decreased NCC activity may have contributed to the maintenance of normotension in RGZ-treated obese rats.<\/jats:p>","DOI":"10.1152\/ajprenal.00335.2004","type":"journal-article","created":{"date-parts":[[2005,4,6]],"date-time":"2005-04-06T20:12:34Z","timestamp":1112818354000},"page":"F442-F450","source":"Crossref","is-referenced-by-count":50,"title":["Regulation of the renal thiazide-sensitive Na-Cl cotransporter, blood pressure, and natriuresis in obese Zucker rats treated with rosiglitazone"],"prefix":"10.1152","volume":"289","author":[{"given":"Osman","family":"Khan","sequence":"first","affiliation":[]},{"given":"Shahla","family":"Riazi","sequence":"additional","affiliation":[]},{"given":"Xinqun","family":"Hu","sequence":"additional","affiliation":[]},{"given":"Jian","family":"Song","sequence":"additional","affiliation":[]},{"given":"James B.","family":"Wade","sequence":"additional","affiliation":[]},{"given":"Carolyn A.","family":"Ecelbarger","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.28.6.1047"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1081\/CEH-120017739"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00353.x"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.281.4.F639"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1159\/000420150"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1161\/01.ATV.0000044461.01844.C9"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.5.F874"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.5.F663"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00379.2001"},{"key":"R10","doi-asserted-by":"crossref","unstructured":"Harker CT\n                      , O'Donnell MP, Kasiske BL, Keane WF, and Katz SA.\n                      The renin-angiotensin system in the type II diabetic obese Zucker rat.\n                      J Am Soc Nephrol\n                      4\n                      : 1354\u20131361, 1993.","DOI":"10.1681\/ASN.V461354"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1001\/archinte.159.15.1811"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1016\/S0739-7240(01)00117-5"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1016\/S0024-3205(03)00646-5"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1136\/gut.52.8.1194"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.24.14552"},{"key":"R16","unstructured":"Komers R\n                      and Vrana A.\n                      Thiazolidinediones\u2013tools for the research of metabolic syndrome X.\n                      Physiol Res\n                      47\n                      : 215\u2013225, 1998."},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.2165\/00003495-200262100-00004"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1172\/JCI7840"},{"key":"R19","unstructured":"Masilamani SM\n                      , Wang X, Nielsen J, Ageloff SA, Brooks HL, and Knepper MA.\n                      Increased abundance of the thiazide-sensitive Na-Cl cotransporter (NCC) in response to dietary NaCl restriction occurs in the absence of changes in NCC mRNA (Abstract).\n                      J Am Soc Nephrol\n                      12\n                      : 36A, 2001."},{"key":"R20","doi-asserted-by":"crossref","unstructured":"McKee JA\n                      , Kumar S, Ecelbarger CA, Fernandez-Llama P, Terris J, and Knepper MA.\n                      Detection of Na\n                      +\n                      transporter proteins in urine.\n                      J Am Soc Nephrol\n                      11\n                      : 2128\u20132132, 2000.","DOI":"10.1681\/ASN.V11112128"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1046\/j.1464-5491.2000.00269.x"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.6.F900"},{"key":"R23","unstructured":"Parving HH\n                      , Osterby R, Anderson PW, and Hsueh WA.\n                      Diabetic nephropathy. In:\n                      The Kidney\n                      (5th ed.)\n                      , edited by Brenner BM. Philadelphia, PA: WB Saunders, 1996, p. 1864\u20131892."},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1291\/hypres.27.417"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.00177.2004"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00063.2004"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.103.058008"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1016\/S0025-7125(03)00128-7"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1345\/aph.10132"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000039963.01288.D3"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.270.1.F211"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.48.7.1448"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1172\/JCI10366"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1998.274.6.R1588"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-140-11-200406010-00036"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1021\/jm990554g"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.6.F966"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00335.2004","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,7,7]],"date-time":"2021-07-07T23:07:12Z","timestamp":1625699232000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00335.2004"}},"issued":{"date-parts":[[2005,8]]},"references-count":37,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2005,8]]}},"alternative-id":["10.1152\/ajprenal.00335.2004"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00335.2004","relation":{"has-review":[{"id-type":"doi","id":"10.3410\/f.1026823.323560","asserted-by":"object"}]},"ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2005,8]]}},{"indexed":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T03:50:03Z","timestamp":1772164203020,"version":"3.50.1"},"reference-count":75,"publisher":"American Physiological Society","issue":"2","funder":[{"DOI":"10.13039\/501100001871","name":"Funda\u00e7\u00e3o para a Ci\u00eancia e a Tecnologia (Foundation for Science and Technology)","doi-asserted-by":"publisher","award":["PTDC\/SAU-OSM\/104369\/2008"],"award-info":[{"award-number":["PTDC\/SAU-OSM\/104369\/2008"]}],"id":[{"id":"10.13039\/501100001871","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001871","name":"Funda\u00e7\u00e3o para a Ci\u00eancia e a Tecnologia (Foundation for Science and Technology)","doi-asserted-by":"publisher","award":["PEst-OE\/SAU\/UI0215\/2014"],"award-info":[{"award-number":["PEst-OE\/SAU\/UI0215\/2014"]}],"id":[{"id":"10.13039\/501100001871","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001871","name":"Funda\u00e7\u00e3o para a Ci\u00eancia e a Tecnologia (Foundation for Science and Technology)","doi-asserted-by":"publisher","award":["REEQ\/1264\/SAU\/2005"],"award-info":[{"award-number":["REEQ\/1264\/SAU\/2005"]}],"id":[{"id":"10.13039\/501100001871","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001871","name":"Funda\u00e7\u00e3o para a Ci\u00eancia e a Tecnologia (Foundation for Science and Technology)","doi-asserted-by":"publisher","award":["SFRH\/BD\/88855\/2012"],"award-info":[{"award-number":["SFRH\/BD\/88855\/2012"]}],"id":[{"id":"10.13039\/501100001871","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Funda\u00e7\u00e3o para a Ci\u00eancia e a Tecnologia","award":["REEQ\/1168\/SAU\/2005"],"award-info":[{"award-number":["REEQ\/1168\/SAU\/2005"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2017,8,1]]},"abstract":"<jats:p>\n                    The direct detrusor relaxant effect of \u03b2\n                    <jats:sub>3<\/jats:sub>\n                    -adrenoceptor agonists as a primary mechanism to improve overactive bladder symptoms has been questioned. Among other targets, activation of \u03b2\n                    <jats:sub>3<\/jats:sub>\n                    -adrenoceptors downmodulate nerve-evoked acetylcholine (ACh) release, but there is insufficient evidence for the presence of these receptors on bladder cholinergic nerve terminals. Our hypothesis is that adenosine formed from the catabolism of cyclic AMP in the detrusor may act as a retrograde messenger via prejunctional A\n                    <jats:sub>1<\/jats:sub>\n                    receptors to explain inhibition of cholinergic activity by \u03b2\n                    <jats:sub>3<\/jats:sub>\n                    -adrenoceptors. Isoprenaline (1 \u00b5M) decreased [\n                    <jats:sup>3<\/jats:sup>\n                    H]ACh release from stimulated (10 Hz, 200 pulses) human (\u221247 \u00b1 5%) and rat (\u221238 \u00b1 1%) detrusor strips. Mirabegron (0.1 \u00b5M, \u221253 \u00b1 8%) and CL316,243 (1 \u00b5M, \u221237 \u00b1 7%) mimicked isoprenaline (1 \u00b5M) inhibition, and their effects were prevented by blocking \u03b2\n                    <jats:sub>3<\/jats:sub>\n                    -adrenoceptors with L748,337 (30 nM) and SR59230A (100 nM), respectively, in human and rat detrusor. Mirabegron and isoprenaline increased extracellular adenosine in the detrusor. Blockage of A\n                    <jats:sub>1<\/jats:sub>\n                    receptors with 1,3-dipropyl-8-cyclopentylxanthine (DPCPX, 100 nM) or the equilibrative nucleoside transporters (ENT) with dipyridamole (0.5 \u00b5M) prevented mirabegron and isoprenaline inhibitory effects. Dipyridamole prevented isoprenaline-induced adenosine outflow from the rat detrusor, and this effect was mimicked by the ENT1 inhibitor, S-(4-nitrobenzyl)-6-thioinosine (NBTI, 30 \u00b5M). Cystometry recordings in anesthetized rats demonstrated that SR59230A, DPCPX, dipyridamole, and NBTI reversed the decrease in the voiding frequency caused by isoprenaline (0.1\u20131,000 nM). Data suggest that inhibition of cholinergic neurotransmission by \u03b2\n                    <jats:sub>3<\/jats:sub>\n                    -adrenoceptors results from adenosine release via equilibrative nucleoside transporters and prejunctional A\n                    <jats:sub>1<\/jats:sub>\n                    -receptor stimulation in human and rat urinary bladder.\n                  <\/jats:p>","DOI":"10.1152\/ajprenal.00392.2016","type":"journal-article","created":{"date-parts":[[2017,4,26]],"date-time":"2017-04-26T20:10:21Z","timestamp":1493237421000},"page":"F388-F403","source":"Crossref","is-referenced-by-count":35,"title":["Inhibition of cholinergic neurotransmission by \u03b2\n                    <sub>3<\/sub>\n                    -adrenoceptors depends on adenosine release and A\n                    <sub>1<\/sub>\n                    -receptor activation in human and rat urinary bladders"],"prefix":"10.1152","volume":"313","author":[{"given":"Isabel","family":"Silva","sequence":"first","affiliation":[{"name":"Laborat\u00f3rio de Farmacologia e Neurobiologia, Universidade do Porto, Porto, Portugal;"},{"name":"Center for Drug Discovery and Innovative Medicines (MedInUP), Instituto de Ci\u00eancias Biom\u00e9dicas de Abel Salazar (ICBAS), Universidade do Porto, Porto, Portugal; and"}]},{"given":"Ana Filipa","family":"Costa","sequence":"additional","affiliation":[{"name":"Laborat\u00f3rio de Farmacologia e Neurobiologia, Universidade do Porto, Porto, Portugal;"},{"name":"Center for Drug Discovery and Innovative Medicines (MedInUP), Instituto de Ci\u00eancias Biom\u00e9dicas de Abel Salazar (ICBAS), Universidade do Porto, Porto, Portugal; and"}]},{"given":"S\u00edlvia","family":"Moreira","sequence":"additional","affiliation":[{"name":"Laborat\u00f3rio de Farmacologia e Neurobiologia, Universidade do Porto, Porto, Portugal;"},{"name":"Center for Drug Discovery and Innovative Medicines (MedInUP), Instituto de Ci\u00eancias Biom\u00e9dicas de Abel Salazar (ICBAS), Universidade do Porto, Porto, Portugal; and"}]},{"given":"F\u00e1tima","family":"Ferreirinha","sequence":"additional","affiliation":[{"name":"Laborat\u00f3rio de Farmacologia e Neurobiologia, Universidade do Porto, Porto, Portugal;"},{"name":"Center for Drug Discovery and Innovative Medicines (MedInUP), Instituto de Ci\u00eancias Biom\u00e9dicas de Abel Salazar (ICBAS), Universidade do Porto, Porto, Portugal; and"}]},{"given":"Maria Teresa","family":"Magalh\u00e3es-Cardoso","sequence":"additional","affiliation":[{"name":"Laborat\u00f3rio de Farmacologia e Neurobiologia, Universidade do Porto, Porto, Portugal;"},{"name":"Center for Drug Discovery and Innovative Medicines (MedInUP), Instituto de Ci\u00eancias Biom\u00e9dicas de Abel Salazar (ICBAS), Universidade do Porto, Porto, Portugal; and"}]},{"given":"Isabel","family":"Calejo","sequence":"additional","affiliation":[{"name":"Laborat\u00f3rio de Farmacologia e Neurobiologia, Universidade do Porto, Porto, Portugal;"},{"name":"Center for Drug Discovery and Innovative Medicines (MedInUP), Instituto de Ci\u00eancias Biom\u00e9dicas de Abel Salazar (ICBAS), Universidade do Porto, Porto, Portugal; and"}]},{"given":"Miguel","family":"Silva-Ramos","sequence":"additional","affiliation":[{"name":"Laborat\u00f3rio de Farmacologia e Neurobiologia, Universidade do Porto, Porto, Portugal;"},{"name":"Servi\u00e7o de Urologia, Centro Hospitalar do Porto (CHP), Porto, Portugal"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6114-9189","authenticated-orcid":false,"given":"Paulo","family":"Correia-de-S\u00e1","sequence":"additional","affiliation":[{"name":"Laborat\u00f3rio de Farmacologia e Neurobiologia, Universidade do Porto, Porto, Portugal;"},{"name":"Center for Drug Discovery and Innovative Medicines (MedInUP), Instituto de Ci\u00eancias Biom\u00e9dicas de Abel Salazar (ICBAS), Universidade do Porto, Porto, Portugal; and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.1992.tb14473.x"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1002\/nau.22571"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1038\/nrurol.2015.297"},{"key":"B4","first-page":"43","volume":"175","author":"Andersson KE","year":"1995","journal-title":"Scand J Urol Nephrol Suppl"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.2010.00754.x"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1002\/nau.20642"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.22-18-08063.2002"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.1979.tb17337.x"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.1978.tb07782.x"},{"key":"B10","doi-asserted-by":"crossref","first-page":"649","DOI":"10.1016\/S0022-3565(24)34946-8","volume":"290","author":"Candelore MR","year":"1999","journal-title":"J Pharmacol Exp Ther"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1111\/bph.12711"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1007\/s00210-012-0767-6"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M104833200"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0707648"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1002\/nau.23224"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/j.autneu.2006.02.004"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejphar.2015.03.074"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0705697"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1111\/j.1464-410X.2012.11421.x"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0702688"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(01)61994-3"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1007\/s00210-015-1136-z"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.300.3.910"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M304059200"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1007\/s00210-003-0860-y"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1111\/j.1464-410X.2011.10400.x"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(05)65729-1"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1007\/s00210-012-0824-1"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-201X.1998.00406.x"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0702358"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1097\/00005392-200101000-00071"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M005463200"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1016\/S0306-3623(96)00573-3"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1002\/nau.22487"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.109.155010"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0701820"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1007\/s00441-010-1053-x"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1161\/ATVBAHA.106.126714"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1002\/nau.20838"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1016\/j.pharmthera.2016.01.007"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0706619"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1111\/j.1464-410X.2006.06679.x"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.1992.tb09032.x"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1016\/j.juro.2013.05.062"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1097\/01.ju.0000067621.62736.7c"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1111\/luts.12007"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1007\/s00210-008-0274-y"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(05)67420-4"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1016\/j.autneu.2016.05.006"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1016\/j.phrs.2013.12.006"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2680.1998.1820099.x"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1172\/JCI74349"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1016\/j.juro.2015.05.080"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1007\/s11302-015-9478-z"},{"key":"B55","volume-title":"Adenosine Receptors: Pharmacology, Functions and Therapeutic Aspects","author":"Silva-Ramos M","year":"2015"},{"key":"B56","first-page":"384","volume":"6","author":"Stehle JH","year":"1992","journal-title":"Mol Endocrinol"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.106.115840"},{"key":"B58","doi-asserted-by":"crossref","first-page":"939","DOI":"10.1016\/S0022-3565(24)39317-6","volume":"293","author":"Takeda H","year":"2000","journal-title":"J Pharmacol Exp Ther"},{"key":"B59","doi-asserted-by":"crossref","first-page":"1367","DOI":"10.1016\/S0022-3565(24)38094-2","volume":"288","author":"Takeda M","year":"1999","journal-title":"J Pharmacol Exp Ther"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1517\/13543784.2015.1076390"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1016\/j.bcp.2013.11.007"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejphar.2005.06.029"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1126\/science.1260419"},{"key":"B64","doi-asserted-by":"crossref","first-page":"595","DOI":"10.1681\/ASN.V133595","volume":"13","author":"van Aubel RA","year":"2002","journal-title":"J Am Soc Nephrol"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1016\/j.autneu.2010.07.008"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1155\/2014\/254640"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1155\/2014\/297295"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(05)65936-8"},{"key":"B69","doi-asserted-by":"publisher","DOI":"10.1016\/j.ceca.2011.03.008"},{"key":"B70","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.108.142562"},{"key":"B71","doi-asserted-by":"publisher","DOI":"10.1002\/nau.20420"},{"key":"B72","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0701870"},{"key":"B73","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(05)67952-9"},{"key":"B74","doi-asserted-by":"publisher","DOI":"10.1016\/j.urology.2003.11.003"},{"key":"B75","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00025.2006"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00392.2016","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,6,17]],"date-time":"2025-06-17T20:40:25Z","timestamp":1750192825000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00392.2016"}},"issued":{"date-parts":[[2017,8,1]]},"references-count":75,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2017,8,1]]}},"alternative-id":["10.1152\/ajprenal.00392.2016"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00392.2016","relation":{"has-review":[{"id-type":"doi","id":"10.3410\/f.727559740.793537998","asserted-by":"object"}]},"ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2017,8,1]]}},{"indexed":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T03:50:27Z","timestamp":1772164227735,"version":"3.50.1"},"reference-count":23,"publisher":"American Physiological Society","issue":"3","funder":[{"name":"Australian Governemnt Research Training Program"},{"DOI":"10.13039\/501100001067","name":"Juvenile Diabetes Research Foundation Australia","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100001067","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2020,3,1]]},"abstract":"<jats:p>\n                    Alterations in gut homeostasis may contribute to the progression of diabetic nephropathy. There has been recent attention on the renoprotective effects of metabolite-sensing receptors in chronic renal injury, including the G protein-coupled receptor (GPR)109a, which ligates the short-chain fatty acid butyrate. However, the role of GPR109a in the development of diabetic nephropathy, a milieu of diminished microbiome-derived metabolites, has not yet been determined. The present study aimed to assess the effects of insufficient GPR109a signaling, via genetic deletion of GPR109a, on the development of renal injury in diabetic nephropathy. Gpr109a\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice or their wild-type littermates ( Gpr109a\n                    <jats:sup>+\/+<\/jats:sup>\n                    ) were rendered diabetic with streptozotocin. Mice received a control diet or an isocaloric high-fiber diet (12.5% resistant starch) for 24 wk, and gastrointestinal permeability and renal injury were determined. Diabetes was associated with increased albuminuria, glomerulosclerosis, and inflammation. In comparison, Gpr109a\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice with diabetes did not show an altered renal phenotype. Resistant starch supplementation did not afford protection from renal injury in diabetic nephropathy. While diabetes was associated with alterations in intestinal morphology, intestinal permeability assessed in vivo using the FITC-dextran test was unaltered. GPR109a deletion did not worsen gastrointestinal permeability. Furthermore, 12.5% resistant starch supplementation, at physiological concentrations, had no effect on intestinal permeability or morphology. The results of this study indicate that GPR109a does not play a critical role in intestinal homeostasis in a model of type 1 diabetes or in the development of diabetic nephropathy.\n                  <\/jats:p>","DOI":"10.1152\/ajprenal.00505.2019","type":"journal-article","created":{"date-parts":[[2020,2,18]],"date-time":"2020-02-18T11:58:39Z","timestamp":1582027119000},"page":"F835-F842","source":"Crossref","is-referenced-by-count":13,"title":["Exploring the role of the metabolite-sensing receptor GPR109a in diabetic nephropathy"],"prefix":"10.1152","volume":"318","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4829-9550","authenticated-orcid":false,"given":"Matthew","family":"Snelson","sequence":"first","affiliation":[{"name":"Department of Diabetes, Central Clinical School, Alfred Medical Research and Education Precinct, Monash University, Melbourne, Victoria, Australia"}]},{"given":"Sih Min","family":"Tan","sequence":"additional","affiliation":[{"name":"Department of Diabetes, Central Clinical School, Alfred Medical Research and Education Precinct, Monash University, Melbourne, Victoria, Australia"}]},{"given":"Gavin C.","family":"Higgins","sequence":"additional","affiliation":[{"name":"Department of Diabetes, Central Clinical School, Alfred Medical Research and Education Precinct, Monash University, Melbourne, Victoria, Australia"}]},{"given":"Runa S. J.","family":"Lindblom","sequence":"additional","affiliation":[{"name":"Department of Diabetes, Central Clinical School, Alfred Medical Research and Education Precinct, Monash University, Melbourne, Victoria, Australia"}]},{"given":"Melinda T.","family":"Coughlan","sequence":"additional","affiliation":[{"name":"Department of Diabetes, Central Clinical School, Alfred Medical Research and Education Precinct, Monash University, Melbourne, Victoria, Australia"},{"name":"Baker Heart and Diabetes Institute, Melbourne, Victoria, Australia"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.11491116"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2017.142"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009070721"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1136\/gut.2008.165886"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/j.ebiom.2018.03.030"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.2337\/db15-0864"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-016-3527-x"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1096\/fj.201901080R"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1159\/000490981"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1038\/nature15766"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-017-02989-2"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1021\/acs.jafc.6b03808"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.3945\/jn.114.198200"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.3791\/57280"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1186\/1743-7075-6-11"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1038\/ncomms7734"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.3390\/toxins10070298"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.54.9.2628"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1093\/advances\/nmy068"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/j.celrep.2016.05.047"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1146\/annurev-immunol-051116-052235"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0114881"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1159\/000360010"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00505.2019","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2020,3,9]],"date-time":"2020-03-09T09:19:15Z","timestamp":1583745555000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00505.2019"}},"issued":{"date-parts":[[2020,3,1]]},"references-count":23,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2020,3,1]]}},"alternative-id":["10.1152\/ajprenal.00505.2019"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00505.2019","relation":{"has-preprint":[{"id-type":"doi","id":"10.1101\/713354","asserted-by":"object"}]},"ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2020,3,1]]}},{"indexed":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T03:49:37Z","timestamp":1772164177805,"version":"3.50.1"},"reference-count":52,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2010,8]]},"abstract":"<jats:p>Urothelium that lines almost the entire urinary tract performs important functions and is prone to assaults by urinary microbials, metabolites, and carcinogens. To improve our understanding of urothelial physiology and disease pathogenesis, we sought to develop two novel transgenic systems, one that would allow inducible and urothelium-specific gene expression, and another that would allow inducible and urothelium-specific knockout. Toward this end, we combined the ability of the mouse uroplakin II promoter (mUPII) to drive urothelium-specific gene expression with a versatile tetracycline-mediated inducible system. We found that, when constructed under the control of mUPII, only a modified, reverse tetracycline trans-activator (rtTA-M2), but not its original version (rtTA), could efficiently trans-activate reporter gene expression in mouse urothelium on doxycycline (Dox) induction. The mUPII\/rtTA-M2-inducible system retained its strict urothelial specificity, had no background activity in the absence of Dox, and responded rapidly to Dox administration. Using a reporter gene whose expression was secondarily controlled by histone remodeling, we were able to identify, colocalize with 5-bromo-2-deoxyuridine incorporation, and semiquantify newly divided urothelial cells. Finally, we established that, when combined with a Cre recombinase under the control of the tetracycline operon, the mUPII-driven rtTA-M2 could inducibly inactivate any gene of interest in mouse urothelium. The establishment of these two new transgenic mouse systems enables the manipulation of gene expression and\/or inactivation in adult mouse urothelium at any given time, thus minimizing potential compensatory effects due to gene overexpression or loss and allowing more accurate modeling of urothelial diseases than previously reported constitutive systems.<\/jats:p>","DOI":"10.1152\/ajprenal.00185.2010","type":"journal-article","created":{"date-parts":[[2010,4,28]],"date-time":"2010-04-28T22:14:22Z","timestamp":1272492862000},"page":"F387-F395","source":"Crossref","is-referenced-by-count":14,"title":["Temporally and spatially controllable gene expression and knockout in mouse urothelium"],"prefix":"10.1152","volume":"299","author":[{"given":"Haiping","family":"Zhou","sequence":"first","affiliation":[{"name":"Departments of 1Urology,"}]},{"given":"Yan","family":"Liu","sequence":"additional","affiliation":[{"name":"Departments of 1Urology,"}]},{"given":"Feng","family":"He","sequence":"additional","affiliation":[{"name":"Departments of 1Urology,"}]},{"given":"Lan","family":"Mo","sequence":"additional","affiliation":[{"name":"Departments of 1Urology,"}]},{"given":"Tung-Tien","family":"Sun","sequence":"additional","affiliation":[{"name":"Departments of 1Urology,"},{"name":"Cell Biology,"},{"name":"Dermatology, and"},{"name":"Pharmacology, New York University School of Medicine, New York; New York University Cancer Institute, New York; and"}]},{"given":"Xue-Ru","family":"Wu","sequence":"additional","affiliation":[{"name":"Departments of 1Urology,"},{"name":"Pathology,"},{"name":"New York Harbor Healthcare System, Manhattan Campus, New York, New York"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1046\/j.1600-0854.2003.00156.x"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002439"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/j.autneu.2009.07.005"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/nm1572"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1093\/carcin\/bgl120"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/23.16.3083"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.2436350100"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.53.1.92"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/j.tice.2006.07.001"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1007\/s11934-006-0051-8"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-0854.2009.00950.x"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.151.5.961"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00043.2002"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/j.urology.2006.03.083"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1038\/nrc777"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.93.9.4465"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(05)00977-8"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/S0960-9822(98)70156-3"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1186\/1471-213X-7-108"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1167\/iovs.04-1237"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00327.2009"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0805636105"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1111\/j.1464-410X.2008.08097.x"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200406025"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.4.F540"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.6.F867"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200505035"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/S0090-4295(01)01160-8"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.3.679"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1002\/ssu.2980080507"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1002\/gene.20175"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.77.3.685"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00368.2004"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1172\/JCI30062"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.4.F886"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1016\/j.urology.2006.03.084"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1101\/gad.1772909"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1016\/j.gene.2003.10.029"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1016\/S0958-1669(98)80028-1"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1677\/joe.0.1710001"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.53.38071"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00035.2006"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.01-09-0435"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1126\/science.1092436"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.130192197"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(02)00621-9"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1242\/dev.011270"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2009.73"},{"key":"B50","doi-asserted-by":"crossref","first-page":"13716","DOI":"10.1016\/S0021-9258(17)36889-8","volume":"269","author":"Wu XR","year":"1994","journal-title":"J Biol Chem"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.E08-04-0439"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1204315"},{"key":"B53","first-page":"3512","volume":"59","author":"Zhang ZT","year":"1999","journal-title":"Cancer Res"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00185.2010","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,10,26]],"date-time":"2021-10-26T17:13:12Z","timestamp":1635268392000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00185.2010"}},"issued":{"date-parts":[[2010,8]]},"references-count":52,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2010,8]]}},"alternative-id":["10.1152\/ajprenal.00185.2010"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00185.2010","relation":{"has-review":[{"id-type":"doi","id":"10.3410\/f.5345956.5297054","asserted-by":"object"}]},"ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2010,8]]}},{"indexed":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T03:49:40Z","timestamp":1772164180743,"version":"3.50.1"},"reference-count":77,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2009,6]]},"abstract":"<jats:p>\n                    NH\n                    <jats:sub>3<\/jats:sub>\n                    movement across plasma membranes has traditionally been ascribed to passive, lipid-phase diffusion. However, ammonia-specific transporters, Mep\/Amt proteins, are present in primitive organisms and mammals express orthologs of Mep\/Amt proteins, the Rh glycoproteins. These findings suggest that the mechanisms of NH\n                    <jats:sub>3<\/jats:sub>\n                    movement in mammalian tissues should be reexamined. Rh C glycoprotein (Rhcg) is expressed in the collecting duct, where NH\n                    <jats:sub>3<\/jats:sub>\n                    secretion is necessary for both basal and acidosis-stimulated ammonia transport. To determine whether the collecting duct secretes NH\n                    <jats:sub>3<\/jats:sub>\n                    via Rhcg or via lipid-phase diffusion, we generated mice with collecting duct-specific Rhcg deletion (CD-KO). CD-KO mice had loxP sites flanking exons 5 and 9 of the Rhcg gene (Rhcg\n                    <jats:sup>fl\/fl<\/jats:sup>\n                    ) and expressed Cre-recombinase under control of the Ksp-cadherin promoter (Ksp-Cre). Control (C) mice were Rhcg\n                    <jats:sup>fl\/fl<\/jats:sup>\n                    but Ksp-Cre negative. We confirmed kidney-specific genomic recombination using PCR analysis and collecting duct-specific Rhcg deletion using immunohistochemistry. Under basal conditions, urinary ammonia excretion was less in KO vs. C mice; urine pH was unchanged. After acid-loading for 7 days, CD-KO mice developed more severe metabolic acidosis than did C mice. Urinary ammonia excretion did not increase significantly on the first day of acidosis in CD-KO mice, despite an intact ability to increase urine acidification, whereas it increased significantly in C mice. On subsequent days, urinary ammonia excretion slowly increased in CD-KO mice, but was always significantly less than in C mice. We conclude that collecting duct Rhcg expression contributes to both basal and acidosis-stimulated renal ammonia excretion, indicating that collecting duct ammonia secretion is, at least in part, mediated by Rhcg and not solely by lipid diffusion.\n                  <\/jats:p>","DOI":"10.1152\/ajprenal.90667.2008","type":"journal-article","created":{"date-parts":[[2009,3,25]],"date-time":"2009-03-25T21:06:59Z","timestamp":1238015219000},"page":"F1364-F1375","source":"Crossref","is-referenced-by-count":85,"title":["Collecting duct-specific Rh C glycoprotein deletion alters basal and acidosis-stimulated renal ammonia excretion"],"prefix":"10.1152","volume":"296","author":[{"given":"Hyun-Wook","family":"Lee","sequence":"first","affiliation":[]},{"given":"Jill W.","family":"Verlander","sequence":"additional","affiliation":[]},{"given":"Jesse M.","family":"Bishop","sequence":"additional","affiliation":[]},{"given":"Peter","family":"Igarashi","sequence":"additional","affiliation":[]},{"given":"Mary E.","family":"Handlogten","sequence":"additional","affiliation":[]},{"given":"I. David","family":"Weiner","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"crossref","unstructured":"Amlal H\n                      , Paillard M, Bichara M.\n                      NH\n                      4\n                      +\n                      transport pathways in cells of medullary thick ascending limb of rat kidney. NH\n                      4\n                      +\n                      conductance and K\n                      +\n                      \/NH\n                      4\n                      +\n                      (H\n                      +\n                      ) antiport.\n                      J Biol Chem\n                      269\n                      : 21962\u201321971, 1994.","DOI":"10.1016\/S0021-9258(17)31742-8"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1016\/S1471-4914(01)01949-9"},{"key":"R3","unstructured":"Avent ND\n                      , Reid ME.\n                      The Rh blood group system: a review.\n                      Blood\n                      95\n                      : 375\u2013387, 2000."},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M308528200"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-005-1381-y"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1038\/nature07518"},{"key":"R7","doi-asserted-by":"crossref","unstructured":"Bruce LJ\n                      , Guizouarn H, Burton NM, Gabillat N, Poole J, Flatt JF, Brady RL, Borgese F, Delaunay J, Stewart GW.\n                      The monovalent cation leak in over-hydrated stomatocytic red blood cells results from amino acid substitutions in the Rh associated glycoprotein (RhAG).\n                      Blood\n                      113\n                      : 1350\u20131357, 2008.","DOI":"10.1182\/blood-2008-07-171140"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00172.2005"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1016\/S0009-9120(72)80014-6"},{"key":"R10","unstructured":"DuBose TD\n                      , Good DW, Hamm LL, Wall SM.\n                      Ammonium transport in the kidney: new physiological concepts and their clinical implications.\n                      J Am Soc Nephrol\n                      1\n                      : 1193\u20131203, 1991."},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000025280.02386.9D"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.260.2.F264"},{"key":"R13","doi-asserted-by":"crossref","unstructured":"Frank AE\n                      , Weiner ID.\n                      Effects of ammonia on acid-base transport by the B-type intercalated cell.\n                      J Am Soc Nephrol\n                      12\n                      : 1607\u20131614, 2001.","DOI":"10.1681\/ASN.V1281607"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00266.2001"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.2.F219"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1988.255.1.F78"},{"key":"R17","doi-asserted-by":"crossref","unstructured":"Good DW\n                      .\n                      Ammonium transport by the loop of Henle.\n                      Miner Electrolyte Metab\n                      16\n                      : 291\u2013298, 1990.","DOI":"10.5840\/pdp19901618"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1159\/000415692"},{"key":"R19","unstructured":"Good DW\n                      , Knepper MA.\n                      Mechanisms of ammonium excretion: role of the renal medulla.\n                      Semin Nephrol\n                      10\n                      : 166\u2013173, 1990."},{"key":"R20","unstructured":"Hamm LL\n                      , Nakhoul NL.\n                      Renal acidification. In:\n                      Brenner and Rector's The Kidney\n                      , edited by Brenner BM. Philadelphia, PA: Saunders Elsevier, 2007, p. 248\u2013279."},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.253.4.F595"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1172\/JCI111723"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00363.2003"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00253.2004"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.00418.2004"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1038\/81532"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2141.2003.04425.x"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0507886102"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.4.F599"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1038\/339478a0"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.99.3.435"},{"key":"R32","doi-asserted-by":"crossref","unstructured":"Kim HY\n                      , Verlander JW, Bishop JM, Cain BD, Han KH, Igarashi P, Lee HW, Handlogten ME, Weiner ID.\n                      Basolateral expression of the ammonia transporter family member, Rh C glycoprotein, in the mouse kidney.\n                      Am J Physiol Renal Physiol\n                      296\n                      : F545\u2013F555, 2009.","DOI":"10.1152\/ajprenal.90637.2008"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00151.2007"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00206.2005"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1981.241.5.C220"},{"key":"R36","unstructured":"Knepper MA\n                      .\n                      NH\n                      4\n                      +\n                      transport in the kidney.\n                      Kidney Int\n                      40\n                      : S95\u2013S102, 1991."},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1984.247.5.F729"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1985.249.6.F870"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5001851"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1159\/000153245"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M003353200"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M007528200"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2004.067728"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00147.2005"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1038\/81656"},{"key":"R46","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.17.8.4282"},{"key":"R47","doi-asserted-by":"publisher","DOI":"10.1002\/yea.320110505"},{"key":"R48","doi-asserted-by":"publisher","DOI":"10.1002\/j.1460-2075.1994.tb06651.x"},{"key":"R49","doi-asserted-by":"publisher","DOI":"10.1172\/JCI113287"},{"key":"R50","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00419.2003"},{"key":"R51","doi-asserted-by":"publisher","DOI":"10.1002\/ajh.2830240306"},{"key":"R52","doi-asserted-by":"publisher","DOI":"10.1002\/j.1460-2075.1994.tb06652.x"},{"key":"R53","doi-asserted-by":"publisher","DOI":"10.1159\/000096979"},{"key":"R54","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000050413.43662.55"},{"key":"R55","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0403704101"},{"key":"R56","doi-asserted-by":"crossref","unstructured":"Sajo IM\n                      , Goldstein MB, Sonnenberg H, Stinebaugh BJ, Wilson DR, Halperin ML.\n                      Sites of ammonia addition to tubular fluid in rats with chronic metabolic acidosis.\n                      Kidney Int\n                      20\n                      : 353\u2013358, 1982.","DOI":"10.1038\/ki.1981.146"},{"key":"R57","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00162.2005"},{"key":"R58","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00459.2005"},{"key":"R59","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000016444.90348.50"},{"key":"R60","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.256.6.F1104"},{"key":"R61","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.262.1.F36"},{"key":"R62","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0401809101"},{"key":"R63","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.112225599"},{"key":"R64","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.252.6.F1148"},{"key":"R65","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.253.6.F1232"},{"key":"R66","doi-asserted-by":"publisher","DOI":"10.1016\/j.blre.2005.04.002"},{"key":"R67","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00050.2002"},{"key":"R68","doi-asserted-by":"publisher","DOI":"10.1016\/S1369-5266(00)00073-X"},{"key":"R69","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.270.3.F432"},{"key":"R70","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.273.6.F857"},{"key":"R71","doi-asserted-by":"publisher","DOI":"10.1053\/ajkd.2000.19115"},{"key":"R72","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.267.4.F660"},{"key":"R73","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.69.040705.142215"},{"key":"R74","doi-asserted-by":"publisher","DOI":"10.1016\/S0016-5085(03)00277-4"},{"key":"R75","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.C200060200"},{"key":"R76","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M311853200"},{"key":"R77","doi-asserted-by":"publisher","DOI":"10.1016\/j.ab.2005.01.045"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.90667.2008","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,10,3]],"date-time":"2021-10-03T12:06:48Z","timestamp":1633262808000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.90667.2008"}},"issued":{"date-parts":[[2009,6]]},"references-count":77,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2009,6]]}},"alternative-id":["10.1152\/ajprenal.90667.2008"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.90667.2008","relation":{"has-review":[{"id-type":"doi","id":"10.3410\/f.1160770.622179","asserted-by":"object"}]},"ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2009,6]]}},{"indexed":{"date-parts":[[2026,4,1]],"date-time":"2026-04-01T16:11:15Z","timestamp":1775059875683,"version":"3.50.1"},"reference-count":67,"publisher":"American Physiological Society","issue":"1","funder":[{"DOI":"10.13039\/501100001659","name":"Deutsche Forschungsgemeinschaft","doi-asserted-by":"publisher","award":["KO 1057\/10-1"],"award-info":[{"award-number":["KO 1057\/10-1"]}],"id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2022,1,1]]},"abstract":"<jats:p> ROMK-mediated renal K<jats:sup>+<\/jats:sup> secretion is essential for maintaining K<jats:sup>+<\/jats:sup> balance and requires a lumen negative transepithelial potential critically dependent on activity of the ENaC. Using microdissected distal mouse tubules, we demonstrated that baseline apical ROMK activity is high in the DCT2\/CNT. Aldosterone-independent baseline ENaC activity is also high in the DCT2\/CNT and downregulated by a low-K<jats:sup>+<\/jats:sup> diet, which highlights the important role of the DCT2\/CNT in regulating K<jats:sup>+<\/jats:sup> secretion in an aldosterone-independent manner. <\/jats:p>","DOI":"10.1152\/ajprenal.00252.2021","type":"journal-article","created":{"date-parts":[[2021,11,30]],"date-time":"2021-11-30T00:45:07Z","timestamp":1638233107000},"page":"F42-F54","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":18,"title":["High baseline ROMK activity in the mouse late distal convoluted and early connecting tubule probably contributes to aldosterone-independent K<sup>+<\/sup> secretion"],"prefix":"10.1152","volume":"322","author":[{"given":"Viatcheslav","family":"Nesterov","sequence":"first","affiliation":[{"name":"Institut f\u00fcr Zellul\u00e4re und Molekulare Physiologie, Friedrich-Alexander-Universit\u00e4t Erlangen-N\u00fcrnberg, Erlangen, Germany"}]},{"given":"Marko","family":"Bertog","sequence":"additional","affiliation":[{"name":"Institut f\u00fcr Zellul\u00e4re und Molekulare Physiologie, Friedrich-Alexander-Universit\u00e4t Erlangen-N\u00fcrnberg, Erlangen, Germany"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2127-4185","authenticated-orcid":true,"given":"Christoph","family":"Korbmacher","sequence":"additional","affiliation":[{"name":"Institut f\u00fcr Zellul\u00e4re und Molekulare Physiologie, Friedrich-Alexander-Universit\u00e4t Erlangen-N\u00fcrnberg, Erlangen, Germany"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/B978-0-12-381462-3.00049-5"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/B978-012088488-9.50035-8"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1997.77.2.359"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/j.coph.2013.11.010"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1146\/annurev-physiol-021115-105423"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.268.6.F1124"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.268.6.F1132"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.0085.2001"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.05920613"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0095149"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00118.2006"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90528.2008"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00044.2005"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-008-0593-3"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1016\/j.febslet.2013.05.013"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00592.2010"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90527.2008"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-009-0656-0"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/j.mce.2011.11.003"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1985.248.6.F858"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1983.244.1.f28"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.104.4.693"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.258"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M212301200"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013111156"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1172\/jci.insight.126910"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00204.2020"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.102.1.25"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.258.3.f562"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00247.2012"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.115.07061"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1161\/JAHA.119.014996"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00420.2016"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00050.2018"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajplegacy.1964.206.4.674"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00031.2008"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00139.2021"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1172\/JCI80304"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.98.1.35"},{"key":"B40","unstructured":"Nesterov V. Nest-O-Patch 2.1. User\u2019s guide. https:\/\/www.researchgate.net\/publication\/326450502_Nest-O-Patch_21_User's_guide. [2021 Dec 2] doi:10.13140\/RG.2.2.16080.00001."},{"key":"B42","volume-title":"R: A Language and Environment for Statistical Computing","author":"R Team","year":"2020"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1021\/bi991206j"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010060617"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.66.032102.150822"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.275.6.f972"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00705.2010"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00185.2013"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0000000000000253"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1007\/bf00585057"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-016-1906-6"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1152\/ajplegacy.1971.221.2.632"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1146\/annurev-physiol-021115-105431"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1172\/JCI200316956"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00258.2015"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00288.2007"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1111\/apha.12703.Role"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00412.2018"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2001.012961"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00072.2021"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00368.2011"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.113.01797"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.1.f143"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2017.10.023"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1007\/s11886-020-01359-1"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1172\/JCI73935.Introduction"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.202112902"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.1161\/hy1101.095010"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00252.2021","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,12,24]],"date-time":"2021-12-24T04:32:15Z","timestamp":1640320335000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00252.2021"}},"issued":{"date-parts":[[2022,1,1]]},"references-count":67,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2022,1,1]]}},"alternative-id":["10.1152\/ajprenal.00252.2021"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00252.2021","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2022,1,1]]},"assertion":[{"value":"2021-07-01","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2021-11-18","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2021-12-23","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,4,3]],"date-time":"2026-04-03T21:33:45Z","timestamp":1775252025229,"version":"3.50.1"},"reference-count":42,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2005,9]]},"abstract":"<jats:p>Glomerular capillary hypertension is a final common pathway to glomerulosclerosis. Because podocyte loss is an early event in the development of glomerulosclerosis, it is logical that the deleterious effects of glomerular capillary hypertension involve podocyte injury. Yet, the mechanisms by which elevated intraglomerular pressure is translated into a maladaptive podocyte response remain poorly understood. Secreted protein acidic and rich in cysteine (SPARC) is a matricellular protein activated in various disease states of the podocyte and accelerates renal injury, as evidenced by the milder course of experimental diabetic nephropathy in SPARC-null mice compared with diabetic SPARC wild-type mice. Accordingly, we tested the hypothesis that mechanical strain activates SPARC in podocytes and thus is a putative mediator of podocyte injury in states of intraglomerular capillary hypertension. Conditionally immortalized mouse podocytes were subjected to 10% cyclical stretch while nonstretched cells served as controls. SPARC levels were measured in whole cell lysate and cell media. Immunostaining was performed for SPARC in an experimental model of glomerular capillary hypertension. Our results demonstrate cyclical stretch of podocytes markedly increased SPARC levels in cell lysate, through activation of p38, as well as secreted SPARC. Relevance was shown by demonstrating increased podocyte staining for SPARC in the uninephrectomized spontaneously hypertensive rat. In conclusion, we have made the novel observation that mechanical forces characteristic of states of glomerular capillary hypertension lead to increased levels of SPARC in podocytes. We speculate that the increase in SPARC may be maladaptive and lead to a progressive reduction in podocyte number, thus fueling the future development of glomerulosclerosis.<\/jats:p>","DOI":"10.1152\/ajprenal.00393.2004","type":"journal-article","created":{"date-parts":[[2005,8,10]],"date-time":"2005-08-10T18:48:45Z","timestamp":1123699725000},"page":"F577-F584","source":"Crossref","is-referenced-by-count":33,"title":["Mechanical strain increases SPARC levels in podocytes: implications for glomerulosclerosis"],"prefix":"10.1152","volume":"289","author":[{"given":"Raghu V.","family":"Durvasula","sequence":"first","affiliation":[]},{"given":"Stuart J.","family":"Shankland","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00680.x"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1006\/exer.1998.0608"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00811.x"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.10.5.1569"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1172\/JCI12939"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1016\/S0945-053X(00)00133-5"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1985.249.3.F324"},{"key":"R8","doi-asserted-by":"crossref","unstructured":"Brenner BMand Zagrobelny J.Clinical renoprotection trials involving angiotensin II-receptor antagonists and angiotensin-converting-enzyme inhibitors.Kidney Int Suppl83: S77\u2013S85, 2003.","DOI":"10.1046\/j.1523-1755.63.s83.16.x"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1042\/bj3510095"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00362.x"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1172\/JCI112377"},{"key":"R12","doi-asserted-by":"crossref","unstructured":"Endlich N, Kress KR, Reiser J, Uttenweiler D, Kriz W, Mundel P, and Endlich K.Podocytes respond to mechanical stress in vitro.J Am Soc Nephrol12: 413\u2013422, 2001.","DOI":"10.1681\/ASN.V123413"},{"key":"R13","unstructured":"Floege J, Alpers CE, Sage EH, Pritzl P, Gordon K, Johnson RJ, and Couser WG.Markers of complement-dependent and complement-independent glomerular visceral epithelial cell injury in vivo. Expression of antiadhesive proteins and cytoskeletal changes.Lab Invest67: 486\u2013497, 1992."},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1002\/jcb.20008"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1016\/j.cellbi.2003.12.007"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1097-4644(19990801)74:2<152::AID-JCB2>3.0.CO;2-4"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)63378-0"},{"key":"R18","unstructured":"Harris RC, Haralson MA, and Badr KF.Continuous stretch-relaxation in culture alters rat mesangial cell morphology, growth characteristics, and metabolic activity.Lab Invest66: 548\u2013554, 1992."},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00057.x"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1007\/s001250051493"},{"key":"R21","doi-asserted-by":"crossref","unstructured":"Kretzler M, Koeppen-Hagemann I, and Kriz W.Podocyte damage is a critical step in the development of glomerulosclerosis in the uninephrectomised-desoxycorticosterone hypertensive rat.Virchows Arch425: 181\u2013193, 1994.","DOI":"10.1007\/BF00230355"},{"key":"R22","unstructured":"Kriz W, Elger M, Nagata M, Kretzler M, Uiker S, Koeppen-Hageman I, Tenschert S, and Lemley KV.The role of podocytes in the development of glomerular sclerosis.Kidney Int Suppl45: S64\u2013S72, 1994."},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00269.x"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199311113292004"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-98-5-832"},{"key":"R25A","unstructured":"Martineau LC, McVeigh LI, Jasmin BJ, and Kennedy CR.p38 MAP kinase mediates mechanically induced COX-2 and PG EP4receptor expression in podocytes: implications for the actin cytoskeleton.Am J Physiol Renal Physiol286: F693\u2013F701, 2004."},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1006\/excr.1997.3739"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-199212007-00010"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119163"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00020.2002"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)63228-2"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00102.x"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00217.x"},{"key":"R33","unstructured":"Pichler RH, Bassuk JA, Hugo C, Reed MJ, Eng E, Gordon KL, Pippin J, Alpers CE, Couser WG, Sage EH, and Johnson RJ.SPARC is expressed by mesangial cells in experimental mesangial proliferative nephritis and inhibits platelet-derived-growth-factor-mediated mesangial cell proliferation in vitro.Am J Pathol148: 1153\u20131167, 1996."},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1177\/37.6.2723400"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.E03-01-0001"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1172\/JCI200112367"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M314155200"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000054498.83125.90"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.5.F839"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00404.2002"},{"key":"R41","unstructured":"Ziyadeh FNand Sharma K.Role of transforming growth factor-\u03b2 in diabetic glomerulosclerosis and renal hypertrophy.Kidney Int Suppl51: S34\u2013S36, 1995."}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00393.2004","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,7,15]],"date-time":"2021-07-15T06:17:45Z","timestamp":1626329865000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00393.2004"}},"issued":{"date-parts":[[2005,9]]},"references-count":42,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2005,9]]}},"alternative-id":["10.1152\/ajprenal.00393.2004"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00393.2004","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2005,9]]}},{"indexed":{"date-parts":[[2026,4,3]],"date-time":"2026-04-03T22:05:37Z","timestamp":1775253937938,"version":"3.50.1"},"reference-count":60,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2011,11]]},"abstract":"<jats:p>The claudin family of proteins is required for the formation of tight junctions that are contact points between epithelial cells. Although little is known of the cellular events by which epithelial cells of the ureteric bud form tubules and branch, tubule formation is critical for kidney development. We hypothesize that if claudin-3 (Cldn3) is expressed within tight junctions of the ureteric bud, this will affect ureteric bud cell shape and tubule formation. Using transmission electron microscopy, we identified tight junctions within epithelial cells of the ureteric bud. Whole mount in situ hybridization and immunoassays were performed in the mouse and chick and demonstrated that Cldn3 transcript and protein were expressed in the nephric duct, the ureteric bud, and its derivatives at critical time points during tubule formation and branching. Mouse inner medullary collecting duct cells (mIMCD-3) form tubules when seeded in a type I collagen matrix and were found to coexpress CLDN3 and the tight junction marker zonula occludens-1 in the cell membrane. When these cells were stably transfected with Cldn3 fused to the enhanced green fluorescent protein reporter, multiple clones showed a significant increase in tubule formation compared with controls ( P &lt; 0.05) due in part to an increase in cell proliferation ( P &lt; 0.01). Cldn3 may therefore promote tubule formation and expansion of the ureteric bud epithelium.<\/jats:p>","DOI":"10.1152\/ajprenal.00497.2010","type":"journal-article","created":{"date-parts":[[2011,7,21]],"date-time":"2011-07-21T02:24:52Z","timestamp":1311215092000},"page":"F1057-F1065","source":"Crossref","is-referenced-by-count":16,"title":["The tight junction protein claudin-3 shows conserved expression in the nephric duct and ureteric bud and promotes tubulogenesis in vitro"],"prefix":"10.1152","volume":"301","author":[{"given":"Nicholas","family":"Haddad","sequence":"first","affiliation":[{"name":"Departments of 1Human Genetics and"}]},{"given":"Jasmine El","family":"Andalousi","sequence":"additional","affiliation":[{"name":"Pediatrics, McGill University, and The Research Institute of McGill University Health Centre, Montreal Children's Hospital, Montr\u00e9al, Qu\u00e9bec, Canada"}]},{"given":"Halim","family":"Khairallah","sequence":"additional","affiliation":[{"name":"Departments of 1Human Genetics and"}]},{"given":"Melissa","family":"Yu","sequence":"additional","affiliation":[{"name":"Pediatrics, McGill University, and The Research Institute of McGill University Health Centre, Montreal Children's Hospital, Montr\u00e9al, Qu\u00e9bec, Canada"}]},{"given":"Aimee K.","family":"Ryan","sequence":"additional","affiliation":[{"name":"Pediatrics, McGill University, and The Research Institute of McGill University Health Centre, Montreal Children's Hospital, Montr\u00e9al, Qu\u00e9bec, Canada"}]},{"given":"Indra R.","family":"Gupta","sequence":"additional","affiliation":[{"name":"Pediatrics, McGill University, and The Research Institute of McGill University Health Centre, Montreal Children's Hospital, Montr\u00e9al, Qu\u00e9bec, Canada"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00063.2006"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1158\/0008-5472.CAN-05-1036"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002329"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90264.2008"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/0012-1606(67)90036-X"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1172\/JCI4586"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1089\/dna.2006.25.79"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1111\/j.1432-0436.2004.07207001.x"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1006\/dbio.2000.0116"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1002\/dvdy.20143"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbamem.2007.08.017"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1111\/j.1432-0436.2006.00106.x"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M502003200"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1242\/dev.034876"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.cellbio.22.010305.104340"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1038\/381789a0"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/S0896-6273(00)80541-3"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200110122"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.143.2.391"},{"key":"B20","doi-asserted-by":"crossref","first-page":"269","DOI":"10.1242\/jcs.113.2.269","volume":"113","author":"Gupta IR","year":"2000","journal-title":"J Cell Sci"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.37.26305"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1111\/j.1399-0004.2010.01397.x"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1016\/j.modgep.2005.05.002"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1158\/1078-0432.CCR-04-0073"},{"key":"B25","first-page":"6281","volume":"60","author":"Hough CD","year":"2000","journal-title":"Cancer Res"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0813348106"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1242\/dev.02442"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1186\/1465-9921-11-59"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/j.ydbio.2007.04.051"},{"key":"B30","doi-asserted-by":"crossref","first-page":"875","DOI":"10.1681\/ASN.V134875","volume":"13","author":"Kiuchi-Saishin Y","year":"2002","journal-title":"J Am Soc Nephrol"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.171325898"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbamem.2007.10.018"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1016\/S0960-9822(99)80452-7"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0002715"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1007\/s00418-007-0322-6"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1016\/j.ydbio.2004.07.022"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbamem.2010.07.014"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M103083200"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1016\/j.ydbio.2007.09.049"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1016\/S0091-679X(08)60630-5"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008020132"},{"key":"B42","doi-asserted-by":"crossref","first-page":"1103","DOI":"10.1242\/dev.126.6.1103","volume":"126","author":"Obara-Ishihara T","year":"1999","journal-title":"Development"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1292\/jvms.68.149"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.273.6.F961"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.5.F891"},{"key":"B46","first-page":"1","volume":"63","author":"Poole TJ","year":"1981","journal-title":"J Embryol Exp Morphol"},{"key":"B47","first-page":"2567","volume":"9","author":"Rangel LB","year":"2003","journal-title":"Clin Cancer Res"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1207008"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.265.3.F416"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004121127"},{"key":"B51","doi-asserted-by":"crossref","first-page":"1919","DOI":"10.1242\/dev.122.6.1919","volume":"122","author":"Schuchardt A","year":"1996","journal-title":"Development"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00276.x"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1016\/j.modgep.2004.10.009"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00383.x"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.2000.tb05235.x"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1038\/onc.2008.344"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.01235"},{"key":"B58","doi-asserted-by":"crossref","first-page":"1775","DOI":"10.1242\/dev.129.7.1775","volume":"129","author":"Turksen K","year":"2002","journal-title":"Development"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.68.040104.131404"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0306924101"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00497.2010","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,11,28]],"date-time":"2021-11-28T12:24:26Z","timestamp":1638102266000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00497.2010"}},"issued":{"date-parts":[[2011,11]]},"references-count":60,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2011,11]]}},"alternative-id":["10.1152\/ajprenal.00497.2010"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00497.2010","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2011,11]]}},{"indexed":{"date-parts":[[2026,4,2]],"date-time":"2026-04-02T18:18:20Z","timestamp":1775153900947,"version":"3.50.1"},"reference-count":196,"publisher":"American Physiological Society","issue":"6","funder":[{"DOI":"10.13039\/100017749","name":"Cardiovascular Center, Medical College of Wisconsin","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100017749","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"HHS | NIH | National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["R01HL128332"],"award-info":[{"award-number":["R01HL128332"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"HHS | NIH | National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["T32 HL134643"],"award-info":[{"award-number":["T32 HL134643"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2022,6,1]]},"abstract":"<jats:p> The 5\/6 nephrectomy rat remnant kidney model is commonly used to study chronic kidney disease (CKD). This model requires the removal of one whole kidney and two-thirds of the other kidney. The two most common ways of producing the remnant kidney are surgical resection of poles, known as the polectomy model, or ligation of superior and inferior segmental renal arteries, resulting in pole infarction. These models have much in common, but also major phenotypic differences, and thus respectively model unique aspects of human CKD. The purpose of this review is to summarize phenotypic similarities and differences between these two models and their relation to human CKD while emphasizing their vascular phenotype. In this article, we review studies that have evaluated arterial blood pressure, the renin-angiotensin-aldosterone-system, autoregulation, nitric oxide, single-nephron physiology, angiogenic and antiangiogenic factors, and capillary rarefaction in these two models. In terms of phenotypic similarities, both models spontaneously develop hallmarks of human CKD including uremia, fibrosis, capillary rarefaction, and progressive renal function decline. They both undergo whole organ hypertrophy, hyperfiltration of functional nephrons, reduced renal expression of vascular endothelial growth factor, increased renal expression of antiangiogenic thrombospondin-1, impaired renal autoregulation, and abnormal vascular nitric oxide physiology. In terms of key phenotypic differences, the infarction model develops rapid-onset, moderate to severe systemic hypertension and the polectomy model develops early normotension followed by mild to moderate hypertension. Rats subjected to the infarction model have a markedly more active renin-angiotensin-aldosterone system. Comparison of these two models facilitates understanding of how they can be used for studying CKD pathophysiology. <\/jats:p>","DOI":"10.1152\/ajprenal.00398.2021","type":"journal-article","created":{"date-parts":[[2022,4,5]],"date-time":"2022-04-05T01:28:41Z","timestamp":1649122121000},"page":"F639-F654","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":44,"title":["Comparison of the surgical resection and infarct 5\/6 nephrectomy rat models of chronic kidney disease"],"prefix":"10.1152","volume":"322","author":[{"given":"Ryan J.","family":"Adam","sequence":"first","affiliation":[{"name":"Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin"},{"name":"Cardiovascular Center, Medical College of Wisconsin, Milwaukee, Wisconsin"}]},{"given":"Adaysha C.","family":"Williams","sequence":"additional","affiliation":[{"name":"Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3961-9893","authenticated-orcid":true,"given":"Alison J.","family":"Kriegel","sequence":"additional","affiliation":[{"name":"Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin"},{"name":"Department of Pediatrics, Medical College of Wisconsin, Milwaukee, Wisconsin"},{"name":"Cardiovascular Center, Medical College of Wisconsin, Milwaukee, Wisconsin"},{"name":"Center of Systems Molecular Medicine, Medical College of Wisconsin, Milwaukee, Wisconsin"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00117.2021"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00343.2020"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(16)32064-5"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1001\/jama.298.17.2038"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2017.05.014"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.V4122023"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00288.2020"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1159\/000066302"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118125"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00679.2020"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2019.07.017"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00592.2015"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00759.x"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.V113497"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.V9172"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/j.freeradbiomed.2013.03.017"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.V1271434"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5001880"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005121379"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1976.50"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1992.222"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)64175-2"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1007\/s10735-013-9521-8"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1016\/j.lfs.2018.05.034"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1002\/path.2961"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1155\/2012\/269039"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1159\/000025837"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1159\/000174072"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/s0046-8177(70)80061-2"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1078\/0940-2993-00276"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00407.2019"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00661.2011"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1097\/FJC.0b013e31802f9923"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1111\/j.1699-0463.1992.tb04046.x"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1016\/s1043-6618(02)00321-3"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000146121.72699.86"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000448"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1973.57"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.4.F642"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1161\/HYP.0000000000000066"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1001\/jama.2010.650"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2009.09.014"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199311113292004"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199604113341502"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1001\/jama.2013.284427"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00653.2011"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00325.2015"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00356.x"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1093\/ajh\/1.2.190"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1172\/JCI112528"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.2009.05253.x"},{"key":"B52","first-page":"S11","volume":"12","author":"Mackenzie HS","year":"1994","journal-title":"J Hypertens Suppl"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1016\/j.lfs.2021.119362"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00419.2019"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1172\/JCI112013"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2019070718"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00614.x"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014050518"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1161\/01.hyp.20.5.659"},{"key":"B60","first-page":"807","volume":"88","author":"Ylitalo P","year":"1976","journal-title":"J Lab Clin Med"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.258.5.F1409"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1016\/j.nut.2012.02.008"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1797.2006.00533.x"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1007\/s11418-011-0625-8"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.252.6.F1003"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.265.3.F391"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1038\/labinvest.3700328"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199212313272704"},{"key":"B69","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199904293401704"},{"key":"B70","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-198906000-00002"},{"key":"B71","doi-asserted-by":"publisher","DOI":"10.1159\/000336095"},{"key":"B72","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(87)91292-3"},{"key":"B73","doi-asserted-by":"publisher","DOI":"10.3109\/08037059709062092"},{"key":"B74","doi-asserted-by":"publisher","DOI":"10.1016\/0002-9149(82)90243-0"},{"key":"B75","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM197801262980403"},{"key":"B76","doi-asserted-by":"publisher","DOI":"10.1186\/s13550-016-0209-4"},{"key":"B77","doi-asserted-by":"publisher","DOI":"10.1093\/ajh\/1.3.298"},{"key":"B78","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90430.2008"},{"key":"B79","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005030297"},{"key":"B80","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00367.2018"},{"key":"B81","doi-asserted-by":"publisher","DOI":"10.1159\/000334952"},{"key":"B82","doi-asserted-by":"publisher","DOI":"10.1186\/s40360-019-0340-8"},{"key":"B83","doi-asserted-by":"publisher","DOI":"10.1016\/s1357-2725(02)00271-6"},{"key":"B84","doi-asserted-by":"publisher","DOI":"10.1161\/01.hyp.25.5.913"},{"key":"B85","doi-asserted-by":"publisher","DOI":"10.1097\/01.asn.0000095248.91994.d3"},{"key":"B86","doi-asserted-by":"publisher","DOI":"10.1097\/01.asn.0000045049.72965.b7"},{"key":"B87","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa011161"},{"key":"B88","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006121372"},{"key":"B89","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa053107"},{"key":"B90","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000145180.38707.84"},{"key":"B91","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.109.133777"},{"key":"B92","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.117.08314"},{"key":"B93","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0b013e32835b36c1"},{"key":"B94","doi-asserted-by":"publisher","DOI":"10.1007\/BF00276965"},{"key":"B95","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.463"},{"key":"B96","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00676.x"},{"key":"B97","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.02231205"},{"key":"B98","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1990.163"},{"key":"B99","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00070.2011"},{"key":"B100","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.06745.x"},{"key":"B101","doi-asserted-by":"publisher","DOI":"10.4103\/0971-4065.147376"},{"key":"B102","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.5.F794"},{"key":"B103","doi-asserted-by":"publisher","DOI":"10.1016\/j.cardiores.2006.09.019"},{"key":"B104","doi-asserted-by":"publisher","DOI":"10.2174\/187152507780363214"},{"key":"B105","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00673.x"},{"key":"B106","doi-asserted-by":"publisher","DOI":"10.1016\/s0008-6363(00)00267-4"},{"key":"B107","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00281.x"},{"key":"B108","doi-asserted-by":"publisher","DOI":"10.1016\/0140-6736(92)90865-z"},{"key":"B109","doi-asserted-by":"publisher","DOI":"10.3390\/ijms20153668"},{"key":"B110","doi-asserted-by":"publisher","DOI":"10.1016\/s0140-6736(01)07217-8"},{"key":"B111","doi-asserted-by":"publisher","DOI":"10.1097\/01.asn.0000086476.48686.7d"},{"key":"B112","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006070696"},{"key":"B113","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.317"},{"key":"B114","doi-asserted-by":"publisher","DOI":"10.1016\/j.lfs.2009.03.018"},{"key":"B115","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00260.x"},{"key":"B116","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00260.2006"},{"key":"B117","doi-asserted-by":"publisher","DOI":"10.1016\/s0168-8227(01)00260-1"},{"key":"B118","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfm797"},{"key":"B119","doi-asserted-by":"publisher","DOI":"10.3109\/0886022X.2014.900601"},{"key":"B120","doi-asserted-by":"publisher","DOI":"10.3109\/0886022X.2013.773834"},{"key":"B121","doi-asserted-by":"publisher","DOI":"10.1016\/s0272-6386(12)80546-4"},{"key":"B122","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.214"},{"key":"B123","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2002.kid555.x"},{"key":"B124","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00582.x"},{"key":"B125","doi-asserted-by":"publisher","DOI":"10.4103\/0971-4065.103907"},{"key":"B126","first-page":"S42","volume":"43","author":"Wolf SC","year":"1995","journal-title":"Clin Nephrol"},{"key":"B127","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1993.264.6.R1254"},{"key":"B128","first-page":"273","volume":"122","author":"Kimura K","year":"1993","journal-title":"J Lab Clin Med"},{"key":"B129","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000163"},{"key":"B130","first-page":"S74","volume":"65","author":"Fine LG","year":"1998","journal-title":"Kidney Int Suppl"},{"key":"B131","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0024695"},{"key":"B132","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.V1271448"},{"key":"B133","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.V133806"},{"key":"B134","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1992.42"},{"key":"B135","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfq200"},{"key":"B136","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(68)90589-8"},{"key":"B137","doi-asserted-by":"publisher","DOI":"10.1053\/hupa.2000.20373"},{"key":"B138","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-013-2430-y"},{"key":"B139","doi-asserted-by":"publisher","DOI":"10.34067\/kid.0001212020"},{"key":"B140","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118143"},{"key":"B141","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00395.x"},{"key":"B142","doi-asserted-by":"publisher","DOI":"10.1016\/j.ajpath.2014.06.014"},{"key":"B143","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00610.x"},{"key":"B144","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00422.x"},{"key":"B145","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)61731-2"},{"key":"B146","doi-asserted-by":"publisher","DOI":"10.1159\/000054735"},{"key":"B147","doi-asserted-by":"publisher","DOI":"10.1136\/jcp.52.10.735"},{"key":"B148","doi-asserted-by":"publisher","DOI":"10.1159\/000088405"},{"key":"B149","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00533.2008"},{"key":"B150","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfn399"},{"key":"B151","first-page":"14","volume":"81","author":"Shvetsov M","year":"2009","journal-title":"Ter Arkh"},{"key":"B152","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1096-9896(199601)178:1<89::AID-PATH457>3.0.CO;2-4"},{"key":"B153","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2017.181"},{"key":"B154","doi-asserted-by":"publisher","DOI":"10.1097\/MD.0000000000004203"},{"key":"B155","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00292.2015"},{"key":"B156","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/13.6.1430"},{"key":"B157","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfg317"},{"key":"B158","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00156.2020"},{"key":"B159","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.V112319"},{"key":"B160","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007040422"},{"key":"B161","doi-asserted-by":"publisher","DOI":"10.1159\/000368915"},{"key":"B162","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2015080886"},{"key":"B163","doi-asserted-by":"publisher","DOI":"10.1016\/0272-6386(95)90119-1"},{"key":"B164","first-page":"427","volume":"3","author":"Staessen J","year":"1989","journal-title":"J Hum Hypertens"},{"key":"B165","doi-asserted-by":"publisher","DOI":"10.1042\/CS20160047"},{"key":"B166","doi-asserted-by":"publisher","DOI":"10.1097\/01.asn.0000060573.77611.73"},{"key":"B167","doi-asserted-by":"publisher","DOI":"10.1002\/bdd.1909"},{"key":"B168","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/18.1.54"},{"key":"B169","doi-asserted-by":"publisher","DOI":"10.1016\/0531-5565(94)90017-5"},{"key":"B170","doi-asserted-by":"publisher","DOI":"10.1161\/01.hyp.35.1.484"},{"key":"B171","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00354.2011"},{"key":"B172","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-85-4-447"},{"key":"B173","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2002.kid590.x"},{"key":"B174","doi-asserted-by":"publisher","DOI":"10.6118\/jmm.2018.24.2.75"},{"key":"B175","doi-asserted-by":"publisher","DOI":"10.1046\/j.1440-1681.1999.02996.x"},{"key":"B176","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00424.2006"},{"key":"B177","doi-asserted-by":"publisher","DOI":"10.1016\/s0020-7292(97)90193-4"},{"key":"B178","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00793.x"},{"key":"B179","doi-asserted-by":"publisher","DOI":"10.1038\/hr.2011.155"},{"key":"B180","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-0528.2000.tb10406.x"},{"key":"B181","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.107.105767"},{"key":"B182","doi-asserted-by":"publisher","DOI":"10.1093\/oxfordjournals.ndt.a027910"},{"key":"B183","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCOUTCOMES.110.868307"},{"key":"B184","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00206.2017"},{"key":"B185","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCOUTCOMES.115.001756"},{"key":"B186","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00575.2019"},{"key":"B187","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.264"},{"key":"B188","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.V491690"},{"key":"B189","doi-asserted-by":"publisher","DOI":"10.1016\/j.etp.2005.09.005"},{"key":"B190","first-page":"945","volume":"59","author":"Bleiler RE","year":"1962","journal-title":"J Lab Clin Med"},{"key":"B191","doi-asserted-by":"publisher","DOI":"10.1016\/s0272-6386(98)70074-5"},{"key":"B192","doi-asserted-by":"publisher","DOI":"10.1078\/0940-2993-00271"},{"key":"B193","doi-asserted-by":"publisher","DOI":"10.1159\/000156715"},{"key":"B194","doi-asserted-by":"publisher","DOI":"10.1007\/BF01321533"},{"key":"B195","first-page":"578","volume":"50","author":"Li C","year":"2020","journal-title":"Ann Clin Lab Sci"},{"key":"B196","doi-asserted-by":"publisher","DOI":"10.2337\/diacare.26.1.156"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00398.2021","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,5,4]],"date-time":"2022-05-04T17:28:50Z","timestamp":1651685330000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00398.2021"}},"issued":{"date-parts":[[2022,6,1]]},"references-count":196,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2022,6,1]]}},"alternative-id":["10.1152\/ajprenal.00398.2021"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00398.2021","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2022,6,1]]},"assertion":[{"value":"2021-10-29","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2022-03-29","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2022-03-29","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2022-05-04","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,4,2]],"date-time":"2026-04-02T16:30:21Z","timestamp":1775147421493,"version":"3.50.1"},"reference-count":52,"publisher":"American Physiological Society","issue":"5","funder":[{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health","doi-asserted-by":"publisher","award":["R01 DK117495"],"award-info":[{"award-number":["R01 DK117495"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health","doi-asserted-by":"publisher","award":["R01 DK 061578"],"award-info":[{"award-number":["R01 DK 061578"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2023,11,1]]},"abstract":"<jats:p> Endotoxin such as lipopolysaccharide (LPS) induces acute kidney injury (AKI), which is a risk factor for and often leads to chronic kidney diseases. The present study revealed that bone marrow-derived macrophage activation of the angiotensin II type 2 receptor (AT<jats:sub>2<\/jats:sub>R) contributes to the anti-inflammation and partial renoprotection against early stages of LPS-induced AKI. Since AT<jats:sub>2<\/jats:sub>R is an emerging anti-inflammatory and organ-protective target, this study advances our understanding of AT<jats:sub>2<\/jats:sub>R\u2019s anti-inflammatory mechanisms associated with renoprotection. <\/jats:p>","DOI":"10.1152\/ajprenal.00177.2022","type":"journal-article","created":{"date-parts":[[2023,8,24]],"date-time":"2023-08-24T08:00:29Z","timestamp":1692864029000},"page":"F552-F563","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":12,"title":["Macrophage angiotensin AT<sub>2<\/sub> receptor activation is protective against early phases of LPS-induced acute kidney injury"],"prefix":"10.1152","volume":"325","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7839-8827","authenticated-orcid":false,"given":"Naureen","family":"Fatima","sequence":"first","affiliation":[{"name":"Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, Texas, United States"}]},{"given":"Riyasat","family":"Ali","sequence":"additional","affiliation":[{"name":"Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, Texas, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5523-407X","authenticated-orcid":false,"given":"Tahmid","family":"Faisal","sequence":"additional","affiliation":[{"name":"Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, Texas, United States"}]},{"given":"Kalyani","family":"Kulkarni","sequence":"additional","affiliation":[{"name":"Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, Texas, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1674-711X","authenticated-orcid":false,"given":"Sanket","family":"Patel","sequence":"additional","affiliation":[{"name":"Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, Texas, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6353-2317","authenticated-orcid":false,"given":"Tahir","family":"Hussain","sequence":"additional","affiliation":[{"name":"Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, Texas, United States"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-021-94946-3"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/s41581-018-0052-0"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/j.biopha.2019.109070"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1155\/2018\/6717212"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1038\/srep11822"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1002\/mnfr.201400819"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/j.celrep.2020.108245"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.7554\/eLife.62270"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1038\/nri3523"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.3389\/fphar.2021.600163"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1042\/BSR20190429"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.3892\/mmr.2021.12094"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-017-3883-1"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00507.2020"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.111.00422"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1038\/hr.2014.132"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejphar.2019.172855"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.3317\/jraas.2007.007"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.2000561"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-199917040-00012"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1007\/s10753-015-0146-9"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.0903681"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1111\/jcmm.12574"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.3389\/fimmu.2022.921488"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejphar.2017.02.016"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1038\/hr.2012.13"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.3791\/50323"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00717.x"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/j.xpro.2021.101004"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2016.06.058"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002275"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1172\/JCI39421"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2006-03-013557"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1189\/jlb.0906545"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1159\/000477181"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1016\/j.imbio.2017.10.005"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1002\/jlb.45.2.97"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1038\/nature01326"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.3390\/ijms21020379"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1038\/srep18687"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1007\/s12017-021-08687-7"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.25122\/jml-2022-0299"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0095762"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1097\/MOP.0b013e328343f4dd"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1053\/j.ackd.2008.04.003"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.04851107"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.5402\/2013\/394582"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00291.2005"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1155\/2019\/6265307"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1159\/000493816"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.3892\/mmr.2019.10416"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.3892\/mmr.2019.10178"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00177.2022","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,9,27]],"date-time":"2023-09-27T13:09:02Z","timestamp":1695820142000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00177.2022"}},"issued":{"date-parts":[[2023,11,1]]},"references-count":52,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2023,11,1]]}},"alternative-id":["10.1152\/ajprenal.00177.2022"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00177.2022","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2023,11,1]]},"assertion":[{"value":"2022-06-27","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2023-07-27","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2023-08-17","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2023-09-27","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,4,2]],"date-time":"2026-04-02T21:34:36Z","timestamp":1775165676949,"version":"3.50.1"},"reference-count":27,"publisher":"American Physiological Society","issue":"12","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2012,6,15]]},"abstract":"<jats:p> The complement cascade is an important part of the innate immune system, but pathological activation of this system causes tissue injury in several autoimmune and inflammatory diseases, including immune complex glomerulonephritis. We examined whether mice with targeted deletion of the gene for factor B ( fB<jats:sup>\u2212\/\u2212<\/jats:sup> mice) and selective deficiency in the alternative pathway of complement are protected from injury in the nephrotoxic serum (NTS) nephritis model of antibody-mediated glomerulonephritis. When the acute affects of the anti-glomerular basement membrane antibody were assessed, fB<jats:sup>\u2212\/\u2212<\/jats:sup> mice developed a degree of injury similar to wild-type controls. If the mice were presensitized with sheep IgG or if the mice were followed for 5 mo postinjection, however, the fB<jats:sup>\u2212\/\u2212<\/jats:sup> mice developed milder injury than wild-type mice. The immune response of fB<jats:sup>\u2212\/\u2212<\/jats:sup> mice exposed to sheep IgG was similar to that of wild-type mice, but the fB<jats:sup>\u2212\/\u2212<\/jats:sup> mice had less glomerular C3 deposition and lower levels of albuminuria. These results demonstrate that fB<jats:sup>\u2212\/\u2212<\/jats:sup> mice are not significantly protected from acute heterologous injury in NTS nephritis but are protected from autologous injury in response to a planted glomerular antigen. Thus, although the glomerulus is resistant to antibody-initiated, alternative pathway-mediated injury, inhibition of this complement pathway may be beneficial in chronic immune complex-mediated diseases. <\/jats:p>","DOI":"10.1152\/ajprenal.00422.2011","type":"journal-article","created":{"date-parts":[[2012,4,5]],"date-time":"2012-04-05T00:32:39Z","timestamp":1333585959000},"page":"F1529-F1536","source":"Crossref","is-referenced-by-count":13,"title":["Complement alternative pathway activation in the autologous phase of nephrotoxic serum nephritis"],"prefix":"10.1152","volume":"302","author":[{"given":"Joshua M.","family":"Thurman","sequence":"first","affiliation":[{"name":"Department of Medicine, University of Colorado School of Medicine, Aurora, Colorado;"}]},{"given":"Svetlana N.","family":"Tchepeleva","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Colorado School of Medicine, Aurora, Colorado;"}]},{"given":"Mark","family":"Haas","sequence":"additional","affiliation":[{"name":"Department of Pathology and Laboratory Medicine, Cedars Sinai Medical Center, Los Angeles, California; and"}]},{"given":"Sarah","family":"Panzer","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Colorado School of Medicine, Aurora, Colorado;"}]},{"given":"Susan A.","family":"Boackle","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Colorado School of Medicine, Aurora, Colorado;"}]},{"given":"Magdalena J.","family":"Glogowska","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Colorado School of Medicine, Aurora, Colorado;"}]},{"given":"Richard J.","family":"Quigg","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Chicago, Chicago, Illinois"}]},{"given":"V. Michael","family":"Holers","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Colorado School of Medicine, Aurora, Colorado;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.179.6.4101"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000051597.27127.A1"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/S0952-7915(97)80160-4"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.168.3.1036"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00371.x"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1084\/jem.192.9.1353"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2249.2004.02627.x"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/13.11.2799"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00403.2006"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1038\/labinvest.3780451"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-6143.2008.02451.x"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.01090209"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.94.16.8720"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMc0808527"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1038\/ng912"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1084\/jem.188.7.1321"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.166.11.6820"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.166.10.6444"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1002\/1521-4141(200104)31:4<1255::AID-IMMU1255>3.0.CO;2-W"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.167.5.2791"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/j.molimm.2004.07.043"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1172\/JCI24521"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005070698"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM200104053441406"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.164.2.786"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1126\/science.287.5452.498"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMc1001060"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00422.2011","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:22:51Z","timestamp":1567974171000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00422.2011"}},"issued":{"date-parts":[[2012,6,15]]},"references-count":27,"journal-issue":{"issue":"12","published-print":{"date-parts":[[2012,6,15]]}},"alternative-id":["10.1152\/ajprenal.00422.2011"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00422.2011","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2012,6,15]]}},{"indexed":{"date-parts":[[2026,4,4]],"date-time":"2026-04-04T17:01:00Z","timestamp":1775322060389,"version":"3.50.1"},"reference-count":36,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2018,4,1]]},"abstract":"<jats:p> The fluid volume balance between intracellular water (ICW) and extracellular water (ECW) gradually changes with age and various medical conditions. Comprehension of these physiological changes would aid in clinical decision-making related to body fluid assessments. A total of 1,992 individuals (753 men and 1,239 women) aged \u226515 yr included in this study had their body composition measurements performed at training gyms in 2014. We developed a regression formula to assess the association of age with the ratio of ECW to ICW in these subjects. The mean ages of male and female subjects were 51.2\u2009\u00b1\u200915.2 and 57.4\u2009\u00b1\u200915.2 yr, and their mean body mass indexes were 23.4\u2009\u00b1\u20093.3 and 21.1\u2009\u00b1\u20092.8 kg\/m<jats:sup>2<\/jats:sup>, respectively. The total fluid volumes of male and female subjects were 39.6\u2009\u00b1\u20094.9 and 27.7\u2009\u00b1\u20093.0 liters, whereas the percent body fat mass per kilogram of body weight were 19 and 26%, respectively. The ECW-to-ICW ratio increased with age because of the steeper decrease in the ICW content than in the ECW content, especially after the age of 70 yr. The regression formulas used for calculating the age-adjusted ECW\/ICW ratio were as follows: 0.5857 + 7.4334\u2009\u00d7\u200910<jats:sup>\u22126<\/jats:sup>\u2009\u00d7\u2009(age)<jats:sup>2<\/jats:sup> in men and 0.6062 + 5.5775\u2009\u00d7\u200910<jats:sup>\u22126<\/jats:sup>\u2009\u00d7\u2009(age)<jats:sup>2<\/jats:sup> in women. In conclusion, the fluid imbalance between ICW and ECW contents is driven by decreased cell volume associated with aging and muscle attenuation. Therefore, our proposed formula may serve as a useful assessment tool for the calculation of body fluid composition. <\/jats:p>","DOI":"10.1152\/ajprenal.00477.2017","type":"journal-article","created":{"date-parts":[[2017,12,6]],"date-time":"2017-12-06T07:15:25Z","timestamp":1512544525000},"page":"F614-F622","source":"Crossref","is-referenced-by-count":69,"title":["Changes in the fluid volume balance between intra- and extracellular water in a sample of Japanese adults aged 15\u201388 yr old: a cross-sectional study"],"prefix":"10.1152","volume":"314","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1670-9498","authenticated-orcid":false,"given":"Yasushi","family":"Ohashi","sequence":"first","affiliation":[{"name":"Department of Nephrology, Sakura Medical Center, Toho University, Chiba, Japan"}]},{"given":"Nobuhiko","family":"Joki","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Toho University Ohashi Medical Center, Tokyo, Japan"}]},{"given":"Keisuke","family":"Yamazaki","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Sakura Medical Center, Toho University, Chiba, Japan"}]},{"given":"Takeshi","family":"Kawamura","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Sakura Medical Center, Toho University, Chiba, Japan"}]},{"given":"Reibin","family":"Tai","sequence":"additional","affiliation":[{"name":"School of Medicine, Department of Nephrology, School of Medicine, Faculty of Medicine, Toho University, Tokyo, Japan"}]},{"given":"Hideyo","family":"Oguchi","sequence":"additional","affiliation":[{"name":"School of Medicine, Department of Nephrology, School of Medicine, Faculty of Medicine, Toho University, Tokyo, Japan"}]},{"given":"Rena","family":"Yuasa","sequence":"additional","affiliation":[{"name":"School of Medicine, Department of Nephrology, School of Medicine, Faculty of Medicine, Toho University, Tokyo, Japan"}]},{"given":"Ken","family":"Sakai","sequence":"additional","affiliation":[{"name":"School of Medicine, Department of Nephrology, School of Medicine, Faculty of Medicine, Toho University, Tokyo, Japan"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.09001209"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/j.abb.2007.01.020"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1088\/0967-3334\/15\/4\/011"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00377.x"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1159\/000101699"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1520-6300(1999)11:2<167::AID-AJHB4>3.0.CO;2-G"},{"key":"B7","first-page":"305","volume":"105","author":"Cohn SH","year":"1985","journal-title":"J Lab Clin Med"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2014.207"},{"key":"B9","first-page":"303","volume":"5","author":"Du Bois D","year":"1989","journal-title":"Nutrition"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/0002-9343(59)90346-8"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.5301\/ijao.5000080"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1093\/ajcn\/35.5.1169"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1249\/00003677-199500230-00016"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ejcn.1601198"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.7762\/cnr.2015.4.1.32"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1980.238.1.R82"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1979.236.3.R215"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1177\/039139880202500803"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/jappl.1999.87.1.294"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1097\/00000658-199207000-00010"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2013.273"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/sj.cdd.4400296"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1016\/j.jacc.2004.06.068"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-149-9-200811040-00003"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1159\/000368376"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1159\/000447024"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1007\/s12603-015-0658-x"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1984.246.2.F234"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1093\/ajcn\/50.5.1176"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1093\/gerona\/59.8.B796"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1007\/s00421-017-3686-x"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1007\/s11255-016-1371-3"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1093\/ajcn\/69.5.833"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1093\/ajcn\/56.1.19"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1111\/ggi.12209"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.00772.2013"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00477.2017","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T12:58:39Z","timestamp":1567947519000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00477.2017"}},"issued":{"date-parts":[[2018,4,1]]},"references-count":36,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2018,4,1]]}},"alternative-id":["10.1152\/ajprenal.00477.2017"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00477.2017","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2018,4,1]]}},{"indexed":{"date-parts":[[2026,4,2]],"date-time":"2026-04-02T05:28:48Z","timestamp":1775107728426,"version":"3.50.1"},"reference-count":44,"publisher":"American Physiological Society","issue":"3","funder":[{"DOI":"10.13039\/501100001807","name":"S\u00e3o Paulo Research Foundation","doi-asserted-by":"crossref","award":["2017\/15175-1"],"award-info":[{"award-number":["2017\/15175-1"]}],"id":[{"id":"10.13039\/501100001807","id-type":"DOI","asserted-by":"crossref"}]},{"name":"Coordination of Improvement of Higher Education Personnel","award":["1680776"],"award-info":[{"award-number":["1680776"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2018,9,1]]},"abstract":"<jats:p>Interstitial Cystitis\/Bladder Pain Syndrome (IC\/BPS) is a chronic inflammatory disease without consistently effective treatment. We investigate the role of toll-like receptor 4 (TLR4) on voiding dysfunction and inflammation in the cyclophosphamide (CYP)-induced mouse cystitis. Male C57BL\/6 [wild-type, (WT)] and\/or TLR4 knockout (TLR4<jats:sup>\u2212\/\u2212<\/jats:sup>) mice were treated with an injection of CYP (300 mg\/kg, 24 h) or saline (10 ml\/kg). The pharmacological blockade of the TLR4 by resatorvid (10 mg\/kg) was also performed 1 h prior CYP-injection in WT mice. Urodynamic profiles were assessed by voiding stain on filter paper and filling cystometry. Contractile responses to carbachol were measured in isolated bladders. In CYP-exposed WT mice, mRNA for TLR4, myeloid differentiation primary response 88, and TIR-domain-containing adapter-inducing interferon-\u03b2 increased by 45%, 72%, and 38%, respectively ( P &lt; 0.05). In free-moving mice, CYP-exposed mice exhibited a higher number of urinary spots and smaller urinary volumes. Increases of micturition frequency and nonvoiding contractions, concomitant with decreases of intercontraction intervals and capacity, were observed in the filling cystometry of WT mice ( P &lt; 0.05). Carbachol-induced bladder contractions were significantly reduced in the CYP group, which was paralleled by reduced mRNA for M2 and M3 muscarinic receptors. These functional and molecular alterations induced by CYP were prevented in TLR4<jats:sup>\u2212\/\u2212<\/jats:sup>and resatorvid-treated mice. Additionally, the increased levels of inflammatory markers induced by CYP exposure, myeloperoxidase activity, interleukin-6, and tumor necrosis factor-alpha were significantly reduced by resatorvid treatment. Our findings reveal a central role for the TLR4 signaling pathway in initiating CYP-induced bladder dysfunction and inflammation and thus emphasize that TLR4 receptor blockade may have clinical value for IC\/BPS treatment.<\/jats:p>","DOI":"10.1152\/ajprenal.00100.2018","type":"journal-article","created":{"date-parts":[[2018,5,2]],"date-time":"2018-05-02T13:01:37Z","timestamp":1525266097000},"page":"F460-F468","source":"Crossref","is-referenced-by-count":22,"title":["Deletion or pharmacological blockade of TLR4 confers protection against cyclophosphamide-induced mouse cystitis"],"prefix":"10.1152","volume":"315","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2226-2530","authenticated-orcid":false,"given":"Mariana G.","family":"de Oliveira","sequence":"first","affiliation":[{"name":"Department of Pharmacology, Faculty of Medical Sciences, University of Campinas, Campinas, Brazil"}]},{"given":"Fabiola Z.","family":"M\u00f3nica","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Faculty of Medical Sciences, University of Campinas, Campinas, Brazil"}]},{"given":"Fabiano B.","family":"Calmasini","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Faculty of Medical Sciences, University of Campinas, Campinas, Brazil"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9482-6799","authenticated-orcid":false,"given":"Eduardo C.","family":"Alexandre","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Faculty of Medical Sciences, University of Campinas, Campinas, Brazil"}]},{"given":"Edith B. G.","family":"Tavares","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Faculty of Medical Sciences, University of Campinas, Campinas, Brazil"}]},{"given":"Antonio G.","family":"Soares","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Institute of Biomedical Sciences, University of S\u00e3o Paulo, S\u00e3o Paulo, Brazil"}]},{"given":"Soraia K. P.","family":"Costa","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Institute of Biomedical Sciences, University of S\u00e3o Paulo, S\u00e3o Paulo, Brazil"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2201-8247","authenticated-orcid":false,"given":"Edson","family":"Antunes","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Faculty of Medical Sciences, University of Campinas, Campinas, Brazil"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1464-410X.2007.07205.x"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/nri1391"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00013.2017"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/bjp.2008.6"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1046\/j.1464-410X.2000.00096.x"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejphar.2013.03.008"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1002\/nau.21180"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1002\/nau.23171"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00047.2006"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00041.2016"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1002\/nau.23072"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1111\/bph.12467"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1005333107"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1097\/ALN.0b013e31820b8b44"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1016\/j.autneu.2005.07.005"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1111\/1440-1681.12583"},{"key":"B17","first-page":"1103","volume":"28","author":"Gomes TN","year":"1995","journal-title":"Braz J Med Biol Res"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/j.juro.2015.01.086"},{"key":"B19","doi-asserted-by":"crossref","first-page":"3749","DOI":"10.4049\/jimmunol.162.7.3749","volume":"162","author":"Hoshino K","year":"1999","journal-title":"J Immunol"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1038\/jcbfm.2014.240"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00297.2013"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/j.neulet.2008.02.065"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1038\/ni.1863"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.3389\/fimmu.2014.00461"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1111\/iju.12090"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/physiolgenomics.00117.2001"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1124\/mol.110.068064"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1016\/j.juro.2013.10.097"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1517\/14728214.2015.1105216"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1126\/science.282.5396.2085"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0067976"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.71.3.1470-1480.2003"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbi.2015.03.003"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1016\/j.pain.2014.05.029"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1016\/j.urology.2015.12.040"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejphar.2007.06.027"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1016\/j.chom.2007.05.007"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1007\/s11255-015-0926-z"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1093\/intimm\/dxh186"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1038\/ncpuro0874"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1161\/STROKEAHA.113.001038"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00075.2017"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00469.2013"},{"key":"B44","first-page":"11202","volume":"8","author":"Zhao Y","year":"2015","journal-title":"Int J Clin Exp Med"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00100.2018","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,9,2]],"date-time":"2023-09-02T11:08:29Z","timestamp":1693652909000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00100.2018"}},"issued":{"date-parts":[[2018,9,1]]},"references-count":44,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2018,9,1]]}},"alternative-id":["10.1152\/ajprenal.00100.2018"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00100.2018","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2018,9,1]]}},{"indexed":{"date-parts":[[2026,4,2]],"date-time":"2026-04-02T09:46:31Z","timestamp":1775123191081,"version":"3.50.1"},"reference-count":108,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2016,12,1]]},"abstract":"<jats:p>Pregnancy is characterized by avid renal sodium retention and plasma volume expansion in the presence of decreased blood pressure. Decreased maternal blood pressure is a consequence of reduced systemic vascular tone, which results from an increased production of vasodilators [nitric oxide (NO), prostaglandins, and relaxin] and decreased vascular responsiveness to the potent vasoconstrictor (angiotensin II). The kidneys participate in this vasodilatory response, resulting in marked increases in renal plasma flow and glomerular filtration rate (GFR) during pregnancy. In women, sodium retention drives plasma volume expansion (\u223c40%) and is necessary for perfusion of the growing uterus and fetus. For there to be avid sodium retention in the presence of the potent natriuretic influences of increased NO and elevated GFR, there must be modifications of the tubules to prevent salt wasting. The purpose of this review is to summarize these adaptations.<\/jats:p>","DOI":"10.1152\/ajprenal.00129.2016","type":"journal-article","created":{"date-parts":[[2016,10,6]],"date-time":"2016-10-06T02:38:43Z","timestamp":1475721523000},"page":"F1125-F1134","source":"Crossref","is-referenced-by-count":70,"title":["The enigma of continual plasma volume expansion in pregnancy: critical role of the renin-angiotensin-aldosterone system"],"prefix":"10.1152","volume":"311","author":[{"given":"Crystal A.","family":"West","sequence":"first","affiliation":[{"name":"Department of Medicine, Georgetown University, Washington, District of Columbia;"}]},{"given":"Jennifer M.","family":"Sasser","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi; and"}]},{"given":"Chris","family":"Baylis","sequence":"additional","affiliation":[{"name":"Department of Physiology and Functional Genomics, University of Florida, Gainesville, Florida"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1080\/10641950701825887"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/0006-291X(79)90945-8"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1980.126"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/0168-8278(92)90033-L"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/0140-6736(93)91224-A"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.3109\/10641959309031053"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.1.4.410"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(12)70344-X"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/S0950-3552(05)80320-7"},{"key":"B10","first-page":"263","volume-title":"Clinical Physiology in Obstetrics","author":"Baylis C","year":"1998"},{"key":"B11","first-page":"117","volume":"11","author":"Baylis C","year":"1992","journal-title":"Clin Exp Hypertens"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1995.75.4.725"},{"key":"B13","first-page":"117","volume-title":"Handbook of Hypertension","volume":"10","author":"Broughton-Pipkin F","year":"1988"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.261.1.F51"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1016\/S0950-3552(05)80322-0"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.4.F592"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1113\/expphysiol.1998.sp004133"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00217.x"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1172\/JCI112723"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1097\/MAJ.0b013e318063c6e4"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118059"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.3389\/fphys.2016.00012"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1172\/JCI106926"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2011.15"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00478.2010"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(87)80126-9"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1677\/joe.0.1130435"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1146\/annurev-physiol-012110-142247"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00216.2013"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-0528.1973.tb02981.x"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.115.06071"},{"key":"B32","first-page":"S35","volume":"55","author":"Hall JE","year":"1996","journal-title":"Kidney Int Suppl"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1210\/jcem-54-5-1010"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-0528.1963.tb04922.x"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.1.F239"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.22.2.113"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.2.F353"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1016\/j.amjhyper.2005.04.022"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1016\/j.yjmcc.2004.10.013"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00155.2007"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.2003.tb07254.x"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00309.2006"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1172\/JCI40145"},{"key":"B44","first-page":"520","volume":"17","author":"Levy M","year":"1997","journal-title":"Semin Nephrol"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.257.2.F159"},{"key":"B46","first-page":"633","volume":"78","author":"Lindheimer MD","year":"1971","journal-title":"J Lab Clin Med"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.09712.x"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.275.5.F812"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1016\/S0895-7061(01)02073-8"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.264.1.F79"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199808203390807"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1994.267.6.R1611"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9378(98)70384-9"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1172\/JCI7840"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00016.2002"},{"key":"B56","doi-asserted-by":"crossref","first-page":"1813","DOI":"10.1681\/ASN.V8121813","volume":"8","author":"May A","year":"1997","journal-title":"J Am Soc Nephrol"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0014227"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1016\/S0016-5085(88)80090-8"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.1996.270.4.E601"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1988.254.5.R793"},{"key":"B61","doi-asserted-by":"crossref","first-page":"2110","DOI":"10.1681\/ASN.V7102110","volume":"7","author":"Ni X","year":"1996","journal-title":"J Am Soc Nephrol"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.0590041264.x"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000125613.96927.38"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00015.2002"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1016\/j.jsgi.2003.12.005"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.30.3.580"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1530\/acta.0.1200519"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.268.3.F416"},{"key":"B69","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1984.247.1.H100"},{"key":"B70","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009121257"},{"key":"B71","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00564.2014"},{"key":"B72","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-198612000-00013"},{"key":"B73","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1989.256.4.H1060"},{"key":"B74","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000200042.64517.19"},{"key":"B75","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-013-1252-x"},{"key":"B76","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00067.2008"},{"key":"B77","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00198.2009"},{"key":"B78","doi-asserted-by":"publisher","DOI":"10.1517\/14728214.2015.1062875"},{"key":"B79","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00117.2010"},{"key":"B80","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM198810203191606"},{"key":"B81","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM198810273191705"},{"key":"B82","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(87)80123-3"},{"key":"B83","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2826.2010.01948.x"},{"key":"B84","author":"Sinning A","journal-title":"J Am Soc Nephrol"},{"key":"B85","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00300.2010"},{"key":"B86","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1202671109"},{"key":"B87","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.111.186270"},{"key":"B88","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-0528.1991.tb13369.x"},{"key":"B89","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.491"},{"key":"B90","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.259.3.F519"},{"key":"B91","doi-asserted-by":"publisher","DOI":"10.1016\/0028-2243(88)90123-2"},{"key":"B92","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-012-1145-4"},{"key":"B93","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115995"},{"key":"B94","doi-asserted-by":"crossref","first-page":"582","DOI":"10.1681\/ASN.V74582","volume":"7","author":"Valentin JP","year":"1996","journal-title":"J Am Soc Nephrol"},{"key":"B95","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005101054"},{"key":"B96","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000088321.67254.B7"},{"key":"B97","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00114.2011"},{"key":"B98","doi-asserted-by":"publisher","DOI":"10.1210\/jcem-44-1-69"},{"key":"B99","doi-asserted-by":"publisher","DOI":"10.1113\/expphysiol.2013.076273"},{"key":"B100","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00147.2015"},{"key":"B101","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00003.2013"},{"key":"B102","doi-asserted-by":"publisher","DOI":"10.1113\/EP085396"},{"key":"B103","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00082.2010"},{"key":"B104","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1997.272.2.H748"},{"key":"B105","doi-asserted-by":"publisher","DOI":"10.1172\/JCI109918"},{"key":"B106","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.010908.163241"},{"key":"B107","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.252.3.F551"},{"key":"B108","doi-asserted-by":"publisher","DOI":"10.1007\/s11906-999-0016-7"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00129.2016","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,7,9]],"date-time":"2022-07-09T20:27:55Z","timestamp":1657398475000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00129.2016"}},"issued":{"date-parts":[[2016,12,1]]},"references-count":108,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2016,12,1]]}},"alternative-id":["10.1152\/ajprenal.00129.2016"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00129.2016","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2016,12,1]]}},{"indexed":{"date-parts":[[2026,3,18]],"date-time":"2026-03-18T04:01:34Z","timestamp":1773806494984,"version":"3.50.1"},"reference-count":40,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2006,2]]},"abstract":"<jats:p>Atrial natriuretic peptide (ANP) acutely promotes water and sodium excretion, whereas subchronic effects involve water retention. Renal hemodynamics, water and sodium excretion, and aquaporin-2 (AQP2) and epithelial Na channel (ENaC) subcellular trafficking were determined in response to continuous ANP infusion in conscious rats, where body sodium and fluid balance was constantly maintained. ANP (0.5 \u03bcg\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7min<jats:sup>\u22121<\/jats:sup>) evoked a transient (peak at 10 min) fivefold diuresis followed by reduced urine production to control levels (30- to 90-min period). The fractional distal water excretion was significantly increased initially and then decreased in response to ANP. There was no change in the subcellular localization of AQP2 and AQP2 phosphorylated in PKA consensus site S256 (p-AQP2) 10 min after ANP infusion. In contrast, after 90 min a marked increase in apical labeling of AQP2 and p-AQP2 was observed in the inner and outer medullary collecting ducts but not in cortical collecting ducts. In support of this, ANP induced plasma membrane targeting of AQP2 in transiently AQP2-transfected cells. ANP infusion evoked an instant increase in renal sodium excretion, which persisted for 90 min. Ten minutes of ANP infusion induced no changes in the subcellular localization of ENaC subunits, whereas a marked increase in apical targeting of \u03b1- and \u03b3-subunits was observed after 90 min. In conclusion, 1) ANP infusion induced a sustained natriuresis and transient diuresis; 2) there were no changes in the subcellular localization of AQP2 and ENaC subunits after 10 min of ANP infusion; and 3) there was a marked increase in apical targeting of AQP2, p-AQP2, and \u03b1- and \u03b3-ENaC after 90 min of ANP infusion. The increased targeting of ENaC and AQP2 likely represents direct or compensatory effects to increase sodium and water reabsorption and to prevent volume depletion in response to prolonged ANP infusion.<\/jats:p>","DOI":"10.1152\/ajprenal.00070.2005","type":"journal-article","created":{"date-parts":[[2005,9,21]],"date-time":"2005-09-21T03:13:46Z","timestamp":1127272426000},"page":"F530-F541","source":"Crossref","is-referenced-by-count":48,"title":["Biphasic effects of ANP infusion in conscious, euvolumic rats: roles of AQP2 and ENaC trafficking"],"prefix":"10.1152","volume":"290","author":[{"given":"Weidong","family":"Wang","sequence":"first","affiliation":[]},{"given":"Chunling","family":"Li","sequence":"additional","affiliation":[]},{"given":"Lene N.","family":"Nejsum","sequence":"additional","affiliation":[]},{"given":"Hongyan","family":"Li","sequence":"additional","affiliation":[]},{"given":"Soo Wan","family":"Kim","sequence":"additional","affiliation":[]},{"given":"Tae-Hwan","family":"Kwon","sequence":"additional","affiliation":[]},{"given":"Thomas E. N.","family":"Jonassen","sequence":"additional","affiliation":[]},{"given":"Mark A.","family":"Knepper","sequence":"additional","affiliation":[]},{"given":"Klaus","family":"Thomsen","sequence":"additional","affiliation":[]},{"given":"J\u00f8rgen","family":"Fr\u00f8ki\u00e6r","sequence":"additional","affiliation":[]},{"given":"S\u00f8ren","family":"Nielsen","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"crossref","unstructured":"Abraham WT, Hensen J, Kim JK, Durr J, Lesnefsky EJ, Groves BM, and Schrier RW.Atrial natriuretic peptide and urinary cyclic guanosine monophosphate in patients with chronic heart failure.J Am Soc Nephrol2: 1697\u20131703, 1992.","DOI":"10.1681\/ASN.V2121697"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1139\/y98-152"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000066129.12106.E2"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1172\/JCI9594"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00337.2004"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1990.70.3.665"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1677\/joe.0.1380413"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1677\/joe.0.1350431"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1984.247.5.F863"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.3181\/00379727-189-42813"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1210\/endo-115-5-2026"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.1.F29"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1016\/0024-3205(81)90370-2"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1126\/science.3006248"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.3181\/00379727-185-3-RC2"},{"key":"R16","doi-asserted-by":"crossref","unstructured":"Granger JP, Opgenorth TJ, Salazar J, Romero JC, and Burnett JC Jr.Long-term hypotensive and renal effects of atrial natriuretic peptide.Hypertension8: II112-II116, 1986.","DOI":"10.1161\/01.HYP.8.6_Pt_2.II112"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.6.F1093"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.83.20.8015"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.16.7212"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.266.3.F506"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1126\/science.2463673"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.4.F675"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1172\/JCI7840"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.4.1013"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00024.2001"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1172\/JCI112840"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1172\/JCI113742"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.256.1.F179"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1172\/JCI112433"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.260.1.F86"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1988.255.3.F421"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.6.F1158"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1172\/JCI112154"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.256.5.F862"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1139\/y91-230"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1016\/0006-291X(86)90424-9"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.261.6.F1080"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1172\/JCI111935"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1210\/jcem-62-5-956"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1983.245.1.F67"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00070.2005","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,7,17]],"date-time":"2021-07-17T22:46:27Z","timestamp":1626561987000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00070.2005"}},"issued":{"date-parts":[[2006,2]]},"references-count":40,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2006,2]]}},"alternative-id":["10.1152\/ajprenal.00070.2005"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00070.2005","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2006,2]]}},{"indexed":{"date-parts":[[2026,3,18]],"date-time":"2026-03-18T02:50:19Z","timestamp":1773802219797,"version":"3.50.1"},"reference-count":45,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2000,8,1]]},"abstract":"<jats:p>The role of AVP-V<jats:sub>2<\/jats:sub>receptor (AVP-V<jats:sub>2<\/jats:sub>R)-dependent regulation of aquaporin-2 (AQP2) expression was evaluated in vasopressin-deficient Brattleboro (BB) rats. AQP2 levels were relatively high in BB rats (52 \u00b1 8% of levels in Wistar rats), and treatment with the AVP-V<jats:sub>2<\/jats:sub>R antagonist SR-121463A (0.8 mg\/day) for 48 h was associated with 1) increased urine output (170 \u00b1 9%), 2), reduced AQP2 protein levels (42 \u00b1 10% in whole kidney and 53 \u00b1 8% in inner medulla), and 3) reduced AQP2 mRNA levels (36 \u00b1 7%). In addition, the levels of AQP2 phosphorylated in the protein kinase A (PKA) consensus site (Ser<jats:sup>256<\/jats:sup>of AQP2) was reduced to 3 \u00b1 1% of control levels. Lithium (Li) treatment of BB rats for 1 mo, known to reduce adenylyl cyclase (AC) activity, downregulated AQP2 protein levels (15 \u00b1 6%) and increased urine output (220%). Downregulation of AQP2 expression in response to SR-121463A or Li treatment indicates that AQP2 expression in BB rats depends in part on activation of AVP-V<jats:sub>2<\/jats:sub>Rs and that the signaling cascade(s) involves AC and hence cAMP. Complete water restriction of BB rats produced only a small increase in AQP2 mRNA (235 \u00b1 33%) and AQP2 protein (156 \u00b1 22%) levels. Immunoelectron microscopy confirmed the increase in AQP2 abundance but revealed no change in AQP2 apical plasma membrane labeling in response to thirsting. In conclusion, the expression and phosphorylation of AQP2 in BB rats are in part dependent on AVP-V<jats:sub>2<\/jats:sub>R signaling, and AVP-V<jats:sub>2<\/jats:sub>-mediated regulation of AQP2 trafficking and expression is effectively decoupled in BB rats, indicating differences in AVP-V<jats:sub>2<\/jats:sub>R-mediated regulation of AQP2 trafficking and expression.<\/jats:p>","DOI":"10.1152\/ajprenal.2000.279.2.f370","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T12:44:35Z","timestamp":1514033075000},"page":"F370-F382","source":"Crossref","is-referenced-by-count":46,"title":["Vasopressin V<sub>2<\/sub>-receptor-dependent regulation of AQP2 expression in Brattleboro rats"],"prefix":"10.1152","volume":"279","author":[{"given":"Dominique","family":"Promeneur","sequence":"first","affiliation":[{"name":"Department of Cell Biology, Institute of Anatomy, University of Aarhus, DK-8000;"}]},{"given":"Tae-Hwan","family":"Kwon","sequence":"additional","affiliation":[{"name":"Department of Cell Biology, Institute of Anatomy, University of Aarhus, DK-8000;"}]},{"given":"J\u00f8rgen","family":"Fr\u00f8ki\u00e6r","sequence":"additional","affiliation":[{"name":"Department of Clinical Physiology, Aarhus University Hospital, and Institute of Experimental Clinical Research, DK-8200 Aarhus N, Denmark; and"}]},{"given":"Mark A.","family":"Knepper","sequence":"additional","affiliation":[{"name":"Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892"}]},{"given":"S\u00f8ren","family":"Nielsen","sequence":"additional","affiliation":[{"name":"Department of Cell Biology, Institute of Anatomy, University of Aarhus, DK-8000;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.1982.tb37432.x"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.1.F70"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.1.F29"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1172\/JCI111901"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1986.251.2.F290"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.91.19.8984"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119352"},{"key":"B9","first-page":"275","volume":"6","author":"Edwards BR","year":"1983","journal-title":"Ren Physiol"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1984.247.3.F453"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00984.x"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.2.F179"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1038\/361549a0"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1979.237.2.F100"},{"key":"B15","doi-asserted-by":"crossref","first-page":"255","DOI":"10.1152\/ajplegacy.1966.211.1.255","volume":"211","author":"Grantham JJ","year":"1966","journal-title":"Am J Physiol"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0701653"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.265.1.F26"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117525"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.261.2.F345"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1996.270.6.C1695"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1172\/JCI114676"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118731"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.1.F62"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.3.F413"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.275.5.F724"},{"key":"B26","first-page":"18A","volume":"10","author":"Kwon T-H","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1007\/BF01950026"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.1987.252.5.E637"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.275.3.F400"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117863"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.3.F331"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1995.269.3.C655"},{"key":"B33","doi-asserted-by":"crossref","first-page":"574","DOI":"10.1152\/ajplegacy.1968.214.3.574","volume":"214","author":"Morgan T","year":"1968","journal-title":"Am J Physiol"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.4.1013"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.90.24.11663"},{"key":"B36","doi-asserted-by":"crossref","first-page":"647","DOI":"10.1681\/ASN.V103647","volume":"10","author":"Nielsen S","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.275.6.F885"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.2.F254"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1007\/BF00233445"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119098"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.2.F414"},{"key":"B42","doi-asserted-by":"crossref","first-page":"23451","DOI":"10.1016\/S0021-9258(17)31537-5","volume":"269","author":"Uchida S","year":"1994","journal-title":"J Biol Chem"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1007\/BF00371002"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1995.268.6.C1546"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.10.5808"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.272.4.F443"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.2000.279.2.F370","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:40:00Z","timestamp":1660189200000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.2000.279.2.F370"}},"issued":{"date-parts":[[2000,8,1]]},"references-count":45,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2000,8,1]]}},"alternative-id":["10.1152\/ajprenal.2000.279.2.F370"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.2000.279.2.f370","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2000,8,1]]}},{"indexed":{"date-parts":[[2026,3,18]],"date-time":"2026-03-18T22:34:36Z","timestamp":1773873276124,"version":"3.50.1"},"reference-count":32,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2000,12,1]]},"abstract":"<jats:p>Podocytes are highly specialized cells that make up a major portion of the glomerular filtration barrier in the kidney. They are also believed to play a pivotal role in the progression of chronic renal disease due to diverse causes that include diabetes (3, 20, 24) and aging (1, 7). Despite the importance of podocytes for kidney function and disease, studies of this cell type have been hindered due to a lack of model systems. Recently, the gene responsible for congenital Finnish nephropathy was identified and named nephrin (13). Nephrin expression is restricted to slit diaphragms of podocytes (11, 30). Infants with congenital Finnish nephropathy develop massive proteinuria and subsequent kidney failure due to podocyte injury. We have identified a 1.25-kb DNA fragment from the human nephrin promoter and 5\u2032-flanking region that is capable of directing podocyte-specific expression in transgenic mice; this represents the first glomerular-specific promoter to be identified. Use of this transgene will facilitate studies of the podocyte in vivo and allow the identification of transacting factors that are required for podocyte-specific expression.<\/jats:p>","DOI":"10.1152\/ajprenal.2000.279.6.f1027","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T13:30:06Z","timestamp":1514035806000},"page":"F1027-F1032","source":"Crossref","is-referenced-by-count":44,"title":["Identification and characterization of a glomerular-specific promoter from the human nephrin gene"],"prefix":"10.1152","volume":"279","author":[{"given":"M. Andrew","family":"Wong","sequence":"first","affiliation":[{"name":"Department of Maternal and Fetal Health, The Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario M5G 1X5; and"}]},{"given":"Shiying","family":"Cui","sequence":"additional","affiliation":[{"name":"Department of Maternal and Fetal Health, The Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario M5G 1X5; and"}]},{"given":"Susan E.","family":"Quaggin","sequence":"additional","affiliation":[{"name":"Department of Maternal and Fetal Health, The Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario M5G 1X5; and"},{"name":"Division of Nephrology, St. Michael's Hospital, Toronto, Ontario, Canada M5B 1W8"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/S1073-4449(00)70001-X"},{"key":"B2","doi-asserted-by":"crossref","first-page":"51","DOI":"10.1681\/ASN.V10151","volume":"10","author":"Barisoni L","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00836.x"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.388"},{"key":"B5","first-page":"447","volume":"13","author":"Dehbi M","year":"1996","journal-title":"Oncogene"},{"key":"B6","doi-asserted-by":"crossref","first-page":"787","DOI":"10.1242\/dev.109.4.787","volume":"109","author":"Dressler GR","year":"1990","journal-title":"Development"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.28"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1999.1854"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/26.1.362"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00719.x"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1038\/ng0393-241"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1016\/S1097-2765(00)80057-X"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2559.1999.00670.x"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1159\/000174083"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-199907000-00014"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1086\/302182"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/S0925-4773(98)00030-6"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1002\/bies.950181111"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1007\/s001250051447"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1007\/BF00240371"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1006\/excr.1997.3739"},{"key":"B23","doi-asserted-by":"crossref","first-page":"697","DOI":"10.1681\/ASN.V85697","volume":"8","author":"Mundel P","year":"1997","journal-title":"J Am Soc Nephrol"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119163"},{"key":"B25","doi-asserted-by":"crossref","first-page":"3013","DOI":"10.1242\/dev.122.10.3013","volume":"122","author":"Partanen J","year":"1996","journal-title":"Development"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1002\/j.1460-2075.1995.tb00276.x"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/S0925-4773(97)00201-3"},{"key":"B28","doi-asserted-by":"crossref","first-page":"5771","DOI":"10.1242\/dev.126.24.5771","volume":"126","author":"Quaggin SE","year":"1999","journal-title":"Development"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1097-0177(199809)213:1<105::AID-AJA10>3.0.CO;2-1"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.14.7962"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1007\/BF00267823"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1126\/science.286.5438.312"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1126\/science.286.5438.225"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.2000.279.6.F1027","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:43:02Z","timestamp":1660189382000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.2000.279.6.F1027"}},"issued":{"date-parts":[[2000,12,1]]},"references-count":32,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2000,12,1]]}},"alternative-id":["10.1152\/ajprenal.2000.279.6.F1027"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.2000.279.6.f1027","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2000,12,1]]}},{"indexed":{"date-parts":[[2026,3,19]],"date-time":"2026-03-19T07:55:25Z","timestamp":1773906925647,"version":"3.50.1"},"reference-count":34,"publisher":"American Physiological Society","issue":"5","funder":[{"DOI":"10.13039\/501100003725","name":"National Research Foundation of Korea","doi-asserted-by":"publisher","award":["NRF-2018R1C1B6003481"],"award-info":[{"award-number":["NRF-2018R1C1B6003481"]}],"id":[{"id":"10.13039\/501100003725","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2021,5,1]]},"abstract":"<jats:p> It is unclear whether antipsychotic drugs can retain water in the kidney in the absence of vasopressin. This study demonstrates that haloperidol, sertraline, and carbamazepine can produce nephrogenic syndrome of inappropriate antidiuresis because they directly upregulate vasopressin-2 receptor and aquaporin-2 (AQP2) via cAMP\/PKA signaling. We showed that, in addition to AQP2 trafficking, AQP2 protein abundance was rapidly increased by treatment with antipsychotic drugs in association with dephosphorylation of AQP2 at Ser<jats:sup>261<\/jats:sup> and accelerated AQP2 transcription. <\/jats:p>","DOI":"10.1152\/ajprenal.00576.2020","type":"journal-article","created":{"date-parts":[[2021,4,12]],"date-time":"2021-04-12T10:16:47Z","timestamp":1618222607000},"page":"F963-F971","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":11,"title":["Psychotropic drugs upregulate aquaporin-2 via vasopressin-2 receptor\/cAMP\/protein kinase A signaling in inner medullary collecting duct cells"],"prefix":"10.1152","volume":"320","author":[{"given":"Sua","family":"Kim","sequence":"first","affiliation":[{"name":"Institute of Biomedical Science, Hanyang University College of Medicine, Seoul, Republic of Korea"}]},{"given":"Chor Ho","family":"Jo","sequence":"additional","affiliation":[{"name":"Institute of Biomedical Science, Hanyang University College of Medicine, Seoul, Republic of Korea"}]},{"given":"Gheun-Ho","family":"Kim","sequence":"additional","affiliation":[{"name":"Institute of Biomedical Science, Hanyang University College of Medicine, Seoul, Republic of Korea"},{"name":"Department of Internal Medicine, Hanyang University College of Medicine, Seoul, Republic of Korea"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejim.2018.11.011"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1001\/jama.2014.13967"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.2165\/11532560-000000000-00000"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/j.psym.2014.01.010"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/j.maturitas.2013.08.010"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1080\/14740338.2017.1248399"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1136\/bmj.1.6069.1134"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1136\/bmj.2.6090.804"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1042\/cs0470289"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1111\/ene.13069"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfq317"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfm714"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00477.2014"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/j.tiv.2017.07.011"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.3109\/00498254.2016.1151088"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejmech.2014.11.012"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2018060668"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009111190"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.275.5.F796"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfp657"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000143476.93376.04"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00617.2013"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1172\/JCI89812"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2008.03.004"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00102.2016"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00418.2016"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014010118"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00001.2011"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00337.2004"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2015080903"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.23876\/j.krcp.19.002"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1007\/s10157-013-0789-5"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2015.181"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1111\/cen.13011"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00576.2020","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,6,23]],"date-time":"2021-06-23T08:49:54Z","timestamp":1624438194000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00576.2020"}},"issued":{"date-parts":[[2021,5,1]]},"references-count":34,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2021,5,1]]}},"alternative-id":["10.1152\/ajprenal.00576.2020"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00576.2020","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2021,5,1]]},"assertion":[{"value":"2020-10-28","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2021-04-07","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2021-05-17","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,3,19]],"date-time":"2026-03-19T22:18:41Z","timestamp":1773958721362,"version":"3.50.1"},"reference-count":39,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2006,9]]},"abstract":"<jats:p> Sodium bicarbonate cotransporter 1 (NBC1) mediates 80% of bicarbonate reabsorption by the kidney, but the molecular determinants for activity, targeting, and cell membrane stability are poorly understood. We generated truncation mutants involving the entire NH<jats:sub>2<\/jats:sub> (\u0394N424) or the entire COOH (\u0394C92) terminus and examined the effects of these truncations on targeting, cell membrane stability, and NBC1 activity. \u0394N424 and \u0394C92 targeted to the plasma membrane of HEK293 cells or to the basolateral membrane of opossum kidney (OK) cells at 24 h but did not display NBC1 activity. Unlike the NBC1 wild-type and the \u0394N424, \u0394C92 expression was significantly decreased in the basolateral membrane at 48 h and yet the total \u0394C92 expression in the cell was constant. We found that decreased \u0394C92 expression in the basolateral membrane was due to increased endocytosis and mistargeting to the apical membrane. Increased endocytosis was prevented when both \u0394N424 and \u0394C92 were cotransfected together and more stable expression of \u0394C92 was observed. Immunoprecipitation studies using NBC1 antibody specific for the COOH epitope were able to detect the COOH truncated NBC1 when probed with NH<jats:sub>2<\/jats:sub> epitope-specific antibody or vice versa. Similar findings were observed with Ni-NTA pull-down assay. Cotransfection of both mutants partially restored NBC1 activity. In summary, NBC1 targets to the basolateral membrane of OK cells by a default mechanism and the COOH terminus plays a role on NBC1 stability in the basolateral membrane. <\/jats:p>","DOI":"10.1152\/ajprenal.00361.2005","type":"journal-article","created":{"date-parts":[[2006,4,18]],"date-time":"2006-04-18T21:46:30Z","timestamp":1145396790000},"page":"F588-F596","source":"Crossref","is-referenced-by-count":15,"title":["Role of NH<sub>2<\/sub> and COOH termini in targeting, stability, and activity of sodium bicarbonate cotransporter 1"],"prefix":"10.1152","volume":"291","author":[{"given":"Doris Joy D.","family":"Espiritu","sequence":"first","affiliation":[]},{"given":"Angelito A.","family":"Bernardo","sequence":"additional","affiliation":[]},{"given":"Jose A. L.","family":"Arruda","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1007\/s00232-002-1051-3"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.81.1.53"},{"key":"R3","doi-asserted-by":"crossref","unstructured":"Burnham CE, Amlal H, Wang ZH, Shull GE, and Soleimani M. Cloning and functional expression of a human kidney Na+\/HCO3\u2212 cotransporter. J Biol Chem 272: 19222\u201319224, 1997.","DOI":"10.1074\/jbc.272.31.19111"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1038\/nature02261"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00338.2001"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1007\/s00232-004-0675-x"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.87.20.7917"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2001.012956"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M110904200"},{"key":"R10","doi-asserted-by":"crossref","unstructured":"Horita S, Yamada H, Inatomi J, Sekine T, Igarashi T, Seki G, and Fugita T. Mechanism of NBC1 inactivation by mutations identified in patients with proximal renal tubular acidosis and ocular abnormalities (Abstract). J Am Soc Nephrol 16: 123A, 2005.","DOI":"10.1681\/ASN.2004080667"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1210\/me.2004-0190"},{"key":"R12","doi-asserted-by":"crossref","unstructured":"Igarashi T. Mutations in SLC4A4 cause permanent isolated proximal renal tubular acidosis with ocular abnormalities. Nature 23: 264\u2013265, 1999.","DOI":"10.1038\/15440"},{"key":"R13","unstructured":"Igarashi T, Inatomi J, Sekine T, Seki G, Yamada H, Horita S, and Fujita T. Mutational and functional analysis of the Na\/HCO3 cotransporter gene (SLC4AC) in patients with permanent isolated proximal renal tubular acidosis and ocular abnormalities. J Am Soc Nephrol 13: 302A, 2003."},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M211662200"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0409114102"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.1.92"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M405780200"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1980.238.3.F166"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-3495(04)74272-1"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2004.065110"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1038\/387409a0"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.256.3.F414"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.231"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1006\/jmbi.1999.3489"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1007\/BF01871942"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.33.20515"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1002\/j.1460-2075.1996.tb00470.x"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.20028641"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.2001.280.6.G1305"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M206964200"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1021\/bi026826q"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.00974"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1182\/blood.V99.1.342"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.47.33393"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M106153200"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.2000.279.2.C410"},{"key":"R37","doi-asserted-by":"crossref","unstructured":"Zhang D, Kiyatkin A, Bolin JT, and Low P. Crystallographic structure and functional interpretation of the cytoplasmic domain of erythrocyte membrane band 3. Blood 96: 2925\u20132933, 2000.","DOI":"10.2210\/pdb1hyn\/pdb"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.23-22-08167.2003"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M207797200"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00361.2005","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:24:52Z","timestamp":1567970692000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00361.2005"}},"issued":{"date-parts":[[2006,9]]},"references-count":39,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2006,9]]}},"alternative-id":["10.1152\/ajprenal.00361.2005"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00361.2005","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2006,9]]}},{"indexed":{"date-parts":[[2026,3,20]],"date-time":"2026-03-20T05:38:18Z","timestamp":1773985098281,"version":"3.50.1"},"reference-count":52,"publisher":"American Physiological Society","issue":"6","funder":[{"DOI":"10.13039\/100000050","name":"HHS | NIH | National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["ZIA-HL001285"],"award-info":[{"award-number":["ZIA-HL001285"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"HHS | NIH | National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["ZIA-HL006129"],"award-info":[{"award-number":["ZIA-HL006129"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2025,12,1]]},"abstract":"<jats:p>We developed an inducible Avp knockout mouse line that will be shared with the research community and is likely to be useful for further study of the regulation of water balance and polycystic kidney disease, as well as neural, vascular, and metabolic roles of vasopressin.<\/jats:p>","DOI":"10.1152\/ajprenal.00340.2025","type":"journal-article","created":{"date-parts":[[2025,10,6]],"date-time":"2025-10-06T17:20:22Z","timestamp":1759771222000},"page":"F784-F795","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["Inducible\n                    <i>Avp<\/i>\n                    knockout mouse line"],"prefix":"10.1152","volume":"329","author":[{"given":"Shaza","family":"Khan","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/01cwqze88","id-type":"ROR","asserted-by":"publisher"}],"name":"National Institutes of Health","place":["United States"]},{"name":"Howard University College of Medicine","place":["United States"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6207-6364","authenticated-orcid":false,"given":"Lihe","family":"Chen","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/01cwqze88","id-type":"ROR","asserted-by":"publisher"}],"name":"National Institutes of Health","place":["United States"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4878-9501","authenticated-orcid":false,"given":"Chung-Lin","family":"Chou","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/01cwqze88","id-type":"ROR","asserted-by":"publisher"}],"name":"National Institutes of Health","place":["United States"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0364-0412","authenticated-orcid":false,"given":"Syed J.","family":"Khundmiri","sequence":"additional","affiliation":[{"name":"Howard University College of Medicine","place":["United States"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2276-8091","authenticated-orcid":false,"given":"Mark A.","family":"Knepper","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/01cwqze88","id-type":"ROR","asserted-by":"publisher"}],"name":"National Institutes of Health","place":["United States"]}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1007\/BF01534707"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1159\/000133420"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1002\/j.1460-2075.1984.tb02291.x"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1126\/science.6153132"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2006.03.003"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1002\/j.1460-2075.1983.tb01497.x"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1136\/bmj.2.5808.282"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuron.2016.11.021"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1093\/bjaceaccp\/mkn021"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1172\/JCI105038"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1006\/frne.1997.0153"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1038\/356523a0"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1038\/357333a0"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.15.6783"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1038\/357336a0"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2020101407"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1210\/endo.133.4.8404628"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1210\/endo.131.1.1535312"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1710964114"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1530\/acta.0.1290489"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1981.240.4.F311"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/0303-7207(84)90096-0"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.ph.56.030194.003431"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.4.1013"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1995.268.6.C1546"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.16.7212"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.91.19.8984"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1038\/srep34863"},{"key":"B29","first-page":"193","volume":"3","author":"Yamamoto T","year":"1995","journal-title":"Exp Nephrol"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M111880200"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1530\/jrf.0.0610273"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-4939-8831-0_11"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-0716-3016-7_10"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1006\/dbio.2002.0597"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00436.2017"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M803074200"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0401704101"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1093\/bioinformatics\/bts635"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1186\/1471-2105-12-323"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00053.2006"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.59.1.437"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/ajplegacy.1964.206.2.425"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1210\/endo-77-4-701"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1038\/308705a0"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1002\/j.1460-2075.1986.tb04311.x"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1677\/joe.0.0560111"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.1974.tb09708.x"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.1982.tb37407.x"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00057.2024"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1172\/JCI39680"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.3389\/fphys.2019.00948"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00068.2007"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00340.2025","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,11,18]],"date-time":"2025-11-18T18:46:54Z","timestamp":1763491614000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00340.2025"}},"issued":{"date-parts":[[2025,12,1]]},"references-count":52,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2025,12,1]]}},"alternative-id":["10.1152\/ajprenal.00340.2025"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00340.2025","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2025,12,1]]},"assertion":[{"value":"2025-09-03","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2025-09-15","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2025-09-29","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2025-11-18","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,3,18]],"date-time":"2026-03-18T11:32:55Z","timestamp":1773833575260,"version":"3.50.1"},"reference-count":36,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2008,10]]},"abstract":"<jats:p> Urotensin II (UII) has been implicated widely in cardiovascular disease. The mechanism(s) through which it contributes to elevated blood pressure is unknown, but its emerging role as a regulator of mammalian renal function suggests that the kidney might be involved. The aim of this study was to determine the effect of UII on renal function in the spontaneously hypertensive rat (SHR). UII infusion (6 pmol\u00b7min<jats:sup>\u22121<\/jats:sup>\u00b7100 g body wt<jats:sup>\u22121<\/jats:sup>) in anesthetized SHR and control Wistar-Kyoto (WKY) rats produced marked reductions in glomerular filtration rate (\u0394GFR WKY, n = 7, \u22120.3 \u00b1 0.1 vs. SHR, n = 7, \u22120.6 \u00b1 0.1 ml\u00b7min<jats:sup>\u22121<\/jats:sup>\u00b7100 g body wt<jats:sup>\u22121<\/jats:sup>, P = 0.03), urine flow, and sodium excretion rates, which were greater in SHR by comparison with WKY rats. WKY rats also showed an increase in fractional excretion of sodium (\u0394FE<jats:sub>Na<\/jats:sub>; +0.6 \u00b1 0.1%, P = 0.02) in contrast to SHR in which no such change was observed (\u0394FE<jats:sub>Na<\/jats:sub> \u22120.6 \u00b1 0.2%). Blockade of the UII receptor (UT), and thus endogenous UII activity, with urantide evoked an increase in GFR which was greater in SHR (+0.3 \u00b1 0.1) compared with WKY rats (+0.1 \u00b1 0.1 ml\u00b7min<jats:sup>\u22121<\/jats:sup>\u00b7100 g body wt<jats:sup>\u22121<\/jats:sup>, P = 0.04) and was accompanied by a diuresis and natriuresis. UII and UT mRNA expression were greater in the renal medulla than the cortex of both strains; however, expression levels were up to threefold higher in SHR tissue. SHR are more sensitive than WKY to UII, which acts primarily to lower GFR thus favoring salt retention in this model of hypertension. <\/jats:p>","DOI":"10.1152\/ajprenal.90374.2008","type":"journal-article","created":{"date-parts":[[2008,10,9]],"date-time":"2008-10-09T11:57:43Z","timestamp":1223553463000},"page":"F1239-F1247","source":"Crossref","is-referenced-by-count":13,"title":["Enhanced renal sensitivity of the spontaneously hypertensive rat to urotensin II"],"prefix":"10.1152","volume":"295","author":[{"given":"Alaa E. S.","family":"Abdel-Razik","sequence":"first","affiliation":[]},{"given":"Richard J.","family":"Balment","sequence":"additional","affiliation":[]},{"given":"Nick","family":"Ashton","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1677\/JOE-08-0260"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1038\/45809"},{"key":"R3","unstructured":"Bern HA, Pearson D, Larson BA, Nishioka RS. Neurohormones from fish tails: the caudal neurosecretory system. I. \u201cUrophysiology\u201d and the caudal neurosecretory system of fishes. Recent Prog Horm Res 41: 533\u2013552, 1985."},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0704448"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejphar.2004.07.089"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1016\/j.peptides.2005.03.043"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1097\/01.hjh.0000125452.28861.f1"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-5793(99)01003-0"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.26.15803"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1016\/j.peptides.2005.10.004"},{"key":"R11","unstructured":"Douglas SA, Ohlstein EH. Urotensin receptors. In: The IUPHAR Compendium of Receptor Characterization and Classification, edited by Girdlestone D. London: IUPHAR Media, 2000, p. 365\u2013372."},{"key":"R12","unstructured":"Dworkin LD, Brenner BM. The renal circulations. In: The Kidney (5th ed.), edited by Brenner BM. Philadelphia: W. B. Saunders, 1996, p. 247\u2013285."},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1007\/s002130100715"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1016\/j.peptides.2005.03.012"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1016\/S0168-8278(02)00295-7"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000121326.69153.98"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1291\/hypres.26.839"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1999.1796"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1006\/meth.2001.1262"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0703601"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-200112000-00011"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000044388.19119.02"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1038\/14081"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfk049"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0705555"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1016\/j.peptides.2007.10.027"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00217.2003"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1016\/j.peptides.2008.02.015"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1016\/j.amjhyper.2005.03.748"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000290"},{"key":"R31","unstructured":"Thompson JP, Watt P, Sanghavi S, Strupish JW, Lambert DG. A comparison of cerebrospinal fluid and plasma urotensin II concentrations in normotensive and hypertensive patients undergoing urological surgery during spinal anesthesia: a pilot study. Anesth Analg 97: 1501\u20131503, 2003."},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1016\/j.peptides.2004.06.024"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1016\/S0008-6363(01)00485-0"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1006\/gcen.1998.7245"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1177\/147323000603400306"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00342.2002"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.90374.2008","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T23:02:54Z","timestamp":1567983774000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.90374.2008"}},"issued":{"date-parts":[[2008,10]]},"references-count":36,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2008,10]]}},"alternative-id":["10.1152\/ajprenal.90374.2008"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.90374.2008","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2008,10]]}},{"indexed":{"date-parts":[[2026,3,19]],"date-time":"2026-03-19T13:36:48Z","timestamp":1773927408182,"version":"3.50.1"},"reference-count":63,"publisher":"American Physiological Society","issue":"3","funder":[{"DOI":"10.13039\/100000968","name":"American Heart Association","doi-asserted-by":"crossref","award":["19EIA34660135"],"award-info":[{"award-number":["19EIA34660135"]}],"id":[{"id":"10.13039\/100000968","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["R01DK109570"],"award-info":[{"award-number":["R01DK109570"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["5U24DK128851"],"award-info":[{"award-number":["5U24DK128851"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["1R56DK128271"],"award-info":[{"award-number":["1R56DK128271"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2024,3,1]]},"abstract":"<jats:p> Circadian rhythms are endogenous biological oscillations that regulate various physiological processes in organisms, including kidney function. The kidney plays a vital role in maintaining homeostasis by regulating water and electrolyte balance, blood pressure, and excretion of metabolic waste products, all of which display circadian rhythmicity. For this reason, studying the circadian regulation of the kidney is important, and the time of day is a biological and experimental variable that must be considered. Over the past decade, considerable progress has been made in understanding the molecular mechanisms underlying circadian regulation within the kidney. In this review, the current knowledge regarding circadian rhythms in the kidney is explored, focusing on the molecular clock machinery, circadian control of renal functions, and the impact of disrupted circadian rhythms on kidney health. In addition, parameters that should be considered and future directions are outlined in this review. <\/jats:p>","DOI":"10.1152\/ajprenal.00214.2023","type":"journal-article","created":{"date-parts":[[2024,1,4]],"date-time":"2024-01-04T09:01:11Z","timestamp":1704358871000},"page":"F382-F393","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":16,"title":["Recent advances in understanding the kidney circadian clock mechanism"],"prefix":"10.1152","volume":"326","author":[{"ORCID":"https:\/\/orcid.org\/0009-0009-8175-0738","authenticated-orcid":false,"given":"Alexandria","family":"Juffre","sequence":"first","affiliation":[{"name":"Department of Physiology and Aging, University of Florida, Gainesville, Florida, United States"},{"name":"Center for Integrative Cardiovascular and Metabolic Diseases, University of Florida, Gainesville, Florida, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1342-0878","authenticated-orcid":false,"given":"Michelle L.","family":"Gumz","sequence":"additional","affiliation":[{"name":"Department of Physiology and Aging, University of Florida, Gainesville, Florida, United States"},{"name":"Center for Integrative Cardiovascular and Metabolic Diseases, University of Florida, Gainesville, Florida, United States"},{"name":"Division of Nephrology, Hypertension, and Renal Transplantation, Department of Medicine, University of Florida, Gainesville, Florida, United States"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1530\/JME-19-0153"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/gks1161"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1408886111"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/j.celrep.2022.111982"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/j.tcb.2013.07.002"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00045.2021"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1986.250.5.R737"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1523629113"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1111\/apha.12804"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0611680104"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00385.2021"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00014.2020"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbadis.2022.166572"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2021.11.016"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1038\/nm.1865"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.119.13908"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.122.19316"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1096\/fj.202002452R"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1038\/s41419-020-2655-1"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/j.labinv.2022.100008"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1111\/jcmm.17223"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/j.abb.2023.109736"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00126.2023"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00364.2019"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2015091055"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-020-02361-w"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1111\/j.1464-5491.2009.02894.x"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1016\/j.cbpb.2005.11.007"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00381.2017"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1139\/cjpp-2019-0688"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1016\/j.lfs.2014.03.028"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1096\/fasebj.26.1_supplement.lb82"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.3389\/fphys.2020.00209"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00060.2009"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1139\/cjpp-2022-0134"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00207.2011"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1101\/cshperspect.a039107"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1016\/j.biopsych.2021.03.005"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00231.2022"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1016\/j.exger.2022.112076"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.3389\/fphys.2022.991705"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00227.2022"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00296.2022"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1172\/JCI167133"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbapap.2009.10.024"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1017\/S0029665116000288"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1161\/JAHA.116.003896"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(23)02230-4"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(23)02302-4"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1126\/sciadv.abb5202"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1016\/j.celrep.2022.111514"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1016\/j.apsb.2020.10.001"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1080\/13880209.2022.2058558"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1016\/j.metabol.2019.154013"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.2337\/db17-0816"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1097\/CCM.0000000000004697"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1111\/apha.13962"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.3389\/fgene.2022.872920"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.3390\/ijerph19095732"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1172\/JCI148277"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2022.04.010"},{"key":"B62","first-page":"109","volume":"103","author":"Choi JS","year":"1999","journal-title":"Res Commun Mol Pathol Pharmacol"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1007\/BF00626363"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00214.2023","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,2,21]],"date-time":"2024-02-21T14:23:06Z","timestamp":1708525386000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00214.2023"}},"issued":{"date-parts":[[2024,3,1]]},"references-count":63,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2024,3,1]]}},"alternative-id":["10.1152\/ajprenal.00214.2023"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00214.2023","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2024,3,1]]},"assertion":[{"value":"2023-07-24","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2023-12-14","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2023-12-15","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2024-02-21","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,3,25]],"date-time":"2026-03-25T12:57:37Z","timestamp":1774443457430,"version":"3.50.1"},"reference-count":54,"publisher":"American Physiological Society","issue":"9","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,11,1]]},"abstract":"<jats:p>\n                    Chemokine (C-C motif) receptor 2 (CCR2) is central for the migration of monocytes into inflamed tissues. The novel CCR2 antagonist CCX140-B, which is currently in two separate phase 2 clinical trials in diabetic nephropathy, has recently been shown to reduce hemoglobin A\n                    <jats:sub>1c<\/jats:sub>\n                    and fasting blood glucose levels in type 2 diabetics. In this report, we describe the effects of this compound on glycemic and renal function parameters in diabetic mice. Since CCX140-B has a low affinity for mouse CCR2, transgenic human CCR2 knockin mice were generated and rendered diabetic with either a high-fat diet (diet-induced obesity) or by deletion of the leptin receptor gene ( db\/ db). CCX140-B treatment in both models resulted in decreased albuminuria, which was associated with decreased glomerular hypertrophy and increased podocyte density. Moreover, treatment of diet-induced obese mice with CCX140-B resulted in decreased levels of fasting blood glucose and insulin, normalization of homeostatic model assessment of insulin resistance values, and decreased numbers of adipose tissue inflammatory macrophages. Unlike other CCR2 antagonists, CCX140-B had no effect on plasma levels of the CCR2 ligand CCL2 or on the numbers of blood monocytes. These results support the ongoing evaluation of this molecule in diabetic subjects with impaired renal function.\n                  <\/jats:p>","DOI":"10.1152\/ajprenal.00316.2013","type":"journal-article","created":{"date-parts":[[2013,8,28]],"date-time":"2013-08-28T22:45:03Z","timestamp":1377729903000},"page":"F1288-F1297","source":"Crossref","is-referenced-by-count":78,"title":["CCR2 antagonist CCX140-B provides renal and glycemic benefits in diabetic transgenic human CCR2 knockin mice"],"prefix":"10.1152","volume":"305","author":[{"given":"Timothy","family":"Sullivan","sequence":"first","affiliation":[{"name":"ChemoCentryx Incorporated, Mountain View, California; and"}]},{"given":"Zhenhua","family":"Miao","sequence":"additional","affiliation":[{"name":"ChemoCentryx Incorporated, Mountain View, California; and"}]},{"given":"Daniel J.","family":"Dairaghi","sequence":"additional","affiliation":[{"name":"ChemoCentryx Incorporated, Mountain View, California; and"}]},{"given":"Antoni","family":"Krasinski","sequence":"additional","affiliation":[{"name":"ChemoCentryx Incorporated, Mountain View, California; and"}]},{"given":"Yu","family":"Wang","sequence":"additional","affiliation":[{"name":"ChemoCentryx Incorporated, Mountain View, California; and"}]},{"given":"Bin N.","family":"Zhao","sequence":"additional","affiliation":[{"name":"ChemoCentryx Incorporated, Mountain View, California; and"}]},{"given":"Trageen","family":"Baumgart","sequence":"additional","affiliation":[{"name":"ChemoCentryx Incorporated, Mountain View, California; and"}]},{"given":"Linda S.","family":"Ertl","sequence":"additional","affiliation":[{"name":"ChemoCentryx Incorporated, Mountain View, California; and"}]},{"given":"Andrew","family":"Pennell","sequence":"additional","affiliation":[{"name":"ChemoCentryx Incorporated, Mountain View, California; and"}]},{"given":"Lisa","family":"Seitz","sequence":"additional","affiliation":[{"name":"ChemoCentryx Incorporated, Mountain View, California; and"}]},{"given":"Jay","family":"Powers","sequence":"additional","affiliation":[{"name":"ChemoCentryx Incorporated, Mountain View, California; and"}]},{"given":"Ruiping","family":"Zhao","sequence":"additional","affiliation":[{"name":"ChemoCentryx Incorporated, Mountain View, California; and"}]},{"given":"Solomon","family":"Ungashe","sequence":"additional","affiliation":[{"name":"ChemoCentryx Incorporated, Mountain View, California; and"}]},{"given":"Zheng","family":"Wei","sequence":"additional","affiliation":[{"name":"ChemoCentryx Incorporated, Mountain View, California; and"}]},{"given":"Landin","family":"Boring","sequence":"additional","affiliation":[{"name":"Gladstone Institute of Cardiovascular Disease, J. David Gladstone Research Institutes, San Francisco, California"}]},{"given":"Chia-Lin","family":"Tsou","sequence":"additional","affiliation":[{"name":"Gladstone Institute of Cardiovascular Disease, J. David Gladstone Research Institutes, San Francisco, California"}]},{"given":"Israel","family":"Charo","sequence":"additional","affiliation":[{"name":"Gladstone Institute of Cardiovascular Disease, J. David Gladstone Research Institutes, San Francisco, California"}]},{"given":"Robert D.","family":"Berahovich","sequence":"additional","affiliation":[{"name":"ChemoCentryx Incorporated, Mountain View, California; and"}]},{"given":"Thomas J.","family":"Schall","sequence":"additional","affiliation":[{"name":"ChemoCentryx Incorporated, Mountain View, California; and"}]},{"given":"Juan C.","family":"Jaen","sequence":"additional","affiliation":[{"name":"ChemoCentryx Incorporated, Mountain View, California; and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/j.atherosclerosis.2009.08.017"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0b013e3283451901"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00214.x"},{"key":"B4","author":"Basak A","year":"2013","journal-title":"Heteroaryl Sulfonamides and CCR2"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119798"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.54.8.2277"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra052723"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00367.x"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1007\/s00125-006-0497-8"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000014"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1038\/clpt.2011.33"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2009.501"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2796.2007.01852.x"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(12)80393-3"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.2174\/157016110793563816"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.4172\/2155-6156.1000225"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009121290"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.128"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M601284200"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2007.06.148"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1172\/JCI26498"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2010.263"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1084\/jem.186.10.1757"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.94.22.12053"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000135055.61833.A8"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1084\/jem.187.4.601"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1007\/BF00280883"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.64.s86.12.x"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/S1056-8727(02)00176-9"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1172\/JCI27280"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1797.2006.00576.x"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1248\/bpb.b12-00528"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1146\/annurev-physiol-021909-135846"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1161\/ATVBAHA.109.198812"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1021\/jm300682j"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1133870100"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.49.3.466"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2011.102"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1038\/nri2972"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1210\/en.2005-0969"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfs555"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1016\/j.cyto.2009.04.001"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.5551\/jat.3368"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1161\/ATVBAHA.108.168633"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.2337\/db08-0895"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1172\/JCI29919"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1002\/art.23591"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.pharmtox.48.121806.154841"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.110.169714"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1186\/1476-9255-6-32"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1172\/JCI24335"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1172\/JCI200319246"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1172\/JCI20514"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1007\/s00125-009-1309-8"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00316.2013","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:56:07Z","timestamp":1567972567000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00316.2013"}},"issued":{"date-parts":[[2013,11,1]]},"references-count":54,"journal-issue":{"issue":"9","published-print":{"date-parts":[[2013,11,1]]}},"alternative-id":["10.1152\/ajprenal.00316.2013"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00316.2013","relation":{"has-review":[{"id-type":"doi","id":"10.3410\/f.718089072.793518339","asserted-by":"object"}]},"ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2013,11,1]]}},{"indexed":{"date-parts":[[2026,3,23]],"date-time":"2026-03-23T21:43:32Z","timestamp":1774302212729,"version":"3.50.1"},"reference-count":49,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2014,8,1]]},"abstract":"<jats:p>Development of higher rates of nondiabetic glomerulosclerosis (GS) in African Americans has been attributed to two coding sequence variants (G1 and G2) in the APOL1 gene. To date, the cellular function and the role of APOL1 variants (Vs) in GS are still unknown. In this study, we examined the effects of overexpressing wild-type (G0) and kidney disease risk variants (G1 and G2) of APOL1 in human podocytes using a lentivirus expression system. Interestingly, G0 inflicted podocyte injury only at a higher concentration; however, G1 and G2 promoted moderate podocyte injury at lower and higher concentrations. APOL1Vs expressing podocytes displayed diffuse distribution of both Lucifer yellow dye and cathepsin L as manifestations of enhanced lysosomal membrane permeability (LMP). Chloroquine attenuated the APOL1Vs-induced increase in podocyte injury, consistent with targeting lysosomes. The chloride channel blocker DIDS prevented APOL1Vs- induced injury, indicating a role for chloride influx in osmotic swelling of lysosomes. Direct exposure of noninfected podocytes with conditioned media from G1- and G2-expressing podocytes also induced injury, suggesting a contributory role of the secreted component of G1 and G2 as well. Adverse host factors (AHFs) such as hydrogen peroxide, hypoxia, TNF-\u03b1, and puromycin aminonucleoside augmented APOL1- and APOL1Vs-induced podocyte injury, while the effect of human immunodeficiency virus (HIV) on podocyte injury was overwhelming under conditions of APOLVs expression. We conclude that G0 and G1 and G2 APOL1 variants have the potential to induce podocyte injury in a manner which is further augmented by AHFs, with HIV infection being especially prominent.<\/jats:p>","DOI":"10.1152\/ajprenal.00647.2013","type":"journal-article","created":{"date-parts":[[2014,6,5]],"date-time":"2014-06-05T03:50:16Z","timestamp":1401940216000},"page":"F326-F336","source":"Crossref","is-referenced-by-count":164,"title":["APOL1 risk variants enhance podocyte necrosis through compromising lysosomal membrane permeability"],"prefix":"10.1152","volume":"307","author":[{"given":"Xiqian","family":"Lan","sequence":"first","affiliation":[{"name":"Renal Molecular Research Laboratory, Feinstein Institute for Medical Research, Hofstra-North Shore Long Island Jewish School of Medicine School, Hempstead, New York;"}]},{"given":"Aakash","family":"Jhaveri","sequence":"additional","affiliation":[{"name":"Renal Molecular Research Laboratory, Feinstein Institute for Medical Research, Hofstra-North Shore Long Island Jewish School of Medicine School, Hempstead, New York;"}]},{"given":"Kang","family":"Cheng","sequence":"additional","affiliation":[{"name":"Renal Molecular Research Laboratory, Feinstein Institute for Medical Research, Hofstra-North Shore Long Island Jewish School of Medicine School, Hempstead, New York;"}]},{"given":"Hongxiu","family":"Wen","sequence":"additional","affiliation":[{"name":"Renal Molecular Research Laboratory, Feinstein Institute for Medical Research, Hofstra-North Shore Long Island Jewish School of Medicine School, Hempstead, New York;"}]},{"given":"Moin A.","family":"Saleem","sequence":"additional","affiliation":[{"name":"Renal Academic Unit, University of Bristol, Bristol, United Kingdom;"}]},{"given":"Peter W.","family":"Mathieson","sequence":"additional","affiliation":[{"name":"Renal Academic Unit, University of Bristol, Bristol, United Kingdom;"}]},{"given":"Joanna","family":"Mikulak","sequence":"additional","affiliation":[{"name":"Laboratory of Clinical and Experimental Immunology, Humanitas Clinical and Research Center, Rozzano, Milan, Italy; and"}]},{"given":"Sharon","family":"Aviram","sequence":"additional","affiliation":[{"name":"Nephrology and Molecular Medicine, Technion Institute of Technology and Rambam Medical Center, Haifa, Israel"}]},{"given":"Ashwani","family":"Malhotra","sequence":"additional","affiliation":[{"name":"Renal Molecular Research Laboratory, Feinstein Institute for Medical Research, Hofstra-North Shore Long Island Jewish School of Medicine School, Hempstead, New York;"}]},{"given":"Karl","family":"Skorecki","sequence":"additional","affiliation":[{"name":"Nephrology and Molecular Medicine, Technion Institute of Technology and Rambam Medical Center, Haifa, Israel"}]},{"given":"Pravin C.","family":"Singhal","sequence":"additional","affiliation":[{"name":"Renal Molecular Research Laboratory, Feinstein Institute for Medical Research, Hofstra-North Shore Long Island Jewish School of Medicine School, Hempstead, New York;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200511103"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1053\/j.ackd.2009.08.005"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1159\/000332378"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20021952"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1038\/onc.2008.310"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1038\/sj.cdd.4401372"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00717.2012"},{"key":"B8","doi-asserted-by":"crossref","first-page":"620","DOI":"10.1016\/S0022-2275(20)31171-8","volume":"42","author":"Duchateau PN","year":"2001","journal-title":"J Lipid Res Lipid Res"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.41.25576"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1038\/990031"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2011060562"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013010113"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2012.217"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(99)70352-5"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2011050519"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2011.306"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1111\/j.1468-1293.2012.01040.x"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2013.34"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1126\/science.1193032"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/j.ccr.2013.08.025"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M109.008482"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0051546"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1007074107"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2013.12.014"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2011040388"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1189\/jlb.0313142"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0055748"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.1100211"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1371\/journal.ppat.1000685"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2012.263"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2011010069"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0b013e328345359a"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000039661.06947.FD"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1128\/EC.5.1.132-139.2006"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1038\/nrmicro1428"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1126\/science.1114566"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2011090932"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-6143.2011.03513.x"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M401973200"},{"key":"B40","doi-asserted-by":"crossref","first-page":"630","DOI":"10.1681\/ASN.V133630","volume":"13","author":"Saleem MA","year":"2002","journal-title":"J Am Soc Nephrol"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1172\/JCI32022"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1007\/s00439-010-0861-0"},{"key":"B43","volume-title":"USRDS Annual Data Report: Atlas of Chronic Kidney Disease and End-Stage Renal Disease in the United States","author":"US Renal Data System","year":"2009"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1038\/nature12516"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2958.2010.07156.x"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1080\/08860220902780101"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M800214200"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.5301\/jn.5000179"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.4161\/auto.7066"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00647.2013","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,4,6]],"date-time":"2022-04-06T01:14:15Z","timestamp":1649207655000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00647.2013"}},"issued":{"date-parts":[[2014,8,1]]},"references-count":49,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2014,8,1]]}},"alternative-id":["10.1152\/ajprenal.00647.2013"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00647.2013","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2014,8,1]]}},{"indexed":{"date-parts":[[2026,3,24]],"date-time":"2026-03-24T06:24:27Z","timestamp":1774333467203,"version":"3.50.1"},"reference-count":76,"publisher":"American Physiological Society","issue":"6","funder":[{"DOI":"10.13039\/100009257","name":"ASN Foundation for Kidney Research","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100009257","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100017540","name":"HHS | NIH | NHLBI | Division of Intramural Research","doi-asserted-by":"publisher","award":["HL147181"],"award-info":[{"award-number":["HL147181"]}],"id":[{"id":"10.13039\/100017540","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100017618","name":"HHS | NIH | NIDDK | Division of Diabetes, Endocrinology, and Metabolic Diseases","doi-asserted-by":"publisher","award":["DK110332"],"award-info":[{"award-number":["DK110332"]}],"id":[{"id":"10.13039\/100017618","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100017618","name":"HHS | NIH | NIDDK | Division of Diabetes, Endocrinology, and Metabolic Diseases","doi-asserted-by":"publisher","award":["DK129285"],"award-info":[{"award-number":["DK129285"]}],"id":[{"id":"10.13039\/100017618","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100017618","name":"HHS | NIH | NIDDK | Division of Diabetes, Endocrinology, and Metabolic Diseases","doi-asserted-by":"publisher","award":["DK061296"],"award-info":[{"award-number":["DK061296"]}],"id":[{"id":"10.13039\/100017618","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100017618","name":"HHS | NIH | NIDDK | Division of Diabetes, Endocrinology, and Metabolic Diseases","doi-asserted-by":"publisher","award":["DK079307"],"award-info":[{"award-number":["DK079307"]}],"id":[{"id":"10.13039\/100017618","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100017618","name":"HHS | NIH | NIDDK | Division of Diabetes, Endocrinology, and Metabolic Diseases","doi-asserted-by":"publisher","award":["DK137329"],"award-info":[{"award-number":["DK137329"]}],"id":[{"id":"10.13039\/100017618","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100006108","name":"HHS | NIH | National Center for Advancing Translational Sciences","doi-asserted-by":"publisher","award":["TR001857"],"award-info":[{"award-number":["TR001857"]}],"id":[{"id":"10.13039\/100006108","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2024,6,1]]},"abstract":"<jats:p> The epithelial Na<jats:sup>+<\/jats:sup> channel (ENaC) is activated in vitro by post-translational proteolysis. In vivo, low Na<jats:sup>+<\/jats:sup> or high K<jats:sup>+<\/jats:sup> diets enhance ENaC proteolysis, and proteolysis is hypothesized to contribute to channel activation in these settings. Using a mouse expressing ENaC with disruption of a key proteolytic cleavage site, this study demonstrates that impaired proteolytic activation of ENaC\u2019s \u03b3 subunit has little impact upon channel open probability or the ability of mice to adapt to low Na<jats:sup>+<\/jats:sup> or high K<jats:sup>+<\/jats:sup> diets. <\/jats:p>","DOI":"10.1152\/ajprenal.00027.2024","type":"journal-article","created":{"date-parts":[[2024,4,18]],"date-time":"2024-04-18T08:01:51Z","timestamp":1713427311000},"page":"F1066-F1077","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":11,"title":["Influence of proteolytic cleavage of ENaC\u2019s \u03b3 subunit upon Na<sup>+<\/sup> and K<sup>+<\/sup> handling"],"prefix":"10.1152","volume":"326","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1491-4869","authenticated-orcid":false,"given":"Evan C.","family":"Ray","sequence":"first","affiliation":[{"name":"Renal-Electrolyte Division, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7604-2344","authenticated-orcid":false,"given":"Andrew","family":"Nickerson","sequence":"additional","affiliation":[{"name":"Renal-Electrolyte Division, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7198-1702","authenticated-orcid":false,"given":"Shaohu","family":"Sheng","sequence":"additional","affiliation":[{"name":"Renal-Electrolyte Division, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, United States"}]},{"given":"Rolando","family":"Carrisoza-Gaytan","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Icahn School of Medicine at Mount Sinai, New York City, New York, United States"}]},{"given":"Tracey","family":"Lam","sequence":"additional","affiliation":[{"name":"Renal-Electrolyte Division, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, United States"}]},{"given":"Allison","family":"Marciszyn","sequence":"additional","affiliation":[{"name":"Renal-Electrolyte Division, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, United States"}]},{"given":"Lei","family":"Zhang","sequence":"additional","affiliation":[{"name":"Renal-Electrolyte Division, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, United States"}]},{"given":"Alexa","family":"Jordahl","sequence":"additional","affiliation":[{"name":"Renal-Electrolyte Division, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, United States"}]},{"given":"Chunming","family":"Bi","sequence":"additional","affiliation":[{"name":"Department of Immunology, University of Pittsburgh, Pittsburgh, Pennsylvania, United States"}]},{"given":"Aaliyah","family":"Winfrey","sequence":"additional","affiliation":[{"name":"Renal-Electrolyte Division, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, United States"}]},{"given":"Zhaohui","family":"Kou","sequence":"additional","affiliation":[{"name":"Department of Immunology, University of Pittsburgh, Pittsburgh, Pennsylvania, United States"}]},{"given":"Sebastien","family":"Gingras","sequence":"additional","affiliation":[{"name":"Department of Immunology, University of Pittsburgh, Pittsburgh, Pennsylvania, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8580-9359","authenticated-orcid":false,"given":"Annet","family":"Kirabo","sequence":"additional","affiliation":[{"name":"Department of Medicine, Vanderbilt University, Nashville, Tennessee, United States"},{"name":"Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, Tennessee, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1744-1748","authenticated-orcid":false,"given":"Lisa M.","family":"Satlin","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Icahn School of Medicine at Mount Sinai, New York City, New York, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2413-5415","authenticated-orcid":false,"given":"Thomas R.","family":"Kleyman","sequence":"additional","affiliation":[{"name":"Renal-Electrolyte Division, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, United States"},{"name":"Department of Cell Biology, University of Pittsburgh, Pittsburgh, Pennsylvania, United States"},{"name":"Department of Pharmacology and Chemical Biology, University of Pittsburgh, Pittsburgh, Pennsylvania, United States"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI3971"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/ng0396-325"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(93)81336-x"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1002\/cphy.c230015"},{"key":"B5","first-page":"2708","volume":"45","author":"Palmer LG","year":"1986","journal-title":"Fed Proc"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1980.239.5.F459"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1038\/39329"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00031.2008"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfs486"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00514.2005"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00422.2005"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1172\/JCI13229"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014060618"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.C400080200"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M610636200"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M803931200"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.V115828"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M105044200"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00330.2011"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajplung.00435.2004"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00133.2012"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1021\/bi2014773"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-012-1138-3"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M111.338574"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M805676200"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008040364"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M114.623496"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00401.2009"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00668.2016"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00596.2012"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00204.2020"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1113\/JP275988"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.201511533"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1172\/JCI7840"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00536.2020"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1172\/jci.insight.156437"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00527.2019"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00705.2011"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90451.2008"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00277.2003"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00138.2015"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013111173"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.112.198879"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1097\/HJH.0000000000000216"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1016\/j.ekir.2018.06.007"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1111\/apha.12047"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1111\/apha.13249"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1053\/j.ackd.2014.11.006"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.1.F121"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00426.2016"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1096\/fasebj.2019.33.1_supplement.751.16"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1016\/j.immuni.2015.01.004"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00559.2020"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1038\/oby.2004.20"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1007\/s00216-003-2224-3"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1172\/jci.insight.172051"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.266.1.F57"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.5.F786"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1172\/jci.insight.130553"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00002.2008"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.4.1732"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.202112902"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.114.1.13"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1007\/BF00870394"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1152\/ajplegacy.1975.228.4.1249"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1172\/JCI106399"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1152\/ajplegacy.1971.221.2.632"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.1152\/ajplegacy.1974.227.2.453"},{"key":"B69","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.20028598"},{"key":"B70","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M604109200"},{"key":"B71","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2008.154435"},{"key":"B72","doi-asserted-by":"publisher","DOI":"10.1097\/01.asn.0000043900.39397.48"},{"key":"B73","doi-asserted-by":"publisher","DOI":"10.1097\/hjh.0b013e328317a762"},{"key":"B74","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2017.07.023"},{"key":"B75","doi-asserted-by":"publisher","DOI":"10.1111\/apha.13448"},{"key":"B76","doi-asserted-by":"publisher","DOI":"10.3390\/cells12192342"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00027.2024","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,5,30]],"date-time":"2024-05-30T14:59:09Z","timestamp":1717081149000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00027.2024"}},"issued":{"date-parts":[[2024,6,1]]},"references-count":76,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2024,6,1]]}},"alternative-id":["10.1152\/ajprenal.00027.2024"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00027.2024","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2024,6,1]]},"assertion":[{"value":"2024-01-23","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2024-03-27","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2024-04-09","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2024-05-30","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,3,24]],"date-time":"2026-03-24T04:04:40Z","timestamp":1774325080133,"version":"3.50.1"},"reference-count":45,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2009,5]]},"abstract":"<jats:p>During metanephric kidney development, renin expression in the renal vasculature begins in larger vessels, shifting to smaller vessels and finally remaining restricted to the terminal portions of afferent arterioles at the entrance into the glomerular capillary network. The mechanisms determining the successive expression of renin along the vascular axis of the kidney are not well understood. Since the cAMP signaling cascade plays a central role in the regulation of both renin secretion and synthesis in the adult kidney, it seemed feasible that this pathway might also be critical for renin expression during kidney development. In the present study we determined the spatiotemporal development of renin expression and the development of the preglomerular arterial tree in mouse kidneys with renin cell-specific deletion of G<jats:sub>s<\/jats:sub>\u03b1, a core element for receptor activation of adenylyl cyclases. We found that in the absence of the G<jats:sub>s<\/jats:sub>\u03b1 protein, renin expression was largely absent in the kidneys at any developmental stage, accompanied by alterations in the development of the preglomerular arterial tree. These data indicate that the maintenance of renin expression following a specific spatiotemporal pattern along the preglomerular vasculature critically depends on the availability of G<jats:sub>s<\/jats:sub>\u03b1. We infer from our data that the cAMP signaling pathway is not only critical for the regulation of renin synthesis and secretion in the mature kidney but that it also is critical for establishing the juxtaglomerular expression site of renin during development.<\/jats:p>","DOI":"10.1152\/ajprenal.90448.2008","type":"journal-article","created":{"date-parts":[[2009,3,5]],"date-time":"2009-03-05T02:10:05Z","timestamp":1236219005000},"page":"F1006-F1012","source":"Crossref","is-referenced-by-count":47,"title":["Development of vascular renin expression in the kidney critically depends on the cyclic AMP pathway"],"prefix":"10.1152","volume":"296","author":[{"given":"Bj\u00f6rn","family":"Neubauer","sequence":"first","affiliation":[]},{"given":"Katharina","family":"Machura","sequence":"additional","affiliation":[]},{"given":"Min","family":"Chen","sequence":"additional","affiliation":[]},{"given":"Lee S.","family":"Weinstein","sequence":"additional","affiliation":[]},{"given":"Mona","family":"Oppermann","sequence":"additional","affiliation":[]},{"given":"Maria Luisa","family":"Sequeira-Lopez","sequence":"additional","affiliation":[]},{"given":"R. Ariel","family":"Gomez","sequence":"additional","affiliation":[]},{"given":"J\u00fcrgen","family":"Schnermann","sequence":"additional","affiliation":[]},{"given":"Hayo","family":"Castrop","sequence":"additional","affiliation":[]},{"given":"Armin","family":"Kurtz","sequence":"additional","affiliation":[]},{"given":"Charlotte","family":"Wagner","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M605720200"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejphar.2006.01.054"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1993.264.3.R591"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00193.2006"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0408268102"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.3.F449"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1210\/endo-113-2-687"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1002\/ar.1092350115"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1203\/00006450-198309000-00016"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.268.6.F1164"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.3109\/10641969709083168"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1988.254.4.F582"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.257.5.F850"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-0528.1992.tb13881.x"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000251057.35537.d3"},{"key":"R16","doi-asserted-by":"crossref","unstructured":"Harding P, Carretero OA, Beierwaltes WH.Chronic cyclooxygenase-2 inhibition blunts low sodium-stimulated renin without changing renal haemodynamics.J Hypertens18: 1107\u20131113, 2001.","DOI":"10.1097\/00004872-200018080-00016"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-199715120-00015"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-201X.2004.01330.x"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1210\/mend-4-3-375"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.107.087577"},{"key":"R21","doi-asserted-by":"crossref","unstructured":"Kim SM, Chen L, Mizel D, Huang YG, Briggs JP, Schnermann J.Low plasma renin and reduced renin secretory responses to acute stimuli in conscious COX-2-deficient mice.Am J Physiol Renal Physiol292: F415\u2013F422, 2007.","DOI":"10.1152\/ajprenal.00317.2006"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-002-0818-9"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1002\/ar.1092390210"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1111\/j.1439-0264.1989.tb00576.x"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1292\/jvms.61.1075"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1016\/j.jsgi.2005.08.007"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00513.2006"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1007\/BF00306489"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000250708.04205.d4"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M103010200"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M414618200"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000149717.55920.45"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M011541200"},{"key":"R34","unstructured":"Phat VN, Camilleri JP, Bariety Galtier M J, Baviera E, Corvol P, Menard J.Immunohistochemical characterization of renin-containing cells in the human juxtaglomerular apparatus during embryonal and fetal development.Lab Invest45: 387\u2013390, 1981."},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1007\/BF00857873"},{"key":"R36","doi-asserted-by":"crossref","unstructured":"Reddi V, Zaglul A, Pentz ES, Gomez RA.Renin-expressing cells are associated with branching of the developing kidney vasculature.J Am Soc Nephrol9: 63\u201371, 1998.","DOI":"10.1681\/ASN.V9163"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002571"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.281.2.F345"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1016\/S1534-5807(04)00134-0"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004060490"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117547"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.1.F110"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.34.1.96"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.4.2412"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M608055200"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.90448.2008","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,10,2]],"date-time":"2021-10-02T17:40:30Z","timestamp":1633196430000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.90448.2008"}},"issued":{"date-parts":[[2009,5]]},"references-count":45,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2009,5]]}},"alternative-id":["10.1152\/ajprenal.90448.2008"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.90448.2008","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2009,5]]}},{"indexed":{"date-parts":[[2026,3,21]],"date-time":"2026-03-21T20:04:02Z","timestamp":1774123442079,"version":"3.50.1"},"reference-count":25,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2008,4]]},"abstract":"<jats:p>Acute kidney injury is an important complication in hospitalized patients often diagnosed late and associated with high mortality and morbidity. Although biomarkers for nephrotoxicity are available, they often lack sensitivity and specificity for detecting tubular injury. Netrin-1 is a laminin-like molecule highly expressed in many organs including kidney. To determine the value of netrin-1 as a biomarker of renal injury, we analyzed its urinary excretion following ischemia-reperfusion-, cisplatin-, folic acid-, and endotoxin-induced renal injury in mice. Urinary netrin-1 levels increased markedly within 3 h of ischemia-reperfusion (40 \u00b1 14-fold, P &lt; 0.01 vs. baseline), reached a peak level at 6 h, and decreased thereafter, returning to near baseline by 72 h. Serum creatinine significantly increased only after 24 h of reperfusion. Similarly, in cisplatin-, folic acid-, and lipopolysaccharide-treated mice, urine netrin-1 excretion increased as early as 1 h and reached a peak level at 6 h after injection. However, serum creatinine was raised significantly after 6, 24, and 72 h after folic acid, lipopolysaccharide, and cisplatin administration, respectively. NGAL excretion in folic acid- and lipopolysaccharide-treated mice urine samples could only be detected by 24 h after drug administration. Furthermore, urinary netrin-1 excretion increased dramatically in 13 acute renal failure patients, whereas none was detected in 6 healthy volunteer urine samples. Immunohistochemical localization showed that netrin-1 is highly expressed in tubular epithelial cells in transplanted human kidney. We conclude that urinary netrin-1 is a promising early biomarker of renal injury.<\/jats:p>","DOI":"10.1152\/ajprenal.00507.2007","type":"journal-article","created":{"date-parts":[[2008,1,30]],"date-time":"2008-01-30T21:09:56Z","timestamp":1201727396000},"page":"F731-F738","source":"Crossref","is-referenced-by-count":93,"title":["Netrin-1 and kidney injury. II. Netrin-1 is an early biomarker of acute kidney injury"],"prefix":"10.1152","volume":"294","author":[{"given":"W.","family":"Brian Reeves","sequence":"first","affiliation":[]},{"given":"Osun","family":"Kwon","sequence":"additional","affiliation":[]},{"given":"Ganesan","family":"Ramesh","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1016\/j.brainresrev.2004.11.003"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2006.050634"},{"key":"R3","unstructured":"Dong L\n                      , Stevens JL, Fabbro D, Jaken S.\n                      Regulation of protein kinase C isozymes in kidney regeneration.\n                      Cancer Res\n                      53\n                      : 4542\u20134549, 1993."},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(03)00744-3"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00433.x"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002189"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000129114.92265.32"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00285.2002"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0506233102"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.21-11-03911.2001"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1038\/nature02788"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(05)74811-X"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000088027.54400.C6"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1159\/000078452"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00633.x"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005030236"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2003.10.040"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-6143.2006.01352.x"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5001527"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(94)90420-0"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00210.x"},{"key":"R22","unstructured":"Taman M\n                      , Liu Y, Tolbert E, Dworkin LD.\n                      Increase urinary hepatocyte growth factor excretion in human acute renal failure.\n                      Clin Nephrol\n                      48\n                      : 241\u2013245, 1997."},{"key":"R22A","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00508.2007"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1126\/science.1124704"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5001874"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00507.2007","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:53:59Z","timestamp":1567968839000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00507.2007"}},"issued":{"date-parts":[[2008,4]]},"references-count":25,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2008,4]]}},"alternative-id":["10.1152\/ajprenal.00507.2007"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00507.2007","relation":{"has-review":[{"id-type":"doi","id":"10.3410\/f.1124893.581994","asserted-by":"object"}]},"ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2008,4]]}},{"indexed":{"date-parts":[[2026,3,25]],"date-time":"2026-03-25T18:54:30Z","timestamp":1774464870762,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1992,8,1]]},"abstract":"<jats:p> Arginine vasopressin (AVP) and oxytocin (OXT) induced contraction in cultured vascular smooth muscle cells (VSMC) and glomerular mesangial cells (GMC). The contractile response of AVP and OXT was paralleled by Ca2+ mobilization as assessed by 45Ca2+ efflux in a dose-dependent manner. The effects of AVP were blocked by pretreating VSMC and GMC with a V1 antagonist. OXT-stimulated effects, however, were not affected by preexposure of VSMC and GMC to an OXT antagonist but were inhibited by the V1 antagonist. Competition studies demonstrated displacement of [3H]AVP from its receptors by unlabeled AVP, the V1 antagonist, and high doses of OXT. The OXT antagonist was the least effective in displacing [3H]AVP. Thus occupancy of the V1 receptor by OXT may initiate signal transduction and contraction in VSMC and GMC in a manner qualitatively similar to that of the AVP agonist. Cultured myometrium cells (MMC) also contracted in response to AVP and OXT. Moreover, 45Ca2+ efflux increased in response to both hormones in a dose-dependent manner. AVP-stimulated contraction and 45Ca2+ efflux were blocked in MMC by pretreatment with V1 antagonist. OXT-induced effects were inhibited by the OXT antagonist but not by the V1 antagonist. Binding experiments showed that [3H]AVP was displaced equally by unlabeled AVP and V1 antagonist. Very high concentrations of OXT antagonist also demonstrated displacement.(ABSTRACT TRUNCATED AT 250 WORDS) <\/jats:p>","DOI":"10.1152\/ajprenal.1992.263.2.f222","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T10:14:44Z","timestamp":1514024084000},"page":"F222-F227","source":"Crossref","is-referenced-by-count":3,"title":["Comparative effects of arginine vasopressin and oxytocin in cell culture systems"],"prefix":"10.1152","volume":"263","author":[{"given":"V. A.","family":"Briner","sequence":"first","affiliation":[{"name":"Department of Medicine, University of Colorado School of Medicine, Denver 80262."}]},{"given":"P.","family":"Tsai","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Colorado School of Medicine, Denver 80262."}]},{"given":"H. L.","family":"Choong","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Colorado School of Medicine, Denver 80262."}]},{"given":"R. W.","family":"Schrier","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Colorado School of Medicine, Denver 80262."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1992.263.2.F222","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:27:17Z","timestamp":1567974437000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1992.263.2.F222"}},"issued":{"date-parts":[[1992,8,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1992,8,1]]}},"alternative-id":["10.1152\/ajprenal.1992.263.2.F222"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1992.263.2.f222","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1992,8,1]]}},{"indexed":{"date-parts":[[2026,3,25]],"date-time":"2026-03-25T18:30:21Z","timestamp":1774463421487,"version":"3.50.1"},"reference-count":13,"publisher":"American Physiological Society","issue":"12","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2014,12,15]]},"abstract":"<jats:p> The zebrafish pronephros is a well-established model to study glomerular development, structure, and function. A few methods have been described to evaluate glomerular barrier function in zebrafish larvae so far. However, there is a need to assess glomerular filtration as well. In the present study, we extended the available methods by simultaneously measuring the intravascular clearances of Alexa fluor 647-conjugated 10-kDa dextran and FITC-conjugated 500-kDa dextran as indicators of glomerular filtration and barrier function, respectively. After intravascular injection of the dextrans, mean fluorescence intensities of both dextrans were measured in the cardinal vein of living zebrafish (4 days postfertilization) by confocal microscopy over time. We demonstrated that injected 10-kDa dextran was rapidly cleared from the circulation, became visible in the lumen of the pronephric tubule, quickly accumulated in tubular cells, and was detectably excreted at the cloaca. In contrast, 500-kDa dextran could not be visualized in the tubule at any time point. To check whether alterations in glomerular function can be quantified by our method, we injected morpholino oligonucleotides (MOs) against zebrafish nonmuscle myosin heavy chain IIA (zMyh9) or apolipoprotein L1 (zApol1). While glomerular filtration was reduced in zebrafish nonmuscle myosin heavy chain IIA MO-injected larvae, glomerular barrier function remained intact. In contrast, in zebrafish apolipoprotein L1 MO-injected larvae, glomerular barrier function was compromised as 500-kDa dextran disappeared from the circulation and became visible in tubular cells. In summary, we present a novel method that allows to simultaneously assess glomerular filtration and barrier function in live zebrafish. <\/jats:p>","DOI":"10.1152\/ajprenal.00029.2014","type":"journal-article","created":{"date-parts":[[2014,10,9]],"date-time":"2014-10-09T00:24:21Z","timestamp":1412814261000},"page":"F1427-F1434","source":"Crossref","is-referenced-by-count":25,"title":["Simultaneous assessment of glomerular filtration and barrier function in live zebrafish"],"prefix":"10.1152","volume":"307","author":[{"given":"Ahmed M.","family":"Kotb","sequence":"first","affiliation":[{"name":"Department of Anatomy and Cell Biology, University Medicine Greifswald, Greifswald, Germany; and"}]},{"given":"Tobias","family":"M\u00fcller","sequence":"additional","affiliation":[{"name":"Department of Anatomy and Cell Biology, University Medicine Greifswald, Greifswald, Germany; and"}]},{"given":"Jing","family":"Xie","sequence":"additional","affiliation":[{"name":"Department of Ophthalmic Research, Cole Eye Institute, Cleveland Clinic, Cleveland, Ohio"}]},{"given":"Bela","family":"Anand-Apte","sequence":"additional","affiliation":[{"name":"Department of Ophthalmic Research, Cole Eye Institute, Cleveland Clinic, Cleveland, Ohio"}]},{"given":"Karlhans","family":"Endlich","sequence":"additional","affiliation":[{"name":"Department of Anatomy and Cell Biology, University Medicine Greifswald, Greifswald, Germany; and"}]},{"given":"Nicole","family":"Endlich","sequence":"additional","affiliation":[{"name":"Department of Anatomy and Cell Biology, University Medicine Greifswald, Greifswald, Germany; and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/B978-0-12-384892-5.00009-8"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013020178"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1126\/science.1193032"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00009.2007"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1038\/ng.568"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/j.ydbio.2005.06.038"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2011.256"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2010.21"},{"key":"B9","volume-title":"The Zebrafish Book","author":"Westerfield M","year":"2000"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/j.stem.2007.11.002"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1186\/1471-213X-10-76"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00218.2006"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2011080776"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00029.2014","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T23:58:55Z","timestamp":1567987135000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00029.2014"}},"issued":{"date-parts":[[2014,12,15]]},"references-count":13,"journal-issue":{"issue":"12","published-print":{"date-parts":[[2014,12,15]]}},"alternative-id":["10.1152\/ajprenal.00029.2014"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00029.2014","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2014,12,15]]}},{"indexed":{"date-parts":[[2026,3,27]],"date-time":"2026-03-27T08:35:44Z","timestamp":1774600544514,"version":"3.50.1"},"reference-count":54,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2011,2]]},"abstract":"<jats:p>In autosomal recessive polycystic kidney disease (ARPKD), progressive enlargement of fluid-filled cysts is due to aberrant proliferation of tubule epithelial cells and transepithelial fluid secretion leading to extensive nephron loss and interstitial fibrosis. Congenital hepatic fibrosis associated with biliary cysts\/dilatations is the most common extrarenal manifestation in ARPKD and can lead to massive liver enlargement. Peroxisome proliferator-activated receptor \u03b3 (PPAR-\u03b3), a member of the ligand-dependent nuclear receptor superfamily, is expressed in a variety of tissues, including the kidneys and liver, and plays important roles in cell proliferation, fibrosis, and inflammation. In the current study, we determined that pioglitazone (PIO), a PPAR-\u03b3 agonist, decreases polycystic kidney and liver disease progression in the polycystic kidney rat, an orthologous model of human ARPKD. Daily treatment with 10 mg\/kg PIO for 16 wk decreased kidney weight (% of body weight), renal cystic area, serum urea nitrogen, and the number of Ki67-, pERK1\/2-, and pS6-positive cells in the kidney. There was also a decrease in liver weight (% of body weight), liver cystic area, fibrotic index, and the number of Ki67-, pERK1\/2-, pERK5-, and TGF-\u03b2-positive cells in the liver. Taken together, these data suggest that PIO inhibits the progression of polycystic kidney and liver disease in a model of human ARPKD by inhibiting cell proliferation and fibrosis. These findings suggest that PPAR-\u03b3 agonists may have therapeutic value in the treatment of the renal and hepatic manifestations of ARPKD.<\/jats:p>","DOI":"10.1152\/ajprenal.00460.2010","type":"journal-article","created":{"date-parts":[[2010,12,9]],"date-time":"2010-12-09T01:47:16Z","timestamp":1291859236000},"page":"F465-F474","source":"Crossref","is-referenced-by-count":75,"title":["PPAR-\u03b3 agonist ameliorates kidney and liver disease in an orthologous rat model of human autosomal recessive polycystic kidney disease"],"prefix":"10.1152","volume":"300","author":[{"given":"Daisuke","family":"Yoshihara","sequence":"first","affiliation":[{"name":"Education and Research Center of Animal Models for Human Diseases,"},{"name":"Division of Molecular Genetics, Institute for Comprehensive Medical Science,"}]},{"given":"Hiroki","family":"Kurahashi","sequence":"additional","affiliation":[{"name":"Division of Molecular Genetics, Institute for Comprehensive Medical Science,"}]},{"given":"Miwa","family":"Morita","sequence":"additional","affiliation":[{"name":"Education and Research Center of Animal Models for Human Diseases,"}]},{"given":"Masanori","family":"Kugita","sequence":"additional","affiliation":[{"name":"Education and Research Center of Animal Models for Human Diseases,"}]},{"given":"Yoshiyuki","family":"Hiki","sequence":"additional","affiliation":[{"name":"School of Health Sciences, Fujita Health University, Toyoake, Aichi, Japan;"}]},{"given":"Harold M.","family":"Aukema","sequence":"additional","affiliation":[{"name":"Department of Human Nutritional Sciences, University of Manitoba, Winnipeg, Manitoba, Canada; and"}]},{"given":"Tamio","family":"Yamaguchi","sequence":"additional","affiliation":[{"name":"Education and Research Center of Animal Models for Human Diseases,"},{"name":"The Kidney Institute, University of Kansas Medical Center, Kansas City, Kansas"}]},{"given":"James P.","family":"Calvet","sequence":"additional","affiliation":[{"name":"The Kidney Institute, University of Kansas Medical Center, Kansas City, Kansas"}]},{"given":"Darren P.","family":"Wallace","sequence":"additional","affiliation":[{"name":"The Kidney Institute, University of Kansas Medical Center, Kansas City, Kansas"}]},{"given":"Shizuko","family":"Nagao","sequence":"additional","affiliation":[{"name":"Education and Research Center of Animal Models for Human Diseases,"},{"name":"The Kidney Institute, University of Kansas Medical Center, Kansas City, Kansas"}]}],"member":"24","reference":[{"key":"B1","first-page":"25","volume":"6","author":"Blanquicett C","year":"2008","journal-title":"Cancer Ther"},{"key":"B2","doi-asserted-by":"crossref","first-page":"1767","DOI":"10.1681\/ASN.V1191767","volume":"11","author":"Chauveau D","year":"2000","journal-title":"J Am Soc Nephrol"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1042\/CS20100113"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/j.vph.2009.05.001"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.01259-08"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.15.8806"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.30.18779"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfn744"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2009.147"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00242.x"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200205000-00007"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1097\/HJH.0b013e328302f0f7"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1038\/labinvest.2008.104"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1210\/jc.2009-0517"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M505649200"},{"key":"B16","doi-asserted-by":"crossref","first-page":"415","DOI":"10.1124\/mol.106.022954","volume":"70","author":"Lee SJ","year":"2006","journal-title":"Mol Pharmacol"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)63427-X"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1002\/hep.21199"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/11.15.1731"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00755.x"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006030251"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002629"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1002\/hep.1840400413"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M805890200"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1053\/jhep.2003.50006"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007050626"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1159\/000242432"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfq384"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)62231-6"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2007.070337"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa0907419"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/ddn039"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0509694103"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009040421"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1053\/j.gastro.2009.09.005"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1016\/j.metabol.2004.06.016"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004080660"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.94.1.237"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2009.128"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1007\/s00247-008-1064-x"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1797.2007.00811.x"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfi181"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M910452199"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa1003491"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000113793.12558.1D"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.00072-07"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004121090"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1038\/ng833"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMe1006925"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00023.x"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(97)90496-0"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1746.2008.05370.x"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2010.250"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1016\/j.bjps.2009.06.032"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00460.2010","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,11,14]],"date-time":"2021-11-14T23:44:47Z","timestamp":1636933487000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00460.2010"}},"issued":{"date-parts":[[2011,2]]},"references-count":54,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2011,2]]}},"alternative-id":["10.1152\/ajprenal.00460.2010"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00460.2010","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2011,2]]}},{"indexed":{"date-parts":[[2026,3,26]],"date-time":"2026-03-26T22:40:53Z","timestamp":1774564853742,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1994,10,1]]},"abstract":"<jats:p> The endosomal pathway of the rat renal cortex was labeled by intravenous infusion of fluorescent dextran small enough to cross the glomerular ultrafiltration barrier and be taken up by luminal endocytosis. A fraction containing entrapped fluorescein was isolated from a cortical homogenate after differential centrifugation and Percoll density gradient centrifugation. This fraction has been dubbed heavy endosomes. To our surprise, small-particle flow cytometry techniques demonstrated that heavy endosomes are homogeneous for entrapped fluorescein dextran and the presence of H(+)-adenosinetriphosphatase activity. The abundance of heavy endosomes, combined with the findings that true endosomal populations are identifiable in other renal cortical fractions, led us to test whether heavy endosomes had the attributes of intermicrovillar clefts. First, we tested whether heavy endosomes vesiculate in vivo or in vitro. Vesicle-by-vesicle flow cytometry analysis of uptake of fluorescein dextran added to the homogenate demonstrated that virtually all the vesicles form in vitro (99 +\/- 2%, n = 4). Second, the fraction contains markers associated with intermicrovillar clefts: clathrin light chains, actin, glycoprotein gp280, and gp330, the \"Heymann antigen.\" The presence of the brush border enzyme markers gamma-glutamyl transpeptidase and leucine aminopeptidase in &gt; 99% of the heavy endosomes confirms that the vesicles are of apical origin. The activity of the enzymes colocalized with entrapped markers but was tenfold less than in brush-border membrane vesicles. Heavy endosomes isolated from the rat renal cortex vesiculate in vitro and contain several intermicrovillar markers. <\/jats:p>","DOI":"10.1152\/ajprenal.1994.267.4.f516","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T23:37:30Z","timestamp":1513985850000},"page":"F516-F527","source":"Crossref","is-referenced-by-count":8,"title":["Heavy endosomes isolated from the rat renal cortex show attributes of intermicrovillar clefts"],"prefix":"10.1152","volume":"267","author":[{"given":"T. G.","family":"Hammond","sequence":"first","affiliation":[{"name":"University of Wisconsin Hospitals and Clinics, William S. MiddletonMemorial Veterans Affairs Hospital, Madison 53792."}]},{"given":"P. J.","family":"Verroust","sequence":"additional","affiliation":[{"name":"University of Wisconsin Hospitals and Clinics, William S. MiddletonMemorial Veterans Affairs Hospital, Madison 53792."}]},{"given":"R. R.","family":"Majewski","sequence":"additional","affiliation":[{"name":"University of Wisconsin Hospitals and Clinics, William S. MiddletonMemorial Veterans Affairs Hospital, Madison 53792."}]},{"given":"K. E.","family":"Muse","sequence":"additional","affiliation":[{"name":"University of Wisconsin Hospitals and Clinics, William S. MiddletonMemorial Veterans Affairs Hospital, Madison 53792."}]},{"given":"T. D.","family":"Oberley","sequence":"additional","affiliation":[{"name":"University of Wisconsin Hospitals and Clinics, William S. MiddletonMemorial Veterans Affairs Hospital, Madison 53792."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1994.267.4.F516","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:55:25Z","timestamp":1567958125000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1994.267.4.F516"}},"issued":{"date-parts":[[1994,10,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1994,10,1]]}},"alternative-id":["10.1152\/ajprenal.1994.267.4.F516"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1994.267.4.f516","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1994,10,1]]}},{"indexed":{"date-parts":[[2026,3,25]],"date-time":"2026-03-25T14:48:47Z","timestamp":1774450127354,"version":"3.50.1"},"reference-count":32,"publisher":"American Physiological Society","issue":"5","funder":[{"name":"Southern Arizona VA Health Care System"},{"DOI":"10.13039\/100007899","name":"University of Arizona","doi-asserted-by":"crossref","id":[{"id":"10.13039\/100007899","id-type":"DOI","asserted-by":"crossref"}]},{"name":"NIH","award":["5T32ES00709137"],"award-info":[{"award-number":["5T32ES00709137"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2020,11,1]]},"abstract":"<jats:p> Diabetes is a prevalent metabolic disease that contributes to \u223c50% of all end-stage renal disease and has limited treatment options. We previously demonstrated that the \u03b2<jats:sub>2<\/jats:sub>-adrenergic receptor agonist formoterol induced mitochondrial biogenesis and promoted recovery from acute kidney injury. Here, we assessed the effects of formoterol on mitochondrial dysfunction and dynamics in renal proximal tubule cells (RPTCs) treated with high glucose and in a mouse model of type 2 diabetes. RPTCs exposed to 17 mM glucose exhibited increased electron transport chain (ETC) complex I, II, III, and V protein levels and reduced ATP levels and uncoupled oxygen consumption rate compared with RPTCs cultured in the absence of glucose or osmotic controls after 96 h. ETC proteins, ATP, and oxygen consumption rate were restored in RPTCs treated with formoterol. RPTCs exposed to high glucose had increased phospho-dynamin-related protein 1 (Drp1), a mitochondrial fission protein, and decreased mitofusin 1 (Mfn1), a mitochondrial fusion protein. Formoterol treatment restored phospho-Drp1 and Mfn1 to control levels. Db\/ db and nondiabetic ( db\/m) mice (10 wk old) were treated with formoterol or vehicle for 3 wk and euthanized. Db\/ db mice showed increased renal cortical ETC protein levels in complexes I, III, and V and decreased ATP; these changes were prevented by formoterol. Phospho-Drp1 was increased and Mfn1 was decreased in db\/ db mice, and formoterol restored both to control levels. Together, these findings demonstrate that hyperglycemic conditions in vivo and exposure of RPTCs to high glucose similarly alter mitochondrial bioenergetic and dynamics profiles and that treatment with formoterol can reverse these effects. Formoterol may be a promising strategy for treating early stages of diabetic kidney disease. <\/jats:p>","DOI":"10.1152\/ajprenal.00427.2020","type":"journal-article","created":{"date-parts":[[2020,9,21]],"date-time":"2020-09-21T10:50:42Z","timestamp":1600685442000},"page":"F773-F779","source":"Crossref","is-referenced-by-count":38,"title":["Regulation of mitochondrial dynamics and energetics in the diabetic renal proximal tubule by the \u03b2<sub>2<\/sub>-adrenergic receptor agonist formoterol"],"prefix":"10.1152","volume":"319","author":[{"given":"Kristan H.","family":"Cleveland","sequence":"first","affiliation":[{"name":"Department of Pharmacology and Toxicology, College of Pharmacy, University of Arizona, Tucson, Arizona"}]},{"suffix":"III","given":"Frank C.","family":"Brosius","sequence":"additional","affiliation":[{"name":"Department of Medicine, College of Medicine, University of Arizona, Tucson, Arizona"},{"name":"Departments of Internal Medicine and Molecular and Integrative Physiology, University of Michigan, Ann Arbor, Michigan"}]},{"given":"Rick G.","family":"Schnellmann","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, College of Pharmacy, University of Arizona, Tucson, Arizona"},{"name":"Southern Arizona Veterans Affairs Health Care System, Tucson, Arizona"},{"name":"Southwest Environmental Health Science Center, University of Arizona, Tucson, Arizona"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1111\/nep.13584"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2019.03.023"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2015101096"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/j.ab.2010.04.040"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2017.107"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.059002515.x"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1172\/JCI37829"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.118.252833"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2011.356"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/j.redox.2016.09.007"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1007\/164_2016_6"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1007\/BF00515567"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2018.9"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/j.molmet.2019.10.005"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2017.05.034"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1172\/JCI127277"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.2337\/db16-0796"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.2337\/db05-1438"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013090952"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.33594\/000000011"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1172\/JCI73943"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/j.ijcard.2010.10.078"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1016\/j.jfma.2018.02.007"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1038\/nrm3877"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2017.02.013"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1995.268.4.C1053"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1038\/embor.2012.132"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1172\/jci.insight.86976"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.3390\/diseases5010001"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00809.2010"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.112.191528"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014050457"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00427.2020","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2020,10,13]],"date-time":"2020-10-13T13:22:29Z","timestamp":1602595349000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00427.2020"}},"issued":{"date-parts":[[2020,11,1]]},"references-count":32,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2020,11,1]]}},"alternative-id":["10.1152\/ajprenal.00427.2020"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00427.2020","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2020,11,1]]}},{"indexed":{"date-parts":[[2026,3,25]],"date-time":"2026-03-25T21:35:41Z","timestamp":1774474541707,"version":"3.50.1"},"reference-count":50,"publisher":"American Physiological Society","issue":"1","funder":[{"name":"NIH","award":["R01HL134711"],"award-info":[{"award-number":["R01HL134711"]}]},{"name":"NIH","award":["R01HL137673"],"award-info":[{"award-number":["R01HL137673"]}]},{"DOI":"10.13039\/100000968","name":"American Heart Association","doi-asserted-by":"publisher","award":["20PRE35120561"],"award-info":[{"award-number":["20PRE35120561"]}],"id":[{"id":"10.13039\/100000968","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2020,7,1]]},"abstract":"<jats:p> Thirty-seven million people in the United States are estimated to have chronic kidney disease (CKD). Hypertension (HTN) is the second leading risk factor for developing kidney disease. A recent study reported that increasing levels of \u03b2-hydroxybutyrate levels by administration of its precursor, 1,3-butanediol, decreased salt-induced HTN in male Dahl salt-sensitive (S) rats. The effect of 1,3-butanediol on hypertensive kidney disease in female rats or the absence of high salt has not been investigated. This study tested the hypothesis that 1,3-butanediol attenuates HTN and the progression of CKD in female S-SHR(11) rats. The S-SHR(11) strain is a congenic rat strain generated from genetic modification of the Dahl S rat, previously characterized as a model of accelerated renal disease. Rats received 1,3-butanediol (20% via drinking water) or control for 10 wk and were maintained on a 0.3% NaCl rodent diet ( n = 12\u201314 rats\/group). Blood pressure was measured after 6 and 9 wk of treatment by tail-cuff plethysmography; after 10 wk, urine and tissues were collected. Activity of the treatment was confirmed by measuring plasma \u03b2-hydroxybutyrate levels, which were greater in the treated group. The 1,3-butanediol-treated group had lower systolic blood pressure, proteinuria, plasma creatinine, and renal fibrosis after 9 wk of treatment compared with controls. The treated group had significantly smaller spleens and increased the renal anti-inflammatory molecules interleukin-10 and granulocyte-macrophage colony-stimulating factor, suggesting reduced inflammation. The present data demonstrate that 1,3-butanediol lowers blood pressure and renal injury in female rats and could be a novel nutritional intervention for the treatment of CKD. <\/jats:p>","DOI":"10.1152\/ajprenal.00141.2020","type":"journal-article","created":{"date-parts":[[2020,6,8]],"date-time":"2020-06-08T09:42:47Z","timestamp":1591609367000},"page":"F106-F114","source":"Crossref","is-referenced-by-count":22,"title":["1,3-Butanediol attenuates hypertension and suppresses kidney injury in female rats"],"prefix":"10.1152","volume":"319","author":[{"given":"Jeanne A.","family":"Ishimwe","sequence":"first","affiliation":[{"name":"Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi"}]},{"given":"Michael R.","family":"Garrett","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7161-5502","authenticated-orcid":false,"given":"Jennifer M.","family":"Sasser","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1007\/s11064-016-2099-2"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1159\/000368940"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0126364"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(96)90512-0"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/0031-9384(83)90038-0"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/j.celrep.2018.09.058"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2017.05.184"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1007\/s40292-015-0096-1"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00646.2012"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.3390\/nu10030261"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1007\/s11892-015-0625-2"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.00453.2013"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1053\/j.ackd.2012.12.007"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/j.matbio.2017.12.013"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.00539.2010"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.3390\/nu10060732"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/j.celrep.2017.02.004"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1161\/JAHA.116.005066"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014060612"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(04)01080-7"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005010063"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1007\/s00395-017-0622-5"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.7326\/M17-2640"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1089\/neu.2017.5192"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1111\/jcmm.14984"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000054"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/j.neulet.2018.06.016"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1053\/j.jrn.2016.03.001"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.7326\/M16-0273"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/s0009-9120(81)90789-x"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1016\/j.seizure.2014.02.015"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.118.036459"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1016\/j.mpmed.2019.06.010"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1038\/hr.2012.157"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1038\/ncomms4944"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005121319"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1152\/physiolgenomics.00015.2012"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.09221.x"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1002\/oby.22468"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006030208"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.13.5_Suppl.I80"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1002\/jbm.a.34902"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1038\/s41581-019-0110-2"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00616.2018"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1155\/2019\/8681959"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfw058"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-017-08055-1"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1038\/nm.3804"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1186\/s12882-019-1586-5"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.5455\/medarh.2016.70.191-192"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00141.2020","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2020,7,6]],"date-time":"2020-07-06T13:26:36Z","timestamp":1594041996000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00141.2020"}},"issued":{"date-parts":[[2020,7,1]]},"references-count":50,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2020,7,1]]}},"alternative-id":["10.1152\/ajprenal.00141.2020"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00141.2020","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2020,7,1]]}},{"indexed":{"date-parts":[[2026,3,25]],"date-time":"2026-03-25T22:01:34Z","timestamp":1774476094452,"version":"3.50.1"},"reference-count":76,"publisher":"American Physiological Society","issue":"4","funder":[{"DOI":"10.13039\/501100006065","name":"Western Australia Department of Health","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100006065","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000925","name":"Department of Health, Australian Government | National Health and Medical Research Council","doi-asserted-by":"publisher","award":["GNT606601"],"award-info":[{"award-number":["GNT606601"]}],"id":[{"id":"10.13039\/501100000925","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000925","name":"Department of Health, Australian Government | National Health and Medical Research Council","doi-asserted-by":"publisher","award":["GNT1122455"],"award-info":[{"award-number":["GNT1122455"]}],"id":[{"id":"10.13039\/501100000925","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2021,10,1]]},"abstract":"<jats:p> Measurement of bladder urine oxygen tension has been proposed as a new method to potentially detect the risk of acute kidney injury in patients. A computational model of oxygen exchange between urine bolus and ureteral tissue shows that it may be technically possible to determine the risk of acute kidney injury based on the measurement of bladder urine oxygen tension, provided that the measurement data are properly interpreted via a computational model. <\/jats:p>","DOI":"10.1152\/ajprenal.00122.2021","type":"journal-article","created":{"date-parts":[[2021,8,30]],"date-time":"2021-08-30T11:59:47Z","timestamp":1630324787000},"page":"F527-F547","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":12,"title":["Predicting oxygen tension along the ureter"],"prefix":"10.1152","volume":"321","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9360-0923","authenticated-orcid":true,"given":"Chang-Joon","family":"Lee","sequence":"first","affiliation":[{"name":"College of Science, Health, Engineering and Education, Murdoch University, Perth, Western Australia, Australia"},{"name":"Faculty of Engineering and Mathematical Sciences, The University of Western Australia, Perth, Western Australia, Australia"}]},{"given":"Bruce S.","family":"Gardiner","sequence":"additional","affiliation":[{"name":"College of Science, Health, Engineering and Education, Murdoch University, Perth, Western Australia, Australia"},{"name":"Faculty of Engineering and Mathematical Sciences, The University of Western Australia, Perth, Western Australia, Australia"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9241-0757","authenticated-orcid":true,"given":"Roger G.","family":"Evans","sequence":"additional","affiliation":[{"name":"Cardiovascular Disease Program, Biomedicine Discovery Institute and Department of Physiology, Monash University, Melbourne, Victoria, Australia"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4864-0288","authenticated-orcid":true,"given":"David W.","family":"Smith","sequence":"additional","affiliation":[{"name":"Faculty of Engineering and Mathematical Sciences, The University of Western Australia, Perth, Western Australia, Australia"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.00710113"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1111\/1440-1681.12031"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1111\/1440-1681.12036"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00315.2019"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00437.2013"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1111\/apha.12995"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/s1053-0770(96)80137-6"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1097\/00000542-196509000-00010"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00195.2016"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1111\/apha.13294"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1002\/jmri.21567"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1148\/radiology.180.2.2068307"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1016\/1056-8719(96)00045-7"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1115\/1.3168367"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/nips.1416.2002"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/s0022-5347(17)58986-7"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.26.1.25"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1089\/end.1996.10.527"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1080\/10255842.2012.761692"},{"key":"B20","volume-title":"Clinical Methods: the History, Physical, and Laboratory Examinations","author":"Billett H","year":"1990"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00363.2018"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1540\/jsmr1965.21.455"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1620\/tjem.146.273"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.2214\/ajr.158.5.1566665"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1016\/s0022-5347(17)45338-9"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00515.2014"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1955.sp005368"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1002\/ar.1092420107"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00659.2016"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/B978-0-12-121250-6.50020-4"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1111\/j.1464-410X.2007.07207.x"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1016\/j.jbiomech.2016.11.067"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1016\/j.jrid.2015.06.006"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1016\/j.jtbi.2011.12.019"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(17)32647-2"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1985.tb07577.x"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1016\/0016-5085(85)90583-9"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1016\/0026-2862(88)90082-9"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1987.252.1.C88"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1007\/BF00926832"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1177\/1756287216675778"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1979.236.5.F423"},{"key":"B43","first-page":"S74","volume":"6","author":"Bottcher W","year":"1976","journal-title":"Kidney Int Suppl"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.71.5.1153"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1161\/01.res.53.3.401"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.75.5.829"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1985.248.3.F347"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1007\/b98841"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1152\/jappl.1976.40.3.487"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1152\/jappl.1966.21.3.1108"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1152\/jappl.1987.63.3.1003"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00544.2010"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00186.2012"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1620\/tjem.97.297"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1152\/ajplegacy.1955.180.2.261"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1089\/end.2006.0161"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(05)67943-8"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1089\/end.2005.19.170"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(17)67508-6"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1111\/j.1464-410x.1989.tb05151.x"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1007\/s00240-007-0100-x"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1182\/blood.V9.10.999.999"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.14814\/phy2.13195"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.2011.05494.x"},{"key":"B65","volume-title":"Principles of Pulmonary Medicine E-Book","author":"Weinberger SE","year":"2017"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1016\/j.urology.2007.11.113"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1152\/ajplegacy.1958.195.1.120"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2008.08.033"},{"key":"B69","doi-asserted-by":"publisher","DOI":"10.1159\/000281192"},{"key":"B70","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1981.241.5.R412"},{"key":"B71","doi-asserted-by":"publisher","DOI":"10.1126\/science.151.3706.78"},{"key":"B72","doi-asserted-by":"publisher","DOI":"10.1007\/BF00498991"},{"key":"B73","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.28.1.21"},{"key":"B74","doi-asserted-by":"publisher","DOI":"10.1016\/j.compbiomed.2020.103676"},{"key":"B75","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00657.2016"},{"key":"B76","doi-asserted-by":"publisher","DOI":"10.1152\/ajplegacy.1955.180.2.261"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00122.2021","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,10,1]],"date-time":"2021-10-01T14:14:48Z","timestamp":1633097688000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00122.2021"}},"issued":{"date-parts":[[2021,10,1]]},"references-count":76,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2021,10,1]]}},"alternative-id":["10.1152\/ajprenal.00122.2021"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00122.2021","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2021,10,1]]},"assertion":[{"value":"2021-03-31","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2021-08-26","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2021-10-01","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,3,25]],"date-time":"2026-03-25T22:01:36Z","timestamp":1774476096984,"version":"3.50.1"},"reference-count":144,"publisher":"American Physiological Society","issue":"11","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2014,12,1]]},"abstract":"<jats:p>Recent clinical and animal studies have shown that acute kidney injury (AKI), even if followed by complete recovery of renal function, can eventually result in chronic kidney disease (CKD). Renal hypoxia is emerging as a key player in the pathophysiology of the AKI-to-CKD transition. Capillary rarefaction after AKI episodes induces renal hypoxia, which can in turn profoundly affect tubular epithelial cells, (myo)fibroblasts, and inflammatory cells, culminating in tubulointerstitial fibrosis, i.e., progression to CKD. Damaged tubular epithelial cells that fail to redifferentiate might supply a decreased amount of vascular endothelial growth factor and contribute to capillary rarefaction, thus aggravating hypoxia and forming a vicious cycle. Mounting evidence also shows that epigenetic changes are closely related to renal hypoxia in the pathophysiology of CKD progression. Animal experiments suggest that targeting hypoxia is a promising strategy to block the transition from AKI to CKD. However, the precise mechanisms by which hypoxia induces the AKI-to-CKD transition and by which hypoxia-inducible factor activation can exert a protective effect in this context should be clarified in further studies.<\/jats:p>","DOI":"10.1152\/ajprenal.00425.2014","type":"journal-article","created":{"date-parts":[[2014,10,2]],"date-time":"2014-10-02T07:59:08Z","timestamp":1412236748000},"page":"F1187-F1195","source":"Crossref","is-referenced-by-count":239,"title":["Hypoxia as a key player in the AKI-to-CKD transition"],"prefix":"10.1152","volume":"307","author":[{"given":"Shinji","family":"Tanaka","sequence":"first","affiliation":[{"name":"Division of Nephrology and Endocrinology, The University of Tokyo Graduate School of Medicine, Tokyo, Japan"}]},{"given":"Tetsuhiro","family":"Tanaka","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Endocrinology, The University of Tokyo Graduate School of Medicine, Tokyo, Japan"}]},{"given":"Masaomi","family":"Nangaku","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Endocrinology, The University of Tokyo Graduate School of Medicine, Tokyo, Japan"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0024695"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2009.332"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1172\/JCI57301"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.602"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000032"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002312"},{"key":"B7","doi-asserted-by":"crossref","first-page":"1303","DOI":"10.1002\/cphy.c110041","volume":"2","author":"Basile DP","year":"2012","journal-title":"Compr Physiol"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00050.2001"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00169.2002"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00596.2007"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00546.2010"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1038\/nm.2135"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1097\/01.mnh.0000441051.36783.f3"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005121302"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1172\/JCI45161"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.267.6.F1063"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199503093321006"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1992.441"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2011.405"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00163.x"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2011.42"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2012.208"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2011.208"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0307574101"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2011.379"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0033258"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00317.2011"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.09909.x"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1159\/000070698"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra0910283"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa0707330"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.57.s75.12.x"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.350"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.113.01425"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2007.10.042"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2009.080295"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1007\/BF02111656"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00241.2013"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1002\/path.1711770308"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1002\/ijc.2910610422"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1016\/j.blre.2012.12.003"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1159\/000146075"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2009.347"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006090998"},{"key":"B44a","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00452.2006"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2012030222"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2010.090517"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1016\/j.stem.2008.01.014"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010111143"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1001\/archinternmed.2010.514"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007080837"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1126\/science.1059817"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1101\/gad.12.2.149"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1126\/science.1059796"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1159\/000341870"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1016\/0891-5849(95)02221-X"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1016\/j.mrfmmm.2008.01.001"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2012.03.014"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00064.2009"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00133.2005"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00667.2011"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1172\/JCI69073"},{"key":"B63","first-page":"1089","volume":"79","author":"Khan S","year":"1999","journal-title":"Lab Invest"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2012080871"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006060639"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2009.68"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0401339101"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013101121"},{"key":"B69","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1310653110"},{"key":"B70","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00660.2011"},{"key":"B71","doi-asserted-by":"publisher","DOI":"10.1038\/nm.3218"},{"key":"B72","doi-asserted-by":"publisher","DOI":"10.2119\/2008-00006.Legrand"},{"key":"B73","doi-asserted-by":"publisher","DOI":"10.1007\/BF00305308"},{"key":"B74","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00099.2008"},{"key":"B75","doi-asserted-by":"crossref","first-page":"1336","DOI":"10.1152\/ajplegacy.1959.196.6.1336","volume":"196","author":"Levy MN","year":"1959","journal-title":"Am J Physiol"},{"key":"B76","doi-asserted-by":"publisher","DOI":"10.1016\/j.ajpath.2010.10.012"},{"key":"B77","doi-asserted-by":"publisher","DOI":"10.1007\/s004240050455"},{"key":"B78","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00697.2013"},{"key":"B79","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2009.289"},{"key":"B80","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008070712"},{"key":"B81","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2011.10.048"},{"key":"B82","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00461.x"},{"key":"B83","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000074239.22357.06"},{"key":"B84","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfq832"},{"key":"B85","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2013.321"},{"key":"B86","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2010.124"},{"key":"B87","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2013.05.009"},{"key":"B88","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M901790200"},{"key":"B89","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009010118"},{"key":"B90","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005070757"},{"key":"B91","doi-asserted-by":"publisher","DOI":"10.1007\/s00109-007-0278-y"},{"key":"B92","doi-asserted-by":"publisher","DOI":"10.1111\/1440-1681.12005"},{"key":"B93","first-page":"1","author":"Nelimarkka O","year":"1984","journal-title":"Acta Chir Scand"},{"key":"B94","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00382.2014"},{"key":"B95","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00419.x"},{"key":"B96","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00560.2006"},{"key":"B97","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00202.2014"},{"key":"B98","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.2011.05532.x"},{"key":"B99","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.140087397"},{"key":"B100","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013040359"},{"key":"B101","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002792"},{"key":"B102","doi-asserted-by":"publisher","DOI":"10.1097\/CCM.0b013e3181e61911"},{"key":"B103","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2011121185"},{"key":"B104","doi-asserted-by":"publisher","DOI":"10.1159\/000314656"},{"key":"B105","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfm808"},{"key":"B106","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.67110.x"},{"key":"B107","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000017223.49823.2A"},{"key":"B108","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006070792"},{"key":"B109","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0509459103"},{"key":"B110","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010121249"},{"key":"B110a","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2009.080687"},{"key":"B111","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00621.x"},{"key":"B112","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2011080851"},{"key":"B113","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.259.6.F910"},{"key":"B115","doi-asserted-by":"publisher","DOI":"10.1038\/ng1266"},{"key":"B116","doi-asserted-by":"crossref","first-page":"661","DOI":"10.1681\/ASN.V75661","volume":"7","author":"Shulman K","year":"1996","journal-title":"J Am Soc Nephrol"},{"key":"B117","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.268.2.F240"},{"key":"B118","doi-asserted-by":"crossref","first-page":"1032","DOI":"10.1681\/ASN.V961032","volume":"9","author":"Simon M","year":"1998","journal-title":"J Am Soc Nephrol"},{"key":"B119","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013010030"},{"key":"B120","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00279.2006"},{"key":"B121","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M112.444059"},{"key":"B122","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-291X(03)01557-2"},{"key":"B123","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00081.2005"},{"key":"B124","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2013.35"},{"key":"B125","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0b013e3283328eed"},{"key":"B126","doi-asserted-by":"publisher","DOI":"10.1096\/fj.13-231837"},{"key":"B127","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.01120211"},{"key":"B128","doi-asserted-by":"publisher","DOI":"10.1101\/gad.12.21.3320"},{"key":"B129","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00017.2010"},{"key":"B130","doi-asserted-by":"publisher","DOI":"10.1016\/j.amjmed.2012.01.016"},{"key":"B131","doi-asserted-by":"publisher","DOI":"10.1001\/jama.2009.1322"},{"key":"B132","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfr379"},{"key":"B133","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007040419"},{"key":"B134","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00483.x"},{"key":"B135","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00475.2005"},{"key":"B136","doi-asserted-by":"publisher","DOI":"10.1096\/fj.02-0445fje"},{"key":"B137","doi-asserted-by":"publisher","DOI":"10.1038\/nm.2144"},{"key":"B138","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejrad.2011.03.045"},{"key":"B139","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfr754"},{"key":"B140","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)63586-9"},{"key":"B141","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gft101"},{"key":"B142","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00061.2009"},{"key":"B143","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2013.157"},{"key":"B144","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00431.2011"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00425.2014","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,4,18]],"date-time":"2022-04-18T18:18:14Z","timestamp":1650305894000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00425.2014"}},"issued":{"date-parts":[[2014,12,1]]},"references-count":144,"journal-issue":{"issue":"11","published-print":{"date-parts":[[2014,12,1]]}},"alternative-id":["10.1152\/ajprenal.00425.2014"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00425.2014","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2014,12,1]]}},{"indexed":{"date-parts":[[2026,3,30]],"date-time":"2026-03-30T15:04:39Z","timestamp":1774883079825,"version":"3.50.1"},"reference-count":58,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2005,11]]},"abstract":"<jats:p> Acute regulation of epithelial sodium channel (ENaC) function at the apical surface of polarized kidney cortical collecting duct (CCD) epithelial cells occurs in large part by changes in channel number, mediated by membrane vesicle trafficking. Several soluble N-ethyl-maleimide-sensitive factor attachment protein receptors (SNARE) have been implicated in this process. A novel SNARE-binding protein, complexin, has been identified in nervous tissue which specifically binds to and stabilizes SNARE complexes at synaptic membranes to promote vesicle fusion. To test whether this protein is present in mouse CCD (mCCD) cells and its possible involvement in acute ENaC regulation, we cloned complexin (isoform II) from a mouse kidney cDNA library. Complexin II mRNA coexpressed with \u03b1-, \u03b2-, and \u03b3-ENaC subunits in Xenopus laevis oocytes reduced sodium currents to 16 \u00b1 3% ( n = 19) of control values. Short-circuit current ( I<jats:sub>sc<\/jats:sub>) measurements on mCCD cell lines stably over- or underexpressing complexin produced similar results. Basal I<jats:sub>sc<\/jats:sub> was reduced from 12.0 \u00b1 1.0 ( n = 15) to 2.0 \u00b1 0.4 ( n = 15) and 1.8 \u00b1 0.3 ( n = 17) \u03bcA\/cm<jats:sup>2<\/jats:sup>, respectively. Similarly forskolin-stimulated I<jats:sub>sc<\/jats:sub> was reduced from control values of 20.0 \u00b1 2 to 2.7 \u00b1 0.5 and 2.3 \u00b1 0.4 \u03bcA\/cm<jats:sup>2<\/jats:sup> by either increasing or decreasing complexin expression. Surface biotinylation demonstrated that the complexin-induced reduction in basal I<jats:sub>sc<\/jats:sub>was due to a reduction in apical membrane-resident ENaC and the inhibition in forskolin stimulation was due to the lack of ENaC insertion into the apical membrane to increase surface channel number. Immunofluorescent localization of SNARE proteins in polarized mCCD epithelia detected the presence of syntaxins 1 and 3 and synaptosomal-associated protein of 23 kDa (SNAP-23) at the apical membrane, and vesicle-associated membrane protein (VAMP2) was localized to intracellular compartments. These findings identify SNAREs that may mediate ENaC-containing vesicle insertion in mCCD epithelia and suggest that stabilization of SNARE interactions by complexin is an essential aspect of the regulated trafficking events that increase apical membrane ENaC density either by constitutive or regulated trafficking pathways. <\/jats:p>","DOI":"10.1152\/ajprenal.00390.2003","type":"journal-article","created":{"date-parts":[[2005,6,22]],"date-time":"2005-06-22T00:44:30Z","timestamp":1119401070000},"page":"F969-F977","source":"Crossref","is-referenced-by-count":42,"title":["PKA-dependent ENaC trafficking requires the SNARE-binding protein complexin"],"prefix":"10.1152","volume":"289","author":[{"given":"M. B.","family":"Butterworth","sequence":"first","affiliation":[]},{"given":"R. A.","family":"Frizzell","sequence":"additional","affiliation":[]},{"given":"J. P.","family":"Johnson","sequence":"additional","affiliation":[]},{"given":"K. W.","family":"Peters","sequence":"additional","affiliation":[]},{"given":"R. S.","family":"Edinger","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.01041"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI5713"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1007\/BF00232519"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M203460200"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.200409124"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.2001.280.4.C752"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.130.5.1063"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1016\/S0896-6273(02)00583-4"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1038\/35052017"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M210772200"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M313592200"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00091.2003"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1006\/exnr.2001.7775"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1097-0029(19980301)40:6<455::AID-JEMT5>3.0.CO;2-O"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1007\/s004240050898"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1042\/bj3450503"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1016\/S0167-4889(03)00090-9"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/17.2.344"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.93.26.15370"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1997.77.2.359"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1042\/bj20021375"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.45.30012"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1210\/jcem-73-5-936"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1254\/jjp.84.179"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1995.2241"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1016\/S0306-4522(98)00223-1"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1999.1756"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(03)00112-0"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.biochem.68.1.863"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00007.2002"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00366.2001"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M403923200"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00185.2002"},{"key":"R34","unstructured":"Liddle GW, Bledsoe T, and Coppage WS. A familial renal disorder simulating primary aldosteronism but with negligible aldosterone secretion. Trans Assoc Am Physicians 76: 199\u2013213, 1963."},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.141.7.1503"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M010626200"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(95)90239-2"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.20018547"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M002571200"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M109507200"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.ph.54.030192.000411"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.43.30345"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(01)00192-1"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.20028638"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.64.082101.143243"},{"key":"R46","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.30.20812"},{"key":"R47","doi-asserted-by":"publisher","DOI":"10.1016\/S0896-6273(00)81177-0"},{"key":"R48","doi-asserted-by":"publisher","DOI":"10.1210\/edrv.23.2.0458"},{"key":"R49","doi-asserted-by":"publisher","DOI":"10.1080\/0968768031000104953"},{"key":"R50","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00919.x"},{"key":"R51","doi-asserted-by":"publisher","DOI":"10.1016\/S0167-4889(03)00095-8"},{"key":"R52","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1996.271.6.C1887"},{"key":"R53","doi-asserted-by":"publisher","DOI":"10.1046\/j.1460-9568.1999.00652.x"},{"key":"R54","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(95)00713-J"},{"key":"R55","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(01)00229-X"},{"key":"R56","doi-asserted-by":"publisher","DOI":"10.1038\/25069"},{"key":"R57","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.E02-11-0720"},{"key":"R58","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M003822200"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00390.2003","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T23:10:52Z","timestamp":1567984252000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00390.2003"}},"issued":{"date-parts":[[2005,11]]},"references-count":58,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2005,11]]}},"alternative-id":["10.1152\/ajprenal.00390.2003"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00390.2003","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2005,11]]}},{"indexed":{"date-parts":[[2026,4,6]],"date-time":"2026-04-06T14:35:59Z","timestamp":1775486159805,"version":"3.50.1"},"reference-count":43,"publisher":"American Physiological Society","issue":"3","funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81770702"],"award-info":[{"award-number":["81770702"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81670470"],"award-info":[{"award-number":["81670470"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100003399","name":"Science and Technology Commission of Shanghai Municipality","doi-asserted-by":"publisher","award":["18XD1403100"],"award-info":[{"award-number":["18XD1403100"]}],"id":[{"id":"10.13039\/501100003399","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100003399","name":"Science and Technology Commission of Shanghai Municipality","doi-asserted-by":"publisher","award":["20140900201"],"award-info":[{"award-number":["20140900201"]}],"id":[{"id":"10.13039\/501100003399","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2021,3,1]]},"abstract":"<jats:p> Primary hyperoxaluria type 1 is a severe inherited disorder that results in recurrent urolithiasis and renal failure. We generated an alanine-glyoxylate aminotransferase ( Agxt) <jats:sup>Q84X<\/jats:sup> nonsense mutant rat model that displayed an early onset of hyperoxaluria, spontaneous renal CaOx precipitation, bladder stone, and kidney injuries. Our results suggest an interaction of renal CaOx crystals with the activation of inflammation-, fibrosis-, and necroptosis-related pathways. In all, the Agxt<jats:sup>Q84X<\/jats:sup> rat strain has broad applicability in mechanistic studies and the development of innovative therapeutics. <\/jats:p>","DOI":"10.1152\/ajprenal.00514.2020","type":"journal-article","created":{"date-parts":[[2021,1,25]],"date-time":"2021-01-25T11:24:20Z","timestamp":1611573860000},"page":"F475-F484","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":8,"title":["Generation and characterization of a novel rat model of primary hyperoxaluria type 1 with a nonsense mutation in alanine-glyoxylate aminotransferase gene"],"prefix":"10.1152","volume":"320","author":[{"given":"Yueyan","family":"Li","sequence":"first","affiliation":[{"name":"Department of Pediatric Urology, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, People\u2019s Republic of China"},{"name":"Children's Stone Treatment Center of National Health and Family Planning Commission of the People's Republic of China, Shanghai, People\u2019s Republic of China"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4446-8724","authenticated-orcid":false,"given":"Rui","family":"Zheng","sequence":"additional","affiliation":[{"name":"Department of Pediatric Urology, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, People\u2019s Republic of China"},{"name":"Children's Stone Treatment Center of National Health and Family Planning Commission of the People's Republic of China, Shanghai, People\u2019s Republic of China"}]},{"given":"Guofeng","family":"Xu","sequence":"additional","affiliation":[{"name":"Department of Pediatric Urology, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, People\u2019s Republic of China"},{"name":"Children's Stone Treatment Center of National Health and Family Planning Commission of the People's Republic of China, Shanghai, People\u2019s Republic of China"}]},{"given":"Yunteng","family":"Huang","sequence":"additional","affiliation":[{"name":"Children's Stone Treatment Center of National Health and Family Planning Commission of the People's Republic of China, Shanghai, People\u2019s Republic of China"},{"name":"Department of Urology, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, People\u2019s Republic of China"}]},{"given":"Yongmei","family":"Li","sequence":"additional","affiliation":[{"name":"Shanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai, People\u2019s Republic of China"}]},{"given":"Dali","family":"Li","sequence":"additional","affiliation":[{"name":"Shanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai, People\u2019s Republic of China"}]},{"given":"Hongquan","family":"Geng","sequence":"additional","affiliation":[{"name":"Department of Pediatric Urology, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, People\u2019s Republic of China"},{"name":"Children's Stone Treatment Center of National Health and Family Planning Commission of the People's Republic of China, Shanghai, People\u2019s Republic of China"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1517\/13543784.2013.741587"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2012.113"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1007\/s00345-018-2563-5"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014070698"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMicm1609986"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.07430711"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.4103\/1319-2442.160216"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0607218103"},{"key":"B9","first-page":"59","volume":"107","author":"Khan SR","year":"1982","journal-title":"Am J Pathol"},{"key":"B10","first-page":"707","volume":"5","author":"Khan SR","year":"1991","journal-title":"Scanning Microsc"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1038\/nbt.2661"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1038\/nprot.2014.171"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1007\/s13238-018-0568-x"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.2174\/1566524019666181212092440"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2020.04.049"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2014.222"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-8993(02)02933-5"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1177\/12.5.333"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.V10112323"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/S0021-9258(19)39143-4"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbadis.2019.04.017"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbamcr.2006.08.021"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1159\/000086357"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM195812042592302"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1136\/adc.35.179.108"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfy239"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1038\/ncomms10274"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2015111271"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/j.juro.2012.04.103"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1172\/JCI128503"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2016040486"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1038\/mt.2015.224"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1038\/s41467-018-07827-1"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1002\/ctm2.261"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfr776"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1038\/mt.2016.4"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1016\/j.ymthe.2018.05.016"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2016030338"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1038\/nature24644"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1038\/nature17946"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1038\/s41587-019-0178-z"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1210\/endo-74-1-128"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(01)61992-X"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00514.2020","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,8,24]],"date-time":"2021-08-24T17:34:52Z","timestamp":1629826492000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00514.2020"}},"issued":{"date-parts":[[2021,3,1]]},"references-count":43,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2021,3,1]]}},"alternative-id":["10.1152\/ajprenal.00514.2020"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00514.2020","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2021,3,1]]},"assertion":[{"value":"2020-09-29","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2021-01-13","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2021-01-14","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2021-03-12","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,4,8]],"date-time":"2026-04-08T01:58:54Z","timestamp":1775613534394,"version":"3.50.1"},"reference-count":27,"publisher":"American Physiological Society","issue":"1","funder":[{"name":"Innovation of science and technology, Fujian province, China","award":["2016Y9012"],"award-info":[{"award-number":["2016Y9012"]}]},{"name":"Natrual science foundation of Fujian province, China","award":["2016J01451"],"award-info":[{"award-number":["2016J01451"]}]},{"name":"Natrual science foundation of Guangdong province, China","award":["2016A030310389"],"award-info":[{"award-number":["2016A030310389"]}]},{"name":"Natrual science foundation of Guangdong province, China","award":["2016A030313561"],"award-info":[{"award-number":["2016A030313561"]}]},{"name":"Medical scientific research foundation of Guangdong province, China","award":["A2016068"],"award-info":[{"award-number":["A2016068"]}]},{"name":"Outstanding youths development scheme of Nanfang Hospital, Southern Medical University","award":["2016J011"],"award-info":[{"award-number":["2016J011"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2019,1,1]]},"abstract":"<jats:p> Sepsis is the leading cause of death in the intensive care unit and continues to lack effective treatment. It is widely accepted that high-mobility group box 1 (HMGB1) is a key inflammatory mediator in the pathogenesis of sepsis. Moreover, some studies indicate that the functions of HMGB1 depend on its molecular localization and posttranslational modifications. Our previous study confirms that sirtuin 1, silent information regulator 2-related enzyme 1 (SIRT1), a type III deacetylase, can ameliorate sepsis-associated acute kidney injury (SA-AKI). We explored the effect and mechanism of SIRT1 on HMGB1 using a mouse model of cecal ligation and puncture-induced sepsis and LPS-treated human kidney (HK-2) cell line. We found that HMGB1 is elevated in the serum but is gradually reduced in kidney cells in the later stages of septic mice. The acetylation modification of HMGB1 is a key process before its nucleus-to-cytoplasm translocation and extracellular secretion in kidney cells, accelerating the development of SA-AKI. Moreover, SIRT1 can physically interact with HMGB1 at the deacetylated lysine sites K28, K29, and K30, subsequently suppressing downstream inflammatory signaling. Thus the SIRT1-HMGB1 signaling pathway is a crucial mechanism in the development of SA-AKI and presents a novel experimental perspective for future SA-AKI research. <\/jats:p>","DOI":"10.1152\/ajprenal.00119.2018","type":"journal-article","created":{"date-parts":[[2018,10,31]],"date-time":"2018-10-31T14:33:08Z","timestamp":1540996388000},"page":"F20-F31","source":"Crossref","is-referenced-by-count":117,"title":["SIRT1-mediated HMGB1 deacetylation suppresses sepsis-associated acute kidney injury"],"prefix":"10.1152","volume":"316","author":[{"given":"Siwei","family":"Wei","sequence":"first","affiliation":[{"name":"Department of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Baiyun District, Guangzhou, Guangdong, China"},{"name":"Guangdong Provincial Key Laboratory of Shock and Microcirculation, School of Basic Medical Sciences, Southern Medical University, Baiyun District, Guangzhou, Guangdong, China"}]},{"given":"Youguang","family":"Gao","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian, China"}]},{"given":"Xingui","family":"Dai","sequence":"additional","affiliation":[{"name":"The First People's Hospital of Chenzhou, Department of Critical Care Medicine, Institute of Translational Medicine, Chenzhou, Hunan, China"}]},{"given":"Weijun","family":"Fu","sequence":"additional","affiliation":[{"name":"Department of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Baiyun District, Guangzhou, Guangdong, China"}]},{"given":"Shumin","family":"Cai","sequence":"additional","affiliation":[{"name":"Department of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Baiyun District, Guangzhou, Guangdong, China"}]},{"given":"Haihong","family":"Fang","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology, Nanfang Hospital, Southern Medical University, Baiyun District, Guangzhou, Guangdong, China"}]},{"given":"Zhenhua","family":"Zeng","sequence":"additional","affiliation":[{"name":"Department of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Baiyun District, Guangzhou, Guangdong, China"},{"name":"Guangdong Provincial Key Laboratory of Shock and Microcirculation, School of Basic Medical Sciences, Southern Medical University, Baiyun District, Guangzhou, Guangdong, China"}]},{"given":"Zhongqing","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Baiyun District, Guangzhou, Guangdong, China"},{"name":"Guangdong Provincial Key Laboratory of Shock and Microcirculation, School of Basic Medical Sciences, Southern Medical University, Baiyun District, Guangzhou, Guangdong, China"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI37829"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2010.02.006"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1177\/09680519050110050901"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1186\/s40560-016-0146-3"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1213\/ANE.0000000000000977"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1517\/14728222.2014.883380"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1038\/ni.1699"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1016\/j.jss.2010.11.883"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1038\/srep15971"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1038\/35066006"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1189\/jlb.0211075"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1159\/000314077"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1016\/j.ajpath.2012.05.013"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2014.217"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1164\/rccm.200708-1269OC"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1158\/0008-5472.CAN-13-2620"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1001\/jama.2016.0287"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.2119\/molmed.2014.00156"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1517\/14728222.2014.863876"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1155\/2016\/7296092"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1097\/SHK.0000000000000225"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/j.immuni.2015.07.003"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1155\/2015\/965961"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1155\/2016\/1737185"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1080\/14728222.2016.1177023"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1155\/2017\/7543973"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1089\/jir.2015.0067"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00119.2018","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:55:05Z","timestamp":1567958105000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00119.2018"}},"issued":{"date-parts":[[2019,1,1]]},"references-count":27,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2019,1,1]]}},"alternative-id":["10.1152\/ajprenal.00119.2018"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00119.2018","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2019,1,1]]}},{"indexed":{"date-parts":[[2022,4,1]],"date-time":"2022-04-01T22:33:35Z","timestamp":1648852415105},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1994,9,1]]},"abstract":"<jats:p> We have previously demonstrated that basolateral addition of the gastric H-K-adenosinetriphosphatase (H-K-ATPase) inhibitor Sch-28080 (10 microM) profoundly reduced net total CO2 flux (JtCO2) in the inner stripe of the outer medullary collecting duct (OMCDi) of K-replete rabbits. In the present studies, we first addressed whether the inhibitory effect of Sch-28080 is dependent on the side of the membrane to which it is added. Second, we reassessed the relative magnitude of contribution of H-K-ATPase. Third, we formally tested whether a bafilomycin-A1 (BAF)-sensitive H-ATPase also contributes to luminal acidification in the OMCDi under K-replete dietary conditions. We found that luminal addition of the structurally and functionally dissimilar gastric H-K-ATPase inhibitor A80915A (10 microM) profoundly reduced JtCO2 while transepithelial voltage (VT) was unchanged. This degree of inhibition was statistically indistinguishable from our previous results when Sch-28080 was applied basolaterally. Inhibition of JtCO2 by the less membrane-permeable N-methyl cation of Sch-28080, H224\/25, was significant when applied luminally but was not significant when applied basolaterally. VT was not significantly affected by either the luminal or basolateral addition of H224\/25. To evaluate the possible contribution of an H-ATPase, the effect of both 5.0 nM and 10.0 nM luminal BAF on JtCO2 and VT was examined. At 5.0 nM, BAF significantly inhibited JtCO2). However, this observation was significantly less (P &lt; 0.05) than the inhibition observed with 10 microM A80915A. No additional inhibition was observed by increasing the concentration of BAF to 10.0 nM.(ABSTRACT TRUNCATED AT 250 WORDS) <\/jats:p>","DOI":"10.1152\/ajprenal.1994.267.3.f450","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T00:50:16Z","timestamp":1513990216000},"page":"F450-F458","source":"Crossref","is-referenced-by-count":13,"title":["Luminal acidification in K-replete OMCDi: contributions of H-K-ATPase and bafilomycin-A1-sensitive H-ATPase"],"prefix":"10.1152","volume":"267","author":[{"given":"F. E.","family":"Armitage","sequence":"first","affiliation":[{"name":"Laboratory of Epithelial Transport, University of Florida,Gainesville."}]},{"given":"C. S.","family":"Wingo","sequence":"additional","affiliation":[{"name":"Laboratory of Epithelial Transport, University of Florida,Gainesville."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1994.267.3.F450","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:57:05Z","timestamp":1567958225000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1994.267.3.F450"}},"issued":{"date-parts":[[1994,9,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1994,9,1]]}},"alternative-id":["10.1152\/ajprenal.1994.267.3.F450"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1994.267.3.f450","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1994,9,1]]}},{"indexed":{"date-parts":[[2022,3,30]],"date-time":"2022-03-30T21:59:22Z","timestamp":1648677562175},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1990,4,1]]},"abstract":"<jats:p> Angiotensin II is an important mediator of renal vasoconstriction resulting from chronic unilateral ureteral obstruction (UUO). Distribution of renin mRNA and immunoreactive renin (IR) was examined in kidneys of 1-mo-old Sprague-Dawley rats subjected to either sham operation (n = 21), left complete UUO (n = 21), or right uninephrectomy (UNX, n = 16) at 2 days of age. There were no differences among the three groups in mean arterial pressure or plasma renin activity. Unlike sham kidneys, in which IR was detected in less than 55% of juxtaglomerular apparatuses (JGA) and was confined to a juxtaglomerular location, IR in both kidneys of animals with UUO appeared in greater than 75% of JGA and extended along most of the length of the afferent arteriole (P less than 0.01). In contrast, IR in kidneys of UNX rats was localized to the JGA as in sham-operated animals. Compared with sham-operated kidneys, renal renin content was increased in the obstructed kidneys (P less than 0.01) but decreased in the intact opposite kidneys of UUO rats and in the remaining kidneys of UNX rats (P less than 0.05). Renin mRNA, detected by in situ hybridization histochemistry, was localized to the JGA in kidneys of all groups. However, the fraction of JGA containing detectable renin mRNA was higher in obstructed kidneys than in intact opposite, UNX, or sham kidneys (P less than 0.05). In conclusion, UUO alters intrarenal renin independent of the systemic renin-angiotensin system. The greater distribution of IR, increased renin content, and renin gene expression of kidneys with ipsilateral UUO are consistent with a role for renin-angiotensin in mediating the vasoconstriction resulting from UUO. <\/jats:p>","DOI":"10.1152\/ajprenal.1990.258.4.f854","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T23:20:11Z","timestamp":1513984811000},"page":"F854-F862","source":"Crossref","is-referenced-by-count":5,"title":["In situ localization of renin and its mRNA in neonatal ureteral obstruction"],"prefix":"10.1152","volume":"258","author":[{"given":"S. S.","family":"el-Dahr","sequence":"first","affiliation":[{"name":"Department of Pediatrics, University of Virginia, Charlottesville22908."}]},{"given":"R. A.","family":"Gomez","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, University of Virginia, Charlottesville22908."}]},{"given":"M. S.","family":"Gray","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, University of Virginia, Charlottesville22908."}]},{"given":"M. J.","family":"Peach","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, University of Virginia, Charlottesville22908."}]},{"given":"R. M.","family":"Carey","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, University of Virginia, Charlottesville22908."}]},{"given":"R. L.","family":"Chevalier","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, University of Virginia, Charlottesville22908."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1990.258.4.F854","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:22:10Z","timestamp":1567970530000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1990.258.4.F854"}},"issued":{"date-parts":[[1990,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1990,4,1]]}},"alternative-id":["10.1152\/ajprenal.1990.258.4.F854"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1990.258.4.f854","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1990,4,1]]}},{"indexed":{"date-parts":[[2022,4,4]],"date-time":"2022-04-04T00:40:56Z","timestamp":1649032856387},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1985,7,1]]},"abstract":"<jats:p> The adaptative response of the renal proximal tubule to a reduction of renal mass was studied in brush border membrane vesicles prepared from the solitary remnant kidney (RK) of subtotally nephrectomized rabbits. The in vivo acid-base status of RK and sham-operated controls (SK) was similar. In the absence of organic solutes, Na+ flux across the membrane demonstrated features of Na+-H+ antiport, i.e., stimulation by a transmembrane pH gradient and inhibition by amiloride. Kinetic parameters for Na+-H+ antiport were derived with different experimental protocols. In the presence of an opposing H+ gradient and over a limited range of Na+ concentration, JNamax was enhanced 65% in RK vesicles compared with SK vesicles and KtNa was unchanged. The enhanced JNamax was not apparent under H+ equilibrium conditions, Comparable values for JNamax and KtNa were obtained by studying RK vesicles at external Na+ concentrations of 0-200 mM and resolving uptake into a substrate component, representing Na+-H+ antiport, and a nonsaturable diffusive component. The apparent Na+ permeability (P'Na) of RK vesicles was identical to the P'Na of normal kidney vesicles, under both H+ gradient and H+ equilibrium conditions. H+ permeability, measured with acridine orange, was also the same in RK and SK vesicles. These studies demonstrate that in the remnant kidney model of chronic renal insufficiency there is an increase in the JNamax of the Na+-H+ antiporter in the luminal membrane of the proximal tubule that is revealed only under transmembrane H+ gradient conditions.(ABSTRACT TRUNCATED AT 250 WORDS) <\/jats:p>","DOI":"10.1152\/ajprenal.1985.249.1.f90","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T00:13:30Z","timestamp":1513988010000},"page":"F90-F98","source":"Crossref","is-referenced-by-count":2,"title":["pH gradient-dependent increased Na+-H+ antiport capacity of the rabbit remnant kidney"],"prefix":"10.1152","volume":"249","author":[{"given":"E. P.","family":"Nord","sequence":"first","affiliation":[]},{"given":"A.","family":"Hafezi","sequence":"additional","affiliation":[]},{"given":"J. D.","family":"Kaunitz","sequence":"additional","affiliation":[]},{"given":"W.","family":"Trizna","sequence":"additional","affiliation":[]},{"given":"L. G.","family":"Fine","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1985.249.1.F90","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:29:52Z","timestamp":1567970992000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1985.249.1.F90"}},"issued":{"date-parts":[[1985,7,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1985,7,1]]}},"alternative-id":["10.1152\/ajprenal.1985.249.1.F90"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1985.249.1.f90","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1985,7,1]]}},{"indexed":{"date-parts":[[2022,3,31]],"date-time":"2022-03-31T02:06:38Z","timestamp":1648692398628},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1982,3,1]]},"abstract":"<jats:p> Ouabain reduces renal oxygen consumption more extensively than ethacrynic acid despite similar natriuretic effects. Therefore, ethacrynic acid, which does not inhibit Na-K-ATPase, might stimulate energy metabolism unrelated to net sodium reabsorption. Experiments were performed on anesthetized dogs that had received isotonic saline intravenously corresponding to 10% of body wt and acetazolamide (100 mg.kg-1 i.v.). Subsequent infusion of ouabain in nine dogs (120 nmol.kg-1 intrarenally) reduced sodium reabsorption and oxygen consumption in parallel, giving a delta Na\/delta O2 ratio of 18.0 +\/- 1.1. With ethacrynic acid (3 mg.kg-1 i.v.) in six other dogs the delta Na\/delta O2 ratio averaged 24.5 +\/- 1.4. In a third group of five dogs, ouabain administered after ethacrynic acid reduced sodium reabsorption and oxygen consumption to the same levels as when ouabain was given alone. Thus, the high oxygen consumption remaining after ethacrynic acid can be inhibited by ouabain. We propose that ethacrynic acid generates a futile cycling of sodium by Na-K-ATPase across the basolateral cell membrane that is not apparent as net sodium reabsorption and is stopped by ouabain.U <\/jats:p>","DOI":"10.1152\/ajprenal.1982.242.3.f254","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T13:45:47Z","timestamp":1513950347000},"page":"F254-F260","source":"Crossref","is-referenced-by-count":1,"title":["Energetics of tubular sodium reabsorption sensitive to ethacrynic acid and ouabain"],"prefix":"10.1152","volume":"242","author":[{"given":"O. M.","family":"Sejersted","sequence":"first","affiliation":[]},{"given":"P. A.","family":"Steen","sequence":"additional","affiliation":[]},{"given":"F.","family":"Kiil","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1982.242.3.F254","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:18:42Z","timestamp":1567966722000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1982.242.3.F254"}},"issued":{"date-parts":[[1982,3,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1982,3,1]]}},"alternative-id":["10.1152\/ajprenal.1982.242.3.F254"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1982.242.3.f254","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1982,3,1]]}},{"indexed":{"date-parts":[[2022,4,3]],"date-time":"2022-04-03T15:25:18Z","timestamp":1648999518892},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1988,3,1]]},"abstract":"<jats:p> The aim of this study was to test the hypothesis that the intrarenal renin-angiotensin system (RAS) modulates glomerular angiotensin II (ANG II) receptors. In one protocol ANG II receptors were measured 7 days after unilateral denervation of the left kidney in rats. There were 50% more receptors in the glomeruli from denervated compared with innervated kidneys (right, 1,037 +\/- 108 vs. left, 1,556 +\/- 143 fmol\/mg; P less than 0.01), which was associated with a 63% reduction (P less than 0.01) in left renal vein renin. The differences in ANG II receptors between the left and right kidneys were no longer present when angiotensin-converting enzyme was inhibited with enalapril or when pharmacological amounts of ANG II (50 ng\/min) were infused. In a second protocol, renal cortical renin content was raised in the left kidney by placing a 0.20-mm clip on the left renal artery (two-kidney, one-clip Goldblatt model). At 7 days, glomerular ANG II receptors were reduced by 72.3% in the clipped compared with the contralateral kidneys (right, 1,232 +\/- 105 vs. left, 341 +\/- 170 fmol\/mg; P less than 0.01). The differences in ANG II receptors were no longer present after enalapril treatment. Pharmacological maneuvers that either blocked ANG II formation or increased circulating ANG II resulted in an equal number of ANG II receptors in the right and left kidneys. The data indicate that the intrarenal RAS modulates the density of glomerular ANG II receptors and is a more important receptor modulator than plasma ANG II. <\/jats:p>","DOI":"10.1152\/ajprenal.1988.254.3.f351","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T03:20:04Z","timestamp":1513999204000},"page":"F351-F357","source":"Crossref","is-referenced-by-count":3,"title":["Transport of tetraethylammonium by a kidney epithelial cell line (LLC-PK1)"],"prefix":"10.1152","volume":"254","author":[{"given":"C.","family":"Fauth","sequence":"first","affiliation":[{"name":"Department of Medicine, North Shore University Hospital, Manhasset, New York."}]},{"given":"B.","family":"Rossier","sequence":"additional","affiliation":[{"name":"Department of Medicine, North Shore University Hospital, Manhasset, New York."}]},{"given":"F.","family":"Roch-Ramel","sequence":"additional","affiliation":[{"name":"Department of Medicine, North Shore University Hospital, Manhasset, New York."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1988.254.3.F351","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:48:48Z","timestamp":1567972128000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1988.254.3.F351"}},"issued":{"date-parts":[[1988,3,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1988,3,1]]}},"alternative-id":["10.1152\/ajprenal.1988.254.3.F351"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1988.254.3.f351","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1988,3,1]]}},{"indexed":{"date-parts":[[2022,3,29]],"date-time":"2022-03-29T09:11:20Z","timestamp":1648545080979},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1986,12,1]]},"abstract":"<jats:p> Electroneutral vs. conductive pathways of Cl transport were examined by measuring transepithelial conductance (GT) and the lumen-to-bath 36Cl rate coefficient (KCl). Experimental conditions minimized both Cl-HCO3 exchange [HCO3\/CO2-free, N-2-hydroxyethylpiperazine-N'-2-ethane-sulfonic acid (HEPES)-buffered solutions] and the electrical driving force for paracellular Cl diffusion (amiloride in the perfusate, transepithelial voltage near zero). Two agents known to inhibit Cl conductances in other epithelia, anthracene-9-carboxylate (9AC, 1 mM) and diphenylamine carboxylate (DPC, 0.1-0.5 mM) reversibly reduced GT and KCl when added to the bath. Both reduced KCl to values consistent with paracellular diffusion. Bath DPC had no effect on GT in the presence of 4 mM lumen Ba2+, suggesting that the DPC-sensitive conductance is in series with an apical K conductance, i.e., resides on the basolateral membrane. Lumen DPC also reduced GT and KCl, but was less potent than bath DPC. Because the lumen DPC effect on GT was also blocked by lumen Ba2+, lumen DPC probably inhibits a basolateral Cl conductance. K removal and ouabain (0.5 mM) had no effect on KCl, suggesting that Cl tracer movement is not predominantly through the principal cell. We assume that these agents are inhibiting Cl conductive pathways and propose a model in which transcellular Cl movement through the intercalated cell occurs via an apical electroneutral entry step in series with a basolateral conductive pathway. <\/jats:p>","DOI":"10.1152\/ajprenal.1986.251.6.f1009","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T21:48:53Z","timestamp":1513979333000},"page":"F1009-F1017","source":"Crossref","is-referenced-by-count":0,"title":["Effects of inhibitors of Cl conductance on Cl self-exchange in rabbit cortical collecting tubule"],"prefix":"10.1152","volume":"251","author":[{"given":"K.","family":"Tago","sequence":"first","affiliation":[]},{"given":"D. H.","family":"Warden","sequence":"additional","affiliation":[]},{"given":"V. L.","family":"Schuster","sequence":"additional","affiliation":[]},{"given":"J. B.","family":"Stokes","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1986.251.6.F1009","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:44:55Z","timestamp":1567957495000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1986.251.6.F1009"}},"issued":{"date-parts":[[1986,12,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1986,12,1]]}},"alternative-id":["10.1152\/ajprenal.1986.251.6.F1009"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1986.251.6.f1009","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1986,12,1]]}},{"indexed":{"date-parts":[[2022,4,1]],"date-time":"2022-04-01T05:29:28Z","timestamp":1648790968026},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1989,12,1]]},"abstract":"<jats:p> Necrosis of the outer two-thirds of the cortex (CN) was induced with boiling water in the left kidney of rats. Two days afterward, morphological damage was shown to be limited to the superficial cortex; deep nephron population was well-preserved. Glucose reabsorption under basal and glucose loading conditions, and extraction of p-aminohippurate, used as indices of proximal tubule integrity, were normal in control and experimental kidneys 48 h after cortical necrosis. Basal fractional water and electrolyte excretion did not differ between control and experimental kidneys. Calculated mean single-nephron glomerular filtration rate (GFR) and plasma flow for superficial (SupGFR and SupNPF) and juxtamedullary nephrons (JMGFR and JMPF) were similar to those obtained by micropuncture and Hanssen's technique for SupGFR, and for JMGFR by Hanssen's. Volume expansion led to a 27% increase in calculated SupGFR, but no change in JMGFR. The JMPF increased by 81%, whereas SupNPF increased by only 23%, suggesting that, in this model, GFR of deep nephrons may be independent of plasma flow. The results indicate that deep nephrons retain their functional integrity 48 h after cortical necrosis. After volume expansion fractional excretion of sodium was greater, and fractional water reabsorption less, in CN than in control kidneys. Thus handling of sodium and water by superficial and deep nephrons under basal conditions was similar, but reabsorptive capacity for deep nephrons of CN was lower during volume expansion. The present studies suggest that deep nephrons can maintain relatively normal function in cortical necrosis. <\/jats:p>","DOI":"10.1152\/ajprenal.1989.257.6.f925","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T21:40:14Z","timestamp":1513978814000},"page":"F925-F936","source":"Crossref","is-referenced-by-count":0,"title":["Functional studies in experimental renal cortical necrosis in the rat"],"prefix":"10.1152","volume":"257","author":[{"given":"M.","family":"Martinez-Maldonado","sequence":"first","affiliation":[{"name":"Renal Metabolic Laboratory, Veterans Administration Medical Center, San Juan, Puerto Rico."}]},{"given":"J. M.","family":"Lopez-Novoa","sequence":"additional","affiliation":[{"name":"Renal Metabolic Laboratory, Veterans Administration Medical Center, San Juan, Puerto Rico."}]},{"given":"E.","family":"Fernandez-Repollet","sequence":"additional","affiliation":[{"name":"Renal Metabolic Laboratory, Veterans Administration Medical Center, San Juan, Puerto Rico."}]},{"given":"C.","family":"Baldizon","sequence":"additional","affiliation":[{"name":"Renal Metabolic Laboratory, Veterans Administration Medical Center, San Juan, Puerto Rico."}]},{"given":"S.","family":"Opava-Stitzer","sequence":"additional","affiliation":[{"name":"Renal Metabolic Laboratory, Veterans Administration Medical Center, San Juan, Puerto Rico."}]},{"given":"J. E.","family":"Benabe","sequence":"additional","affiliation":[{"name":"Renal Metabolic Laboratory, Veterans Administration Medical Center, San Juan, Puerto Rico."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1989.257.6.F925","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:12:18Z","timestamp":1567969938000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1989.257.6.F925"}},"issued":{"date-parts":[[1989,12,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1989,12,1]]}},"alternative-id":["10.1152\/ajprenal.1989.257.6.F925"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1989.257.6.f925","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1989,12,1]]}},{"indexed":{"date-parts":[[2022,4,2]],"date-time":"2022-04-02T00:18:32Z","timestamp":1648858712113},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1983,5,1]]},"abstract":"<jats:p> Earlier studies employed colchicine to demonstrate the need for microtubules in the ADH-induced initiation of increased water permeability in toad bladder. We have used colchicine and hydrostatic pressure together to determine whether formed or growing microtubules are required for initiation of the ADH response in Bufo marinus. When ADH and 8,000 psi were administered simultaneously, the ADH-induced increase in water flow was inhibited while under pressure by 107 +\/- 7% (n = 6). Application of 8,000 psi for 10 min before ADH administration resulted in an increased initiation of the ADH osmotic response over the non-pressure-treated control (average acceleration, rate of water flow increase during first 3 min after ADH stimulation, 1.25 +\/- 0.27 vs. 0.43 +\/- 0.12 mg X cm-2 X min-2, n = 6). In addition, the inhibition of the ADH response brought about by colchicine incubation was overcome with pretreatment of the colchicine-incubated bladders with 8,000 psi for 10 min (average 3-min acceleration, 0.18 +\/- 0.04 vs. 1.13 +\/- 0.06 mg X cm-2 X min-2, respectively). Repeating the experiments with dibutyryl cAMP gave similar results. We interpret these data as suggesting that growing microtubules are required for initiation. The proposed model is as follows. Pressure removes colchicine inhibition by introducing, through disassembly of formed microtubules, more colchicine-free tubulin subunits. These subunits are then available following decompression to reassemble when the tissue is challenged with hormone. <\/jats:p>","DOI":"10.1152\/ajprenal.1983.244.5.f547","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T10:00:13Z","timestamp":1513936813000},"page":"F547-F553","source":"Crossref","is-referenced-by-count":0,"title":["Pressure effects on the ADH-induced initiation of water flow in toad bladder"],"prefix":"10.1152","volume":"244","author":[{"given":"L. M.","family":"Coluccio","sequence":"first","affiliation":[]},{"given":"R. J.","family":"Brady","sequence":"additional","affiliation":[]},{"given":"R. H.","family":"Parsons","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1983.244.5.F547","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T14:25:24Z","timestamp":1567952724000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1983.244.5.F547"}},"issued":{"date-parts":[[1983,5,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1983,5,1]]}},"alternative-id":["10.1152\/ajprenal.1983.244.5.F547"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1983.244.5.f547","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1983,5,1]]}},{"indexed":{"date-parts":[[2022,4,1]],"date-time":"2022-04-01T02:55:50Z","timestamp":1648781750492},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1980,6,1]]},"DOI":"10.1152\/ajprenal.1980.238.6.f509","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T08:15:49Z","timestamp":1513930549000},"page":"F509-F514","source":"Crossref","is-referenced-by-count":1,"title":["Effect of increased NaCl or KCl intake on response to chronic furosemide administration"],"prefix":"10.1152","volume":"238","author":[{"given":"T.","family":"Kahn","sequence":"first","affiliation":[]},{"given":"B.","family":"Von Albertini","sequence":"additional","affiliation":[]},{"given":"M.","family":"Goldstein","sequence":"additional","affiliation":[]},{"given":"M. F.","family":"Levitt","sequence":"additional","affiliation":[]},{"given":"J. P.","family":"Bosch","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1980.238.6.F509","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T14:13:30Z","timestamp":1567952010000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1980.238.6.F509"}},"issued":{"date-parts":[[1980,6,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1980,6,1]]}},"alternative-id":["10.1152\/ajprenal.1980.238.6.F509"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1980.238.6.f509","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1980,6,1]]}},{"indexed":{"date-parts":[[2022,4,2]],"date-time":"2022-04-02T02:53:02Z","timestamp":1648867982178},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1987,12,1]]},"abstract":"<jats:p> Urinary prostaglandin E (UPGE) excretion increased significantly after 1 and 2 wk of potassium depletion (KD) in female New Zealand White rabbits on ad libitum water intake [UPGE control, 21.3 +\/- 4.6 ng PGE\/mg creatinine; 1 wk KD, 40.4 +\/- 6.1 ng PGE\/mg creatinine (P less than 0.01); 2 wk KD, 31.9 +\/- 14.9 ng PGE\/mg creatinine (P less than 0.05)]. In vivo prostaglandin inhibition with indomethacin or meclofenamate significantly increased urinary osmolality after 12 h of dehydration and exogenous vasopressin (1.25 U) from 794 +\/- 59 to 1,163 +\/- 113 mosmol\/kgH2O (P less than 0.01). In vitro prostaglandin inhibition with indomethacin or meclofenamate corrected the antidiuretic hormone (ADH) unresponsiveness of isolated perfused cortical collecting tubules (CCTs) from KD rabbits. Furthermore, preincubation with pertussis toxin, an agent that inactivates the guanine nucleotide inhibitory (Ni) subunit of adenylate cyclase, normalized the ADH response of KD CCTs, suggesting that prostaglandins may attenuate ADH action on the CCT through activation of Ni and contribute to the urinary concentrating defect associated with KD. <\/jats:p>","DOI":"10.1152\/ajprenal.1987.253.6.f1113","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T03:25:22Z","timestamp":1513999522000},"page":"F1113-F1119","source":"Crossref","is-referenced-by-count":3,"title":["Prostaglandins and the urinary concentrating defect in potassium-depleted rabbits"],"prefix":"10.1152","volume":"253","author":[{"given":"K. H.","family":"Raymond","sequence":"first","affiliation":[{"name":"Research Service, Audie L. Murphy Memorial Veteran's Hospital, SanAntonio, Texas."}]},{"given":"M. D.","family":"Lifschitz","sequence":"additional","affiliation":[{"name":"Research Service, Audie L. Murphy Memorial Veteran's Hospital, SanAntonio, Texas."}]},{"given":"T. D.","family":"McKinney","sequence":"additional","affiliation":[{"name":"Research Service, Audie L. Murphy Memorial Veteran's Hospital, SanAntonio, Texas."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1987.253.6.F1113","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:51:12Z","timestamp":1567972272000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1987.253.6.F1113"}},"issued":{"date-parts":[[1987,12,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1987,12,1]]}},"alternative-id":["10.1152\/ajprenal.1987.253.6.F1113"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1987.253.6.f1113","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1987,12,1]]}},{"indexed":{"date-parts":[[2022,4,5]],"date-time":"2022-04-05T03:18:02Z","timestamp":1649128682326},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1978,1,1]]},"DOI":"10.1152\/ajprenal.1978.234.1.f64","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T14:56:00Z","timestamp":1513954560000},"page":"F64-F67","source":"Crossref","is-referenced-by-count":2,"title":["Stimulation of prostaglandin biosynthesis in the renal papilla by hypertonic mediums"],"prefix":"10.1152","volume":"234","author":[{"given":"A.","family":"Danon","sequence":"first","affiliation":[]},{"given":"H. R.","family":"Knapp","sequence":"additional","affiliation":[]},{"given":"O.","family":"Oelz","sequence":"additional","affiliation":[]},{"given":"J. A.","family":"Oates","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1978.234.1.F64","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T14:55:39Z","timestamp":1567954539000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1978.234.1.F64"}},"issued":{"date-parts":[[1978,1,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1978,1,1]]}},"alternative-id":["10.1152\/ajprenal.1978.234.1.F64"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1978.234.1.f64","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1978,1,1]]}},{"indexed":{"date-parts":[[2022,4,4]],"date-time":"2022-04-04T22:44:06Z","timestamp":1649112246975},"reference-count":0,"publisher":"American Physiological Society","issue":"8","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2014,4,15]]},"DOI":"10.1152\/ajprenal.00142.2014","type":"journal-article","created":{"date-parts":[[2014,3,13]],"date-time":"2014-03-13T04:09:24Z","timestamp":1394683764000},"page":"F928-F929","source":"Crossref","is-referenced-by-count":0,"title":["2014 Young Investigator Award of the American Physiological Society Renal Section"],"prefix":"10.1152","volume":"306","member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00142.2014","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T23:59:16Z","timestamp":1567987156000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00142.2014"}},"issued":{"date-parts":[[2014,4,15]]},"references-count":0,"journal-issue":{"issue":"8","published-print":{"date-parts":[[2014,4,15]]}},"alternative-id":["10.1152\/ajprenal.00142.2014"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00142.2014","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2014,4,15]]}},{"indexed":{"date-parts":[[2022,3,30]],"date-time":"2022-03-30T10:26:23Z","timestamp":1648635983043},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1996,9,1]]},"abstract":"<jats:p> Adhesion of rat glomerular epithelial cells (GEC) to collagen stimulates production of D-myo-inositol 1,4,5-trisphosphate (IP3) and 1,2-diacylglycerol. This process is mediated via beta 1-integrins, and it modulates GEC proliferation. In this study, we address the changes in inositol-lipid turnover induced by GEC adhesion to extracellular matrix (ECM). The masses of both phosphatidylinositol 4,5-bisphosphate (PIP2) and IP3, as well as [3H]inositol phosphates, were increased in GEC adherent to collagen, compared with plastic substratum. Phosphatidylinositol-4-phosphate (PIP) 5-kinase activity was predominantly membrane associated and was enhanced in GEC on collagen. Phospholipase C (PLC) activity and PLC-gamma 1 protein were increased in membrane fractions of GEC adherent to collagen, compared with plastic. Stable overexpression of PLC-gamma 1 in GEC amplified the effect of ECM on the production of [3H]inositol phosphates. In addition, the PLC-gamma 1 that was membrane associated in collagen-adherent GEC was tyrosine phosphorylated. Thus production of IP3 in GEC adherent to ECM is associated with increased production of PIP2. Moreover, adhesion to ECM increases tyrosine phosphorylation and membrane association of PLC-gamma 1, which may facilitate PIP2 hydrolysis by increasing the catalytic activity of PLC-gamma 1 and the proximity of PLC-gamma 1 and its substrate. Understanding the process of ECM-induced inositol lipid production and breakdown in GEC may provide insights into the regulation of GEC proliferation and differentiated functions in normal conditions and during glomerular injury. <\/jats:p>","DOI":"10.1152\/ajprenal.1996.271.3.f579","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T06:31:13Z","timestamp":1514010673000},"page":"F579-F587","source":"Crossref","is-referenced-by-count":5,"title":["Extracellular matrix stimulates production and breakdown of inositol phospholipids"],"prefix":"10.1152","volume":"271","author":[{"given":"A. V.","family":"Cybulsky","sequence":"first","affiliation":[{"name":"Department of Medicine, Royal Victoria Hospital, McGill University,Montreal, Quebec, Canada."}]},{"given":"A. J.","family":"McTavish","sequence":"additional","affiliation":[{"name":"Department of Medicine, Royal Victoria Hospital, McGill University,Montreal, Quebec, Canada."}]},{"given":"J.","family":"Papillon","sequence":"additional","affiliation":[{"name":"Department of Medicine, Royal Victoria Hospital, McGill University,Montreal, Quebec, Canada."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1996.271.3.F579","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:05:52Z","timestamp":1567973152000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1996.271.3.F579"}},"issued":{"date-parts":[[1996,9,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1996,9,1]]}},"alternative-id":["10.1152\/ajprenal.1996.271.3.F579"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1996.271.3.f579","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1996,9,1]]}},{"indexed":{"date-parts":[[2022,4,4]],"date-time":"2022-04-04T07:53:23Z","timestamp":1649058803393},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1992,7,1]]},"abstract":"<jats:p> We have investigated the relative contribution of hydrolysis, intact transport and urinary excretion to the renal clearance of Gly-Sar, Gly-Sar-Sar, and Gly-Gly-Sar in fed and starved rats. The results obtained from isolated kidney perfusion studies are summarized as follows: 1) clearance was fastest for Gly-Gly-Sar and slowest for Gly-Sar-Sar, 2) urinary excretion of Gly-Sar-Sar exceeded that of Gly-Gly-Sar or Gly-Sar, 3) there was accumulation of products of hydrolysis of Gly-Gly-Sar in the perfusate but not of Gly-Sar or Gly-Sar-Sar, 4) isolated brush-border and basolateral membranes of renal tubular cells lacked hydrolytic activity against Gly-Sar and Gly-Sar-Sar but possessed hydrolytic activity against Gly-Gly-Sar, 5) an excess amount of Gly-Sar-Sar reduced the rate of clearance of Gly-Gly-Sar by approximately 40% and significantly increased urinary excretion of this peptide, 6) the nonfiltering kidney cleared Gly-Gly-Sar at a rate which was 50% of that of the filtering kidney but did not clear Gly-Sar, and 7) starvation for 96 h was without a significant effect on the renal clearance of either Gly-Sar or Gly-Sar-Sar but significantly reduced the renal clearance of Gly-Gly-Sar and the brush-border membrane hydrolase activity against this peptide. We conclude that the molecular structure determines the affinity of oligopeptides for the membrane transport and hydrolytic systems, which, in turn, determines their efficiency for clearance by the kidney. <\/jats:p>","DOI":"10.1152\/ajprenal.1992.263.1.f109","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T10:12:07Z","timestamp":1514023927000},"page":"F109-F115","source":"Crossref","is-referenced-by-count":2,"title":["Oligopeptides: mechanism of renal clearance depends on molecular structure"],"prefix":"10.1152","volume":"263","author":[{"given":"H.","family":"Minami","sequence":"first","affiliation":[{"name":"Department of Medicine, University of Pittsburgh School of Medicine, Pennsylvania 15213."}]},{"given":"H.","family":"Daniel","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Pittsburgh School of Medicine, Pennsylvania 15213."}]},{"given":"E. L.","family":"Morse","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Pittsburgh School of Medicine, Pennsylvania 15213."}]},{"given":"S. A.","family":"Adibi","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Pittsburgh School of Medicine, Pennsylvania 15213."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1992.263.1.F109","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:26:33Z","timestamp":1567974393000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1992.263.1.F109"}},"issued":{"date-parts":[[1992,7,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1992,7,1]]}},"alternative-id":["10.1152\/ajprenal.1992.263.1.F109"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1992.263.1.f109","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1992,7,1]]}},{"indexed":{"date-parts":[[2022,12,17]],"date-time":"2022-12-17T15:50:00Z","timestamp":1671292200519},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1994,3,1]]},"abstract":"<jats:p> The aim of the present report was to examine the effect of several agents on angiotensin II (ANG II) and losartan receptors using 125I-[Sar1,Ala8]ANG II and [3H]losartan as radiolabeled ligand, respectively. ANG II receptors were downregulated in glomeruli from rats infused with ANG II during 3 wk or rats receiving losartan orally during 1 wk. The number of sites (Bmax) was reduced, but the dissociation constant (Kd) value was unchanged. Losartan receptors were downregulated in glomeruli from rats receiving losartan, but remained unchanged in glomeruli from rats infused with ANG II. Since in vivo administration of losartan results in increase of plasma ANG II and formation of metabolites, in vitro studies using human mesangial cells were performed to better analyze the present findings. Treatment of mesangial cells during 4 days by ANG II, losartan, or its metabolite, EXP-3174, also produced downregulation of 125I-[Sar1,Ala8]ANG II binding sites with a decreased Bmax and unchanged Kd value. Only treatment of mesangial cells by ANG II or EXP-3174 produced downregulation of [3H]losartan binding sites. In contrast, exposure of these cells to losartan resulted in upregulation of [3H]losartan binding sites. Under all conditions, only Bmax was modified. Whereas internalization of [3H]losartan in mesangial cells was negligible under all experimental conditions, there was an increase of the percentage of internalized 125I-[Sar1,Ala8]ANG II after exposure of the cells to ANG II or AT1 antagonists. No change was observed in mesangial cell AT1 receptor mRNA levels. This study demonstrates that 1) AT1 mRNA is expressed in human mesangial cells; 2) the characteristics of 125I-[Sar1,Ala8]ANG II and [3H]losartan binding sites in rat glomeruli and human mesangial cells are different, with Kd and Bmax values greater in both preparations when [3H]losartan was utilized; 3) both types of binding sites obey different regulations, and the effects of losartan in vivo are due in part to the associated increase in plasma ANG II levels and the transformation of the drug into its metabolite, EXP-3174; 4) downregulation of AT1 receptors does not depend on changes in mRNA expression but is associated with increased relative internalization. <\/jats:p>","DOI":"10.1152\/ajprenal.1994.266.3.f384","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T06:02:48Z","timestamp":1514008968000},"page":"F384-F393","source":"Crossref","is-referenced-by-count":5,"title":["Differential regulation of angiotensin II and losartan binding sites in glomeruli and mesangial cells"],"prefix":"10.1152","volume":"266","author":[{"given":"D.","family":"Chansel","sequence":"first","affiliation":[{"name":"Institut National de la Sante et de la Recherche Medicale (INSERM) 64,Hopital Tenon, Paris, France."}]},{"given":"T.","family":"Bizet","sequence":"additional","affiliation":[{"name":"Institut National de la Sante et de la Recherche Medicale (INSERM) 64,Hopital Tenon, Paris, France."}]},{"given":"S.","family":"Vandermeersch","sequence":"additional","affiliation":[{"name":"Institut National de la Sante et de la Recherche Medicale (INSERM) 64,Hopital Tenon, Paris, France."}]},{"given":"P.","family":"Pham","sequence":"additional","affiliation":[{"name":"Institut National de la Sante et de la Recherche Medicale (INSERM) 64,Hopital Tenon, Paris, France."}]},{"given":"B.","family":"Levy","sequence":"additional","affiliation":[{"name":"Institut National de la Sante et de la Recherche Medicale (INSERM) 64,Hopital Tenon, Paris, France."}]},{"given":"R.","family":"Ardaillou","sequence":"additional","affiliation":[{"name":"Institut National de la Sante et de la Recherche Medicale (INSERM) 64,Hopital Tenon, Paris, France."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1994.266.3.F384","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:31:36Z","timestamp":1567960296000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1994.266.3.F384"}},"issued":{"date-parts":[[1994,3,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1994,3,1]]}},"alternative-id":["10.1152\/ajprenal.1994.266.3.F384"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1994.266.3.f384","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1994,3,1]]}},{"indexed":{"date-parts":[[2022,4,1]],"date-time":"2022-04-01T23:01:01Z","timestamp":1648854061641},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1996,8,1]]},"abstract":"<jats:p> The proximal tubule epithelial handling of native and glycated albumin was evaluated by quantitative immunocytochemistry. Native bovine serum albumin (BSA) and its glycated form (gBSA), tagged to different haptens, were simultaneously injected in anesthetized mice and maintained in circulation for 10 or 60 min. Both albumins were localized within the capillary lumen, in glomerular and peritubular basement membranes, the urinary space, and cellular compartments of the proximal tubular epithelial cells. In these cells, both forms of albumin were concomitantly found within the same endocytic-lysosomal system. Morphometric evaluations have indicated higher proportions of gBSA in the urinary space, reflecting probably a significant glomerular filtration of this form of albumin combined to a lesser reabsorptive clearance. Indeed, higher proportions of native BSA were found in the endocytic compartment of the tubular epithelial cells, suggesting its preferential reabsorption. The present study thus supports a preferential glomerular filtration of gBSA with a facilitated filtration of native BSA in the presence of the glycated one. It also demonstrates the tubular reabsorption of BSA and gBSA through a common endocytic pathway, in which the native BSA is preferentially reabsorbed with respect to its glycated form. <\/jats:p>","DOI":"10.1152\/ajprenal.1996.271.2.f261","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T06:30:13Z","timestamp":1514010613000},"page":"F261-F268","source":"Crossref","is-referenced-by-count":3,"title":["Reabsorption of native and glycated albumin by renal proximal tubular epithelial cells"],"prefix":"10.1152","volume":"271","author":[{"given":"M.","family":"Bendayan","sequence":"first","affiliation":[{"name":"Department of Anatomy, Universite de Montreal, Quebec, Canada."}]},{"given":"I.","family":"Londono","sequence":"additional","affiliation":[{"name":"Department of Anatomy, Universite de Montreal, Quebec, Canada."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1996.271.2.F261","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:05:30Z","timestamp":1567973130000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1996.271.2.F261"}},"issued":{"date-parts":[[1996,8,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1996,8,1]]}},"alternative-id":["10.1152\/ajprenal.1996.271.2.F261"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1996.271.2.f261","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1996,8,1]]}},{"indexed":{"date-parts":[[2022,4,1]],"date-time":"2022-04-01T13:33:27Z","timestamp":1648820007588},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1992,12,1]]},"abstract":"<jats:p> This study was designed to test the hypothesis that the changes in renal hemodynamics that occur after a high-protein meal involve voltage-dependent calcium channels. In chronically instrumented female dogs, a 10-g\/kg meal of raw beef caused plasma alpha-amino nitrogen levels to increase from 3.9 +\/- 0.2 to 6.7 +\/- 0.5 mg\/dl after 90 min, and glomerular filtration rate (GFR) rose from 59 +\/- 6 to 85 +\/- 7 ml\/min, effective renal plasma flow (ERPF) rose from 130 +\/- 22 to 213 +\/- 36 ml\/min, and sodium excretion rose from 21 +\/- 4 to 84 +\/- 20 mu eq\/min. On another day the dogs were pretreated with verapamil (0.075 mg\/kg + 0.005 mg.kg-1.min-1 iv), which did not change arterial pressure significantly but increased GFR by 25 +\/- 7% and ERPF by 23 +\/- 5%. After a subsequent meat meal, plasma alpha-amino nitrogen increased from 4.0 +\/- 0.3 to 6.6 +\/- 0.1 mg\/dl but GFR, ERPF, and sodium excretion did not change significantly. On the other hand, pretreatment with dopamine, which caused a similar degree of vasodilation to that caused by verapamil, did not prevent the response to a subsequent meat meal. Thus verapamil specifically prevented the normal increases in renal hemodynamics after protein feeding, suggesting that protein-stimulated renal vasodilation requires intact voltage-dependent calcium channels. <\/jats:p>","DOI":"10.1152\/ajprenal.1992.263.6.f1044","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T09:33:38Z","timestamp":1514021618000},"page":"F1044-F1050","source":"Crossref","is-referenced-by-count":1,"title":["Control of renal hemodynamics after protein feeding: role of calcium channels"],"prefix":"10.1152","volume":"263","author":[{"given":"L. L.","family":"Woods","sequence":"first","affiliation":[{"name":"Division of Nephrology and Hypertension, Oregon Health SciencesUniversity, Portland 97201."}]},{"given":"B. E.","family":"Smith","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Oregon Health SciencesUniversity, Portland 97201."}]},{"given":"D. R.","family":"De Young","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Oregon Health SciencesUniversity, Portland 97201."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1992.263.6.F1044","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:22:32Z","timestamp":1567974152000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1992.263.6.F1044"}},"issued":{"date-parts":[[1992,12,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1992,12,1]]}},"alternative-id":["10.1152\/ajprenal.1992.263.6.F1044"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1992.263.6.f1044","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1992,12,1]]}},{"indexed":{"date-parts":[[2022,4,5]],"date-time":"2022-04-05T04:00:10Z","timestamp":1649131210507},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1986,6,1]]},"abstract":"<jats:p> There has been some controversy as to whether in sodium-transporting epithelia (e.g., frog skin, toad urinary bladder) the Na-O2 ratio is independent of the net rate of transepithelial sodium transport or remains constant over a wide range of transport rates. This computer simulation study shows that both views are defensible, depending on whether one wishes to exclude or include \u201cstatic head\u201d energy in the calculations. This energy arises from intramembrane sodium recirculation, as shown here when applying a multicompartment epithelial membrane model. Assuming reasonable kinetic parameters of a transport model whose sodium transport rate is varied over a wide range by a step-by-step simulated amiloride action, the computations have shown the following. When static head energy (O2 consumption) is excluded from the calculations, the Na-O2 ratio is constant over a wide range of transepithelial sodium flux, up to the tested value of 20 neq X cm-2 X min-1, a \u201cnormal\u201d value found in frog skin. The Na-O2 ratios were 19.4 and 28.7 in low- and high-sodium models, respectively. If the static head energy is included in the calculations, the Na-O2 ratios increase with increasing transport rate from zero values to values up to 15.7. These data are in good agreement with laboratory results, as are derived data on phenomenological coefficients and thermodynamic coupling coefficients (LNa = 80, 128; LNa,r = 4.4; Lr = 0.27, 0.58; q = 0.50, 0.90, depending on the chosen model parameters). <\/jats:p>","DOI":"10.1152\/ajprenal.1986.250.6.f1107","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T01:02:46Z","timestamp":1513990966000},"page":"F1107-F1118","source":"Crossref","is-referenced-by-count":0,"title":["Role of topology in bioenergetics of sodium transport in complex epithelia"],"prefix":"10.1152","volume":"250","author":[{"given":"E. G.","family":"Huf","sequence":"first","affiliation":[]},{"given":"D. C.","family":"Mikulecky","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1986.250.6.F1107","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:35:25Z","timestamp":1567971325000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1986.250.6.F1107"}},"issued":{"date-parts":[[1986,6,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1986,6,1]]}},"alternative-id":["10.1152\/ajprenal.1986.250.6.F1107"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1986.250.6.f1107","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1986,6,1]]}},{"indexed":{"date-parts":[[2022,4,4]],"date-time":"2022-04-04T09:54:23Z","timestamp":1649066063420},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1995,4,1]]},"abstract":"<jats:p> Postischemic thyroxin (T<jats:sub>4<\/jats:sub>) enhances restitution of cellular ATP and accelerates recovery of renal function. This effect is not related to global improvement in cell integrity. To determine the mechanism by which recovery of cellular ATP is enhanced, the effect of T<jats:sub>4<\/jats:sub> on mitochondrial ATP production was evaluated using specific inhibitor stop assays for mitochondrial phosphate transport and ADP translocator activity. Rats were subjected to 45-min renal ischemia and given normal saline (NS, 0.5 ml) or T<jats:sub>4<\/jats:sub> (20 \u03bcg\/kg) during the reflow period. By 30-min reflow, the values for apparent endpoint of phosphate transport (PiTm, nmol Pi\/mg mitochondrial protein) had recovered to rates seen in nonischemic animals (10.3 \u00b1 0.9) and remained stable at 120 min. T<jats:sub>4<\/jats:sub> treatment did not affect PiTm. In contrast, the apparent endpoint of ADP transport (ADPTm, nmol ADP\/mg mitochondrial protein) was dramatically decreased in NS rats at 30-min (6.7 \u00b1 0.5) and 120-min (13.7 \u00b1 1.0) reflow compared with nonischemic control rats (24.7 \u00b1 2.4). T<jats:sub>4<\/jats:sub> significantly improved ADPTm by 30 min (10.1 \u00b1 0.6, P &lt; 0.05). By 120 min T<jats:sub>4<\/jats:sub> stimulated ADPTm (37.7 \u00b1 5.2, P &lt; 0.05) to exceed nonischemic control values. These data suggest the following: 1) postischemic mitochondrial PiTm recovers to control values by 30 min of reflow; 2) T<jats:sub>4<\/jats:sub> does not augment PiTm; 3) renal ischemia causes a dramatic decrease in mitochondrial ADPTm; 4) postischemic T<jats:sub>4<\/jats:sub> significantly enhances mitochondrial nucleotide transport at 30-min reflow; 5) by 120-min reflow, T<jats:sub>4<\/jats:sub> rats have ADPTm which exceeds control values. These findings provide an understanding of at least one of the metabolic components that contribute to the enhanced recovery of cellular ATP resulting from postischemic T<jats:sub>4<\/jats:sub> administration. <\/jats:p><jats:p> acute renal failure; mitochondrial transport; cellular adenosine triphosphate recovery <\/jats:p><jats:p> Submitted on January 24, 1994 <\/jats:p><jats:p> Accepted on November 1, 1994 <\/jats:p>","DOI":"10.1152\/ajprenal.1995.268.4.f651","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T06:23:42Z","timestamp":1514010222000},"page":"F651-F656","source":"Crossref","is-referenced-by-count":0,"title":["Postischemic thyroxin stimulates renal mitochondrial adenine nucleotide translocator activity"],"prefix":"10.1152","volume":"268","author":[{"given":"Ivy","family":"Boydstun","sequence":"first","affiliation":[{"name":"Department of Pediatrics and Pathology, Yale University School of Medicine, New Haven, Connecticut 06520-8064"}]},{"given":"Samer","family":"Najjar","sequence":"additional","affiliation":[{"name":"Department of Pediatrics and Pathology, Yale University School of Medicine, New Haven, Connecticut 06520-8064"}]},{"given":"Michael","family":"Kashgarian","sequence":"additional","affiliation":[{"name":"Department of Pediatrics and Pathology, Yale University School of Medicine, New Haven, Connecticut 06520-8064"}]},{"given":"Thomas","family":"Carpenter","sequence":"additional","affiliation":[{"name":"Department of Pediatrics and Pathology, Yale University School of Medicine, New Haven, Connecticut 06520-8064"}]},{"given":"Norman","family":"Siegel","sequence":"additional","affiliation":[{"name":"Department of Pediatrics and Pathology, Yale University School of Medicine, New Haven, Connecticut 06520-8064"}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1995.268.4.F651","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:02:21Z","timestamp":1567972941000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1995.268.4.F651"}},"issued":{"date-parts":[[1995,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1995,4,1]]}},"alternative-id":["10.1152\/ajprenal.1995.268.4.F651"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1995.268.4.f651","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1995,4,1]]}},{"indexed":{"date-parts":[[2022,4,2]],"date-time":"2022-04-02T14:36:11Z","timestamp":1648910171694},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1990,5,1]]},"abstract":"<jats:p> Parathyroid hormone (PTH) produces rapid inhibition of Na(+)-phosphate cotransport, characterized by a decreased maximal rate of transport, and the inhibition is independent of de novo protein synthesis. The present study determined whether the action of PTH on Na(+)-phosphate cotransport is mediated, at least in part, by rapid endocytic internalization of Na(+)-phosphate cotransporters present in the plasma membrane. Horseradish peroxidase, a fluid-phase marker, was used to demonstrate the presence of endocytosis in opossum kidney (OK) epithelial cells in monolayer culture. An increase in medium osmolality to 500 mosmol\/kgH2O, by addition of sucrose, produced 80% inhibition of endocytosis within 1 h. The inhibition was reversed on returning the cells to normal medium. Incubation of OK cell monolayers with PTH (10(-8) M) for 3 h at normal osmolality (281 mosmol\/kgH2O) inhibited Na(+)-phosphate cotransport (4 min uptakes) by 56-67%. In hyperosmolar medium (513 mosmol\/kgH2O), when endocytosis was inhibited, PTH inhibited Na(+)-phosphate cotransport by only 25-39%, a change that was significantly different from the inhibition in normal medium. Hyperosomolality had no effect on PTH inhibition of Na(+)-H+ exchange or on PTH stimulation of intracellular adenosine 3',5'-cyclic monophosphate. We conclude that the full inhibitory action of PTH on Na(+)-phosphate cotransport may require an intact endocytic mechanism. <\/jats:p>","DOI":"10.1152\/ajprenal.1990.258.5.f1336","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T23:21:57Z","timestamp":1513984917000},"page":"F1336-F1344","source":"Crossref","is-referenced-by-count":3,"title":["Parathyroid hormone action on phosphate transport is inhibited by high osmolality"],"prefix":"10.1152","volume":"258","author":[{"given":"S. A.","family":"Kempson","sequence":"first","affiliation":[{"name":"Physiology Institute, University of Zurich, Switzerland."}]},{"given":"C.","family":"Helmle","sequence":"additional","affiliation":[{"name":"Physiology Institute, University of Zurich, Switzerland."}]},{"given":"M. I.","family":"Abraham","sequence":"additional","affiliation":[{"name":"Physiology Institute, University of Zurich, Switzerland."}]},{"given":"H.","family":"Murer","sequence":"additional","affiliation":[{"name":"Physiology Institute, University of Zurich, Switzerland."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1990.258.5.F1336","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:24:01Z","timestamp":1567970641000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1990.258.5.F1336"}},"issued":{"date-parts":[[1990,5,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1990,5,1]]}},"alternative-id":["10.1152\/ajprenal.1990.258.5.F1336"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1990.258.5.f1336","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1990,5,1]]}},{"indexed":{"date-parts":[[2022,4,3]],"date-time":"2022-04-03T20:34:45Z","timestamp":1649018085648},"reference-count":6,"publisher":"American Physiological Society","issue":"5","funder":[{"name":"NIH","award":["HL131577"],"award-info":[{"award-number":["HL131577"]}]},{"name":"AHA","award":["19IPLOI34730020"],"award-info":[{"award-number":["19IPLOI34730020"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2019,11,1]]},"DOI":"10.1152\/ajprenal.00394.2019","type":"journal-article","created":{"date-parts":[[2019,9,18]],"date-time":"2019-09-18T13:16:21Z","timestamp":1568812581000},"page":"F1169-F1170","source":"Crossref","is-referenced-by-count":0,"title":["Cholesterol may not have a special place in kidneys"],"prefix":"10.1152","volume":"317","author":[{"given":"Surya M.","family":"Nauli","sequence":"first","affiliation":[{"name":"Department of Biomedical and Pharmaceutical Sciences, Chapman University, and Department of Medicine, University of California Irvine, Irvine, California"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M110.159194"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/S2213-8587(17)30283-8"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.20.5.651"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.48.32304"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00196.2019"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.119628"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00394.2019","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,10,28]],"date-time":"2019-10-28T13:19:41Z","timestamp":1572268781000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00394.2019"}},"issued":{"date-parts":[[2019,11,1]]},"references-count":6,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2019,11,1]]}},"alternative-id":["10.1152\/ajprenal.00394.2019"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00394.2019","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2019,11,1]]}},{"indexed":{"date-parts":[[2022,3,31]],"date-time":"2022-03-31T18:21:57Z","timestamp":1648750917968},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1983,12,1]]},"abstract":"<jats:p> The effects of variations in renal hemodynamics on the time course of renin secretion were studied in dogs anesthetized with pentobarbital-chloralose. Hemodynamic changes were induced either locally in kidneys perfused in situ via an extracorporeal circuit (with or without a pump system) or systemically by hemorrhage or nitroprusside infusion. In the autoperfused kidney the reduction of renal perfusion pressure to approximately one-half of the arterial pressure by inflow occlusion caused an increase in renal conductance (renal vasodilation) and an increase in renin secretion rate (RSR). In the pump-perfused kidney, a step increase in renal blood flow (RBF) caused renal vasoconstriction and a decrease in RSR; a step decrease in RBF caused renal vasodilation and an increase in RSR. Following step changes in RBF, the time constant of the alterations of renal conductance was 56.5 s, and the time constant of the RSR responses was 80.1 s. The total time required to reach a steady state for RSR lagged behind that for renal conductance by approximately 5 min. These differences reflect the time needed for the kidney to release renin in response to changes in renal vascular caliber. The results suggest that renin release occurs in response to the autoregulatory dilation of the renal arterioles. When systemic hypotension was induced by nitroprusside infusion, RSR also increased together with the renal conductance. Following hemorrhage, however, RSR increased despite a decrease in renal conductance, reflecting the role of neurohumoral factors in causing renin release in this case. The comparison of renin secretion following different types of hemodynamic alterations serves to elucidate the mechanisms of renin secretion. <\/jats:p>","DOI":"10.1152\/ajprenal.1983.245.6.f784","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T10:02:26Z","timestamp":1513936946000},"page":"F784-F791","source":"Crossref","is-referenced-by-count":0,"title":["Effects of variations in renal hemodynamics on the time course of renin secretion rate"],"prefix":"10.1152","volume":"245","author":[{"given":"S.","family":"Simchon","sequence":"first","affiliation":[]},{"given":"S.","family":"Chien","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1983.245.6.F784","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T14:25:34Z","timestamp":1567952734000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1983.245.6.F784"}},"issued":{"date-parts":[[1983,12,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1983,12,1]]}},"alternative-id":["10.1152\/ajprenal.1983.245.6.F784"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1983.245.6.f784","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1983,12,1]]}},{"indexed":{"date-parts":[[2022,4,3]],"date-time":"2022-04-03T18:41:35Z","timestamp":1649011295671},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1991,8,1]]},"abstract":"<jats:p> The effects of maleic acid on renal phosphate (Pi) transport were examined by clearance and brush-border membrane vesicle (BBMV) transport studies. In normal rats, maleic acid 50 mg.kg body wt-1.h-1 increased the phosphaturia (P less than 0.001). Intraperitoneal administration of a similar dose of maleic acid decreased the BBMV uptake of Pi but not glucose. In rats fed a low-phosphate diet (0.03%), the maleic acid-induced phosphaturia was blunted, but the inhibitory effect on the BBMV transport of Pi persisted. In chronic parathyroidectomized rats fed a low-phosphate diet, where the filtered load of Pi was higher than in the previous groups, the phosphaturia was abolished, but the inhibition of the BBMV transport of Pi was sustained. Both the in vitro incubation of BBMVV and in vivo administration of maleic acid were associated with a competitive inhibition of Pi transport. These studies indicate that the maleic acid-induced phosphaturia is expressed at the apical membrane entry step of Pi, and the enhanced distal tubular reabsorption accounts for the lack of phosphaturia in dietary Pi deprivation. <\/jats:p>","DOI":"10.1152\/ajprenal.1991.261.2.f227","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T23:29:45Z","timestamp":1513985385000},"page":"F227-F237","source":"Crossref","is-referenced-by-count":0,"title":["Effects of maleic acid on renal phosphorus transport: role of dietary phosphorus"],"prefix":"10.1152","volume":"261","author":[{"given":"J.","family":"Guntupalli","sequence":"first","affiliation":[{"name":"Department of Medicine, University of Texas Medical School, Houston77025."}]},{"given":"V.","family":"Delaney","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Texas Medical School, Houston77025."}]},{"given":"E. J.","family":"Weinman","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Texas Medical School, Houston77025."}]},{"given":"D.","family":"Lyle","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Texas Medical School, Houston77025."}]},{"given":"M.","family":"Allon","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Texas Medical School, Houston77025."}]},{"given":"E.","family":"Bourke","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Texas Medical School, Houston77025."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1991.261.2.F227","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:22:39Z","timestamp":1567970559000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1991.261.2.F227"}},"issued":{"date-parts":[[1991,8,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1991,8,1]]}},"alternative-id":["10.1152\/ajprenal.1991.261.2.F227"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1991.261.2.f227","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1991,8,1]]}},{"indexed":{"date-parts":[[2022,4,3]],"date-time":"2022-04-03T22:11:03Z","timestamp":1649023863382},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1986,11,1]]},"abstract":"<jats:p> The effects of glucocorticoid agonists RU 26988 (G) and dexamethasone (D) and antagonist RU 486 (AG) on aortic and renal prostaglandin (PG) production were studied in Wistar rats. Blood pressure increased in rats administered G (20 mg X kg-1 X day-1) during 1 or 3 days; such increase was prevented by AG (100 mg X kg-1 X day-1). Renal papillary PGE2 release was increased after a 3-day administration of G, and this was prevented by AG. Neither G nor AG altered basal 6-keto-PGF1 alpha aortic production. However, G inhibited and AG magnified the stimulatory effect of ionophore A 23187, added in vitro, on 6-keto-PGF1 alpha production; AG reversed G inhibition. In addition, AG alone (20 mg X kg-1 X day-1 X 3 days) enhanced the stimulatory effect of angiotensin II (10(-8) M), added in vitro, on 6-keto-PGF1 alpha release. In vitro studies were performed on renomedullary interstitial cells grown in culture; G and D depressed PGE2 production in a dose-dependent manner; AG at equimolar 10(-8) M concentration inhibited this effect. In conclusion, AG inhibits the effects of G on blood pressure and PG synthesis. G exerts strong depressor activity on in vitro PGE2 renal production, whereas in vivo effects are more complex. Endogenous G inhibits aortic prostacyclin production, an action unmasked by AG administration. Diminished stimulation of vascular prostacyclin synthesis may contribute to vascular hyperreactivity in G-induced hypertension. <\/jats:p>","DOI":"10.1152\/ajprenal.1986.251.5.f810","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T00:52:48Z","timestamp":1513990368000},"page":"F810-F816","source":"Crossref","is-referenced-by-count":1,"title":["Effects of gluco- and antiglucocorticoids on renal and aortic prostaglandin synthesis"],"prefix":"10.1152","volume":"251","author":[{"given":"J. P.","family":"Grunfeld","sequence":"first","affiliation":[]},{"given":"L.","family":"Eloy","sequence":"additional","affiliation":[]},{"given":"A.","family":"Araujo","sequence":"additional","affiliation":[]},{"given":"F.","family":"Russo-Marie","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1986.251.5.F810","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:34:24Z","timestamp":1567971264000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1986.251.5.F810"}},"issued":{"date-parts":[[1986,11,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1986,11,1]]}},"alternative-id":["10.1152\/ajprenal.1986.251.5.F810"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1986.251.5.f810","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1986,11,1]]}},{"indexed":{"date-parts":[[2022,3,31]],"date-time":"2022-03-31T20:26:09Z","timestamp":1648758369305},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1987,6,1]]},"abstract":"<jats:p> Urinary kallikrein activity, intake, and excretion of sodium and water were measured in metabolic balance studies on spontaneously hypertensive rats (SHR) of the Okamoto-Aoki strain and normotensive Wistar-Kyoto rats (WKY) on a normal sodium diet from 4 through 15 wk of age. Urinary excretion of active and total kallikrein was significantly lower in SHR at all ages examined and represented a stable percentage of the values in age-matched WKY throughout development, on the average 69.5 and 67.4%, respectively. SHR exhibited a lower urinary excretion of sodium and water than WKY, a higher cumulative sodium balance at all ages studied, and a higher cumulative water balance only at ages 7 and 8 wk. The slopes of the regression lines correlating urinary kallikrein to systolic arterial pressure and to urinary excretion and cumulative balance of sodium and water were always significantly less in SHR than in WKY. The results of the present study indicate that SHR developing hypertension exhibit a precocious and stable abnormality in renal excretion of kallikrein activity. <\/jats:p>","DOI":"10.1152\/ajprenal.1987.252.6.f964","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T21:04:41Z","timestamp":1513976681000},"page":"F964-F969","source":"Crossref","is-referenced-by-count":1,"title":["Reduced urinary kallikrein activity in rats developing spontaneous hypertension"],"prefix":"10.1152","volume":"252","author":[{"given":"J. L.","family":"Ader","sequence":"first","affiliation":[]},{"given":"T.","family":"Tran-Van","sequence":"additional","affiliation":[]},{"given":"F.","family":"Praddaude","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1987.252.6.F964","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:41:57Z","timestamp":1567957317000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1987.252.6.F964"}},"issued":{"date-parts":[[1987,6,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1987,6,1]]}},"alternative-id":["10.1152\/ajprenal.1987.252.6.F964"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1987.252.6.f964","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1987,6,1]]}},{"indexed":{"date-parts":[[2022,3,31]],"date-time":"2022-03-31T19:47:18Z","timestamp":1648756038284},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1994,12,1]]},"abstract":"<jats:p> Chronic rejection necessitates a return to dialysis or retransplantation for a significant number of patients with renal allografts. Although alloresponses between donor organ and recipient importantly determine this process, the detailed immunologic processes and organ physiology of chronic rejection are unclear; in consequence its mechanism and therapy are uncertain. A model of chronic rejection in the rat was used to examine several facets of this process. Fisher-to-Lewis (F-L), allogeneic, and Lewis-to-Lewis (L-L), syngeneic, renal transplants were performed in nephrectomized recipients. All rats were treated with cyclosporin A (5 mg.kg-1.day-1) for 10 days from the time of grafting. At 6 wk, allogeneically grafted animals had a higher protein excretion rate (F-L, 47 +\/- 30 mg\/day; L-L, 17 +\/- 6 mg\/day; P &lt;0.05) and an increase in glomerular capillary pressure (F-L, 69 +\/- 5 mmHg; L-L, 58 +\/- 8 mmHg; P &lt;0.05) and fractional cortical interstitial volume (F-L, 29.8 +\/- 4.3%; L-L, 19.5 +\/- 4.0%; P &lt; 0.01). This model of chronic rejection is characterized by glomerular capillary hypertension, proteinuria, and cortical interstitial expansion. Because these findings are also present in other models of chronic renal injury, mechanisms in addition to alloresponses may operate in chronic rejection. <\/jats:p>","DOI":"10.1152\/ajprenal.1994.267.6.f1102","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T04:54:01Z","timestamp":1514004841000},"page":"F1102-F1106","source":"Crossref","is-referenced-by-count":2,"title":["Physiological and structural responses to chronic experimental renal allograft injury"],"prefix":"10.1152","volume":"267","author":[{"given":"A.","family":"Junaid","sequence":"first","affiliation":[{"name":"Department of Medicine, University of Minnesota, Minneapolis 55455."}]},{"given":"S. M.","family":"Kren","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Minnesota, Minneapolis 55455."}]},{"given":"M. E.","family":"Rosenberg","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Minnesota, Minneapolis 55455."}]},{"given":"K. A.","family":"Nath","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Minnesota, Minneapolis 55455."}]},{"given":"T. H.","family":"Hostetter","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Minnesota, Minneapolis 55455."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1994.267.6.F1102","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:55:53Z","timestamp":1567972553000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1994.267.6.F1102"}},"issued":{"date-parts":[[1994,12,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1994,12,1]]}},"alternative-id":["10.1152\/ajprenal.1994.267.6.F1102"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1994.267.6.f1102","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1994,12,1]]}},{"indexed":{"date-parts":[[2022,3,31]],"date-time":"2022-03-31T08:31:28Z","timestamp":1648715488917},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1990,3,1]]},"abstract":"<jats:p> The effect of parathyroid hormone (PTH) on cytosolic Ca2+ was studied on suspensions of purified rat renal proximal tubules using the fluorescent indicator quin-2. Rat PTH-(1-34) produced a transient 40% increase in apparent cytosolic Ca2+ at 20 s, followed by a rapid return toward the basal level. The half-maximal dose for both the rate of rise and peak apparent Ca2+ was 3 X 10(-8) M for rat PTH-(1-34). Unlike PTH, forskolin and dibutyryl adenosine 3',5'-cyclic monophosphate had no immediate effect. Bovine PTH-(3-34) blocked the effect of PTH in a concentration-dependent manner. Acute reduction of medium Ca2+ to less than 10(-6) M had no effect on either PTH- or angiotensin II (ANG II)-induced transients, but prevented any sustained increases. Washing tubules in nominally Ca2(+)-free medium followed by ethylene glycol-bis (beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid reduced both transients by 50%. PTH at 2 X 10(-7) caused small (6-9%) increases in accumulation of [3H]inositol phosphates comparable with that produced by norepinephrine at 10(-7) M. At 10(-7) M, norepinephrine produced increases in Ca2+ and inositol phosphates similar to PTH; at 10(-5) M much larger increases in inositol phosphates occurred. Exposure to high levels of either norepinephrine or ANG II before PTH administration prevented any subsequent stimulation by PTH or other agonists. A submaximal dose of norepinephrine only slightly blunted the effect of PTH or ANG II.(ABSTRACT TRUNCATED AT 250 WORDS) <\/jats:p>","DOI":"10.1152\/ajprenal.1990.258.3.f545","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T21:37:30Z","timestamp":1513978650000},"page":"F545-F552","source":"Crossref","is-referenced-by-count":2,"title":["Parathyroid hormone regulation of cytosolic Ca2+ in rat proximal tubules"],"prefix":"10.1152","volume":"258","author":[{"given":"C. R.","family":"Filburn","sequence":"first","affiliation":[{"name":"Laboratory of Biological Chemistry, Gerontology Research Center,National Institute on Aging, National Institutes of Health, Baltimore,Maryland 21224."}]},{"given":"S.","family":"Harrison","sequence":"additional","affiliation":[{"name":"Laboratory of Biological Chemistry, Gerontology Research Center,National Institute on Aging, National Institutes of Health, Baltimore,Maryland 21224."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1990.258.3.F545","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:12:03Z","timestamp":1567969923000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1990.258.3.F545"}},"issued":{"date-parts":[[1990,3,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1990,3,1]]}},"alternative-id":["10.1152\/ajprenal.1990.258.3.F545"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1990.258.3.f545","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1990,3,1]]}},{"indexed":{"date-parts":[[2022,3,31]],"date-time":"2022-03-31T06:19:40Z","timestamp":1648707580697},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1994,12,1]]},"abstract":"<jats:p> A method is described for gaining access to the basolateral membranes of confluent Madin-Darby canine kidney (MDCK) cells by surgical reflection of the cell layer overlying fluid-filled domes. Single-channel recordings from cell-attached inside-out and outside-out configurations revealed two K+ channels located in the basal membranes of the highly differentiated monolayers. With 140 mmol\/l KCl in pipette, the intermediate-conductance K+ channel displayed outward rectification in cell-attached configuration with channel conductances of 65 pS for outward part and 17 pS for inward part. In excised-patch recording, this channel had a conductance of 92 pS with 140 mmol\/l KCl on the extracellular side of the patch and 5 mmol\/l KCl on the cytosolic side. The maximum conductance obtained in symmetrical KCl (140 mmol\/l) solution was 140 pS. Ba2+ (1 mmol\/l) and tetraethylammonium (5 mmol\/l) blocked this channel reversibly. Channel open probability (Po) was reduced from 0.41 at cytosolic pH 7.4 to 0.14 at pH 6.8 and increased to 0.64 at pH 8.0. The channel activity was significantly inhibited by elevation of intracellular Ca2+. A small-conductance K+ channel was also observed mainly in excised patches with single-channel conductance of 48 pS in symmetrical KCl solutions. However, the activity of this channel was partially obscured by the intermediate-conductance K+ channel and further analysis was not possible. A physiological role of these channels in mediating K+ recycling through the monolayer is suggested. <\/jats:p>","DOI":"10.1152\/ajprenal.1994.267.6.f1007","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T23:54:01Z","timestamp":1513986841000},"page":"F1007-F1014","source":"Crossref","is-referenced-by-count":0,"title":["Ba(2+)-sensitive K+ channels in basal membrane of confluent Madin-Darby canine kidney cells"],"prefix":"10.1152","volume":"267","author":[{"given":"X. Y.","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Physiology, University of Melbourne, Parkville, Victoria, Australia."}]},{"given":"P. J.","family":"Harris","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Melbourne, Parkville, Victoria, Australia."}]},{"given":"R. E.","family":"Kemm","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Melbourne, Parkville, Victoria, Australia."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1994.267.6.F1007","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:55:46Z","timestamp":1567958146000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1994.267.6.F1007"}},"issued":{"date-parts":[[1994,12,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1994,12,1]]}},"alternative-id":["10.1152\/ajprenal.1994.267.6.F1007"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1994.267.6.f1007","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1994,12,1]]}},{"indexed":{"date-parts":[[2022,4,2]],"date-time":"2022-04-02T20:13:06Z","timestamp":1648930386839},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1993,11,1]]},"abstract":"<jats:p> To examine functional changes of the transporters in the inner stripe of the outer medullary collecting ducts (OMCDis) by the peritubular acid-base status, in vitro microperfusion using the acetoxymethyl ester of 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein was performed. Cell alkalinization systems were assessed by the recovery rate (dpHi\/dt) of intracellular pH (pHi) after intracellular acid loading by NH(4+)-NH3 prepulse with bath amiloride. In alkali-loaded rabbits (0.15 M NaHCO3 drinking for 14 days), dpHi\/dt showed a significant decrease (1.80 +\/- 0.29 pH units\/s x 10(3)) compared with either control (3.30 +\/- 0.59) or acid-loaded rabbits (0.15 M NH4Cl drinking for 14 days, 3.05 +\/- 0.46). The difference of dpHi\/dt between control and alkali-loaded rabbits was eliminated by lumen N-ethylmaleimide (NEM), suggesting that H+ pump activity was decreased. The effect of in vitro alkali treatment (50 mM HCO3-, pH 7.7) for 3-4 h was also examined. This incubation significantly decreased the dpHi\/dt (1.83 +\/- 0.35) compared with the time control experiments (3.18 +\/- 0.28), whereas no significant difference was seen in the presence of lumen NEM. Anion exchanger activity, as determined from the pHi changes after Cl- addition to the bath, showed no significant change with in vivo or in vitro alkali treatment. The results indicate that cell function of the OMCDis is regulated in response to the peritubular acid-base environment via changes in the H(+)-adenosinetriphosphatase. <\/jats:p>","DOI":"10.1152\/ajprenal.1993.265.5.f729","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T06:05:15Z","timestamp":1514009115000},"page":"F729-F735","source":"Crossref","is-referenced-by-count":0,"title":["Effects of in vivo and in vitro alkali treatment on intracellular pH regulation of OMCDis cells"],"prefix":"10.1152","volume":"265","author":[{"given":"M.","family":"Hayashi","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, School of Medicine, Keio University,Tokyo, Japan."}]},{"given":"M.","family":"Iyori","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, School of Medicine, Keio University,Tokyo, Japan."}]},{"given":"Y.","family":"Yamaji","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, School of Medicine, Keio University,Tokyo, Japan."}]},{"given":"T.","family":"Saruta","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, School of Medicine, Keio University,Tokyo, Japan."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1993.265.5.F729","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:31:32Z","timestamp":1567960292000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1993.265.5.F729"}},"issued":{"date-parts":[[1993,11,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1993,11,1]]}},"alternative-id":["10.1152\/ajprenal.1993.265.5.F729"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1993.265.5.f729","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1993,11,1]]}},{"indexed":{"date-parts":[[2022,4,2]],"date-time":"2022-04-02T21:53:47Z","timestamp":1648936427965},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1978,2,1]]},"abstract":"<jats:p> The effects of chronic single nephron or mesonephric duct obstruction on renal pressures were measured in anesthetized Necturi by servo-null techniques. Glomerular capillary hydrostatic pressure (PGC) averaged 11.3 +\/- 1.2 (SD) cmH2O in 18 normal nephrons. Chronic tubule blockade for 2-6 days produced no significant change in PGC. Light and electron microscopy of the juxtaglomerular apparatus (JGA) revealed juxtaglomerular cell granules widely dispersed along the course of preglomerular arterioles, a deficient macula densa, and no polkissen. The absence of a detectable change in PGC with chronic tubule blockade, i.e., a tubuloglomerular feedback response, may reflect poor development of the JGA in this amphibian. <\/jats:p>","DOI":"10.1152\/ajprenal.1978.234.2.f112","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T14:59:39Z","timestamp":1513954779000},"page":"F112-F116","source":"Crossref","is-referenced-by-count":1,"title":["Effects of chronic tubular obstruction in Necturus kidney"],"prefix":"10.1152","volume":"234","author":[{"given":"G. A.","family":"Tanner","sequence":"first","affiliation":[]},{"given":"M. N.","family":"Yum","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1978.234.2.F112","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T14:55:48Z","timestamp":1567954548000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1978.234.2.F112"}},"issued":{"date-parts":[[1978,2,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1978,2,1]]}},"alternative-id":["10.1152\/ajprenal.1978.234.2.F112"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1978.234.2.f112","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1978,2,1]]}},{"indexed":{"date-parts":[[2022,4,2]],"date-time":"2022-04-02T20:53:44Z","timestamp":1648932824262},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1996,9,1]]},"abstract":"<jats:p> We characterized bradykinin (BK) receptors in a human line of glomerular visceral epithelial cells (hGVEC) transfected by the SV40 virus. [3H]BK bound specifically in a manner consistent with a single high-affinity site. Scatchard analysis yielded dissociation constant and maximum binding values of 0.28 +\/- 0.04 nM and 76.6 +\/- 4.9 fmol\/mg, respectively. Competition binding studies with selective BK type 2 (Hoe-140) receptor antagonist and type 1 ([des-Arg9]BK) receptor agonist showed that hGVEC only expressed type 2 receptors, and this was confirmed by reverse transcriptase-polymerase chain reaction and ribonuclease protection assay. BK stimulated intracellular calcium ion concentration ([Ca2+]i) release in a dose-dependent manner with a threshold at 1 nM. Hoe-140, in contrast with [des-Arg9]BK, abolished this effect. [Ca2+]i stimulation was also inhibited by thapsigargin, an inhibitor of Ca(2+)-adenosinetriphosphatase. Ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid attenuated but did not suppress the [Ca2+]i peak. These results associated with the stimulatory effect of BK on inositol phosphate production indicated that [Ca2+]i stimulation was produced both by [Ca2+] mobilization from its intracellular stores and by [Ca2+] entry into the cells. In conclusion, hGVEC express specific type 2 BK receptors that enable specific BK-induced responses. <\/jats:p>","DOI":"10.1152\/ajprenal.1996.271.3.f754","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T01:31:13Z","timestamp":1513992673000},"page":"F754-F761","source":"Crossref","is-referenced-by-count":2,"title":["Characterization of a B2-bradykinin receptor in human glomerular podocytes"],"prefix":"10.1152","volume":"271","author":[{"given":"N.","family":"Ardaillou","sequence":"first","affiliation":[{"name":"Institut National de la Sante et de la Recherche Medicale Unite 64,Hopital Tenon, Paris, France."}]},{"given":"V.","family":"Blaise","sequence":"additional","affiliation":[{"name":"Institut National de la Sante et de la Recherche Medicale Unite 64,Hopital Tenon, Paris, France."}]},{"given":"K.","family":"Costenbader","sequence":"additional","affiliation":[{"name":"Institut National de la Sante et de la Recherche Medicale Unite 64,Hopital Tenon, Paris, France."}]},{"given":"Y.","family":"Vassitch","sequence":"additional","affiliation":[{"name":"Institut National de la Sante et de la Recherche Medicale Unite 64,Hopital Tenon, Paris, France."}]},{"given":"R.","family":"Ardaillou","sequence":"additional","affiliation":[{"name":"Institut National de la Sante et de la Recherche Medicale Unite 64,Hopital Tenon, Paris, France."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1996.271.3.F754","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:06:08Z","timestamp":1567958768000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1996.271.3.F754"}},"issued":{"date-parts":[[1996,9,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1996,9,1]]}},"alternative-id":["10.1152\/ajprenal.1996.271.3.F754"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1996.271.3.f754","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1996,9,1]]}},{"indexed":{"date-parts":[[2022,4,1]],"date-time":"2022-04-01T02:18:19Z","timestamp":1648779499733},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1978,5,1]]},"abstract":"<jats:p> In order to study the effect of potassium on the renal tubule, proximal convoluted tubules were dissected from rabbit kidneys and perfused in vitro. Omitting potassium from both the perfusate and bath caused the rate of fluid absorption and the transtubular potential difference to fall to zero. This effect was due to the absence of potassium in the bathing medium since no change was observed when potassium was omitted from the perfusate only. With 0.5 and 1.0 meq\/liter of potassium in the bath, there was still a significant decrease from control in both the potential difference and the rate of fluid absorption. With 2.5 meq\/liter of potassium in the bath, the results did not differ from control. In further studies, tubules were perfused with 10 meq\/liter of potassium in both perfusate and bath. There was no change in the potential difference of fluid absorption. These results are consistent with the view that active transtubular transport of sodium is linked to the influx of potassium into the cell at the peritubular membrane and that this is probably mediated by sodium-potassium-ATPase. Our results also suggest that the variations of potassium concentration in the physiological range do not affect proximal tubular function. <\/jats:p>","DOI":"10.1152\/ajprenal.1978.234.5.f381","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T15:46:30Z","timestamp":1513957590000},"page":"F381-F385","source":"Crossref","is-referenced-by-count":1,"title":["Effect of potassium on proximal tubular function"],"prefix":"10.1152","volume":"234","author":[{"given":"J.","family":"Cardinal","sequence":"first","affiliation":[]},{"given":"D.","family":"Duchesneau","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1978.234.5.F381","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:01:40Z","timestamp":1567954900000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1978.234.5.F381"}},"issued":{"date-parts":[[1978,5,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1978,5,1]]}},"alternative-id":["10.1152\/ajprenal.1978.234.5.F381"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1978.234.5.f381","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1978,5,1]]}},{"indexed":{"date-parts":[[2024,5,17]],"date-time":"2024-05-17T14:18:27Z","timestamp":1715955507131},"reference-count":39,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2006,8]]},"abstract":"<jats:p>Basic fibroblast growth factor (bFGF) is a heparin-binding growth factor that is accumulated in human dysplastic and cystic renal diseases. Previous studies have shown that bFGF can modulate the growth of developing renal tubules; however, its role in the pathogenesis of renal cyst formation is not clearly understood. Here, we tested the hypothesis that overexpression of bFGF in developing rodent kidneys induces cyst formation in vivo. We used two different adenoviral-mediated gene-transferring approaches to overexpress bFGF in developing rodent kidneys. Initially, metanephric kidney (MK) explants harvested from embryonic day 15 Sprague-Dawley rats were infected with adenoviral vectors (rAd) encoding human bFGF or LacZ genes and transplanted under the renal capsule of adult female rats. Subsequently, to determine whether bFGF could induce renal cysts in developing kidneys with an intact renal collecting system, we injected rAd-bFGF or LacZ vectors in the retroorbital plexus of newborn mice. Basic FGF induced a more efficient integration of the MK explants into the host kidneys and increased the vascularization and proliferation of developing tubules, leading to tubular dilatation and rapid formation of renal cysts. In addition, we successfully expressed human bFGF in the kidney of newborn mice in vivo and induced tubular dilatation and renal cysts. In contrast, mice injected with rAd- lacZ did not develop tubular dilatation or renal cysts. To the best of our knowledge, these experiments show for the first time that overexpression of bFGF in developing rodent kidneys can induce the formation of renal cysts in vivo.<\/jats:p>","DOI":"10.1152\/ajprenal.00382.2005","type":"journal-article","created":{"date-parts":[[2006,4,6]],"date-time":"2006-04-06T13:52:08Z","timestamp":1144331528000},"page":"F289-F296","source":"Crossref","is-referenced-by-count":16,"title":["Novel cystogenic role of basic fibroblast growth factor in developing rodent kidneys"],"prefix":"10.1152","volume":"291","author":[{"given":"Zhuangwu","family":"Li","sequence":"first","affiliation":[]},{"given":"Marina","family":"Jerebtsova","sequence":"additional","affiliation":[]},{"given":"Xue-Hui","family":"Liu","sequence":"additional","affiliation":[]},{"given":"Pingtao","family":"Tang","sequence":"additional","affiliation":[]},{"given":"Patricio E.","family":"Ray","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.273.5.F757"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/17.6.1642"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00723.x"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1159\/000020567"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1101\/gad.13.12.1601"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1096\/fasebj.6.15.1464370"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.110.3.753"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1002\/1521-2254(200105\/06)3:3<252::AID-JGM185>3.0.CO;2-S"},{"key":"R9","unstructured":"Gupta GK, Milner L, Linshaw MA, McCauley RG, Connors S, Folkman J, and Bianchi DW.Urinary basic fibroblast growth factor: a noninvasive marker of progressive cystic renal disease in a child.Am J Med Genet17: 132\u2013135, 2000."},{"key":"R10","doi-asserted-by":"crossref","unstructured":"Hanaoka Kand Guggino WB.cAMP regulates cells proliferation and cyst formation in autosomal polycystic kidney disease cells.J Am Soc Nephrol11: 1179\u20131187, 2000.","DOI":"10.1681\/ASN.V1171179"},{"key":"R11","doi-asserted-by":"crossref","unstructured":"Izevbigie EB, Gutkind JS, and Ray PE.Isoproterenol inhibits fibroblast growth factor-2 induced growth of renal epithelial cells.Pediatr Nephrol14: 726\u2013734, 2001.","DOI":"10.1007\/PL00013426"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-005-1882-0"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1053\/ajkd.2001.26886"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.1998.00854.x"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1007\/BF01233250"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.0590051850.x"},{"key":"R17","doi-asserted-by":"crossref","unstructured":"Lovicu FJand Overbeek PA.Overlapping effects of different members of the FGF family on lens fiber differentiation in transgenic mice.Development125: 3365\u20133377, 1998.","DOI":"10.1242\/dev.125.17.3365"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00834.x"},{"key":"R19","unstructured":"Morita H, Shizato T, David G, Mizutani A, Habuchi H, Fujita Y, Ito M, Asai Maeda KJ, and Kimata K.Basic fibroblast growth factor-binding domain of heparan sulfate in the human glomerulosclerosis and renal tubulointerstitial fibrosis.Lab Invest71: 528\u2013535, 1994."},{"key":"R20","unstructured":"Nguyen HQ, Danilenko DM, Bucay N, DeRose ML, Van GY, Thomason A, and Simonet WS.Expression of keratinocyte growth factor in embryonic liver of transgenic mice causes changes in epithelial growth and differentiation resulting in polycystic kidneys and other organs malformations.Oncogene16: 2109\u20132119, 1996."},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.10.4696"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1677\/erc.0.0070165"},{"key":"R23","doi-asserted-by":"crossref","unstructured":"Qiao J, Uzo R, Obara-Ishihara T, Degenstein L, and Fuchs E.FGF-7 modulates ureteric bud growth and nephron number in the developing kidney.Development126: 547\u2013554, 1999.","DOI":"10.1242\/dev.126.3.547"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.331"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00028.x"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1007\/s004670050749"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00971.x"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.113.6.1447"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1126\/science.3018928"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1007\/s003830050750"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1016\/j.ydbio.2004.04.029"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00997.x"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00333.x"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.060002484.x"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-005-2018-2"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00991.x"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M405079200"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1089\/10430340050015806"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1089\/104303401750061203"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00382.2005","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,7,25]],"date-time":"2021-07-25T10:58:06Z","timestamp":1627210686000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00382.2005"}},"issued":{"date-parts":[[2006,8]]},"references-count":39,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2006,8]]}},"alternative-id":["10.1152\/ajprenal.00382.2005"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00382.2005","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2006,8]]}},{"indexed":{"date-parts":[[2022,3,29]],"date-time":"2022-03-29T03:39:06Z","timestamp":1648525146494},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1978,3,1]]},"abstract":"<jats:p> The permeability of Necturus proximal tubule to hydrophilic nonelectrolytes of varying molecular size was studied under control conditions and during isotonic expansion of the animal's extracellular volume. Transepithelial permeability was measured in perfused tubular segments under conditions of zero net water flux. During volume expansion, tubular permeability to urea increased slightly, whereas mannitol decreased slightly and permeability to sucrose was significantly decreased. Volume expansion had a greater effect on osmotic flow parameters; the NaCl reflection coefficient decreased from 0.64 to 0.47 (summer animals) and from 0.41 to 0.27 (winter animals). Osmotic water flux and hydraulic conductivity increased but only in the lumen-to-capillary direction. Reflection coefficients of nonelectrolytes measured at the apical surface were reduced during volume expansion for probing molecules greater than 3 A in radius and were unchanged for smaller molecules, less than 3 A, suggesting two pore populations. We propose that an increase in tight-junction permeability can account for modification of osmotic flow parameters, whereas the whole thickness of the epithelium, particularly the intercellular space, plays the dominant role in regulation of diffusional permeability. <\/jats:p>","DOI":"10.1152\/ajprenal.1978.234.3.f225","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T15:02:23Z","timestamp":1513954943000},"page":"F225-F234","source":"Crossref","is-referenced-by-count":2,"title":["Permeability changes in Necturus proximal tubule during volume expansion"],"prefix":"10.1152","volume":"234","author":[{"given":"C. J.","family":"Bentzel","sequence":"first","affiliation":[]},{"given":"P. R.","family":"Reczek","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1978.234.3.F225","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T14:57:25Z","timestamp":1567954645000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1978.234.3.F225"}},"issued":{"date-parts":[[1978,3,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1978,3,1]]}},"alternative-id":["10.1152\/ajprenal.1978.234.3.F225"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1978.234.3.f225","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1978,3,1]]}},{"indexed":{"date-parts":[[2022,3,31]],"date-time":"2022-03-31T19:00:54Z","timestamp":1648753254157},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1985,9,1]]},"abstract":"<jats:p> Parathyroid hormone (PTH), through the generation of cAMP, inhibits the transport of sodium, bicarbonate, and water in the proximal convoluted tubule. The present studies were designed to determine whether the response to PTH or dibutyryl cAMP by proximal renal tubules requires an influx of calcium into the cells or an alteration in the cytosolic concentration of calcium. O2 consumption was determined in an enriched suspension of rabbit proximal convoluted tubules, and the ouabain-sensitive component of O2 consumption was taken as a measure of sodium transport. PTH (1 IU\/ml) inhibited the ouabain-sensitive component of O2 consumption from 14.2 +\/- 1.6 to 8.9 +\/- 1.1 nmol O2 X min-1 X mg protein-1 (P less than 0.005). Dibutyryl cAMP (10(-4) M) inhibited ouabain-sensitive O2 consumption from 12.0 +\/- 1.1 to 8.4 +\/- 0.8 nmol O2 X min-1 X mg protein-1 (P less than 0.005). In the presence of lanthanum (5-50 microM) or verapamil (20-200 microM), PTH inhibited ouabain-sensitive O2 consumption by 21.3 +\/- 3.4% (P less than 0.025) and 33.9 +\/- 5.5% (P less than 0.025), respectively. Dibutyryl cAMP inhibited the ouabain-sensitive O2 consumption by 22.6 +\/- 7.1% (P less than 0.025) in the presence of lanthanum and 35.4 +\/- 3.1% (P less than 0.01) in the presence of verapamil. To more directly assess the cytosolic concentration of calcium, the fluorescent intensity of quin 2-loaded tubules was determined. As compared with timed controls, exposure to PTH resulted in a lower cytosolic concentration of calcium over the 10 min of incubation. Dibutyryl cAMP had a similar effect.(ABSTRACT TRUNCATED AT 250 WORDS) <\/jats:p>","DOI":"10.1152\/ajprenal.1985.249.3.f409","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T19:12:48Z","timestamp":1513969968000},"page":"F409-F416","source":"Crossref","is-referenced-by-count":5,"title":["Relationship among parathyroid hormone, cAMP, and calcium on proximal tubule sodium transport"],"prefix":"10.1152","volume":"249","author":[{"given":"G. M.","family":"Dolson","sequence":"first","affiliation":[]},{"given":"M. K.","family":"Hise","sequence":"additional","affiliation":[]},{"given":"E. J.","family":"Weinman","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1985.249.3.F409","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:31:10Z","timestamp":1567956670000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1985.249.3.F409"}},"issued":{"date-parts":[[1985,9,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1985,9,1]]}},"alternative-id":["10.1152\/ajprenal.1985.249.3.F409"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1985.249.3.f409","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1985,9,1]]}},{"indexed":{"date-parts":[[2022,4,1]],"date-time":"2022-04-01T00:42:43Z","timestamp":1648773763512},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1982,1,1]]},"abstract":"<jats:p> The uptake and excretion of endogenous dopa, dopamine, norepinephrine, and epinephrine by the kidney were studied. Blood samples were taken from the aorta at the origin of the renal artery and from the renal vein during a timed urine collection in each of six anesthetised greyhound dogs. Arterial plasma dopa (1,043 +\/- 129 pg\/ml) and epinephrine (218 +\/- 96 pg\/ml) were consistently higher than venous levels of dopa (591 +\/- 80) and epinephrine (54 +\/- 16 pg\/ml), showing extraction of these by the kidney, whereas arterial plasma norepinephrine (329 +\/- 89 pg\/ml) and dopamine (64 +\/- 9 pg\/ml) were lower than the venous levels of norepinephrine (695 +\/- 161 pg\/ml) and dopamine (239 +\/- 45 pg\/ml), indicating secretion of these catecholamines into the circulation. The dopa extracted did not appear in the urine. Norepinephrine (7.2 +\/- 1.7 ng\/min), epinephrine (4.5 +\/- 1.7 ng\/min), and dopamine (3.2 +\/- 0.7 ng\/min) were excreted in the urine. These rates of urinary excretion could be accounted for by glomerular filtration and tubular secretion of the three catecholamines. The kidney extracts circulating dopa. It extracts and excretes epinephrine, norepinephrine, and dopamine, and, in addition, secretes both dopamine and norepinephrine into the circulation. These observations emphasize the important relationship between renal function and the peripheral sympathetic nervous system. <\/jats:p>","DOI":"10.1152\/ajprenal.1982.242.1.f56","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T09:09:25Z","timestamp":1513933765000},"page":"F56-F62","source":"Crossref","is-referenced-by-count":3,"title":["Renal handling of dopa, dopamine, norepinephrine, and epinephrine in the dog"],"prefix":"10.1152","volume":"242","author":[{"given":"S. G.","family":"Ball","sequence":"first","affiliation":[]},{"given":"I. G.","family":"Gunn","sequence":"additional","affiliation":[]},{"given":"I. H.","family":"Douglas","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1982.242.1.F56","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T14:19:21Z","timestamp":1567952361000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1982.242.1.F56"}},"issued":{"date-parts":[[1982,1,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1982,1,1]]}},"alternative-id":["10.1152\/ajprenal.1982.242.1.F56"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1982.242.1.f56","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1982,1,1]]}},{"indexed":{"date-parts":[[2022,3,31]],"date-time":"2022-03-31T21:28:48Z","timestamp":1648762128513},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1992,5,1]]},"abstract":"<jats:p> To assess the possibility of an enhanced role of renal nerves in the control of urinary sodium excretion (UNaV) and fluid homeostasis during pregnancy, urine output, UNaV, and urinary potassium excretion were assessed hourly for 3 days before and for 6 days after a step reduction in total daily sodium intake from 400 to 40 mmol. Studies were performed in normal conscious sheep (4 nonpregnant and 4 pregnant). Each animal was prepared with a divided bladder so that urine could be collected simultaneously from one normally innervated and one denervated kidney. In nonpregnant ewes, ratios of the rates of excretion by denervated vs. innervated kidneys for UNaV averaged 1.00 +\/- 0.07 under steady-state conditions at high levels of sodium intake. This ratio was not different at the low-sodium-intake state. In contrast, this ratio was 1.15 +\/- 0.07 at high sodium intake and 1.13 +\/- 0.03 at low sodium intake in pregnant ewes. The ratios at both steady-state intake levels were different (P less than 0.05) between nonpregnant and pregnant sheep. During the transition between sodium intake states, these ratios were unchanged in nonpregnant animals, whereas pregnant animals exhibited peak ratios of 2.20 +\/- 0.39 (P less than 0.05), indicating sodium wasting by the denervated kidneys. In summary, the data suggest that renal nerve activity may not be completely suppressed by high sodium intakes in pregnant sheep. Furthermore, the renal nerves have an enhanced influence on sodium conservation during and after the transition from high- to low-sodium-intake states during pregnancy.(ABSTRACT TRUNCATED AT 250 WORDS) <\/jats:p>","DOI":"10.1152\/ajprenal.1992.262.5.f823","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T08:53:48Z","timestamp":1514019228000},"page":"F823-F829","source":"Crossref","is-referenced-by-count":0,"title":["Renal nerve effects on renal adaptation to changes in sodium intake during ovine pregnancy"],"prefix":"10.1152","volume":"262","author":[{"given":"G. W.","family":"Aberdeen","sequence":"first","affiliation":[{"name":"Department of Obstetrics and Gynecology, McGill University, Montreal,Quebec, Canada."}]},{"given":"S. C.","family":"Cha","sequence":"additional","affiliation":[{"name":"Department of Obstetrics and Gynecology, McGill University, Montreal,Quebec, Canada."}]},{"given":"S.","family":"Mukaddam-Daher","sequence":"additional","affiliation":[{"name":"Department of Obstetrics and Gynecology, McGill University, Montreal,Quebec, Canada."}]},{"given":"B. S.","family":"Nuwayhid","sequence":"additional","affiliation":[{"name":"Department of Obstetrics and Gynecology, McGill University, Montreal,Quebec, Canada."}]},{"suffix":"Jr","given":"E. W.","family":"Quillen","sequence":"additional","affiliation":[{"name":"Department of Obstetrics and Gynecology, McGill University, Montreal,Quebec, Canada."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1992.262.5.F823","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:16:49Z","timestamp":1567973809000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1992.262.5.F823"}},"issued":{"date-parts":[[1992,5,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1992,5,1]]}},"alternative-id":["10.1152\/ajprenal.1992.262.5.F823"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1992.262.5.f823","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1992,5,1]]}},{"indexed":{"date-parts":[[2022,4,3]],"date-time":"2022-04-03T07:17:01Z","timestamp":1648970221295},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1983,9,1]]},"abstract":"<jats:p> The effects of pharmacologic doses of synthetic salmon calcitonin on the renal tubular capacity of phosphate (Pi) transport were determined in the presence and absence of maximally phosphaturic doses of parathyroid hormone (PTH). Thyroparathyroidectomized rats were given graded infusions of Pi (1, 2, and 3 mumol\/min) to prevent the hypophosphatemic effects of calcitonin and to determine the maximum transport of Pi for the kidney (TmPi\/GFR). The maximum transport of Pi for the rats treated with calcitonin was 2.46 +\/- 0.27 mumol\/ml. This value was significantly less than that of 3.88 +\/- 0.32 mumol\/ml (P less than 0.05) for the control animals but was significantly greater than the maximum transport of Pi of 1.16 +\/- 0.05 mumol\/ml (P less than 0.05) for the rats treated with PTH. Furthermore, there was no significant difference between the maximum transport of Pi for the rats treated with PTH and that of 1.04 +\/- 0.05 mumol\/ml for the rats treated with PTH plus calcitonin. We conclude that pharmacologic doses of calcitonin decrease the tubular capacity for Pi reabsorption of the kidney and that the effect is significantly smaller than that of maximally phosphaturic doses of PTH. <\/jats:p>","DOI":"10.1152\/ajprenal.1983.245.3.f345","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T14:38:37Z","timestamp":1513953517000},"page":"F345-F348","source":"Crossref","is-referenced-by-count":1,"title":["Calcitonin decreases the renal tubular capacity for phosphate reabsorption"],"prefix":"10.1152","volume":"245","author":[{"given":"R. K.","family":"Zalups","sequence":"first","affiliation":[]},{"given":"F. G.","family":"Knox","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1983.245.3.F345","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:23:26Z","timestamp":1567967006000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1983.245.3.F345"}},"issued":{"date-parts":[[1983,9,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1983,9,1]]}},"alternative-id":["10.1152\/ajprenal.1983.245.3.F345"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1983.245.3.f345","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1983,9,1]]}},{"indexed":{"date-parts":[[2022,4,4]],"date-time":"2022-04-04T17:43:50Z","timestamp":1649094230533},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1984,11,1]]},"abstract":"<jats:p> Prostaglandin E2 (PGE2) inhibits the ADH-stimulated components of the lumen-positive transepithelial voltage (Ve) and of net chloride absorption (JnetCl) in the isolated microperfused mouse medullary thick ascending limb of Henle (mTALH), presumably by interfering with the ADH-dependent intracellular accumulation of cAMP. These experiments examined the interactions of PGE2 with two nonhormonal stimulators of adenylate cyclase--cholera toxin and forskolin--in an attempt to evaluate the means by which PGE2 inhibits ADH-stimulated transport in these mTALH segments. Forskolin (FSK) stimulated Ve in the mTALH with half-maximal stimulation at 1.4 X 10(-7) M FSK. PGE2 had no effect on FSK stimulation of Ve; 10(-6) M FSK reversed completely the PGE2 inhibition of ADH-stimulated Ve. A low concentration of cholera toxin, 5 X 10(-13) M, stimulated Ve and JnetCl in the mTALH; 10(-6) M PGE2 inhibited the stimulation by cholera toxin; and 10(-6) M FSK reversed the PGE2 inhibition of both Ve and JnetCl in cholera toxin-stimulated mTALH. A higher concentration of cholera toxin, 10(-10) M, stimulated Ve and JnetCl to values identical to those seen with maximal concentrations of ADH, but PGE2 did not inhibit the increments in either Ve or JnetCl produced by 10(-10) M cholera toxin. PGE2 appears to inhibit ADH stimulation of NaCl transport in mTALH by an action distal to hormone-receptor interactions yet proximal to the catalytic subunit of adenylate cyclase. <\/jats:p>","DOI":"10.1152\/ajprenal.1984.247.5.f784","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T15:59:48Z","timestamp":1513958388000},"page":"F784-F792","source":"Crossref","is-referenced-by-count":9,"title":["PGE2, forskolin, and cholera toxin interactions in modulating NaCl transport in mouse mTALH"],"prefix":"10.1152","volume":"247","author":[{"given":"R. M.","family":"Culpepper","sequence":"first","affiliation":[]},{"given":"T. E.","family":"Andreoli","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1984.247.5.F784","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:29:35Z","timestamp":1567967375000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1984.247.5.F784"}},"issued":{"date-parts":[[1984,11,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1984,11,1]]}},"alternative-id":["10.1152\/ajprenal.1984.247.5.F784"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1984.247.5.f784","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1984,11,1]]}},{"indexed":{"date-parts":[[2022,4,3]],"date-time":"2022-04-03T08:29:29Z","timestamp":1648974569877},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1980,12,1]]},"abstract":"<jats:p> The time course of the water permeability response to synthetic arginine vasopressin (AVP) was examined in isolated perfused rabbit collecting tubules. When experiments were conducted at 37 degrees C, addition of AVP in a concentration of 100 microU\/ml increased hydraulic water permeability (Lp) from 18 +\/- 4 X 10(-7) to 153 +\/- 15 X 10(-7) cm x s-1 x atm-1. However, in contrast to results obtained at 25 degrees C, the Lp immediately decreased in spite of the continued presence of AVP, reaching half the peak value in 67 +\/- 6 (SE) min. A similar decline was observed at 37 degrees C when a cyclic 3',5'-adenosine monophosphate analogue was added to the bathing medium. Corticosteroids greatly enhanced the peak water absorption but did not stabilize the subsequent response to AVP at 37 degrees C. A decline in diffusional water permeability measured in the absence of a transtubule osmotic gradient excluded the possible roles of cellular hypotonicity, increased cell volume, or osmotic water absorption in the unstable response to hormone. The peritubular membrane remained highly permeable to water, independent of AVP and temperature. Duration of exposure to 37 degrees C was more important than AVP in determining the unstable response. On the basis of these studies we conclude that isolated rabbit cortical collecting tubules progressively become insensitive to AVP at 37 degrees C, possibly due to alterations in the responsiveness of the urinary plasma membrane to cAMP. <\/jats:p>","DOI":"10.1152\/ajprenal.1980.239.6.f595","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T07:41:08Z","timestamp":1513928468000},"page":"F595-F601","source":"Crossref","is-referenced-by-count":1,"title":["Temperature effect on ADH response of isolated perfused rabbit collecting tubules"],"prefix":"10.1152","volume":"239","author":[{"given":"D. A.","family":"Hall","sequence":"first","affiliation":[]},{"given":"J. J.","family":"Grantham","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1980.239.6.F595","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T14:08:03Z","timestamp":1567951683000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1980.239.6.F595"}},"issued":{"date-parts":[[1980,12,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1980,12,1]]}},"alternative-id":["10.1152\/ajprenal.1980.239.6.F595"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1980.239.6.f595","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1980,12,1]]}},{"indexed":{"date-parts":[[2023,8,31]],"date-time":"2023-08-31T10:46:21Z","timestamp":1693478781881},"reference-count":66,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1999,1,1]]},"abstract":"<jats:p>Gene transfer approaches offer the promise of revolutionizing medicine. In this review, we focus on the current and future prospects of somatic gene transfer into the kidney. The advantages and disadvantages of current vector systems are described, and the ex vivo and in vitro approaches applicable to the kidney are reviewed. We discuss uses of gene transfer approaches to dissect the pathogenesis of kidney disease and the future directions and applications of gene transfer to combat kidney destruction.<\/jats:p>","DOI":"10.1152\/ajprenal.1999.276.1.f1","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T16:10:27Z","timestamp":1514045427000},"page":"F1-F9","source":"Crossref","is-referenced-by-count":7,"title":["Gene transfer in the kidney"],"prefix":"10.1152","volume":"276","author":[{"given":"Vicki Rubin","family":"Kelley","sequence":"first","affiliation":[{"name":"Renal Division, Molecular Autoimmunity, Brigham and Women\u2019s Hospital, Harvard Medical School, and"}]},{"given":"Vikas P.","family":"Sukhatme","sequence":"additional","affiliation":[{"name":"Renal Division, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215"}]}],"member":"24","reference":[{"key":"B1","first-page":"367","volume":"1","author":"Ali M.","year":"1994","journal-title":"Gene Ther."},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1038\/377630a0"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1089\/hum.1997.8.10-1243"},{"key":"B5","first-page":"49","volume":"1","author":"Bosch R. J.","year":"1993","journal-title":"Exp. Nephrol."},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.94.5.1645"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(94)90137-6"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(95)90339-9"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1993.79"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1126\/science.270.5235.404"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.85.17.6460"},{"key":"B12","doi-asserted-by":"crossref","first-page":"4626","DOI":"10.1128\/JVI.71.6.4626-4637.1997","volume":"71","author":"Dedieu J.-F.","year":"1997","journal-title":"J. Virol."},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1089\/hum.1994.5.8-979"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.88"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1089\/hum.1996.7.15-1907"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117859"},{"key":"B17","first-page":"21","volume":"3","author":"Heikkila P.","year":"1996","journal-title":"Gene Ther."},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1038\/nm0496-418"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1172\/JCI116874"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1084\/jem.186.4.613"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1126\/science.2911748"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1126\/science.278.5341.1322"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1038\/nm0797-738"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1089\/hum.1997.8.1-45"},{"key":"B25","first-page":"693","volume":"139","author":"Kaspareit-Rittinghausen J.","year":"1991","journal-title":"Am. J. Pathol."},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1177\/030098588902600302"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.93.14.7387"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117361"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.473"},{"key":"B30","first-page":"56","volume":"4","author":"Kitamura M.","year":"1994","journal-title":"Exp. Nephrol."},{"key":"B31","first-page":"S86","volume":"60","author":"Kitamura M.","year":"1997","journal-title":"Kidney Int. Suppl."},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119659"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1097\/00007890-199404150-00002"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.93.12.5731"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1172\/JCI1694"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1038\/sj.gt.3300406"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1126\/science.273.5271.109"},{"key":"B39","first-page":"S85","volume":"61","author":"Lein Y. H.","year":"1997","journal-title":"Kidney Int. Suppl."},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1126\/science.1323143"},{"key":"B41","doi-asserted-by":"crossref","first-page":"8944","DOI":"10.1128\/JVI.70.12.8944-8960.1996","volume":"70","author":"Lieber A.","year":"1996","journal-title":"J. Virol."},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(96)90457-6"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1038\/332161a0"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1089\/hum.1996.7.1-79"},{"key":"B45","doi-asserted-by":"crossref","first-page":"433","DOI":"10.4049\/jimmunol.157.1.433","volume":"157","author":"Moore K. J.","year":"1996","journal-title":"J. Immunol."},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.13.5855"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.162"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1126\/science.8493530"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.8.3194"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)81874-7"},{"issue":"40","key":"B52","first-page":"F603","volume":"271","author":"Naito T.","year":"1996","journal-title":"Am. J. Physiol."},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1007\/BF03401628"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1126\/science.272.5259.263"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1038\/nm0298-194"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.93.21.11400"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1038\/380364a0"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1097\/00000658-199410000-00009"},{"key":"B59","doi-asserted-by":"crossref","first-page":"2946","DOI":"10.1182\/blood.V84.9.2946.2946","volume":"84","author":"Setoguchi Y.","year":"1994","journal-title":"Blood"},{"key":"B60","first-page":"1537","volume":"57","author":"Simons J. W.","year":"1997","journal-title":"Cancer Res."},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.167"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-291X(05)80784-3"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1038\/nm0596-545"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.93.20.10876"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.205"},{"key":"B69","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1996.1444"},{"key":"B70","doi-asserted-by":"publisher","DOI":"10.1097\/00007890-199603150-00023"},{"key":"B71","first-page":"298","volume":"3","author":"Zhu G.","year":"1996","journal-title":"Gene Ther."},{"key":"B72","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.421"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1999.276.1.F1","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,8,30]],"date-time":"2023-08-30T05:41:16Z","timestamp":1693374076000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1999.276.1.F1"}},"issued":{"date-parts":[[1999,1,1]]},"references-count":66,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1999,1,1]]}},"alternative-id":["10.1152\/ajprenal.1999.276.1.F1"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1999.276.1.f1","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1999,1,1]]}},{"indexed":{"date-parts":[[2022,3,29]],"date-time":"2022-03-29T17:45:00Z","timestamp":1648575900655},"reference-count":10,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2007,7]]},"DOI":"10.1152\/ajprenal.00218.2007","type":"journal-article","created":{"date-parts":[[2007,5,16]],"date-time":"2007-05-16T20:55:09Z","timestamp":1179348909000},"page":"F50-F51","source":"Crossref","is-referenced-by-count":2,"title":["How to keep kidneys safe while shrinking tumors: the conundrum of cisplatin action"],"prefix":"10.1152","volume":"293","author":[{"given":"Michael S.","family":"Goligorsky","sequence":"first","affiliation":[]}],"member":"24","reference":[{"key":"R1","unstructured":"Berthet C, Kaldis P. Cell-specific responses to loss of cyclin-dependent kinases. Oncogene. In press."},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1016\/S1535-6108(03)00080-1"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1208619"},{"key":"R4","unstructured":"Dong Y, Yang H, Elliott M, McMasters K. Adenovirus-mediated E2F1 gene transfer sensitizes melanoma cells to apoptosis induced by topoisomerase II inhibitors. Cancer Res 62: 1776\u20131783, 2002."},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1172\/JCI1497"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1203540"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1158\/1078-0432.CCR-06-0780"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1158\/0008-5472.CAN-05-3725"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1158\/0008-5472.CAN-05-0888"},{"key":"R10","doi-asserted-by":"crossref","unstructured":"Yu F, Megyesi J, Safirstein R, Price P. Involvement of the CDK2-E2F1 pathway in cysplatin cytotoxicity in vitro and in vivo. Am J Physiol Renal Physiol. First published April 25, 2007; doi:10.1152.ajprenal.00119.2007.","DOI":"10.1152\/ajprenal.00119.2007"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00218.2007","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:35:32Z","timestamp":1567967732000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00218.2007"}},"issued":{"date-parts":[[2007,7]]},"references-count":10,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2007,7]]}},"alternative-id":["10.1152\/ajprenal.00218.2007"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00218.2007","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2007,7]]}},{"indexed":{"date-parts":[[2022,3,29]],"date-time":"2022-03-29T14:41:36Z","timestamp":1648564896926},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1977,11,1]]},"abstract":"<jats:p> To investigate the effects of uninephrectomy on renal concentrating ability, studies were performed on unanesthetized rats 5-11 days after uninephrectomy (UN) or a sham operation (SO). Female rats were deprived of water for 27 h prior to the infusion of inulin and para-aminohippurate and urine collection. They were also preconditioned to being handled and to the experimental locale. During a nondiuretic state urine osmolality was the same for all UN and SO groups (mean about 1,700 micro osmol\/g H2O), whereas the mean solute excretion rate (micro osmol\/min per kg body wt per kidney) was 74 in the UN and 35 in the SO rats. When SO rats were infused with mannitol or isotonic saline to increase their solute excretion rate per kidney to the level of the UN rats, urine osmolality dropped 200-1,000 micro osmol\/g H2O; when urea was infused, urine osmolality did not drop. Thus, after uninephrectomy and a consequent doubling of the solute excretion rate per kidney, renal concentrating ability was higher than predicted on the basis of a comparable but acute elevation of the solute excretion rate. The glomerular filtration rate was about 17 ml\/min per kg body wt in the SO rats and was 1.2 times greater (on a per kidney basis) in the UN rats. These exceptionally high glomerular filtration rats are attributed to preexperimental conditioning of the rats and the absence of stress during urine collection. <\/jats:p>","DOI":"10.1152\/ajprenal.1977.233.5.f428","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T20:08:13Z","timestamp":1513973293000},"page":"F428-F437","source":"Crossref","is-referenced-by-count":0,"title":["Renal concentrating ability in the uninephrectomized rat"],"prefix":"10.1152","volume":"233","author":[{"given":"E.","family":"Sachtjen","sequence":"first","affiliation":[]},{"given":"L.","family":"Rabinowitz","sequence":"additional","affiliation":[]},{"given":"P. E.","family":"Binkerd","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1977.233.5.F428","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:56:08Z","timestamp":1567968968000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1977.233.5.F428"}},"issued":{"date-parts":[[1977,11,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1977,11,1]]}},"alternative-id":["10.1152\/ajprenal.1977.233.5.F428"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1977.233.5.f428","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1977,11,1]]}},{"indexed":{"date-parts":[[2022,3,29]],"date-time":"2022-03-29T18:30:52Z","timestamp":1648578652355},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1990,4,1]]},"abstract":"<jats:p> The ionic conductive properties of the nonperfused rabbit proximal straight tubule (S2) basolateral membrane were assessed by microelectrode techniques. The response of the basolateral membrane electrical potential difference, Vbl, to rapid changes in the peritubular bath concentration of K, HCO3, Na, and Cl were monitored with microelectrodes. The control steady-state Vbl averaged -41 mV (cell negative). An increase in peritubular bathing medium K concentration from 5 to 40 mM resulted in an instantaneous and sustained depolarization of +14.6 mV (27% of delta EK). Addition of barium (2 mM) depolarized the Vbl by +15.8 mV and abolished the Vbl response to the high-K medium. In other studies, reduction of peritubular bicarbonate at constant pH from 25 to 2.5 mM instantaneously and transiently depolarized Vbl by +15.8 mV (26% of delta EHCO3). In these same tubules reduction of peritubular Na from 126 to 2.2 mM resulted in an instantaneous and paradoxical depolarization of Vbl of +21.5 mV. Both depolarization transients resulting from reduction of Na and HCO3 were simultaneously inhibited by the addition of 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (SITS; 0.5 mM), consistent with the presence of a SITS-sensitive Na-HCO3-coupled conductive pathway. In the absence of the bicarbonate buffer, reduction of Na resulted in a small sustained hyperpolarization of -5.8 mV (5% of delta ENa). Reduction of peritubular Cl from 120 to 4 mM resulted in an instantaneous and sustained depolarization of Vbl of +5.3 mV (6% of ECl) and was not affected by the addition of bumetanide (0.1 mM). It is concluded that the basolateral membrane of the nonperfused proximal straight tubule is characterized by a major barium-sensitive K conductance and a SITS-sensitive Na-coupled HCO3 conductance that carries net negative charge. These pathways are paralleled by relatively minor, but important, Na-conductive and Cl-conductive pathways. <\/jats:p>","DOI":"10.1152\/ajprenal.1990.258.4.f940","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T23:20:11Z","timestamp":1513984811000},"page":"F940-F950","source":"Crossref","is-referenced-by-count":1,"title":["Ionic conductive properties of rabbit proximal straight tubule basolateral membrane"],"prefix":"10.1152","volume":"258","author":[{"given":"P. A.","family":"Welling","sequence":"first","affiliation":[{"name":"Department of Physiology and Cell Biology, University of Texas MedicalSchool, Houston 77225."}]},{"given":"R. G.","family":"O'Neil","sequence":"additional","affiliation":[{"name":"Department of Physiology and Cell Biology, University of Texas MedicalSchool, Houston 77225."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1990.258.4.F940","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:22:16Z","timestamp":1567970536000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1990.258.4.F940"}},"issued":{"date-parts":[[1990,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1990,4,1]]}},"alternative-id":["10.1152\/ajprenal.1990.258.4.F940"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1990.258.4.f940","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1990,4,1]]}},{"indexed":{"date-parts":[[2022,3,29]],"date-time":"2022-03-29T11:16:18Z","timestamp":1648552578853},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1977,2,1]]},"abstract":"<jats:p> The maturation of renal function was investigated by clearance studies in 11 fetal, 9 young, and 4 adult guinea pigs undergoing salt loading (NaCl 1.5%, 75 mul min-1 100 g-1) and in 10 young and 4 adult animals under nondiuretic conditions. The fetal preparation described makes it possible to obtain two to four steady clearance periods for each animal. In the fetus, GFR increased significantly with age, but less than in the newborn. Fractional water and sodium reabsorption was generally low, and net renal secretion of potassium was observed in some cases. Fetal urine was sometimes slightly hypertonic. The effectiveness of the diuretic and natriuretic response following saline expansion was smaller in young than adult animals. The fractional excretion rate of solutes and water increased as a function of age in the young animal and the urinary Na\/K concentration ratio showed a marked drop around birth. This latter observation suggests that during the first days of life the effect of saline expansion on the proximal tubule is partially blunted by enhanced sodium reabsorption from the distal nephron due to the high concentration of circulating aldosterone. <\/jats:p>","DOI":"10.1152\/ajprenal.1977.232.2.f178","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T20:21:42Z","timestamp":1513974102000},"page":"F178-F185","source":"Crossref","is-referenced-by-count":3,"title":["Renal clearance studies in fetal and young guinea pigs: effect of salt loading"],"prefix":"10.1152","volume":"232","author":[{"given":"C.","family":"Merlet-Benichou","sequence":"first","affiliation":[]},{"given":"C.","family":"de Rouffignac","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1977.232.2.F178","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:58:54Z","timestamp":1567969134000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1977.232.2.F178"}},"issued":{"date-parts":[[1977,2,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1977,2,1]]}},"alternative-id":["10.1152\/ajprenal.1977.232.2.F178"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1977.232.2.f178","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1977,2,1]]}},{"indexed":{"date-parts":[[2023,10,5]],"date-time":"2023-10-05T22:44:03Z","timestamp":1696545843719},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1997,2,1]]},"abstract":"<jats:p> Differential display-polymerase chain reaction (DD-PCR) was used to identify genes that are expressed in kidney following induction of acute ischemic renal injury. The receptor for activated C kinase (RACK1) mRNA expression in kidneys obtained from rats 12 h following ischemia is enhanced twofold compared with sham-operated rats. The maximal enhancement of expression (3.3-fold) is at 7 days following reperfusion. Expression remains elevated at 14 days. RACK1 transcripts and protein are localized to the damaged and regenerating segments of proximal tubules. At 1 day following injury, RACK1 protein is present in the epithelial cells of the damaged S3 segment and in cells sloughed into the tubular lumen. By 5 days following injury, RACK1 protein expression is enhanced in the regenerating cells relining the injured tubules of the S3 segment and in papillary proliferations within regenerating tubules. Increased expression of RACK1 could enhance the activity of PKC and, in so doing, regulate the process of regeneration of the proximal tubule following ischemic renal injury. <\/jats:p>","DOI":"10.1152\/ajprenal.1997.272.2.f160","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T08:43:57Z","timestamp":1514018637000},"page":"F160-F166","source":"Crossref","is-referenced-by-count":7,"title":["Ischemia-induced receptor for activated C kinase (RACK1) expression in rat kidneys"],"prefix":"10.1152","volume":"272","author":[{"given":"B. J.","family":"Padanilam","sequence":"first","affiliation":[{"name":"George M. O'Brien Kidney and Urological Diseases Center, WashingtonUniversity School of Medicine, St. Louis, Missouri 63110, USA."}]},{"given":"M. R.","family":"Hammerman","sequence":"additional","affiliation":[{"name":"George M. O'Brien Kidney and Urological Diseases Center, WashingtonUniversity School of Medicine, St. Louis, Missouri 63110, USA."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1997.272.2.F160","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:16:23Z","timestamp":1567973783000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1997.272.2.F160"}},"issued":{"date-parts":[[1997,2,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1997,2,1]]}},"alternative-id":["10.1152\/ajprenal.1997.272.2.F160"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1997.272.2.f160","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1997,2,1]]}},{"indexed":{"date-parts":[[2023,10,17]],"date-time":"2023-10-17T21:22:55Z","timestamp":1697577775988},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1985,2,1]]},"abstract":"<jats:p> Plasma volume expansion alters renal tubular sodium chloride transport and renal nerve activity. The purpose of this study was to determine the mechanism(s) for inhibition of renin secretion by acute volume expansion with albumin in the anesthetized dog. In dogs with a single intact kidney, albumin infusion decreased renin release by 86% and significantly increased renal blood flow, glomerular filtration rate, and sodium excretion. Albumin volume expansion inhibited renin secretion to a lesser extent in dogs with denervated filtering kidneys and in dogs with innervated nonfiltering kidneys. In dogs with denervated nonfiltering kidneys, albumin infusion did not change renin secretion. Comparable volume expansion was produced in all groups. Thus, inhibition of renin release by acute plasma volume expansion is dependent on both a renal tubular mechanism and the integrity of the renal nerves. Partial inhibition of renin release was observed with interruption of either one of the mechanisms, whereas interruption of both mechanisms totally abolished the effect of acute plasma volume expansion on renin secretion. <\/jats:p>","DOI":"10.1152\/ajprenal.1985.248.2.f206","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T00:43:27Z","timestamp":1513989807000},"page":"F206-F211","source":"Crossref","is-referenced-by-count":1,"title":["Mechanism for inhibition of renin release by acute plasma volume expansion in the dog"],"prefix":"10.1152","volume":"248","author":[{"given":"M. W.","family":"Roy","sequence":"first","affiliation":[]},{"given":"C. E.","family":"Ott","sequence":"additional","affiliation":[]},{"given":"W. J.","family":"Welch","sequence":"additional","affiliation":[]},{"given":"J. H.","family":"Downs","sequence":"additional","affiliation":[]},{"given":"T. A.","family":"Kotchen","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1985.248.2.F206","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:33:22Z","timestamp":1567971202000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1985.248.2.F206"}},"issued":{"date-parts":[[1985,2,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1985,2,1]]}},"alternative-id":["10.1152\/ajprenal.1985.248.2.F206"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1985.248.2.f206","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1985,2,1]]}},{"indexed":{"date-parts":[[2022,6,17]],"date-time":"2022-06-17T00:07:31Z","timestamp":1655424451615},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1989,10,1]]},"abstract":"<jats:p> Growth hormone (GH) exerts a variety of metabolic and anabolic effects on skeletal and soft tissues including kidney. Some of these actions are mediated directly, whereas others result from GH-dependent synthesis and release of polypeptide growth factors designated insulin-like growth factors (IGFs). Receptors for GH are present in proximal tubule and GH directly stimulates gluconeogenesis at this site. IGF receptors are found in glomerulus and proximal tubule. Mechanisms for signal transduction by GH and IGFs have been characterized using proximal tubular basolateral membranes. IGFs regulate metabolic and transport processes in cultured glomerular mesangial cells and in isolated proximal tubular cells. IGF I is synthesized in cultured mesangial cells and is produced in a GH-dependent manner in cortical and medullary collecting duct. Evidence has accumulated that IGF I of renal origin functions as a paracrine growth factor in the settings of GH-induced hypertrophy and compensatory hypertrophy of the kidney, and in the setting of proximal tubular regeneration following ischemic injury. IGFs are embryonal mitogens and IGF II may act as a transforming agent for Wilms' tumor. Further characterization of the GH-IGF axis in kidney will provide additional insights into the roles of these peptides as regulators of renal function, growth, and development. <\/jats:p>","DOI":"10.1152\/ajprenal.1989.257.4.f503","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T21:53:58Z","timestamp":1513979638000},"page":"F503-F514","source":"Crossref","is-referenced-by-count":3,"title":["The growth hormone-insulin-like growth factor axis in kidney"],"prefix":"10.1152","volume":"257","author":[{"given":"M. R.","family":"Hammerman","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, Washington University School of Medicine, St. Louis, Missouri 63110."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1989.257.4.F503","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:14:35Z","timestamp":1567970075000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1989.257.4.F503"}},"issued":{"date-parts":[[1989,10,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1989,10,1]]}},"alternative-id":["10.1152\/ajprenal.1989.257.4.F503"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1989.257.4.f503","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1989,10,1]]}},{"indexed":{"date-parts":[[2024,6,19]],"date-time":"2024-06-19T11:18:19Z","timestamp":1718795899862},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1996,5,1]]},"abstract":"<jats:p> Animal studies have implicated an important role of nitric oxide (NO) in the regulation of blood pressure, renal hemodynamics, and renal excretion of sodium. NG-monomethyl-L-arginine (L-NMMA) is a specific, competitive inhibitor of NO synthesis interfering with NO synthase. The purpose of the present study was to investigate the effect of L-NMMA on renal plasma flow (RPF), glomerular filtration rate (GFR), urinary sodium excretion (UNa), fractional sodium excretion (FENa), fractional lithium excretion (FELi), mean arterial blood pressure (MAP), and heart rate (HR) in healthy humans. In a randomized placebo-controlled study, 23 healthy subjects were randomized to receive either bolus injection of L-NMMA (3 mg\/kg in 10 ml saline, n = 12 subjects) or placebo (10 ml saline, n = 11). GFR and RPF were measured using the renal clearances of 51Cr-labeled EDTA and 125I-labeled hippuran by the constant infusion technique. L-NMMA treatment induced 60 min after injection a 14.6% decrease in RPF, a 5.8% decrease in GFR, a 9.8% increase in filtration fraction, a 34.7% decrease in UNa a 28.6% decrease in FENa, and a 12.1% decrease in FELi. These changes were still evident 120 min after injection. None of the effect parameters were changed after placebo, except FENa, which increased 9.9% 60 min after injection. Ten minutes after L-NMMA injection, MAP increased significantly (80 vs. 88 mmHg), and HR decreased (58 vs. 47 beats\/min). The changes in HR and MAP normalized within 30 min. L-NMMA significantly reduced the plasma level of cGMP 60 min (3.0 vs. 3.7 pmol\/l) and 120 min after injection (2.5 vs. 3.7 pmol\/l). It is concluded that, in healthy humans, NO is a regulator of renal hemodynamics as a tonic vasodilator and a regulator of sodium excretion, due at least in part to a proximal tubular effect. <\/jats:p>","DOI":"10.1152\/ajprenal.1996.270.5.f845","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T06:59:33Z","timestamp":1514012373000},"page":"F845-F851","source":"Crossref","is-referenced-by-count":18,"title":["Effects of systemic NO synthesis inhibition on RPF, GFR, UNa, and vasoactive hormones in healthy humans"],"prefix":"10.1152","volume":"270","author":[{"given":"J. N.","family":"Bech","sequence":"first","affiliation":[{"name":"Research Laboratory for Hypertension and Nephrology, Skejby Hospital,University Hospital in Aarhus, Denmark."}]},{"given":"C. B.","family":"Nielsen","sequence":"additional","affiliation":[{"name":"Research Laboratory for Hypertension and Nephrology, Skejby Hospital,University Hospital in Aarhus, Denmark."}]},{"given":"E. B.","family":"Pedersen","sequence":"additional","affiliation":[{"name":"Research Laboratory for Hypertension and Nephrology, Skejby Hospital,University Hospital in Aarhus, Denmark."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1996.270.5.F845","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:08:27Z","timestamp":1567973307000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1996.270.5.F845"}},"issued":{"date-parts":[[1996,5,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1996,5,1]]}},"alternative-id":["10.1152\/ajprenal.1996.270.5.F845"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1996.270.5.f845","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1996,5,1]]}},{"indexed":{"date-parts":[[2022,3,29]],"date-time":"2022-03-29T21:04:37Z","timestamp":1648587877015},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2000,2,1]]},"DOI":"10.1152\/ajprenal.2000.278.2.f337","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T11:35:23Z","timestamp":1514028923000},"page":"F337-F337","source":"Crossref","is-referenced-by-count":0,"title":["The Carl W. Gottschalk Distinguished Lectureship of the Renal Section"],"prefix":"10.1152","volume":"278","member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.2000.278.2.F337","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:37:59Z","timestamp":1567975079000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.2000.278.2.F337"}},"issued":{"date-parts":[[2000,2,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2000,2,1]]}},"alternative-id":["10.1152\/ajprenal.2000.278.2.F337"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.2000.278.2.f337","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2000,2,1]]}},{"indexed":{"date-parts":[[2023,10,31]],"date-time":"2023-10-31T07:49:58Z","timestamp":1698738598003},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1984,11,1]]},"abstract":"<jats:p> To measure simultaneously the concentration profiles of bicarbonate, chloride and inulin along the length of the superficial proximal convoluted tubule, free-flow micropuncture measurements were made sequentially from the end-proximal tubule to Bowman's space in 10 tubules of hydropenic Munich-Wistar rats. Bicarbonate and volume reabsorption were 354 +\/- 21 pmol X mm-1 X min-1 and 5.9 +\/- 0.4 nl X mm-1 X min-1 in the first millimeter and fell progressively in the remaining 3.8 mm of tubule, averaging 83 +\/- 4 pmol X mm-1 X min-1 and 2.3 +\/- 0.5 nl X mm-1 X min-1, respectively. The values in the initial millimeter represents a high transport capacity since they exceed rates that have been observed when comparable or even higher mean luminal substrate concentrations were presented to the late proximal tubule. In contrast, chloride reabsorption was only 206 +\/- 55 peq X mm-1 X min-1 in the first millimeter compared with a mean of 306 +\/- 22 peq X mm-1 X min-1 in the rest of the tubule. In conclusion, there is substantial axial transport heterogeneity, with bicarbonate and water reabsorption higher but chloride reabsorption lower in the early compared with the late superficial proximal convoluted tubule. <\/jats:p>","DOI":"10.1152\/ajprenal.1984.247.5.f816","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T15:59:48Z","timestamp":1513958388000},"page":"F816-F821","source":"Crossref","is-referenced-by-count":12,"title":["Axial heterogeneity in the rat proximal convoluted tubule. I. Bicarbonate, chloride, and water transport"],"prefix":"10.1152","volume":"247","author":[{"given":"F. Y.","family":"Liu","sequence":"first","affiliation":[]},{"given":"M. G.","family":"Cogan","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1984.247.5.F816","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:29:37Z","timestamp":1567967377000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1984.247.5.F816"}},"issued":{"date-parts":[[1984,11,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1984,11,1]]}},"alternative-id":["10.1152\/ajprenal.1984.247.5.F816"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1984.247.5.f816","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1984,11,1]]}},{"indexed":{"date-parts":[[2023,10,30]],"date-time":"2023-10-30T19:42:43Z","timestamp":1698694963009},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1993,7,1]]},"abstract":"<jats:p> Hepatic lipid and apolipoprotein synthesis is increased in the nephrotic syndrome. Catabolism of triglyceride-rich lipoproteins is impaired in nephrotic syndrome but not in rats with hereditary analbuminemia (NA), suggesting that lipid synthesis should be increased by analbuminemia in the absence of proteinuria. In this study the rate of cholesterol and fatty acid synthesis in liver and extrahepatic tissue was measured in female NA and control Sprague-Dawley (SD) rats to determine whether lipid synthesis was indeed increased in isolated analbuminemia and to identify the site(s) of increased lipogenesis. We also measured the concentrations of apolipoproteins (apo) AI, B, and E in plasma, as well as the levels of the respective mRNAs in liver. Plasma cholesterol, triglycerides, and apo AI, B, and E were all increased severalfold in the NA rat (P &lt; 0.001). Although liver apolipoprotein mRNA content was significantly increased (P &lt; 0.001) for apo AI (643%), B (273%), and E (299%), 3-hydroxy-3-methylglutaryl-coenzyme A reductase activity in liver microsomes and hepatic cholesterol synthesis were not significantly increased in the NA rats. Hepatic fatty acid synthesis and intestinal cholesterol synthesis were not increased in the NA rats. Surprisingly, intestinal fatty acid synthesis was elevated by 60% (P &lt; 0.01). The NA rats demonstrated approximately fourfold increases in the incorporation of 3H2O into circulating cholesterol and fatty acids (P &lt; 0.001). A 56% increase in the synthesis of total nonsaponifiable lipid was found in the extravisceral carcass (P &lt; 0.01).(ABSTRACT TRUNCATED AT 250 WORDS) <\/jats:p>","DOI":"10.1152\/ajprenal.1993.265.1.f70","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T10:27:23Z","timestamp":1514024843000},"page":"F70-F76","source":"Crossref","is-referenced-by-count":3,"title":["Extrahepatic lipogenesis contributes to hyperlipidemia in the analbuminemic rat"],"prefix":"10.1152","volume":"265","author":[{"given":"J. A.","family":"Joles","sequence":"first","affiliation":[{"name":"Department of Medicine, University of California, Davis 95616."}]},{"given":"K. R.","family":"Feingold","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of California, Davis 95616."}]},{"given":"A.","family":"Van Tol","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of California, Davis 95616."}]},{"given":"L. H.","family":"Cohen","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of California, Davis 95616."}]},{"given":"X.","family":"Sun","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of California, Davis 95616."}]},{"suffix":"Jr","given":"H.","family":"Jones","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of California, Davis 95616."}]},{"given":"R. W.","family":"Davies","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of California, Davis 95616."}]},{"given":"G. A.","family":"Kaysen","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of California, Davis 95616."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1993.265.1.F70","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:27:31Z","timestamp":1567974451000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1993.265.1.F70"}},"issued":{"date-parts":[[1993,7,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1993,7,1]]}},"alternative-id":["10.1152\/ajprenal.1993.265.1.F70"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1993.265.1.f70","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1993,7,1]]}},{"indexed":{"date-parts":[[2024,6,21]],"date-time":"2024-06-21T15:36:30Z","timestamp":1718984190111},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1989,12,1]]},"abstract":"<jats:p> The normal relationship between arterial and venous acid-base composition is altered in hemodynamic compromise. Because the mechanism of this phenomenon remains conjectural, we have studied the acid-base profile and the end-tidal PCO2 of dogs with normal or depressed hemodynamic status in association with either normal ventilation or respiratory arrest. Reductions in cardiac output widened the arteriovenous difference in PCO2 and pH, largely due to arterial hypocapnia but also to venous hypercapnia, and decreased end-tidal PCO2. The arteriovenous gradients for PCO2 and pH of -5.1 +\/- 0.4 mmHg and 0.02 +\/- 0.01, respectively, during normal hemodynamics widened progressively with graded circulatory compromise reaching values of -30 +\/- 5 mmHg for PCO2 (P less than 0.01) and 0.35 +\/- 0.05 for pH (P less than 0.01) during cardiac arrest. Development of this disparity, however, required the presence of substantial pulmonary ventilation, since respiratory arrest obliterated the arteriovenous gradients. We propose that arterial hypocapnia, which occurs in association with reduced CO2 excretion, is secondary to an increased ventilation-to-perfusion ratio that reflects a disproportionate decrement in cardiac output. Venous hypercapnia, on the other hand, results from a greater than normal addition of CO2 per unit of blood traversing the capillaries of the hypoperfused peripheral tissues and a diminished CO2 excretion because of pulmonary hypoperfusion. Titration of bicarbonate stores by ongoing production of organic acids might also contribute to venous hypercapnia. <\/jats:p>","DOI":"10.1152\/ajprenal.1989.257.6.f1087","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T21:40:14Z","timestamp":1513978814000},"page":"F1087-F1093","source":"Crossref","is-referenced-by-count":1,"title":["Arteriovenous acid-base disparity in circulatory failure: studies on mechanism"],"prefix":"10.1152","volume":"257","author":[{"given":"H. J.","family":"Adrogue","sequence":"first","affiliation":[{"name":"Department of Medicine and Anesthesia, Baylor College of Medicine, Houston, Texas."}]},{"given":"M. N.","family":"Rashad","sequence":"additional","affiliation":[{"name":"Department of Medicine and Anesthesia, Baylor College of Medicine, Houston, Texas."}]},{"given":"A. B.","family":"Gorin","sequence":"additional","affiliation":[{"name":"Department of Medicine and Anesthesia, Baylor College of Medicine, Houston, Texas."}]},{"given":"J.","family":"Yacoub","sequence":"additional","affiliation":[{"name":"Department of Medicine and Anesthesia, Baylor College of Medicine, Houston, Texas."}]},{"given":"N. E.","family":"Madias","sequence":"additional","affiliation":[{"name":"Department of Medicine and Anesthesia, Baylor College of Medicine, Houston, Texas."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1989.257.6.F1087","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:12:38Z","timestamp":1567969958000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1989.257.6.F1087"}},"issued":{"date-parts":[[1989,12,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1989,12,1]]}},"alternative-id":["10.1152\/ajprenal.1989.257.6.F1087"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1989.257.6.f1087","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1989,12,1]]}},{"indexed":{"date-parts":[[2023,4,24]],"date-time":"2023-04-24T08:36:04Z","timestamp":1682325364811},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1996,8,1]]},"abstract":"<jats:p> We evaluated renal 131I-hippurate clearance (ERPFhip) as a measure of renal blood flow (RBF) in chronically instrumented conscious dogs. When adjusted for renal hippurate extraction (Ehip, 0.77 +\/- 0.01) and hematocrit (Hct, 39.7 +\/- 1%), calculated RBFhip (656 +\/- 37 ml\/min) markedly exceeded renal blood flow measured with renal artery blood flow probes (RBFprobe, 433 +\/- 27 ml\/min). The discrepancy could not be explained by flow probe calibration, because in vivo comparison of flow probe values with renal venous outflow showed only a slight underestimation of renal blood flow (slope 0.93, 95% confidence interval 0.89-0.97). Redistribution of hippurate from erythrocytes into renal venous plasma during or shortly after blood sampling led to an underestimation of Ehip by 4 +\/- 1% and thus could only explain a small part of the difference. Extrarenal hippurate clearance was excluded, because the amount of 131I-hippurate cleared from plasma equaled that appearing in the urine (303 +\/- 17 and 307 +\/- 17 ml\/min). Applying these corrections, we found that RBFhip still exceeded RBFprobe by 37 +\/- 3%. These data indicate that renal blood flow measured by the hippurate clearance technique markedly overestimates true renal blood flow. Because other errors were excluded, a combination of sampling of nonrenal blood and intrarenal hippurate extraction from erythrocytes might play a role. <\/jats:p>","DOI":"10.1152\/ajprenal.1996.271.2.f269","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T01:30:13Z","timestamp":1513992613000},"page":"F269-F274","source":"Crossref","is-referenced-by-count":1,"title":["Renal 131I-hippurate clearance overestimates true renal blood flow in the instrumented conscious dog"],"prefix":"10.1152","volume":"271","author":[{"given":"C. A.","family":"Visscher","sequence":"first","affiliation":[{"name":"Department of Medicine, Groningen Institute for Drug Studies,University Hospital, The Netherlands."}]},{"given":"D.","family":"De Zeeuw","sequence":"additional","affiliation":[{"name":"Department of Medicine, Groningen Institute for Drug Studies,University Hospital, The Netherlands."}]},{"given":"G.","family":"Navis","sequence":"additional","affiliation":[{"name":"Department of Medicine, Groningen Institute for Drug Studies,University Hospital, The Netherlands."}]},{"given":"A. K.","family":"Van Zanten","sequence":"additional","affiliation":[{"name":"Department of Medicine, Groningen Institute for Drug Studies,University Hospital, The Netherlands."}]},{"given":"P. E.","family":"De Jong","sequence":"additional","affiliation":[{"name":"Department of Medicine, Groningen Institute for Drug Studies,University Hospital, The Netherlands."}]},{"given":"R. M.","family":"Huisman","sequence":"additional","affiliation":[{"name":"Department of Medicine, Groningen Institute for Drug Studies,University Hospital, The Netherlands."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1996.271.2.F269","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:05:31Z","timestamp":1567958731000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1996.271.2.F269"}},"issued":{"date-parts":[[1996,8,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1996,8,1]]}},"alternative-id":["10.1152\/ajprenal.1996.271.2.F269"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1996.271.2.f269","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1996,8,1]]}},{"indexed":{"date-parts":[[2022,4,6]],"date-time":"2022-04-06T01:23:07Z","timestamp":1649208187904},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1984,2,1]]},"abstract":"<jats:p> The effects of physiological doses of human calcitonin (HCT) on renal excretion and tubular transport of water and electrolytes were investigated in hormone-deprived rats, i.e., homozygous DI Brattleboro rats with reduced levels of circulating glucagon, parathyroid hormone, and thyrocalcitonin, as these hormones are believed, together with ADH, to stimulate the same cells of the thick ascending limb. The experimental design was similar to the one used in a preceding study aimed at determining the effects of ADH in hormone-deprived rats [C. de Rouffignac et al. Am. J. Physiol. 244 (Renal Fluid Electrolyte Physiol. 13): F156-F164, 1983]. In the present experiments, HCT consistently increased the reabsorption of Mg, Ca, and K and, to a lesser extent, Na and Cl in the loop of Henle, but phosphate transport did not rise. The urinary excretion rate of Mg and Ca fell significantly. These data are very similar to the findings obtained with ADH on hormone-deprived rats. It is concluded that, in vivo, administration of HCT 1) stimulates reabsorption of Na, Cl, Mg, Ca, and K by the thick ascending limb, and 2) consistently enhances Mg and Ca reabsorption by the whole kidney by enhancing reabsorption in the loop of Henle. The similarity of the physiological responses elicited by ADH and calcitonin on the thick ascending limb supports the hypothesis of multiple hormonal control of electrolyte transport by the thick ascending limb. <\/jats:p>","DOI":"10.1152\/ajprenal.1984.246.2.f213","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T12:14:42Z","timestamp":1513944882000},"page":"F213-F220","source":"Crossref","is-referenced-by-count":3,"title":["ADH-like effects of calcitonin on electrolyte transport by Henle's loop of rat kidney"],"prefix":"10.1152","volume":"246","author":[{"given":"J. M.","family":"Elalouf","sequence":"first","affiliation":[]},{"given":"N.","family":"Roinel","sequence":"additional","affiliation":[]},{"given":"C.","family":"de Rouffignac","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1984.246.2.F213","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T14:36:14Z","timestamp":1567953374000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1984.246.2.F213"}},"issued":{"date-parts":[[1984,2,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1984,2,1]]}},"alternative-id":["10.1152\/ajprenal.1984.246.2.F213"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1984.246.2.f213","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1984,2,1]]}},{"indexed":{"date-parts":[[2022,4,5]],"date-time":"2022-04-05T20:56:47Z","timestamp":1649192207489},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1993,2,1]]},"abstract":"<jats:p> Urodilatin (URO) [ANP-(95-126)] is an analogue of atrial natriuretic peptide (alpha-ANP) [ANP-(99-126)] that was first isolated from human urine. In rat mesangial cells, URO competed with high affinity for non-guanylate cyclase-coupled ANPR-C receptors [concentration at which 50% labeled ligand is displaced (IC50) approximately 70 pM], but with lesser affinity to the guanylate cyclase-linked ANPR-A receptors (IC50 approximately 800 pM). alpha-ANP bound to both receptors with similar affinity [dissociation constant (Kd) approximately 150 pM]. In papillary collecting duct homogenates, which possess only ANPR-A receptors, the apparent Kd value averaged 229 pM for alpha-ANP and 2.7 nM for URO. Intravenous URO was at least as potent and effective as alpha-ANP in inducing diuresis and natriuresis in anesthetized rats, but URO was approximately 10-fold less potent in stimulating guanosine 3',5'-cyclic monophosphate generation in mesangial and inner medullary collecting duct cells. We conclude that URO has a lesser affinity than alpha-ANP for guanylate cyclase-coupled ANP receptors in the kidney and that the relative natriuretic potency of URO in vivo cannot be directly attributed to its binding characteristics with ANPR-A receptors. <\/jats:p>","DOI":"10.1152\/ajprenal.1993.264.2.f267","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T10:21:35Z","timestamp":1514024495000},"page":"F267-F273","source":"Crossref","is-referenced-by-count":0,"title":["Urodilatin: binding properties and stimulation of cGMP generation in rat kidney cells"],"prefix":"10.1152","volume":"264","author":[{"given":"H.","family":"Saxenhofer","sequence":"first","affiliation":[{"name":"Division of Nephrology, Ralph H. Johnson Department of VeteransAffairs Medical Center, Charleston, South Carolina."}]},{"given":"W. R.","family":"Fitzgibbon","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Ralph H. Johnson Department of VeteransAffairs Medical Center, Charleston, South Carolina."}]},{"given":"R. V.","family":"Paul","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Ralph H. Johnson Department of VeteransAffairs Medical Center, Charleston, South Carolina."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1993.264.2.F267","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:28:54Z","timestamp":1567974534000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1993.264.2.F267"}},"issued":{"date-parts":[[1993,2,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1993,2,1]]}},"alternative-id":["10.1152\/ajprenal.1993.264.2.F267"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1993.264.2.f267","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1993,2,1]]}},{"indexed":{"date-parts":[[2024,5,13]],"date-time":"2024-05-13T10:40:08Z","timestamp":1715596808277},"reference-count":36,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2009,9]]},"abstract":"<jats:p>We hypothesized that combination treatment with the mineralocorticoid receptor antagonist eplerenone and the calcium channel blocker amlodipine elicits better renoprotective effects than monotherapy with either drug, via different mechanisms in Dahl salt-sensitive (DS) hypertensive rats. DS rats were fed a high-salt diet (4% NaCl) for 10 wk and were treated with vehicle ( n = 12), eplerenone (50 mg\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7day<jats:sup>\u22121<\/jats:sup>, po, n = 12), amlodipine (3 mg\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7day<jats:sup>\u22121<\/jats:sup>, po, n = 12), or eplerenone plus amlodipine ( n = 12) after 2 wk of salt feeding. Vehicle-treated DS rats developed proteinuria, which was attenuated by eplerenone or amlodipine. Interestingly, eplerenone attenuated the glomerulosclerosis and podocyte injury, but amlodipine did not. Conversely, treatment with amlodipine markedly improved interstitial fibrosis, while the effect of eplerenone was minimal. Combination treatment markedly improved proteinuria, glomerulosclerosis, podocyte injury, and interstitial fibrosis in DS rats. Renal hypoxia estimated by pimonidazole, vascular endothelial growth factor expression, and density of peritubular endothelial cells was exacerbated by salt feeding. Amlodipine, either as monotherapy or in combination, ameliorated the renal hypoxia, whereas eplerenone treatment had no effect. In conclusion, both eplerenone and amlodipine attenuated renal injuries in high salt-fed DS rats, but the targets for renoprotection differed between these two drugs, with eplerenone predominantly acting on glomeruli and amlodipine acting on interstitium. The combination of eplerenone and amlodipine improved renal injury more effectively than either monotherapy in high salt-fed DS rats, presumably by achieving their own renoprotective effects.<\/jats:p>","DOI":"10.1152\/ajprenal.00197.2009","type":"journal-article","created":{"date-parts":[[2009,6,18]],"date-time":"2009-06-18T01:29:44Z","timestamp":1245288584000},"page":"F802-F808","source":"Crossref","is-referenced-by-count":23,"title":["Mineralocorticoid receptor blockade and calcium channel blockade have different renoprotective effects on glomerular and interstitial injury in rats"],"prefix":"10.1152","volume":"297","author":[{"given":"Jun","family":"Du","sequence":"first","affiliation":[]},{"given":"Yu-Yan","family":"Fan","sequence":"additional","affiliation":[]},{"given":"Hirofumi","family":"Hitomi","sequence":"additional","affiliation":[]},{"given":"Hideyasu","family":"Kiyomoto","sequence":"additional","affiliation":[]},{"given":"Shoji","family":"Kimura","sequence":"additional","affiliation":[]},{"given":"Chui-Ze","family":"Kong","sequence":"additional","affiliation":[]},{"given":"Takahisa","family":"Noma","sequence":"additional","affiliation":[]},{"given":"Masakazu","family":"Kohno","sequence":"additional","affiliation":[]},{"given":"Akira","family":"Nishiyama","sequence":"additional","affiliation":[]},{"given":"Daisuke","family":"Nakano","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1001\/archinte.1991.00400070058006"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1080\/10641960500468276"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1053\/hupa.2000.20373"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.107.103580"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.27.2.245"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.350"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1002\/ijc.2910610422"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1248\/bpb.29.2222"},{"key":"R9","unstructured":"Innes A, Johnston PA, Morgan AG, Davison AM, Burden RP.Clinical features of benign hypertensive nephrosclerosis at time of renal biopsy.Q J Med86: 271\u2013275, 1993."},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00244.2003"},{"key":"R11","doi-asserted-by":"crossref","unstructured":"Kang DH, Hughes J, Mazzali M, Schreiner GF, Johnson RJ.Impaired angiogenesis in the remnant kidney model. II. Vascular endothelial growth factor administration reduces renal fibrosis and stabilizes renal function.J Am Soc Nephrol12: 1448\u20131457, 2001.","DOI":"10.1681\/ASN.V1271448"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004080676"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00824.x"},{"key":"R14","doi-asserted-by":"crossref","unstructured":"Kondo N, Kiyomoto H, Yamamoto T, Miyatake A, Sun GP, Rahman M, Hitomi H, Moriwaki K, Hara T, Kimura S, Abe Y, Kohno M, Nishiyama A.Effects of calcium channel blockade on angiotensin II-induced peritubular ischemia in rats.J Pharmacol Exp Ther316: 1047\u20131052, 2006.","DOI":"10.1124\/jpet.105.095331"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000125614.35046.10"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000174593.88899.68"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000222003.28517.99"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000203772.78696.67"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005070757"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1007\/s10157-005-0357-8"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000154681.38944.9a"},{"key":"R22","doi-asserted-by":"crossref","unstructured":"Ohashi R, Kitamura H, Yamanaka N.Peritubular capillary injury during the progression of experimental glomerulonephritis in rats.J Am Soc Nephrol11: 47\u201356, 2000.","DOI":"10.1681\/ASN.V11147"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1016\/j.mce.2003.10.047"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000255636.11931.a2"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1038\/nm.1879"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90488.2008"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000138287.46849.82"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005020129"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007050531"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.34.4.854"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1016\/j.mce.2008.12.008"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1291\/hypres.31.887"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.2006.04478.x"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1016\/j.amjcard.2004.01.007"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1291\/hypres.26.635"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)63586-9"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00197.2009","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,10,7]],"date-time":"2021-10-07T14:23:01Z","timestamp":1633616581000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00197.2009"}},"issued":{"date-parts":[[2009,9]]},"references-count":36,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2009,9]]}},"alternative-id":["10.1152\/ajprenal.00197.2009"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00197.2009","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2009,9]]}},{"indexed":{"date-parts":[[2022,4,5]],"date-time":"2022-04-05T21:23:35Z","timestamp":1649193815719},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1979,8,1]]},"abstract":"<jats:p> Tissue slices prepared from renal cortex of littermate dogs with chronic metabolic acidosis or alkalosis were incubated in media with or without arsenite and containing 1 mM L-[14C]glutamine or [1,5\u201314C]citrate. The presence of arsenite increased the concentration of alpha-ketoglutarate in slices by 5\u2013\u201320 times the values found without this inhibitor. alpha-Ketoglutarate concentrations in acidotic slices were 40% or more greater than those in alkalotic ones when arsenited was present. 14C incorporation into alpha-ketoglutarate was also increased manyfold by arsenite with either labeled glutamine or citrate as substrate. 14CO2 production from labeled glutamine by over 90% and from labeled citrate by over 75%; the difference between 14CO2 production by acidotic and alkalotic slices was greatly reduced or eliminated by arsenite. These results suggest that in chronic metabolic acidosis metabolism of both glutamine and citrate is stimulated at a site or sites preceding formation of alpha-ketoglutarate. <\/jats:p>","DOI":"10.1152\/ajprenal.1979.237.2.f93","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T20:36:53Z","timestamp":1513975013000},"page":"F93-F99","source":"Crossref","is-referenced-by-count":0,"title":["Effect of arsenite on renal tissue slice metabolism in chronic metabolic acidosis and alkalosis"],"prefix":"10.1152","volume":"237","author":[{"given":"D. P.","family":"Simpson","sequence":"first","affiliation":[]},{"given":"J.","family":"Hecker","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1979.237.2.F93","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:02:09Z","timestamp":1567969329000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1979.237.2.F93"}},"issued":{"date-parts":[[1979,8,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1979,8,1]]}},"alternative-id":["10.1152\/ajprenal.1979.237.2.F93"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1979.237.2.f93","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1979,8,1]]}},{"indexed":{"date-parts":[[2024,5,13]],"date-time":"2024-05-13T10:44:22Z","timestamp":1715597062760},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1984,12,1]]},"abstract":"<jats:p> A procedure for isolating a suspension of tubules derived from the rabbit medullary thick ascending limb is described. The purity of the preparation was assessed by microscopy and enzyme assays and the viability of the preparation was assessed by measuring oxygen consumption. Microscopy revealed that the suspension contains 95% thick ascending limbs and that the isolation procedure preserves the structure of the epithelium except for the loss of the basement membrane. The preparation had a high activity of calcitonin-sensitive adenylate cyclase, a marker enzyme for the medullary thick ascending limb. Control oxygen consumption was considerably higher than that reported for proximal tubules in the literature, and nystatin or carbonyl cyanide p-trifluoromethoxyphenylhydrazone addition produced a more than 100% increase in oxygen consumption. Furosemide inhibited the oxygen consumption by 43% and ouabain inhibited it by 42%. Furosemide inhibited sodium chloride entry without directly affecting the Na-K-ATPase or cellular metabolism. Chloride removal depressed oxygen consumption to the same extent as furosemide, but some of this action was through direct inhibition of cellular metabolism. <\/jats:p>","DOI":"10.1152\/ajprenal.1984.247.6.f955","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T15:59:02Z","timestamp":1513958342000},"page":"F955-F964","source":"Crossref","is-referenced-by-count":11,"title":["Suspension of medullary thick ascending limb tubules from the rabbit kidney"],"prefix":"10.1152","volume":"247","author":[{"given":"M. E.","family":"Chamberlin","sequence":"first","affiliation":[]},{"given":"A.","family":"LeFurgey","sequence":"additional","affiliation":[]},{"given":"L. J.","family":"Mandel","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1984.247.6.F955","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:29:26Z","timestamp":1567967366000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1984.247.6.F955"}},"issued":{"date-parts":[[1984,12,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1984,12,1]]}},"alternative-id":["10.1152\/ajprenal.1984.247.6.F955"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1984.247.6.f955","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1984,12,1]]}},{"indexed":{"date-parts":[[2024,5,13]],"date-time":"2024-05-13T10:46:03Z","timestamp":1715597163749},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1986,7,1]]},"abstract":"<jats:p> The effect of streptozotocin-induced diabetes mellitus on rat renal ouabain-sensitive ATPase in six distinct nephron segments was studied. Twenty-four hours after administration of streptozotocin, blood glucose increased threefold (P less than 0.001), and glucosuria was evident. Aldosterone levels increased almost twofold (P less than 0.001). Ouabain-sensitive ATPase increased in the proximal segments PC (proximal convoluted tubule) and PS (proximal straight tubule) by 43 and 62%, respectively, (P less than 0.001) and CD (cortical collecting duct) ouabain-sensitive ATPase increased 77% (P less than 0.001). Ouabain-sensitive ATPase in the cortical (CTAL) and medullary (MTAL) thick ascending limbs of Henle's loop and in the DC (distal convoluted tubule) remained unchanged after 24 h of streptozotocin administration. Eight days after streptozotocin administration, when glomerular filtration rate (GFR) was already markedly elevated, ouabain-sensitive ATPase remained increased in the PC, PS, and CD but was significantly less compared with the activity after 24 h (P less than 0.05), whereas in the CTAL and MTAL a marked increase in ouabain-sensitive ATPase occurred by 54% in the CTAL and 65% in the MTAL (P less than 0.001). Aldosterone levels remained elevated compared with control but less than after 24 h. Pretreatment with deoxycorticosterone acetate abolished the increase in ouabain-sensitive ATPase in the CD. These findings show that streptozotocin-induced diabetes mellitus in the rat is associated with a substantial increase in ouabain-sensitive ATPase activity along most of the nephron. This increase in enzyme activity may represent a mechanism of physiological adaptation of the nephron to maintain electrolyte homeostasis in diabetes in face of the increased GFR and osmotic diuresis. <\/jats:p>","DOI":"10.1152\/ajprenal.1986.251.1.f164","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T20:01:17Z","timestamp":1513972877000},"page":"F164-F170","source":"Crossref","is-referenced-by-count":5,"title":["Enhanced renal tubular ouabain-sensitive ATPase in streptozotocin diabetes mellitus"],"prefix":"10.1152","volume":"251","author":[{"given":"H.","family":"Wald","sequence":"first","affiliation":[]},{"given":"P.","family":"Scherzer","sequence":"additional","affiliation":[]},{"given":"M. M.","family":"Popovtzer","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1986.251.1.F164","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:35:12Z","timestamp":1567956912000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1986.251.1.F164"}},"issued":{"date-parts":[[1986,7,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1986,7,1]]}},"alternative-id":["10.1152\/ajprenal.1986.251.1.F164"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1986.251.1.f164","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1986,7,1]]}},{"indexed":{"date-parts":[[2024,5,13]],"date-time":"2024-05-13T11:14:13Z","timestamp":1715598853506},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1985,8,1]]},"abstract":"<jats:p> To assess the role of cortical collecting duct bicarbonate secretion in the regulation of net acid excretion, we have sought to identify what factors influence the secretion rate. Net and unidirectional bicarbonate fluxes were measured in isolated perfused cortical collecting ducts from deoxycorticosterone-treated rabbits. The collecting ducts secreted bicarbonate at 11-24 pmol X mm-1 X min-1, confirming the high rate seen in earlier studies. Oral acid loading (50 mM NH4Cl drinking water) completely inhibited the net bicarbonate secretion. The bath-to-lumen flux was markedly reduced with acid loading, but the lumen-to-bath flux changed very little. In tubules from rabbits treated with deoxycorticosterone (but not NH4Cl), luminal chloride replacement with either sulfate or gluconate completely and reversibly inhibited the net bicarbonate secretion. The bath-to-lumen flux was greatly inhibited, but there was little change in the lumen-to-bath flux. We conclude: 1) High rates of bicarbonate secretion can be induced in rabbit cortical collecting ducts by chronic treatment of the animals with deoxycorticosterone. 2) When deoxycorticosterone-treated rabbits were made acidotic by oral administration of NH4Cl, the bicarbonate secretion was prevented, indicating that the systemic acid-base state of the animal may be an important factor regulating bicarbonate secretion. 3) Replacement of chloride in the lumen with sulfate inhibits bicarbonate secretion in the cortical collecting duct, an effect which may explain in part the decrease in urinary pH in response to sulfate infusions in mineralocorticoid-stimulated animals. <\/jats:p>","DOI":"10.1152\/ajprenal.1985.249.2.f205","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T00:15:14Z","timestamp":1513988114000},"page":"F205-F212","source":"Crossref","is-referenced-by-count":12,"title":["Deoxycorticosterone-stimulated bicarbonate secretion in rabbit cortical collecting ducts: effects of luminal chloride removal and in vivo acid loading"],"prefix":"10.1152","volume":"249","author":[{"given":"J.","family":"Garcia-Austt","sequence":"first","affiliation":[]},{"given":"D. W.","family":"Good","sequence":"additional","affiliation":[]},{"given":"M. B.","family":"Burg","sequence":"additional","affiliation":[]},{"given":"M. A.","family":"Knepper","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1985.249.2.F205","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:29:39Z","timestamp":1567970979000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1985.249.2.F205"}},"issued":{"date-parts":[[1985,8,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1985,8,1]]}},"alternative-id":["10.1152\/ajprenal.1985.249.2.F205"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1985.249.2.f205","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1985,8,1]]}},{"indexed":{"date-parts":[[2022,9,9]],"date-time":"2022-09-09T15:12:05Z","timestamp":1662736325316},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2022,9,1]]},"DOI":"10.1152\/ajprenal.2022.323.3.au","type":"journal-article","created":{"date-parts":[[2022,9,9]],"date-time":"2022-09-09T14:37:20Z","timestamp":1662734240000},"page":"i-i","update-policy":"http:\/\/dx.doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["First Author Spotlight"],"prefix":"10.1152","volume":"323","member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.2022.323.3.AU","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,9,9]],"date-time":"2022-09-09T14:37:21Z","timestamp":1662734241000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.2022.323.3.AU"}},"issued":{"date-parts":[[2022,9,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2022,9,1]]}},"alternative-id":["10.1152\/ajprenal.2022.323.3.AU"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.2022.323.3.au","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2022,9,1]]},"assertion":[{"value":"2022-09-09","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2022,4,5]],"date-time":"2022-04-05T16:12:40Z","timestamp":1649175160177},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1991,12,1]]},"abstract":"<jats:p> The turtle urinary bladder is composed of different epithelial cell types that are suspected to separately produce electrogenic acid and alkali excretion. We measured the electrical currents produced by individual cells, scanning a two-dimensional vibrating probe over the luminal surface of the bladder. Acidification (outward current) was produced by the type of epithelial cell rich in carbonic anhydrase (CA cells). The measured currents of these cells quantitatively accounted for the total epithelial acidification current. When alkali secretion was induced by adenosine 3',5'-cyclic monophosphate and acidification was inhibited (by luminal pH 4), we measured inward currents localized to a small number of epithelial cells in four bladders but found no localization in the other seven treated bladders. When alkali secretion was localized and induced without inhibiting acidification, we found both cells producing inward current and cells producing outward current, which demonstrated that the two transport functions can occur simultaneously. We conclude that net acid-base secretion can be determined by regulating the transport rates of separate cells. <\/jats:p>","DOI":"10.1152\/ajprenal.1991.261.6.f963","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T04:30:08Z","timestamp":1514003408000},"page":"F963-F974","source":"Crossref","is-referenced-by-count":3,"title":["Localization and regulation of acid-base secretory currents from individual epithelial cells"],"prefix":"10.1152","volume":"261","author":[{"given":"C.","family":"Scheffey","sequence":"first","affiliation":[{"name":"Department of Biological Sciences, Columbia University, New York, NewYork 10027."}]},{"given":"A. M.","family":"Shipley","sequence":"additional","affiliation":[{"name":"Department of Biological Sciences, Columbia University, New York, NewYork 10027."}]},{"given":"J. H.","family":"Durham","sequence":"additional","affiliation":[{"name":"Department of Biological Sciences, Columbia University, New York, NewYork 10027."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1991.261.6.F963","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:20:45Z","timestamp":1567959645000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1991.261.6.F963"}},"issued":{"date-parts":[[1991,12,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1991,12,1]]}},"alternative-id":["10.1152\/ajprenal.1991.261.6.F963"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1991.261.6.f963","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1991,12,1]]}},{"indexed":{"date-parts":[[2022,4,5]],"date-time":"2022-04-05T18:47:32Z","timestamp":1649184452706},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1986,8,1]]},"abstract":"<jats:p> Two groups of Sprague-Dawley rats, Harlan (H) and Charles River (CR), were discovered in that the medullary thick ascending limb (MAL) had a profoundly different adenylate cyclase response to arginine vasopressin (AVP). Using these two groups of rats, we studied the correlation between AVP action on the MAL and maximal urinary concentration. AVP (10(-6) M) significantly stimulated adenylate cyclase in MAL of H rats (7.4 +\/- 0.9 to 43.8 +\/- 4.6 fmol cAMP formed X 30 min-1 X mm-1, P less than 0.001) but not in CR rats (10.3 +\/- 1.4 to 12.7 +\/- 2.0 fmol cAMP formed X 30 min-1 X mm-1, NS). In contrast, AVP significantly stimulated adenylate cyclase of cortical, outer and inner medullary collecting tubules from both H and CR rats. Glucagon (10(-6) M) significantly stimulated adenylate cyclase of MAL from both H and CR rats. After 48 h of fluid deprivation, urinary osmolality was significantly higher (P less than 0.001) in the H (4,504 +\/- 399 mosmol\/kg H2O, n = 14) than CR (2,840 +\/- 176 mosmol\/kg H2O, n = rats. This observation was not attributable to differences in creatinine clearance (CR, 1.30 +\/- 0.24; H, 1.24 +\/- 0.03 ml\/min, NS, n = 4) or plasma AVP (CR, 12.75 +\/- 1.44; H, 12.38 +\/- 1.17 pg\/ml, NS, n = 6) levels. These results therefore suggest that the action of AVP on the MAL, in addition to the effect on collecting tubules, is involved in maximal urinary concentration in rats. <\/jats:p>","DOI":"10.1152\/ajprenal.1986.251.2.f266","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T01:22:44Z","timestamp":1513992164000},"page":"F266-F270","source":"Crossref","is-referenced-by-count":5,"title":["Role of arginine vasopressin in medullary thick ascending limb on maximal urinary concentration"],"prefix":"10.1152","volume":"251","author":[{"given":"J. K.","family":"Kim","sequence":"first","affiliation":[]},{"given":"S. N.","family":"Summer","sequence":"additional","affiliation":[]},{"given":"A. E.","family":"Erickson","sequence":"additional","affiliation":[]},{"given":"R. W.","family":"Schrier","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1986.251.2.F266","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:36:51Z","timestamp":1567971411000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1986.251.2.F266"}},"issued":{"date-parts":[[1986,8,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1986,8,1]]}},"alternative-id":["10.1152\/ajprenal.1986.251.2.F266"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1986.251.2.f266","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1986,8,1]]}},{"indexed":{"date-parts":[[2022,4,5]],"date-time":"2022-04-05T14:59:59Z","timestamp":1649170799720},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1986,5,1]]},"abstract":"<jats:p> The effects of vasoactive substances on the release of prostaglandin (PG) and thromboxane (TX) from isolated rat glomeruli were investigated. The PGE2, PGF2 alpha, 6-keto-PGF1 alpha, and TXB2 release during 60 min into Krebs-Henseleit medium was assessed by radioimmunoassay following extraction. Norepinephrine (NE) stimulated PGE2 (from 2,117 +\/- 117 to 3,968 +\/- 182 pg X mg protein-1 X 60 min-1, P less than 0.01) at a concentration of 10(-4)M and PGF2 alpha (from 2,748 +\/- 285 to 8,535 +\/- 495 pg X mg protein-1 X 60 min-1, P less than 0.01) at a concentration of 10(-5)M. However, neither angiotensin II (ANG II) nor arginine vasopressin (AVP) affected the release of PG and TXB2 at concentrations up to 10(-5)M. In the presence of 10(-5) M NE, ANG II enhanced the release of PGE2 (from 3,307 +\/- 207 to 6,865 +\/- 469 pg X mg protein-1 X 60 min-1., P less than 0.01) and PGF2 alpha (from 3,652 +\/- 252 to 6,612 +\/- 388 pg X mg protein-1 X 60 min-1, P less than 0.01) at a concentration of 10(-8)M, whereas AVP lacked any similar effect. These results indicate that catecholamine acts as a major stimulant for the release of PG from isolated glomeruli via alpha-receptors. ANG II may work in cooperation with catecholamine, but AVP appears to play little role. <\/jats:p>","DOI":"10.1152\/ajprenal.1986.250.5.f811","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T01:02:00Z","timestamp":1513990920000},"page":"F811-F816","source":"Crossref","is-referenced-by-count":0,"title":["Synergistic action of angiotensin II on norepinephrine-induced prostaglandin release from rat glomeruli"],"prefix":"10.1152","volume":"250","author":[{"given":"Y.","family":"Matsumura","sequence":"first","affiliation":[]},{"given":"Y.","family":"Ozawa","sequence":"additional","affiliation":[]},{"given":"H.","family":"Suzuki","sequence":"additional","affiliation":[]},{"given":"T.","family":"Saruta","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1986.250.5.F811","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:34:39Z","timestamp":1567971279000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1986.250.5.F811"}},"issued":{"date-parts":[[1986,5,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1986,5,1]]}},"alternative-id":["10.1152\/ajprenal.1986.250.5.F811"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1986.250.5.f811","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1986,5,1]]}},{"indexed":{"date-parts":[[2023,10,17]],"date-time":"2023-10-17T19:38:57Z","timestamp":1697571537772},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1978,1,1]]},"DOI":"10.1152\/ajprenal.1978.234.1.f59","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T19:56:00Z","timestamp":1513972560000},"page":"F59-F63","source":"Crossref","is-referenced-by-count":9,"title":["Effects of prenatal and early postnatal sodium deprivation on subsequent adult thirst and salt preference in rats"],"prefix":"10.1152","volume":"234","author":[{"given":"D. R.","family":"Mouw","sequence":"first","affiliation":[]},{"given":"A. J.","family":"Vander","sequence":"additional","affiliation":[]},{"given":"J.","family":"Wagner","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1978.234.1.F59","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:55:38Z","timestamp":1567968938000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1978.234.1.F59"}},"issued":{"date-parts":[[1978,1,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1978,1,1]]}},"alternative-id":["10.1152\/ajprenal.1978.234.1.F59"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1978.234.1.f59","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1978,1,1]]}},{"indexed":{"date-parts":[[2023,4,30]],"date-time":"2023-04-30T19:10:15Z","timestamp":1682881815986},"reference-count":46,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2005,1]]},"abstract":"<jats:p>Hepatocyte growth factor (HGF) is a multifunctional cytokine that plays a crucial role in renal development, injury, and repair. HGF also serves a protective role in chronic renal disease by preventing tissue fibrosis. Endothelin-1 (ET-1), produced primarily by endothelial cells, is a potent vasoconstrictor that also acts as a proinflammatory peptide, promoting vascular injury and renal damage. In addition to mediating a variety of epithelial cell responses, HGF also induces hemodynamic changes that are poorly understood. The aim of the present study was to study the acute and chronic effects of HGF on ET-1 production in the kidney. We hypothesized that hemodynamic changes upon HGF treatment are likely mediated by immediate ET-1 release, whereas protection from renal fibrosis in rats chronically treated with HGF is likely due to suppression of ET-1 production. Acute HGF infusion into rats caused a decline in blood pressure that was enhanced by pretreatment with bosentan (an endothelin A and B receptor antagonist). HGF infusion also resulted in a decline in glomerular filtration rate (GFR) that could be entirely prevented by bosentan, suggesting that HGF acutely increases production and\/or release of ET-1, which then mediates the observed decline in GFR. In cultured glomerular endothelial cells, HGF induced ET-1 production in a dose-dependent manner. Moreover, although there was an initial increase in ET-1 production upon HGF treatment, longer administration suppressed ET-1 production. This finding was consistent with the observation in vivo of a decrease in ET-1 production in renal parenchyma of rats chronically treated with HGF. Our data suggest both a hemodynamic and biological role for HGF-mediated ET-1 regulation.<\/jats:p>","DOI":"10.1152\/ajprenal.00435.2003","type":"journal-article","created":{"date-parts":[[2004,12,6]],"date-time":"2004-12-06T23:02:46Z","timestamp":1102374166000},"page":"F8-F15","source":"Crossref","is-referenced-by-count":1,"title":["Hepatocyte growth factor induces an endothelin-mediated decline in glomerular filtration rate"],"prefix":"10.1152","volume":"288","author":[{"given":"Purba","family":"Biswas","sequence":"first","affiliation":[]},{"given":"Abinash","family":"Roy","sequence":"additional","affiliation":[]},{"given":"Rujun","family":"Gong","sequence":"additional","affiliation":[]},{"given":"Angelito","family":"Yango","sequence":"additional","affiliation":[]},{"given":"Evelyn","family":"Tolbert","sequence":"additional","affiliation":[]},{"given":"Jason","family":"Centracchio","sequence":"additional","affiliation":[]},{"given":"Lance D.","family":"Dworkin","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI113880"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.260.3.F331"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1097\/00005344-200000002-00017"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1016\/S0962-8924(98)01359-2"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(95)90279-1"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1126\/science.1846706"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/14.8.1881"},{"key":"R8","doi-asserted-by":"crossref","unstructured":"Cortner J, Vande Woude GF, and Rong S.The Met-HGF\/SF autocrine signaling mechanism is involved in sarcomagenesis.EXS74: 89\u2013121, 1995.","DOI":"10.1007\/978-3-0348-9070-0_6"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00417.x"},{"key":"R10","unstructured":"Fujitani Y, Ueda H, Okada T, Urade Y, and Karaki H.A selective agonist of endothelin type B receptor, IRL 1620, stimulates cyclic GMP increase via nitric oxide formation in rat aorta.J Pharmacol Exp Ther267: 683\u2013689, 1993."},{"key":"R11","unstructured":"Gherardi Eand Stoker M.Hepatocyte growth factor\u2014scatter factor: mitogen, motogen, and met.Cancer Cells3: 227\u2013232, 1991."},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000098686.72971.DB"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.85.1.21"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00132.x"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1097\/00005344-200008000-00016"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/16.12.2310"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.2000.279.6.H2865"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1016\/0024-3205(92)90331-I"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1096\/fj.02-0442fje"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1172\/JCI114079"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00126.x"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200301000-00005"},{"key":"R23","doi-asserted-by":"crossref","unstructured":"Liu QP, Fruit K, Ward J, and Correll PH.Negative regulation of macrophage activation in response to IFN-\u03b3 and lipopolysaccharide by the STK\/RON receptor tyrosine kinase.J Immunol163: 6606\u20136613, 1999.","DOI":"10.4049\/jimmunol.163.12.6606"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200201000-00004"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2000.00375.x"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1998.8676"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.3.F679"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.34.2.279"},{"key":"R29","unstructured":"Matsumoto Kand Nakamura T.Roles of HGF as a pleiotropic factor in organ regeneration.EXS65: 225\u2013249, 1993."},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00199.2003"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(91)90363-4"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1016\/0955-2235(91)90014-U"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1993.265"},{"key":"R34","unstructured":"Ong AC, Jowett TP, Firth JD, Burton S, Kitamura M, and Fine LG.Human tubular-derived endothelin in the paracrine regulation of renal interstitial fibroblast function (Abstract).Exp Nephrol2: 134, 1994."},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1995.269.2.R469"},{"key":"R36","doi-asserted-by":"crossref","unstructured":"Rabkin R, Fervenza F, Tsao T, Sibley R, Friedlaender M, Hsu F, Lassman C, Hausmann M, Huie P, and Schwall RH.Hepatocyte growth factor receptor in acute tubular necrosis.J Am Soc Nephrol12: 531\u2013540, 2001.","DOI":"10.1681\/ASN.V123531"},{"key":"R37","doi-asserted-by":"crossref","unstructured":"Rosen EM, Lamszus K, Laterra J, Polverini PJ, Rubin JS, and Goldberg ID.HGF\/SF in angiogenesis.Ciba Found Symp212: 215\u2013226, 1997.","DOI":"10.1002\/9780470515457.ch14"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.127.6.1783"},{"key":"R39","doi-asserted-by":"crossref","unstructured":"Rubin JS, Bottaro DP, and Aaronson SA.Hepatocyte growth factor\/scatter factor and its receptor, the c-met proto-oncogene product.Biochim Biophys Acta1155: 357\u2013371, 1993.","DOI":"10.1016\/0304-419X(93)90015-5"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1994.1481"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1053\/ajkd.2001.26087"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1054\/bjoc.1999.1023"},{"key":"R43","doi-asserted-by":"crossref","unstructured":"Yang Jand Liu Y.Blockage of tubular epithelial to myofibroblast transition by hepatocyte growth factor prevents renal interstitial fibrosis.J Am Soc Nephrol13: 96\u2013107, 2002.","DOI":"10.1681\/ASN.V13196"},{"key":"R44","doi-asserted-by":"crossref","unstructured":"Yang Jand Liu Y.Delayed administration of hepatocyte growth factor reduces renal fibrosis in obstructive nephropathy.Am J Physiol Renal Physiol284: F349\u2013F357, 2003.","DOI":"10.1152\/ajprenal.00154.2002"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1097\/00005344-199709000-00004"},{"key":"R46","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/16.9.1769"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00435.2003","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,4,30]],"date-time":"2023-04-30T18:30:48Z","timestamp":1682879448000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00435.2003"}},"issued":{"date-parts":[[2005,1]]},"references-count":46,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2005,1]]}},"alternative-id":["10.1152\/ajprenal.00435.2003"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00435.2003","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2005,1]]}},{"indexed":{"date-parts":[[2022,4,5]],"date-time":"2022-04-05T08:44:24Z","timestamp":1649148264447},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1994,9,1]]},"abstract":"<jats:p> The objective of this study was to develop a technique to identify and dissect segments of the rat renal microcirculation and to apply reverse transcription (RT) to specific mRNAs with subsequent amplification of the cDNA by polymerase chain reaction (PCR) to evaluate gene expression. To circumvent the difficulty associated with visualizing specific microvessels, we intrarenally infused blue latex microparticles, 1-5 microns in diameter, with subsequent identification and microdissection of specific segments of the renal microvasculature under stereomicroscopy. To demonstrate its utility, we assessed expression of mRNAs encoding fibronectin and renin. As expected, mRNA encoding fibronectin was localized along the renal microcirculation, and mRNA encoding renin was primarily present in afferent arterioles and interlobular arteries. Identity of the amplified cDNA fragments was verified by sequencing. This perfusion-microdissection technique coupled to RT-PCR should be useful in the evaluation of gene expression along the renal microvasculature. It may also allow bridging of the gap between analysis of gene expression of rare mRNA species by in situ hybridization and physiology of the renal microcirculation. <\/jats:p>","DOI":"10.1152\/ajprenal.1994.267.3.f497","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T00:50:16Z","timestamp":1513990216000},"page":"F497-F503","source":"Crossref","is-referenced-by-count":1,"title":["A method for isolation of rat renal microvessels and mRNA localization"],"prefix":"10.1152","volume":"267","author":[{"given":"J. C.","family":"Pelayo","sequence":"first","affiliation":[{"name":"Department of Pediatrics, University of California, Los Angeles,School of Medicine 90024."}]},{"given":"M. A.","family":"Mobilia","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, University of California, Los Angeles,School of Medicine 90024."}]},{"given":"S.","family":"Tjio","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, University of California, Los Angeles,School of Medicine 90024."}]},{"given":"R.","family":"Singh","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, University of California, Los Angeles,School of Medicine 90024."}]},{"given":"J. M.","family":"Nakamoto","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, University of California, Los Angeles,School of Medicine 90024."}]},{"given":"C.","family":"Van Dop","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, University of California, Los Angeles,School of Medicine 90024."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1994.267.3.F497","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:57:08Z","timestamp":1567958228000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1994.267.3.F497"}},"issued":{"date-parts":[[1994,9,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1994,9,1]]}},"alternative-id":["10.1152\/ajprenal.1994.267.3.F497"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1994.267.3.f497","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1994,9,1]]}},{"indexed":{"date-parts":[[2022,4,5]],"date-time":"2022-04-05T08:49:42Z","timestamp":1649148582570},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1990,5,1]]},"abstract":"<jats:p> Gentamicin nephrotoxicity is associated with impairments in proximal tubular function. This study determined whether gentamicin administration to the rat, before a reduction in glomerular filtration rate (GFR), causes early and selective alterations in renal cortical brush-border membrane (BBM) enzyme and transport activity, lipid composition, and fluidity. Three days of gentamicin administration caused significant decreases in the Vmax of alkaline phosphatase, the Vmax of sodium gradient-dependent phosphate transport (Na-Pi cotransport), and the Vmax of pH gradient-dependent sodium transport (Na-H exchange). Gentamicin did not affect BBM-bound maltase or leucine aminopeptidase activities and sodium gradient-dependent glucose or proline transport activities. Gentamicin also caused a significant decrease in BBM sphingomyelin, significant increases in BBM phosphatidylcholine and phosphatidylinositol, a significant decrease in the phospholipid fatty acid saturation index, and a significant increase in BBM fluidity, i.e., decrease in the fluorescence anisotropy of diphenylhexatriene. These BBM functional and compositional effects of gentamicin were independent of endogenous parathyroid hormone activity. We conclude that gentamicin causes early and specific alterations in BBM enzyme and transport activity and also lipid composition, which may play an important role in the progression of renal cell injury. <\/jats:p>","DOI":"10.1152\/ajprenal.1990.258.5.f1379","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T18:21:57Z","timestamp":1513966917000},"page":"F1379-F1387","source":"Crossref","is-referenced-by-count":1,"title":["Early selective effects of gentamicin on renal brush-border membrane Na-Pi cotransport and Na-H exchange"],"prefix":"10.1152","volume":"258","author":[{"given":"M.","family":"Levi","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, University of Texas SouthwesternMedical Center, Dallas."}]},{"given":"R. E.","family":"Cronin","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Texas SouthwesternMedical Center, Dallas."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1990.258.5.F1379","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:24:04Z","timestamp":1567956244000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1990.258.5.F1379"}},"issued":{"date-parts":[[1990,5,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1990,5,1]]}},"alternative-id":["10.1152\/ajprenal.1990.258.5.F1379"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1990.258.5.f1379","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1990,5,1]]}},{"indexed":{"date-parts":[[2024,9,15]],"date-time":"2024-09-15T22:45:04Z","timestamp":1726440304004},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1997,2,1]]},"abstract":"<jats:p> Animal experiments indicate that inhibition of nitric oxide synthase (NOS) influences renal hemodynamics and that this effect can be reversed by L-arginine, the precursor of NO synthesis. We have therefore studied the effects of an inhibitor of NOS, N(G)-monomethyl-L-arginine (L-NMMA), and a subsequent coinfusion with L-arginine on renal hemodynamics. In a double-blind, randomized crossover design, eight healthy volunteers (means +\/- 1SD, 25.6 +\/- 3.1 yr) received a primed constant infusion of L-NMMA (3 mg\/kg bolus infusion over 5 min, followed by 50 microg x kg(-1) x min(-1) over 120 min) with subsequent coinfusion of L-arginine (17 mg x kg(-1) x min(-1) over 30 min). In the absence of a hypertensive response, L-NMMA decreased renal plasma flow to 79% of baseline (P &lt; 0.005); this effect was abrogated by L-arginine. Glomerular filtration rate was not affected, NO exhalation was reduced to 30% of baseline (P &lt; 0.005) by L-NMMA, and this effect was attenuated by L-arginine. Our results demonstrate that basal NO production maintains renal blood flow in vivo in humans. In addition, the renal vasculature is particularly sensitive to inhibition of NOS, and these pharmacodynamic effects can be reversed by excess doses of L-arginine. <\/jats:p>","DOI":"10.1152\/ajprenal.1997.272.2.f178","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T03:43:57Z","timestamp":1514000637000},"page":"F178-F182","source":"Crossref","is-referenced-by-count":11,"title":["Effect of nitric oxide synthase inhibition on renal hemodynamics in humans: reversal by L-arginine"],"prefix":"10.1152","volume":"272","author":[{"given":"M.","family":"Wolzt","sequence":"first","affiliation":[{"name":"Department of Clinical Pharmacology, Vienna University, Austria."}]},{"given":"L.","family":"Schmetterer","sequence":"additional","affiliation":[{"name":"Department of Clinical Pharmacology, Vienna University, Austria."}]},{"given":"W.","family":"Ferber","sequence":"additional","affiliation":[{"name":"Department of Clinical Pharmacology, Vienna University, Austria."}]},{"given":"E.","family":"Artner","sequence":"additional","affiliation":[{"name":"Department of Clinical Pharmacology, Vienna University, Austria."}]},{"given":"C.","family":"Mensik","sequence":"additional","affiliation":[{"name":"Department of Clinical Pharmacology, Vienna University, Austria."}]},{"given":"H. G.","family":"Eichler","sequence":"additional","affiliation":[{"name":"Department of Clinical Pharmacology, Vienna University, Austria."}]},{"given":"K.","family":"Krejcy","sequence":"additional","affiliation":[{"name":"Department of Clinical Pharmacology, Vienna University, Austria."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1997.272.2.F178","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:16:24Z","timestamp":1567959384000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1997.272.2.F178"}},"issued":{"date-parts":[[1997,2,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1997,2,1]]}},"alternative-id":["10.1152\/ajprenal.1997.272.2.F178"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1997.272.2.f178","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[1997,2,1]]}},{"indexed":{"date-parts":[[2024,9,15]],"date-time":"2024-09-15T22:43:58Z","timestamp":1726440238509},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1983,7,1]]},"abstract":"<jats:p> The short-term effects (within 4 h) of low doses of intravenous aldosterone or deoxycorticosterone on potassium and sodium urinary excretion were studied by clearance techniques in 24-h adrenalectomized, anesthetized male rats. All animals were substituted with a glucocorticoid (dexamethasone; plasma concentration approximately 6 nM) to maintain normal glomerular filtration rate. The mineralocorticoid effects were studied under various conditions of sodium and potassium load. Mineralocorticoid administration uniformly resulted in antinatriuresis, starting within 30-60 min and, at the peak effect, amounting to 1-2% sodium fractional excretion. The level of antinatriuresis was directly related to the control sodium excretion before aldosterone administration. Mineralocorticoids induced a significant kaliuresis in all groups except one, the one receiving the lowest sodium load. The aldosterone-induced kaliuresis was also related to the sodium load and the control fractional sodium excretion level and was simultaneous with the beginning of the reduced sodium excretion. In control, mineralocorticoid-deprived rats, kaliuresis was not enhanced by increasing the sodium load. Control as well as mineralocorticoid-treated rats responded by an increased kaliuresis following an acute potassium load and by a decreased kaliuresis after 3 days of low potassium diet. <\/jats:p>","DOI":"10.1152\/ajprenal.1983.245.1.f89","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T10:05:02Z","timestamp":1513937102000},"page":"F89-F99","source":"Crossref","is-referenced-by-count":12,"title":["Effects of mineralocorticoids on Na+ and K+ excretion in the adrenalectomized rat"],"prefix":"10.1152","volume":"245","author":[{"given":"J. D.","family":"Horisberger","sequence":"first","affiliation":[]},{"given":"J.","family":"Diezi","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1983.245.1.F89","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T14:28:10Z","timestamp":1567952890000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1983.245.1.F89"}},"issued":{"date-parts":[[1983,7,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1983,7,1]]}},"alternative-id":["10.1152\/ajprenal.1983.245.1.F89"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1983.245.1.f89","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[1983,7,1]]}},{"indexed":{"date-parts":[[2024,9,15]],"date-time":"2024-09-15T22:44:16Z","timestamp":1726440256331},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1988,12,1]]},"abstract":"<jats:p> To elucidate the role of the ureter in urinary concentration we studied the effect of partial and complete ureteral excision on urinary osmolality and papillary interstitial osmolality and on sodium, potassium, and urea concentrations in the antidiuretic rat. Urine and descending vasa recta (DVR) plasma samples were obtained by micropuncture of the left renal papilla before (period 1) and 45 min after (period 2) complete (group 1, n = 10 rats) or partial (group 2, n = 10 rats) ureteral excision. Urine osmolality fell from 2,063 +\/- 156 (mean +\/- SE) to 736 +\/- 116 mosmol\/kgH2O after complete ureteral excision (P less than 0.01). After partial ureteral excision, the fall was less than half as great, from 2,038 +\/- 167 to 1,551 +\/- 162 mosmol\/kgH2O (P less than 0.01). Vasa recta plasma osmolality decreased from 1,742 +\/- 133 to 860 +\/- 119 mosmol\/kgH2O after complete excision (P less than 0.01) but only from 1,830 +\/- 146 to 1,504 +\/- 154 mosmol\/kgH2O after partial excision (P less than 0.05). Mean DVR plasma sodium concentration declined from 339 +\/- 25 to 211 +\/- 25 meq\/l (P less than 0.01) in group 1 but did not change in group 2 (348 +\/- 21 to 347 +\/- 28 meq\/l). The fraction of DVR plasma osmolality accounted for by urea decreased significantly from 0.59 +\/- 0.01 to 0.46 +\/- 0.02 mM\/(mosmol\/kgH2O) in group 1 and from 0.59 +\/- 0.02 to 0.49 +\/- 0.03 mM\/(mosmol\/kgH2O) for group 2 (P less than 0.01, both groups). We interpret these findings to show that the remnant ureter moderates the fall in interstitial osmolality at least in part through preservation of the corticomedullary sodium chloride gradient. <\/jats:p>","DOI":"10.1152\/ajprenal.1988.255.6.f1225","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T21:10:56Z","timestamp":1513977056000},"page":"F1225-F1229","source":"Crossref","is-referenced-by-count":8,"title":["Effect of ureteral excision on inner medullary solute concentration in rats"],"prefix":"10.1152","volume":"255","author":[{"given":"T. L.","family":"Pallone","sequence":"first","affiliation":[{"name":"Division of Nephrology, Stanford University, California 94305."}]},{"given":"R. L.","family":"Jamison","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Stanford University, California 94305."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1988.255.6.F1225","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:09:08Z","timestamp":1567969748000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1988.255.6.F1225"}},"issued":{"date-parts":[[1988,12,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1988,12,1]]}},"alternative-id":["10.1152\/ajprenal.1988.255.6.F1225"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1988.255.6.f1225","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[1988,12,1]]}},{"indexed":{"date-parts":[[2022,10,13]],"date-time":"2022-10-13T04:03:14Z","timestamp":1665633794022},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2022,10,1]]},"DOI":"10.1152\/ajprenal.2022.323.4.au","type":"journal-article","created":{"date-parts":[[2022,10,12]],"date-time":"2022-10-12T17:05:46Z","timestamp":1665594346000},"page":"i-ii","update-policy":"http:\/\/dx.doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["First Author Spotlight"],"prefix":"10.1152","volume":"323","member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.2022.323.4.AU","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,10,12]],"date-time":"2022-10-12T17:05:47Z","timestamp":1665594347000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.2022.323.4.AU"}},"issued":{"date-parts":[[2022,10,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2022,10,1]]}},"alternative-id":["10.1152\/ajprenal.2022.323.4.AU"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.2022.323.4.au","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2022,10,1]]},"assertion":[{"value":"2022-10-12","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2022,4,5]],"date-time":"2022-04-05T21:43:30Z","timestamp":1649195010095},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1985,5,1]]},"abstract":"<jats:p> We investigated the possibility that altered cell calcium regulation may affect function of isolated Kyoto spontaneously hypertensive rat (SHR) kidneys as compared with kidneys from Wistar-Kyoto control (WKY) rats. The kidneys were perfused at 120 and 160 mmHg. At 120 mmHg, SHR glomerular filtration rate (GFR) was 0.24 +\/- 0.04 compared with WKY GFR of 0.70 +\/- 0.10 ml\/min (P = 0.001). At 160 mmHg, SHR GFR was 0.48 +\/- 0.05 compared with WKY GFR of 1.09 +\/- 0.05 ml\/min (P less than 0.001). At 120 mmHg, addition of norepinephrine increased renal vascular resistance (RVR) by 50% and decreased SHR GFR by 27% and WKY GFR by 57% (P = 0.04). At 160 mmHg, norepinephrine elicited similar changes. Addition of verapamil, 5-10 microM, in the presence of norepinephrine returned RVR to 100-110% of control. With verapamil at 120 mmHg, SHR GFR increased to 0.84 +\/- 0.23 ml\/min, a value 3.5 times that of control (P = 0.03). In contrast, WKY GFR in the presence of norepinephrine and verapamil was 0.97 +\/- 0.07 ml\/min, unchanged from control (P = 0.07). At 160 mmHg, norepinephrine and verapamil also failed to increase WKY GFR above control (P = 0.4) but increased SHR GFR to 52% above control (P = 0.03). Isolated SHR kidneys exhibited exaggerated GFR responses to verapamil but not to norepinephrine. Abnormal cell calcium regulation may underlie the marked decrease in GFR when SHR kidneys are perfused acutely at normotensive perfusion pressures. <\/jats:p>","DOI":"10.1152\/ajprenal.1985.248.5.f668","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T00:32:13Z","timestamp":1513989133000},"page":"F668-F673","source":"Crossref","is-referenced-by-count":0,"title":["Glomerular response to verapamil by isolated spontaneously hypertensive rat kidney"],"prefix":"10.1152","volume":"248","author":[{"given":"T. H.","family":"Steele","sequence":"first","affiliation":[]},{"given":"L.","family":"Challoner-Hue","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1985.248.5.F668","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:32:06Z","timestamp":1567971126000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1985.248.5.F668"}},"issued":{"date-parts":[[1985,5,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1985,5,1]]}},"alternative-id":["10.1152\/ajprenal.1985.248.5.F668"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1985.248.5.f668","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1985,5,1]]}},{"indexed":{"date-parts":[[2022,4,1]],"date-time":"2022-04-01T16:42:44Z","timestamp":1648831364962},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1992,7,1]]},"abstract":"<jats:p> Antidiuretic hormone (ADH) increases the osmotic water permeability (Pf) of the toad urinary bladder by insertion of water channels into the apical cell membrane. Transepithelial water flow (Jv) reduces Pf by inducing endocytosis of apical water channels despite continuous ADH stimulation. This phenomenon is termed flux inhibition. We wished to determine whether cytoplasmic dilution or transcellular Jv causes flux inhibition because both have been proposed previously as a primary regulatory mechanism for this process. Apical membrane endocytosis was quantified by monitoring the uptake of the fluid phase marker fluorescein isothiocyanate dextran (FITC-dextran). FITC-dextran fluorescence was monitored in Triton X-100 extracts of epithelial cells as the ratio of total tissue fluorescence compared with background fluorescence. The background was defined as cellular autofluorescence and nonspecific tissue staining due to the presence of small amounts of free fluorescein contaminating the FITC-dextran. FITC-dextran uptake measured under symmetric isotonic (220 mosmol\/kgH2O) conditions in either the absence (1.0 +\/- 0.4 SD; n = 14) or presence (1.3 +\/- 0.3; n = 4) of ADH was not statistically different from that of background. In contrast, flux inhibition induced by a 180 mosmol\/kgH2O apical-to-basolateral osmotic gradient increased FITC-dextran uptake to 3.4 +\/- 1.3 (n = 7). FITC-dextran uptake was identical in bladders exposed to symmetric hypotonic (150 mosmol\/kgH2O) solutions during ADH (3.6 +\/- 0.9; n = 6) or adenosine 3',5'-cyclic monophosphate (3.1 +\/- 0.4 fold; n = 3) stimulation.(ABSTRACT TRUNCATED AT 250 WORDS) <\/jats:p>","DOI":"10.1152\/ajprenal.1992.263.1.f163","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T10:12:07Z","timestamp":1514023927000},"page":"F163-F170","source":"Crossref","is-referenced-by-count":1,"title":["Cytoplasmic dilution induces antidiuretic hormone water channel retrieval in toad urinary bladder"],"prefix":"10.1152","volume":"263","author":[{"suffix":"Jr","given":"H. W.","family":"Harris","sequence":"first","affiliation":[{"name":"Division of Nephrology, Children's Hospital, Massachusetts."}]},{"given":"B.","family":"Botelho","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Children's Hospital, Massachusetts."}]},{"given":"M. L.","family":"Zeidel","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Children's Hospital, Massachusetts."}]},{"given":"K.","family":"Strange","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Children's Hospital, Massachusetts."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1992.263.1.F163","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:26:37Z","timestamp":1567974397000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1992.263.1.F163"}},"issued":{"date-parts":[[1992,7,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1992,7,1]]}},"alternative-id":["10.1152\/ajprenal.1992.263.1.F163"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1992.263.1.f163","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1992,7,1]]}},{"indexed":{"date-parts":[[2022,4,2]],"date-time":"2022-04-02T12:44:29Z","timestamp":1648903469285},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1990,3,1]]},"abstract":"<jats:p> We produced maximal or near-maximal acute intrarenal blockade of the renin-angiotensin system (RAS) by combining inhibitors. Intrarenal infusion of the renin inhibitor, ACRIP, the converting enzyme inhibitor, teprotide, and saralasin were administered individually or combined in random order. The inhibitors were infused for 20 min in doses that did not produce systemic effects in uninephrectomized conscious dogs in sodium balance at 10 meq\/day. Significant increases in urine flow rate (UV; F = 97, P less than 0.0001), urinary sodium excretion (UNaV; F = 220, P less than 0.0001), glomerular filtration rate (GFR; F = 64, P less than 0.0001), and renal plasma flow (RPF; F = 108, P less than 0.0001) were observed with each blocker, whether alone or in combination except that ACRIP alone did not alter GFR or RPF. The increase in renal function was related to the number of blockers (3 greater than 2 greater than 1). With the three blockers combined UV increased approximately sixfold (from 0.5 +\/- 0.06 to 2.9 +\/- 0.03 ml\/min), UNaV approximately 10-fold (from 3 +\/- 0.4 to 34 +\/- 2.8 mueq\/min), GFR from 31 +\/- 2 to 49 +\/- 2 ml\/min, RPF from 59 +\/- 1 to 120 +\/- 4 ml\/min, and fractional excretion of sodium from 0.06 +\/- 0.01 to 0.5 +\/- 0.4% (all P less than 0.001). These changes did not occur where the inhibitors were infused systemically and the changes during intrarenal blocker administration were blocked completely with co-administration of angiotensin II intrarenally. The intrarenal RAS is a potent physiological regulator of renal function.(ABSTRACT TRUNCATED AT 250 WORDS) <\/jats:p>","DOI":"10.1152\/ajprenal.1990.258.3.f522","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T16:37:30Z","timestamp":1513960650000},"page":"F522-F529","source":"Crossref","is-referenced-by-count":1,"title":["Combined intrarenal blockade of the renin-angiotensin system in the conscious dog"],"prefix":"10.1152","volume":"258","author":[{"given":"H. M.","family":"Siragy","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, University of Virginia School ofMedicine, Charlottesville 22908."}]},{"given":"N. L.","family":"Howell","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Virginia School ofMedicine, Charlottesville 22908."}]},{"given":"M. J.","family":"Peach","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Virginia School ofMedicine, Charlottesville 22908."}]},{"given":"R. M.","family":"Carey","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Virginia School ofMedicine, Charlottesville 22908."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1990.258.3.F522","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:12:02Z","timestamp":1567955522000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1990.258.3.F522"}},"issued":{"date-parts":[[1990,3,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1990,3,1]]}},"alternative-id":["10.1152\/ajprenal.1990.258.3.F522"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1990.258.3.f522","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1990,3,1]]}},{"indexed":{"date-parts":[[2022,4,2]],"date-time":"2022-04-02T14:01:26Z","timestamp":1648908086773},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1983,12,1]]},"abstract":"<jats:p> Techniques were developed to determine the location of exchangeable K pools that had been identified previously in kinetic studies of the intact perfused bullfrog kidney. Following perfusion of the kidneys with 42K, a washout of the isotope was begun and interrupted at various times; the kidneys were removed, frozen, dried at low pressure and temperature, and then microdissected. Glomerular capillary tufts, small segments of tissue containing early distal tubules (diluting segment), and other segments containing proximal tubular convolutions were removed and analyzed for total content of K and 42K. In the intact kidney 77% of tissue K exchanged in 60 min. The exchangeable K concentration was 95 mu eq\/ml cell water. Correction for the K activity coefficient in Ringer solution yielded an activity of 72 mu eq\/ml. Thirty-two percent of glomerular capillary K exchanged in 60 min; 7% exchanged with a half time of 3.5 min; and the remainder exchanged at a rate too slow to measure. The data from tissue containing proximal tubular segments were too scattered to permit analysis. In segments containing early distal tubules, 67% of tissue K was contained in two exchangeable pools: one pool exchanged at a rate 10-fold greater than did the other. The data for these two distal pools were analyzed in terms of a parallel model (two cell types?) and a nested model (cytoplasm and subcellular organelles?). Pool size and exchange rates were calculated for both models. Electron microscopic analysis revealed that early distal tubular segments contain only one cell type which has a large population of mitochondria. This suggests that the nested model is more plausible. The fast distal pool exchanged at the same rate as the fast-exchanging pool identified in kinetic studies of the intact functioning kidney and is considered to be the K secretory pool. <\/jats:p>","DOI":"10.1152\/ajprenal.1983.245.6.f801","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T15:02:26Z","timestamp":1513954946000},"page":"F801-F812","source":"Crossref","is-referenced-by-count":0,"title":["Localization of tissue potassium pools in the amphibian kidney"],"prefix":"10.1152","volume":"245","author":[{"given":"H. L.","family":"Wilkinson","sequence":"first","affiliation":[]},{"given":"L. P.","family":"Sullivan","sequence":"additional","affiliation":[]},{"given":"D. J.","family":"Welling","sequence":"additional","affiliation":[]},{"given":"L. W.","family":"Welling","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1983.245.6.F801","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:25:35Z","timestamp":1567967135000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1983.245.6.F801"}},"issued":{"date-parts":[[1983,12,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1983,12,1]]}},"alternative-id":["10.1152\/ajprenal.1983.245.6.F801"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1983.245.6.f801","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1983,12,1]]}},{"indexed":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T04:10:35Z","timestamp":1660191035894},"reference-count":21,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1998,1,1]]},"abstract":"<jats:p>Understanding the mechanism of sulfate-dependent, oxalate-stimulated chloride reabsorption in the mammalian proximal tubule is complicated by the presence of multiple oxalate and sulfate transport pathways. Accordingly, we developed a method of reconstituting functional oxalate transport from the rabbit renal cortex so that the individual transporters might be examined. Solubilized microvillus membrane proteins were separated by hydroxyapatite chromatography and then reconstituted into proteoliposomes. Two peaks of oxalate\/oxalate exchange activity were observed. Sulfate (10 mM) cis-inhibits oxalate transport in the early peak by 93% and in the later peak by 41%. In contrast, 20 mM chloride inhibits oxalate\/oxalate exchange by only 32% in the early peak but inhibits oxalate exchange by 70% in the later peak. Oxalate-stimulated sulfate uptake was observed in the early fractions but not in the later fractions. These data are consistent with the recovery of the sulfate\/oxalate exchanger in the early hydroxyapatite fractions and the chloride\/oxalate exchanger in the later fractions. The basolateral membrane sulfate\/oxalate exchanger was also reconstituted. The reconstituted basolateral and apical membrane sulfate\/oxalate exchangers demonstrate nearly identical patterns of substrate specificities. However, 98% of apical sulfate\/oxalate exchange activity is lost following exposure to octylglucoside at room temperature, whereas the basolateral sulfate\/oxalate exchange activity was reduced 67% ( P &lt; 0.05). In conclusion, functional reconstitution of solubilized membrane proteins demonstrates that apical membrane chloride\/oxalate exchange and sulfate\/oxalate exchange are mediated by different transport proteins. Apical and basolateral sulfate\/oxalate exchange may also represent transport on two separate exchangers.<\/jats:p>","DOI":"10.1152\/ajprenal.1998.274.1.f189","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T14:24:43Z","timestamp":1514039083000},"page":"F189-F196","source":"Crossref","is-referenced-by-count":2,"title":["Effects of sulfate and chloride on three separate oxalate transporters reconstituted from rabbit renal cortex"],"prefix":"10.1152","volume":"274","author":[{"given":"Lawrence P.","family":"Karniski","sequence":"first","affiliation":[{"name":"Laboratory of Epithelial Transport, Department of Internal Medicine, Iowa City Veterans Affairs and University of Iowa Hospitals, Iowa City, Iowa 52242"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.ph.51.030189.002223"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/0003-2697(83)90356-1"},{"key":"B3","doi-asserted-by":"crossref","first-page":"8778","DOI":"10.1016\/S0021-9258(19)84448-4","volume":"261","author":"Grassl S. M.","year":"1986","journal-title":"J. Biol. Chem."},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1007\/BF00585601"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/S0076-6879(84)04097-0"},{"key":"B6","doi-asserted-by":"crossref","first-page":"13379","DOI":"10.1016\/S0021-9258(19)38309-7","volume":"265","author":"Kaplan R. S.","year":"1990","journal-title":"J. Biol. Chem."},{"issue":"22","key":"B7","first-page":"F513","volume":"253","author":"Karniski L. P.","year":"1987","journal-title":"Am. J. Physiol."},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1016\/0076-6879(90)91037-7"},{"key":"B9","doi-asserted-by":"crossref","first-page":"9710","DOI":"10.1016\/S0021-9258(19)81576-4","volume":"263","author":"Kuo S.-M.","year":"1988","journal-title":"J. Biol. Chem."},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.26.15491"},{"key":"B11","doi-asserted-by":"crossref","first-page":"265","DOI":"10.1016\/S0021-9258(19)52451-6","volume":"193","author":"Lowry O. H.","year":"1951","journal-title":"J. Biol. Chem."},{"key":"B12","doi-asserted-by":"crossref","first-page":"3022","DOI":"10.1016\/S0021-9258(17)42041-2","volume":"269","author":"Markovich D.","year":"1994","journal-title":"J. Biol. Chem."},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1016\/0003-2697(77)90043-4"},{"issue":"21","key":"B14","first-page":"F346","volume":"252","author":"Pritchard J. B.","year":"1987","journal-title":"Am. J. Physiol."},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.80.9.2603"},{"issue":"12","key":"B16","first-page":"F271","volume":"243","author":"Senekjian H. O.","year":"1982","journal-title":"Am. J. Physiol."},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1111\/j.1432-1033.1987.tb11182.x"},{"issue":"33","key":"B18","first-page":"F730","volume":"264","author":"Wang T.","year":"1993","journal-title":"Am. J. Physiol."},{"issue":"40","key":"B19","first-page":"F446","volume":"271","author":"Wang T.","year":"1996","journal-title":"Am. J. Physiol."},{"issue":"32","key":"B20","first-page":"F37","volume":"263","author":"Wang T.","year":"1992","journal-title":"Am. J. Physiol."},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.83.23.8913"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1998.274.1.F189","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:45:56Z","timestamp":1660189556000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1998.274.1.F189"}},"issued":{"date-parts":[[1998,1,1]]},"references-count":21,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1998,1,1]]}},"alternative-id":["10.1152\/ajprenal.1998.274.1.F189"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1998.274.1.f189","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1998,1,1]]}},{"indexed":{"date-parts":[[2022,3,30]],"date-time":"2022-03-30T18:08:39Z","timestamp":1648663719237},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1995,6,1]]},"abstract":"<jats:p> On the basis of intracellular calcium concentration ([Ca2+]i) measurements, we have previously reported that the parietal sheet of Bowman's capsule was sensitive to cholinergic agonists. The aim of the present work was to investigate whether this structure could be also a target of endothelin and platelet-activating factor (PAF), since we observed [Ca2+]i increases in response to both agonists in the glomerulus, but which were very different from that induced by carbachol. For this purpose, we measured [Ca2+]i on single microdissected parietal sheets, using a fura 2 microfluorescence technique and compared the effects of maximal concentrations of the three agonists (10(-7), 10(-8), and 10(-4) M for endothelin, PAF, and carbachol, respectively) under various experimental conditions. We observed that, like in the glomerulus, endothelin and PAF induced, in the parietal sheet, [Ca2+]i responses that differed in many respects from those found with carbachol. Thus, in the presence of 2 mM external calcium, 1) endothelin and PAF responses spontaneously declined to basal level, whereas a stationary plateau was observed after a sharp peak of [Ca2+]i with carbachol; 2) the magnitude of [Ca2+]i peak was smaller with endothelin and PAF than with carbachol; and 3) endothelin and PAF, but not carbachol, induced a homologous dose-dependent desensitization. Moreover, in the absence of external calcium, endothelin and PAF responses were smaller than carbachol response, although all three responses apparently resulted from release of calcium ions from the same internal pool. In additional experiments, we observed that, like carbachol, endothelin and PAF contracted the parietal sheet, which is only composed of myoepithelial cells.(ABSTRACT TRUNCATED AT 250 WORDS) <\/jats:p>","DOI":"10.1152\/ajprenal.1995.268.6.f1053","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T00:34:24Z","timestamp":1513989264000},"page":"F1053-F1061","source":"Crossref","is-referenced-by-count":3,"title":["The parietal sheet of Bowman's capsule of rat renal glomerulus: a target of endothelin and PAF"],"prefix":"10.1152","volume":"268","author":[{"given":"J.","family":"Marchetti","sequence":"first","affiliation":[{"name":"Laboratoire de Physiologie Cellulaire, Centre National de la Recherche Scientifique, College de France, Paris."}]},{"given":"P.","family":"Meneton","sequence":"additional","affiliation":[{"name":"Laboratoire de Physiologie Cellulaire, Centre National de la Recherche Scientifique, College de France, Paris."}]},{"given":"F.","family":"Lebrun","sequence":"additional","affiliation":[{"name":"Laboratoire de Physiologie Cellulaire, Centre National de la Recherche Scientifique, College de France, Paris."}]},{"given":"M.","family":"Bloch-Faure","sequence":"additional","affiliation":[{"name":"Laboratoire de Physiologie Cellulaire, Centre National de la Recherche Scientifique, College de France, Paris."}]},{"given":"R. M.","family":"Rajerison","sequence":"additional","affiliation":[{"name":"Laboratoire de Physiologie Cellulaire, Centre National de la Recherche Scientifique, College de France, Paris."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1995.268.6.F1053","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:00:55Z","timestamp":1567958455000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1995.268.6.F1053"}},"issued":{"date-parts":[[1995,6,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1995,6,1]]}},"alternative-id":["10.1152\/ajprenal.1995.268.6.F1053"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1995.268.6.f1053","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1995,6,1]]}},{"indexed":{"date-parts":[[2024,8,5]],"date-time":"2024-08-05T00:16:26Z","timestamp":1722816986742},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1991,7,1]]},"abstract":"<jats:p> Mammalian distal tubules adapt structurally and functionally when NaCl concentration in tubule fluid is altered chronically. These experiments were designed to test the hypothesis that chronic administration of hydrochlorothiazide (HCTZ), a drug that blocks Na and Cl uptake across apical membranes of rat distal tubule cells, would reduce intrinsic transport capacity of distal tubules and reduce the number of thiazide-sensitive transporters. Osmotic pumps were implanted into rats to deliver 3.75 mg\/day HCTZ or vehicle for 10-14 days. All animals were offered a solution containing 0.8% NaCl and 0.1% KCl as drinking fluid. Free-flow micropuncture after 10\u201314 days indicated that Na and Cl delivery to distal tubule was not significantly different in HCTZ- and vehicle-treated animals. Microperfusion in vivo with an artificial interstitial solution, with no thiazide, indicated that 10-14 days of HCTZ infusion did reduce Na transport capacity of distal tubules from 390 +\/- 32 to 203 +\/- 24 pmol\/min (P less than 0.01). In contrast, the number of thiazide-sensitive NaCl transporters, determined as high-affinity receptors for [3H]metolazone in renal cortical membranes, was higher in HCTZ group than in controls (2.2 +\/- 0.4 vs. 1.0 +\/- 0.1 pmol\/mg protein, P less than 0.01). These data support the hypothesis that chronic blockade of NaCl entry across apical membranes of distal tubule cells reduces NaCl transport capacity, an effect that occurs despite an increase in the number of thiazide receptors. They indicate that thiazide receptor binding studies should be interpreted in combination with direct functional measurements. <\/jats:p>","DOI":"10.1152\/ajprenal.1991.261.1.f137","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T23:39:32Z","timestamp":1513985972000},"page":"F137-F143","source":"Crossref","is-referenced-by-count":10,"title":["Adaptation of distal convoluted tubule of rats. II. Effects of chronic thiazide infusion"],"prefix":"10.1152","volume":"261","author":[{"given":"P.","family":"Morsing","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, Yale School of Medicine, New Haven, Connecticut 06510."}]},{"given":"H.","family":"Velazquez","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Yale School of Medicine, New Haven, Connecticut 06510."}]},{"given":"F. S.","family":"Wright","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Yale School of Medicine, New Haven, Connecticut 06510."}]},{"given":"D. H.","family":"Ellison","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Yale School of Medicine, New Haven, Connecticut 06510."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1991.261.1.F137","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:25:33Z","timestamp":1567970733000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1991.261.1.F137"}},"issued":{"date-parts":[[1991,7,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1991,7,1]]}},"alternative-id":["10.1152\/ajprenal.1991.261.1.F137"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1991.261.1.f137","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1991,7,1]]}},{"indexed":{"date-parts":[[2022,4,5]],"date-time":"2022-04-05T00:22:27Z","timestamp":1649118147819},"reference-count":11,"publisher":"American Physiological Society","issue":"12","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2012,12,15]]},"DOI":"10.1152\/ajprenal.00505.2012","type":"journal-article","created":{"date-parts":[[2012,9,27]],"date-time":"2012-09-27T11:57:52Z","timestamp":1348747072000},"page":"F1608-F1609","source":"Crossref","is-referenced-by-count":2,"title":["A balancing act: protein-energy wasting in chronic kidney disease"],"prefix":"10.1152","volume":"303","author":[{"given":"Maria R.","family":"Wing","sequence":"first","affiliation":[{"name":"George Washington University School of Medicine"}]},{"given":"Dominic S.","family":"Raj","sequence":"additional","affiliation":[{"name":"George Washington University School of Medicine"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2362.2010.02347.x"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI22521"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006091024"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00341.2012"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1007\/s13539-011-0039-1"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1999.276.3.R864"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M109.070706"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2009.06.022"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5001532"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2012.84"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2009.090275"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00505.2012","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:30:25Z","timestamp":1567974625000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00505.2012"}},"issued":{"date-parts":[[2012,12,15]]},"references-count":11,"journal-issue":{"issue":"12","published-print":{"date-parts":[[2012,12,15]]}},"alternative-id":["10.1152\/ajprenal.00505.2012"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00505.2012","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2012,12,15]]}},{"indexed":{"date-parts":[[2025,1,8]],"date-time":"2025-01-08T05:16:45Z","timestamp":1736313405801,"version":"3.32.0"},"reference-count":40,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2006,9]]},"abstract":"<jats:p>We have previously shown that systemic treatment with the somatostatin analog octreotide has marked beneficial effects on renal function in rats with liver cirrhosis induced by common bile duct ligation (CBL; Jonassen TEN, Christensen S, S\u00f8rensen AM, Marcussen N, Flyvbjerg A, Andreasen F, and Petersen JS. Hepatology 29: 1387\u20131395, 1999). In the present study, we tested the hypothesis that octreotide has a direct effect on renal tubular function. Rats (CBL or Sham-CBL) were intrarenally treated with low-dose octreotide in a long-acting release formulation, which had no systemic actions (100 \u03bcg\/kg body wt as a single dose). Rats receiving low-dose octreotide (sc) were used as controls. The rats were chronically instrumented, and renal function was examined 4 wk after CBL or Sham-CBL. Intrarenal octreotide administration (IROA) prevented sodium retention in CBL rats without changes in renal plasma flow, glomerular filtration rate, or circulating levels of aldosterone and vasopressin. Renal clearance studies revealed that IROA normalized the increased natriuretic efficacy of furosemide found in CBL rats. Furthermore, IROA protected against the development of hypertrophy of the inner stripe of the outer medulla and thereby the increased the volume of thick ascending limb of Henle's loop (TAL) epithelium found in CBL rats. Finally, Western blot analyses of outer medullary homogenates showed increased abundance of the furosemide-sensitive Na-K-2Cl (NKCC2) cotransporter. IROA did not affect the abundance of NCKK2 within the outer medulla. Together with the histological findings, these results indicate that IROA reduces the total number of NKCC2 within the outer medulla. In conclusion, the results indicate a direct intrarenal effect of octreotide on TAL function and morphology in cirrhotic rats.<\/jats:p>","DOI":"10.1152\/ajprenal.00226.2005","type":"journal-article","created":{"date-parts":[[2006,1,18]],"date-time":"2006-01-18T03:14:09Z","timestamp":1137554049000},"page":"F537-F545","source":"Crossref","is-referenced-by-count":1,"title":["Intrarenal octreotide treatment prevents sodium retention in liver cirrhotic rats: evidence for direct effects within the thick ascending limb of Henle's loop"],"prefix":"10.1152","volume":"291","author":[{"given":"Thomas E. N.","family":"Jonassen","sequence":"first","affiliation":[]},{"given":"Sten","family":"Christensen","sequence":"additional","affiliation":[]},{"given":"Niels","family":"Marcussen","sequence":"additional","affiliation":[]},{"given":"J\u00f8rgen S\u00f8berg","family":"Petersen","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"crossref","unstructured":"Albillos A, Colombato LA, Lee FY, and Groszmann RJ.Octreotide ameliorates vasodilatation and Na+retention in portal hypertensive rats.Gastroenterology104: 575\u2013579, 1989.","DOI":"10.1016\/0016-5085(93)90429-G"},{"key":"R2","doi-asserted-by":"crossref","unstructured":"Andreasen F, Christensen CK, Jacobsen FK, and Mogensen CE.The use of HPLC to elucidate the metabolism and urinary excretion of furosemide and its metabolic products.Acta Pharmacol Toxicol49: 223\u2013229, 1981.","DOI":"10.1111\/j.1600-0773.1981.tb00897.x"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.3.F457"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1985.152"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1988.138"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.pa.23.040183.000401"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1210\/endo.133.6.8243278"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1007\/BF00582129"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.3.F619"},{"key":"R10","doi-asserted-by":"crossref","unstructured":"Gillis JC, Noble S, and Goa KL.Octreotide long-acting release (LAR). A review of its pharmacological properties and therapeutic use in the management of acromegaly.Drugs53: 661\u2013699, 1997.","DOI":"10.2165\/00003495-199753040-00009"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1111\/j.1699-0463.1988.tb05320.x"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1111\/j.1699-0463.1988.tb00954.x"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1016\/S0165-6147(00)88988-9"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1988.31"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1136\/bmj.315.7119.1338"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1997.273.2.R568"},{"key":"R17","doi-asserted-by":"crossref","unstructured":"Jonassen TEN, Nielsen S, Christensen S, and Petersen JS.Decreased vasopressin-mediated renal water reabsorption in rats with compensated liver cirrhosis.Am J Physiol Renal Physiol275: F216\u2013F225, 1998.","DOI":"10.1152\/ajprenal.1998.275.2.F216"},{"key":"R18","doi-asserted-by":"crossref","unstructured":"Jonassen TEN, Petersen JS, S\u00f8rensen AM, Andreasen F, and Christensen S.Aldosterone receptor blockade inhibits increased furosemide-sensitive sodium reabsorption in rats with liver cirrhosis.J Pharmacol Exp Ther287: 931\u2013936, 1998.","DOI":"10.1016\/S0022-3565(24)37883-8"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1002\/hep.510290532"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1053\/jhep.2000.7518"},{"key":"R21","doi-asserted-by":"crossref","unstructured":"Jonassen TEN, Br\u00f8nd L, Torp M, Gr\u00e6be M, Nielsen S, Sk\u00f8tt O, Marcussen N, and Christensen S.Effects of renal denervation on thick ascending Na reabsorption in rats with liver cirrhosis.Am J Physiol Renal Physiol284: F555\u2013F563, 2003.","DOI":"10.1152\/ajprenal.00258.2002"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1210\/endo.135.2.8033816"},{"key":"R23","unstructured":"Kountouras J, Billing BH, and Scheuer PJ.Prolonged bile duct obstruction: a new experimental model for cirrhosis in the rat.Br J Exp Path65: 305\u2013311, 1984."},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.267.1.F86"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1002\/hep.510230319"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1016\/S0168-8278(97)80247-4"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1002\/hep.1840210507"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1139\/y82-090"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1016\/0026-0495(85)90204-5"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1093\/oxfordjournals.ndt.a091713"},{"key":"R31","unstructured":"Ottesen LH, Aagaard NK, Kiszka-Kanowitz M, Rehling M, Henriksen JH, Pedersen EB, Flyvbjerg A, and Bendtsen F.Effects of a long-acting formulation of octreotide on renal function and renal sodium handling in cirrhotic patients with portal hypertension: a randomized, double-blind, controlled trial.Hepatology34: 471\u2013477, 2001."},{"key":"R32","unstructured":"Petersen JS, Shalmi M, Lam HR, and Christensen S.Renal response of furosemide in conscious rats: effects of acute instrumentation and peripheral sympathectomy.J Pharmacol Exp Ther258: 1\u20137, 1991."},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.47.6.924"},{"key":"R34","doi-asserted-by":"crossref","unstructured":"Reid IAand Rose JC.An intrarenal effect of somatostatin on water excretion.Endocrinology100: 782\u2013785, 1997.","DOI":"10.1210\/endo-100-3-782"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1023\/A:1026698001921"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1002\/hep.1840080532"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1002\/hep.510230541"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.6.F1095"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1016\/S0168-8278(97)80122-5"},{"key":"R40","unstructured":"Winkler SN, Torikai S, Levine BS, and Kurokawa K.Effect of somatostatin on vasopressin-induced antidiuresis and renal cyclic AMP of rats.Min Electr Metab7: 8\u201314, 1982."}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00226.2005","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,1,7]],"date-time":"2025-01-07T05:49:54Z","timestamp":1736228994000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00226.2005"}},"issued":{"date-parts":[[2006,9]]},"references-count":40,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2006,9]]}},"alternative-id":["10.1152\/ajprenal.00226.2005"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00226.2005","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2006,9]]}},{"indexed":{"date-parts":[[2024,6,17]],"date-time":"2024-06-17T20:35:41Z","timestamp":1718656541664},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1985,11,1]]},"abstract":"<jats:p> An isotopic method was developed to measure the intracellular Na+ content of the transepithelial Na+ transport pool of frog skin. Isolated epithelia (no corium) were labeled with 24Na either asymmetrically, from apical (Aa) or basolateral (Ab) solutions, or symmetrically (Aab). Transport pool Na+ could be identified from the kinetics of washout of 24Na carried out in the presence of 1 mM ouabain, 100 microM amiloride, and 1 mM furosemide that served to trap cold Na+ and 24Na within the transport pool. In control epithelia, Aab averaged 64.1 neq\/cm2 (13.9 mM), and maximal inhibition of apical membrane Na+ entry with 100 microM amiloride caused Aab to decrease to 24.3 neq\/cm2 (5.3 mM). Ouabain caused Aab to increase markedly to 303 neq\/cm2 in 30 min, whereas amiloride inhibition of apical membrane Na+ entry reduced markedly the rate of increase of Aab caused by ouabain (7.3 neq X cm-2 X min-1 in control and 1.7 neq X cm-2 X min-1 in the presence of amiloride). These data, in part, confirmed the existence of an important basolateral membrane permeability to Na+ that was measured in separate studies of the bidirectional 24Na fluxes at the basolateral membranes of the cells. Both sets of data were supportive of the idea that a significant Na+ recycling exists at the basolateral membranes of the cells that contributes to the Na+ load on the pump and Na+ recycling participates in the regulation of the Na+ concentration of the Na+ transport pool of these epithelial cells. <\/jats:p>","DOI":"10.1152\/ajprenal.1985.249.5.f662","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T19:00:57Z","timestamp":1513969257000},"page":"F662-F671","source":"Crossref","is-referenced-by-count":1,"title":["Dependence of intracellular Na+ concentration on apical and basolateral membrane Na+ influx in frog skin"],"prefix":"10.1152","volume":"249","author":[{"given":"J. S.","family":"Stoddard","sequence":"first","affiliation":[]},{"given":"S. I.","family":"Helman","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1985.249.5.F662","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:29:36Z","timestamp":1567956576000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1985.249.5.F662"}},"issued":{"date-parts":[[1985,11,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1985,11,1]]}},"alternative-id":["10.1152\/ajprenal.1985.249.5.F662"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1985.249.5.f662","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1985,11,1]]}},{"indexed":{"date-parts":[[2024,6,17]],"date-time":"2024-06-17T20:33:47Z","timestamp":1718656427829},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1995,9,1]]},"abstract":"<jats:p> Recently, it has been hypothesized that the proximal tubular Na(+)-Pi transporter may play a role in murine X-linked hypophosphatemic vitamin D-resistant rickets. In the present investigation, Western blot analysis of renal brush-border membrane proteins, utilizing polyclonal antisera raised against the mouse Na(+)-Pi transporter, revealed a predominant band at 87 kDa in normal and hypophosphatemic (Hyp) mice. The intensity of this band was reduced in the Hyp mouse by 4.5-fold (Hyp\/normal = 0.22 +\/- 0.04, n = 3, P &lt; 0.05). Additionally, immunohistochemical analysis of kidney cortex in both mice localized the protein to the apical membrane of the proximal tubules. Relative transcription rates of the Na(+)-Pi transporter gene in the normal and Hyp mouse were then investigated. Nuclear run-on assays showed a 51 +\/- 0.02% decreased rate of transcription of the Na(+)-Pi transporter gene in the Hyp mice (n = 3). Thus abnormal transcriptional control of this gene in the Hyp mouse likely plays a role in X-linked hypophosphatemia. <\/jats:p>","DOI":"10.1152\/ajprenal.1995.269.3.f439","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T00:25:28Z","timestamp":1513988728000},"page":"F439-F448","source":"Crossref","is-referenced-by-count":7,"title":["Decreased transcription of the sodium-phosphate transporter gene in the hypophosphatemic mouse"],"prefix":"10.1152","volume":"269","author":[{"given":"J. F.","family":"Collins","sequence":"first","affiliation":[{"name":"Department of Pediatrics, Vanderbilt University School of Medicine,Nashville, Tennessee 37232-2576, USA."}]},{"given":"L. A.","family":"Scheving","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Vanderbilt University School of Medicine,Nashville, Tennessee 37232-2576, USA."}]},{"given":"F. K.","family":"Ghishan","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Vanderbilt University School of Medicine,Nashville, Tennessee 37232-2576, USA."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1995.269.3.F439","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:58:25Z","timestamp":1567958305000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1995.269.3.F439"}},"issued":{"date-parts":[[1995,9,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1995,9,1]]}},"alternative-id":["10.1152\/ajprenal.1995.269.3.F439"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1995.269.3.f439","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1995,9,1]]}},{"indexed":{"date-parts":[[2023,9,10]],"date-time":"2023-09-10T23:51:32Z","timestamp":1694389892430},"reference-count":32,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2001,11,1]]},"abstract":"<jats:p> First published July 12, 2001; 10.1152\/ajprenal.00138.2001.\u2014Nitric oxide (NO) production by endothelial nitric oxide synthase (eNOS) regulates renal O<jats:sub>2<\/jats:sub>consumption. This mechanism is impaired in heart and kidney of dogs with heart failure (CHF). Simvastatin, an inhibitor of 3-hydroxy-3-methylglutaryl-CoA reductase, increases eNOS expression in the endothelium. Therefore, we studied whether simvastatin treatment could restore the regulation of renal O<jats:sub>2<\/jats:sub> consumption by stimulators of NO production in dogs with CHF. Renal O<jats:sub>2<\/jats:sub>consumption was measured after stimulation of NO production with bradykinin, ramiprilat, or amlodipine or the NO donor S-nitroso- N-acetylpenicillamine (SNAP). Simvastatin delayed the time to euthanasia in dogs with CHF (35 \u00b1 1.0 vs. 29 \u00b1 1.2 days; P &lt; 0.01). In normal dogs, bradykinin (10<jats:sup>\u22124<\/jats:sup> M), ramiprilat (10<jats:sup>\u22124<\/jats:sup>M), amlodipine (10<jats:sup>\u22125<\/jats:sup> M), and SNAP (10<jats:sup>\u22124<\/jats:sup> M) significantly reduced O<jats:sub>2<\/jats:sub> consumption in the renal cortex (\u221231.8 \u00b1 0.9, \u221230.3 \u00b1 1.1, \u221230.1 \u00b1 2.0, \u221246.9 \u00b1 1.0%) and renal medulla (\u221229.7 \u00b1 2.1, \u221233.0 \u00b1 2.7, \u221230.8 \u00b1 2.2, \u221246.8 \u00b1 1.1%). Responses to bradykinin, ramiprilat, and amlodipine were significantly attenuated in CHF but were partially or completely restored by simvastatin. Responses to SNAP were unaffected. These data demonstrate that treatment with simvastatin improves renal production of NO in CHF, restoring the normal regulation of renal O<jats:sub>2<\/jats:sub> consumption by NO. <\/jats:p>","DOI":"10.1152\/ajprenal.00138.2001","type":"journal-article","created":{"date-parts":[[2018,3,25]],"date-time":"2018-03-25T20:21:12Z","timestamp":1522009272000},"page":"F802-F809","source":"Crossref","is-referenced-by-count":2,"title":["Simvastatin reverses impaired regulation of renal oxygen consumption in congestive heart failure"],"prefix":"10.1152","volume":"281","author":[{"given":"Stephen","family":"Adler","sequence":"first","affiliation":[{"name":"Division of Nephrology, Department of Medicine, and the"}]},{"given":"Harer","family":"Huang","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, and the"}]},{"given":"Jean Noel","family":"Trochu","sequence":"additional","affiliation":[{"name":"Department of Physiology, New York Medical College, Valhalla, New York 10532"}]},{"given":"Xiaobin","family":"Xu","sequence":"additional","affiliation":[{"name":"Department of Physiology, New York Medical College, Valhalla, New York 10532"}]},{"given":"Shabnam","family":"Gupta","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, and the"}]},{"given":"Thomas H.","family":"Hintze","sequence":"additional","affiliation":[{"name":"Department of Physiology, New York Medical College, Valhalla, New York 10532"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.96.10.3655"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.4.F766"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.5.F838"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.267.5.F748"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(12)80170-3"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1042\/bj3150295"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115316"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00292.x"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.95.2.527"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1172\/JCI1500"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.349"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/jappl.1994.76.3.1166"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00474.x"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(97)90275-4"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.272.5.F561"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.97.12.1129"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.82.12.1263"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.100.12.1291"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.84.7.840"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.35.1.337"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.2000.279.6.H2649"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.318"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.95.5.1126"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.35.1.319"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.83.10.969"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00281.x"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.75.6.1086"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.78.1.58"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1991.260.5.C910"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(96)05190-2"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.79.3.381"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.95.1.176"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00138.2001","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T22:01:50Z","timestamp":1567980110000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00138.2001"}},"issued":{"date-parts":[[2001,11,1]]},"references-count":32,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2001,11,1]]}},"alternative-id":["10.1152\/ajprenal.00138.2001"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00138.2001","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2001,11,1]]}},{"indexed":{"date-parts":[[2022,3,30]],"date-time":"2022-03-30T17:27:00Z","timestamp":1648661220693},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1994,11,1]]},"abstract":"<jats:p> This study examined the ontogeny of the mRNA for three atrial natriuretic peptide (ANP) receptors in the ovine fetal kidney and the effect of systemic ANP infusion in the very immature ovine fetus. mRNA was isolated from the kidneys of 60-, 100-, and 140-day fetuses (n = 4 at each age). Northern blots [5 micrograms poly(A)+ RNA per track] were probed for the guanylate cyclase (GC)-A, GC-B, and clearance receptors, using beta-actin as a control for variations in loading. The results were quantitated using laser densitometry. Levels of clearance receptor mRNA were significantly higher in 140-day than 60-day fetal kidneys (P &lt; 0.05), whereas levels of mRNA for the GC-A and GC-B receptors remained steady. We propose that binding of ANP to an increased number of C receptors in the late-gestation fetal kidney could explain the previously documented increase in total ANP receptor number in late-gestation ovine kidneys without increased ANP biological activity. Systemic ANP infusion into four fetuses of approximately 74 days gestation resulted in a natriuresis and diuresis, indicating the presence of functional ANP receptors in the ovine kidney early in gestation. <\/jats:p>","DOI":"10.1152\/ajprenal.1994.267.5.f825","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T23:51:59Z","timestamp":1513986719000},"page":"F825-F830","source":"Crossref","is-referenced-by-count":2,"title":["Atrial natriuretic peptide receptors are present and functional by midgestation in fetal sheep"],"prefix":"10.1152","volume":"267","author":[{"given":"M. B.","family":"Fraenkel","sequence":"first","affiliation":[{"name":"Howard Florey Institute of Experimental Physiology and Medicine,University of Melbourne, Victoria, Australia."}]},{"given":"S. J.","family":"Potocnik","sequence":"additional","affiliation":[{"name":"Howard Florey Institute of Experimental Physiology and Medicine,University of Melbourne, Victoria, Australia."}]},{"given":"E. M.","family":"Wintour","sequence":"additional","affiliation":[{"name":"Howard Florey Institute of Experimental Physiology and Medicine,University of Melbourne, Victoria, Australia."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1994.267.5.F825","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:55:40Z","timestamp":1567958140000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1994.267.5.F825"}},"issued":{"date-parts":[[1994,11,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1994,11,1]]}},"alternative-id":["10.1152\/ajprenal.1994.267.5.F825"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1994.267.5.f825","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1994,11,1]]}},{"indexed":{"date-parts":[[2023,10,1]],"date-time":"2023-10-01T12:42:21Z","timestamp":1696164141759},"reference-count":13,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2012,7,1]]},"DOI":"10.1152\/ajprenal.00225.2012","type":"journal-article","created":{"date-parts":[[2012,4,26]],"date-time":"2012-04-26T02:51:06Z","timestamp":1335408666000},"page":"F35-F36","source":"Crossref","is-referenced-by-count":4,"title":["Protein kinase C-\u03b1 comes to the rescue of aquaporin-2"],"prefix":"10.1152","volume":"303","author":[{"given":"Serena M.","family":"Bagnasco","sequence":"first","affiliation":[{"name":"Department of Pathology, The Johns Hopkins School of Medicine, Baltimore, Maryland"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00102.2008"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.262.6.F1061"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00617.2009"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00358.2011"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.5.F835"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00664.2011"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00376.2011"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00469.2010"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00721.2010"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/S0167-4781(00)00311-0"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M004678200"},{"key":"B12","author":"Thai TL","journal-title":"Am J Physiol Renal Physiol"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008121225"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00225.2012","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T00:20:03Z","timestamp":1567988403000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00225.2012"}},"issued":{"date-parts":[[2012,7,1]]},"references-count":13,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2012,7,1]]}},"alternative-id":["10.1152\/ajprenal.00225.2012"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00225.2012","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2012,7,1]]}},{"indexed":{"date-parts":[[2024,7,26]],"date-time":"2024-07-26T13:20:12Z","timestamp":1722000012760},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1990,7,1]]},"abstract":"<jats:p> The distribution of atrial natriuretic peptide (ANP) clearance receptors in rat kidney was investigated by in vitro autoradiography using des[Gln18,Ser19,Gly20,Leu21,Gly22]-ANP-(4- 23) (C-ANP) and 125I-Tyr0-ANP-(5-25) as relatively specific ligands of this receptor. Alpha-125I-ANP (100 pM) bound reversibly but with high affinity to glomeruli, outer medullary vasa recta bundles, and inner medulla. C-ANP (10 microM) inhibited greater than 60% of this glomerular binding but did not inhibit the binding of alpha-125I-ANP to medullary tissues. Alpha-125I-ANP also bound reversibly to the renal arteries up to the glomerulus. This arterial binding was only partly inhibited by 10 microM C-ANP. In the presence of 10 microM C-ANP, increasing concentrations of alpha-125I-ANP bound to a residue of glomerular sites with apparent dissociation constants of 0.82 +\/- 0.16 to 2.73 +\/- 1.20 nM at different cortical levels. 125I-Tyr0-ANP-(5-25) bound significantly to glomeruli and intrarenal arteries but not to vasa recta bundles or inner medulla. This glomerular binding also occurred with nanomolar dissociation constants. It was completely inhibited by 1 microM alpha-ANP and 10 microM C-ANP, but not by unrelated peptides such as gastrin. These results suggest that renal ANP clearance receptors are restricted in vivo to the glomeruli and renal arterial system of the rat. <\/jats:p>","DOI":"10.1152\/ajprenal.1990.259.1.f26","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T17:23:09Z","timestamp":1513963389000},"page":"F26-F39","source":"Crossref","is-referenced-by-count":4,"title":["Autoradiographic localization of atrial natriuretic peptide receptor subtypes in rat kidney"],"prefix":"10.1152","volume":"259","author":[{"given":"J.","family":"Brown","sequence":"first","affiliation":[{"name":"Physiological Laboratory, University of Cambridge, United Kingdom."}]},{"given":"S. P.","family":"Salas","sequence":"additional","affiliation":[{"name":"Physiological Laboratory, University of Cambridge, United Kingdom."}]},{"given":"A.","family":"Singleton","sequence":"additional","affiliation":[{"name":"Physiological Laboratory, University of Cambridge, United Kingdom."}]},{"given":"J. M.","family":"Polak","sequence":"additional","affiliation":[{"name":"Physiological Laboratory, University of Cambridge, United Kingdom."}]},{"given":"C. T.","family":"Dollery","sequence":"additional","affiliation":[{"name":"Physiological Laboratory, University of Cambridge, United Kingdom."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1990.259.1.F26","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:17:05Z","timestamp":1567955825000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1990.259.1.F26"}},"issued":{"date-parts":[[1990,7,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1990,7,1]]}},"alternative-id":["10.1152\/ajprenal.1990.259.1.F26"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1990.259.1.f26","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1990,7,1]]}},{"indexed":{"date-parts":[[2024,6,17]],"date-time":"2024-06-17T20:00:03Z","timestamp":1718654403346},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1990,4,1]]},"abstract":"<jats:p> Dopamine receptors have been identified in many tissues including the kidney. To establish an in vitro system as a model for dopamine action, we studied the effect of dopamine (DA) receptor agonists and antagonists on adenosine 3',5'-cyclic monophosphate (cAMP) formation in opossum kidney (OK) cells. The stimulation of cAMP production in these cells by dopamine was dose dependent, and markedly higher levels were observed in the presence of dopamine plus a phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine. Half-maximal stimulation was found with 1.15 +\/- 0.22 microM dopamine. A DA1-receptor agonist, SKF 82526J, stimulated cAMP production, whereas a DA2-receptor agonist, Ly 171555, did not. The stimulatory effects of dopamine and SKF 82526J were abolished by a specific DA1-receptor antagonist, Sch 23390 with half-maximal inhibition concentrations of 1.24 +\/- 0.18 and 4.0 +\/- 0.5 nM, respectively. In contrast, the DA2-receptor antagonist, spiperone, had no inhibitory effect on dopamine- and SKF 82526J-stimulated cAMP production. Beta-Adrenergic antagonists failed to attenuate the stimulatory effects of dopamine and SKF 82526J on cAMP production. In addition, the beta-adrenergic receptor agonist, isoproterenol, did not stimulate cAMP production. These results suggest that the action of dopamine was not mediated through beta-adrenergic receptors. Furthermore, our results clearly demonstrated the existence of DA1-receptors linked to adenylate cyclase in OK cells. <\/jats:p>","DOI":"10.1152\/ajprenal.1990.258.4.f877","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T18:20:11Z","timestamp":1513966811000},"page":"F877-F882","source":"Crossref","is-referenced-by-count":6,"title":["Dopamine stimulation of cAMP production in cultured opossum kidney cells"],"prefix":"10.1152","volume":"258","author":[{"given":"L.","family":"Cheng","sequence":"first","affiliation":[{"name":"Laboratory of Biological Chemistry, National Institute on Aging,National Institutes of Health, Baltimore, Maryland 21224."}]},{"given":"P.","family":"Precht","sequence":"additional","affiliation":[{"name":"Laboratory of Biological Chemistry, National Institute on Aging,National Institutes of Health, Baltimore, Maryland 21224."}]},{"given":"D.","family":"Frank","sequence":"additional","affiliation":[{"name":"Laboratory of Biological Chemistry, National Institute on Aging,National Institutes of Health, Baltimore, Maryland 21224."}]},{"given":"C. T.","family":"Liang","sequence":"additional","affiliation":[{"name":"Laboratory of Biological Chemistry, National Institute on Aging,National Institutes of Health, Baltimore, Maryland 21224."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1990.258.4.F877","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:22:12Z","timestamp":1567956132000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1990.258.4.F877"}},"issued":{"date-parts":[[1990,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1990,4,1]]}},"alternative-id":["10.1152\/ajprenal.1990.258.4.F877"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1990.258.4.f877","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1990,4,1]]}},{"indexed":{"date-parts":[[2024,6,17]],"date-time":"2024-06-17T19:20:02Z","timestamp":1718652002672},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1996,10,1]]},"abstract":"<jats:p> Expression of aquaporin-2 (AQP2) is exclusively limited to kidney collecting duct cells, and this strictly limited expression could be mediated by transcription of the gene. We first examined AQP2 mRNA expression in many cultured epithelial cells derived from kidney. Northern blot using OK, LLC-PK1, Madin-Darby canine kidney, and outer medullary collecting duct (OMCD) cells and primary culture of inner medullary collecting duct (IMCD) cells did not reveal any significant signal. A more sensitive method, ribonuclease protection assay, could detect a faint signal in OMCD cells when they were bathed in a hypertonic medium. Reverse-transcribed polymerase chain reaction applied to primary culture of IMCD cells showed a rapid dissipation of AQP2 mRNA within 4 days after culture. A reporter gene assay performed in the 1st day of primary culture of IMCD cells showed that the 5' region up to -2.9 kb worked as a promoter. Deletion experiments showed that at least two regions, from -434 to -364 and from -153 to -84, contain negatively acting cis-elements. When connected to a heterologous promoter, these regions repressed the activity in an orientation-dependent manner. These results suggest that transcription of AQP2 gene is strictly regulated and its ability is rapidly depressed in culture condition. This cell differentiation-specific expression of the gene may be, at least in part, mediated by the repressors present in its 5'-flanking region. <\/jats:p>","DOI":"10.1152\/ajprenal.1996.271.4.f854","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T01:41:53Z","timestamp":1513993313000},"page":"F854-F860","source":"Crossref","is-referenced-by-count":14,"title":["Repressive regulation of the aquaporin-2 gene"],"prefix":"10.1152","volume":"271","author":[{"given":"M.","family":"Furuno","sequence":"first","affiliation":[{"name":"Second Department of Internal Medicine, Tokyo Medical and Dental University, School of Medicine, Japan."}]},{"given":"S.","family":"Uchida","sequence":"additional","affiliation":[{"name":"Second Department of Internal Medicine, Tokyo Medical and Dental University, School of Medicine, Japan."}]},{"given":"F.","family":"Marumo","sequence":"additional","affiliation":[{"name":"Second Department of Internal Medicine, Tokyo Medical and Dental University, School of Medicine, Japan."}]},{"given":"S.","family":"Sasaki","sequence":"additional","affiliation":[{"name":"Second Department of Internal Medicine, Tokyo Medical and Dental University, School of Medicine, Japan."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1996.271.4.F854","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:06:10Z","timestamp":1567958770000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1996.271.4.F854"}},"issued":{"date-parts":[[1996,10,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1996,10,1]]}},"alternative-id":["10.1152\/ajprenal.1996.271.4.F854"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1996.271.4.f854","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1996,10,1]]}},{"indexed":{"date-parts":[[2024,6,17]],"date-time":"2024-06-17T19:57:30Z","timestamp":1718654250827},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1989,9,1]]},"abstract":"<jats:p> Uptake of calcium by brush-border membrane vesicles from rat small intestine is composed of saturable and nonsaturable components. We studied regulation of calcium uptake using the divalent cations strontium, a foreign ion that mimics calcium biologically and magnesium, a physiologically important ion that resembles calcium physically, although not biologically. Strontium present outside the vesicle inhibited saturable calcium uptake competitively, consistent with binding to the transporter at the same site as calcium. Strontium inside the vesicle accelerated saturable calcium uptake from the outside (countertransport), also consistent with binding to the same transporter site as calcium. Thus the calcium transporter shows functional characteristics of a mobile carrier. In the uptake medium (extracellular), magnesium was a noncompetitive inhibitor of saturable calcium transport, consistent with a regulatory role in calcium uptake by binding to the transporter at a locus other than that for calcium. Magnesium at 1 mM concentration inside the vesicle had no effect on saturable calcium uptake and a high concentrations functioned as a week uncompetitive inhibitor. Thus intracellular magnesium appears to have no major role in regulating saturable calcium uptake at the brush border of the enterocyte. <\/jats:p>","DOI":"10.1152\/ajprenal.1989.257.3.f446","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T22:10:00Z","timestamp":1513980600000},"page":"F446-F453","source":"Crossref","is-referenced-by-count":3,"title":["Calcium uptake by brush-border membrane vesicles from the rat intestine"],"prefix":"10.1152","volume":"257","author":[{"given":"H. D.","family":"Wilson","sequence":"first","affiliation":[{"name":"Medical Service, Veterans Administration, Iowa City, Iowa."}]},{"given":"H. P.","family":"Schedl","sequence":"additional","affiliation":[{"name":"Medical Service, Veterans Administration, Iowa City, Iowa."}]},{"given":"K.","family":"Christensen","sequence":"additional","affiliation":[{"name":"Medical Service, Veterans Administration, Iowa City, Iowa."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1989.257.3.F446","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:16:06Z","timestamp":1567970166000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1989.257.3.F446"}},"issued":{"date-parts":[[1989,9,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1989,9,1]]}},"alternative-id":["10.1152\/ajprenal.1989.257.3.F446"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1989.257.3.f446","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1989,9,1]]}},{"indexed":{"date-parts":[[2024,6,17]],"date-time":"2024-06-17T20:39:12Z","timestamp":1718656752149},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1992,8,1]]},"abstract":"<jats:p> Phorbol 12-myristate 13-acetate (PMA) decreases the tight junction conductance (TJC) during the reorganization of LLC-PK1A monolayers, but has the opposite effect in LLC-PK1B4, MDCK, and MDCK4 cells. Because no protein synthesis was required for the effects of PMA on the TJC of LLC-PK1A monolayers, we conclude that the regulation of the tight junction by protein kinase C (PKC) is a posttranslational event. In LLC-PK1A monolayers with existing tight junctions, PMA produced an initial increase in the TJC that reverted later to control values despite the continuous presence of PMA and cycloheximide. The inhibitory effect of PMA on the other cell lines was not revertible. A downregulation of total PKC activity and phorbol ester receptors was only observed during the reorganization of LLC-PK1A monolayers. PMA further increases this downregulation. This indicates that the peculiar response to PMA observed in LLC-PK1A monolayers is the result of two concurrent events: 1) the early activation of the enzyme just before the reorganization of the tight junctions begin, and 2) its late downregulation induced after prolonged exposure to phorbol esters. We conclude that PKC regulates the development of the occluding junctions, but through different mechanisms dependent on the characteristics of the cells. <\/jats:p>","DOI":"10.1152\/ajprenal.1992.263.2.f293","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T05:14:44Z","timestamp":1514006084000},"page":"F293-F300","source":"Crossref","is-referenced-by-count":9,"title":["Cellular variability in the development of tight junctions after activation of protein kinase C"],"prefix":"10.1152","volume":"263","author":[{"given":"B.","family":"Ellis","sequence":"first","affiliation":[{"name":"Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston 02114."}]},{"given":"E. E.","family":"Schneeberger","sequence":"additional","affiliation":[{"name":"Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston 02114."}]},{"given":"C. A.","family":"Rabito","sequence":"additional","affiliation":[{"name":"Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston 02114."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1992.263.2.F293","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:27:23Z","timestamp":1567960043000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1992.263.2.F293"}},"issued":{"date-parts":[[1992,8,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1992,8,1]]}},"alternative-id":["10.1152\/ajprenal.1992.263.2.F293"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1992.263.2.f293","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1992,8,1]]}},{"indexed":{"date-parts":[[2024,6,17]],"date-time":"2024-06-17T17:56:12Z","timestamp":1718646972072},"reference-count":47,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2008,3]]},"abstract":"<jats:p>The sodium-phosphate cotransporter 2a (NPT2a) is the principal phosphate transporter expressed in the brush border of renal proximal tubules and is downregulated by parathyroid hormone (PTH) through an endocytic mechanism. Apical membrane expression of NPT2a is dependent on interactions with the sodium-hydrogen exchanger regulatory factor 1 (NHERF-1). An LLC-PK1 renal cell line stably expressing the PTH receptor (PTH1R) and NHERF-1, termed B28-N1, fails to functionally express NPT2a. In B28-N1 cells, NHERF-1 and NPT2a are inappropriately localized to the cytoplasm. Ezrin, in the activated state, is capable at linking NHERF-1-assembled complexes to the actin cytoskeleton. Early-passage LLC-PK1 cells stably transfected with either empty vector or wild-type ezrin express a comparable level of the active, T567 phosphorylated form of ezrin and are capable of functionally expressing NPT2a. Colocalization of the PTH1R, NPT2a, and ezrin exists and is prominently associated with actin-containing microvilli in apical domains of these cells. Upon PTH treatment, the PTH1R, NPT2a, NHERF-1, and ezrin colocalize to endocytic vesicles and NPT2a-dependent phosphate uptake is markedly inhibited. LLC-PK1 cells expressing the constitutively active ezrin (T567D) display enhanced NPT2a functional expression and PTH-mediated regulation of phosphate. Expression of a dominant-negative ezrin, consisting of the NH<jats:sub>2<\/jats:sub>-terminal half of the protein, markedly disrupts NPT2a-dependent phosphate uptake. PTH does not appear to alter ezrin phosphorylation at T567. Instead, PTH perhaps initiates NPT2a endocytosis by inducing reorganization of the actin-containing microvilli in a process that is blocked by the actin-stabilizing compound jasplakinolide.<\/jats:p>","DOI":"10.1152\/ajprenal.00276.2007","type":"journal-article","created":{"date-parts":[[2008,1,10]],"date-time":"2008-01-10T01:54:14Z","timestamp":1199930054000},"page":"F667-F675","source":"Crossref","is-referenced-by-count":17,"title":["Ezrin promotes functional expression and parathyroid hormone-mediated regulation of the sodium-phosphate cotransporter 2a in LLC-PK1 cells"],"prefix":"10.1152","volume":"294","author":[{"given":"Matthew J.","family":"Mahon","sequence":"first","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1210\/endo.138.1.4845"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00249.2003"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1097-4644(199705)65:2<276::AID-JCB13>3.0.CO;2-G"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.cellbio.16.1.113"},{"key":"R5","unstructured":"Bretscher A, Reczek D, Berryman M.Ezrin: a protein requiring conformational activation to link microfilaments to the plasma membrane in the assembly of cell surface structures.J Cell Sci110: 3011\u20133018, 1997."},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1210\/endo.132.5.8386606"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.E04-10-0877"},{"key":"R8","doi-asserted-by":"crossref","unstructured":"Caverzasio J, Rizzoli R, Bonjour JP.Sodium-dependent phosphate transport inhibited by parathyroid hormone and cyclic AMP stimulation in an opossum kidney cell line.J Biol Chem261: 3233\u20133237, 1986.","DOI":"10.1016\/S0021-9258(17)35773-3"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1021\/bi0480382"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1210\/endo-122-6-2981"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.256.4.F672"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.138.2.423"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00036.2006"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1016\/j.addr.2003.07.011"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00456.2004"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200307032"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5001813"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.150.1.193"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1007\/BF01870704"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1210\/endo.136.9.7649096"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.15.8496"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.182412699"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1210\/endo.134.3.8119156"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M414071200"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M502305200"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1210\/me.2003-0043"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1038\/nature00816"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M313229200"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1986.251.1.C23"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.140.3.647"},{"key":"R31","unstructured":"Murray EJ, Tram KK, Spencer MJ, Tidball JG, Murray SS, Lee DB.PTH-mediated osteoblast retraction: possible participation of the calpain pathway.Miner Electrolyte Metab21: 184\u2013188, 1995."},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00505.x"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.5.F720"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.32.20125"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.270.1.F220"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.29.18452"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1007\/BF01994356"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.162232699"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M106827200"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1021\/bi027237n"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M106724200"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M511435200"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.2001.280.1.C192"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.68.040104.131050"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1172\/JCI204"},{"key":"R46","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1986.250.5.C682"},{"key":"R47","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.E04-09-0774"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00276.2007","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,9,1]],"date-time":"2021-09-01T11:03:19Z","timestamp":1630494199000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00276.2007"}},"issued":{"date-parts":[[2008,3]]},"references-count":47,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2008,3]]}},"alternative-id":["10.1152\/ajprenal.00276.2007"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00276.2007","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2008,3]]}},{"indexed":{"date-parts":[[2024,8,7]],"date-time":"2024-08-07T11:50:57Z","timestamp":1723031457298},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1993,9,1]]},"abstract":"<jats:p> The time course for the increases in soluble renal epidermal growth factor (EGF) after ischemia has been established. These elevated levels of EGF have been compared with the degree of tissue injury as well as the extent of cell proliferation in the recovering tissue. Levels of soluble immunoreactive EGF (irEGF) in control animals were 9.74 +\/- 1.1 ng\/g wet wt (n = 4-8 for all values) and rose to 83.9 +\/- 30 ng\/g within 12 h after injury. Soluble irEGF content peaked at 88.8 +\/- 15 ng\/g at 24 h postinjury and returned to control values by 72 h. We previously reported that trypsin digestion of crude renal membranes (CRM) generates rat EGF that is indistinguishable from that isolated from the submandibular gland. Initial levels of trypsin-releasable membrane-associated irEGF were 439 +\/- 26 ng\/g. These levels fell to 46.6 +\/- 9.6 ng\/g at 48 h after injury. The total renal EGF demonstrated an 80% decline 48 h after injury but returned to 50% of the initial values after 72 h representing significant new synthesis of EGF-containing proteins between 48 and 72 h postinjury. Immunohistochemical staining of kidney paraffin sections for EGF immunoreactivity demonstrated staining intensities that paralleled the amount of irEGF in the trypsin-digested CRM fraction, suggesting that the membrane-associated irEGF is the predominant form detected by this technique. Regenerative hyperplasia subsequent to tubular insult was monitored by immunostaining nuclei of S phase cells after pulse labeling with the thymidine analogue 5-bromo-2'-deoxyuridine. Cell proliferation was particularly prominent in the outer stripe of outer medulla of kidneys exposed to ischemia and reached a maximum (19-fold higher than the baseline value) 48 h after reperfusion. Renal cell turnover returned to control values by day 7. The observation that the peak in soluble EGF levels (24 h) precedes the peak in tubular regeneration (48 h) by 24 h is consistent with the hypothesis that EGF is one of the mitogenic signals triggering regenerative hyperplasia after renal injury. <\/jats:p>","DOI":"10.1152\/ajprenal.1993.265.3.f425","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T10:17:13Z","timestamp":1514024233000},"page":"F425-F434","source":"Crossref","is-referenced-by-count":3,"title":["Endogenous EGF as a potential renotrophic factor in ischemia-induced acute renal failure"],"prefix":"10.1152","volume":"265","author":[{"given":"R. P.","family":"Schaudies","sequence":"first","affiliation":[{"name":"Department of Nephrology, Walter Reed Army Institute of Research,Washington, District of Columbia 20307-5100."}]},{"given":"D.","family":"Nonclercq","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Walter Reed Army Institute of Research,Washington, District of Columbia 20307-5100."}]},{"given":"L.","family":"Nelson","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Walter Reed Army Institute of Research,Washington, District of Columbia 20307-5100."}]},{"given":"G.","family":"Toubeau","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Walter Reed Army Institute of Research,Washington, District of Columbia 20307-5100."}]},{"given":"J.","family":"Zanen","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Walter Reed Army Institute of Research,Washington, District of Columbia 20307-5100."}]},{"given":"J. A.","family":"Heuson-Stiennon","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Walter Reed Army Institute of Research,Washington, District of Columbia 20307-5100."}]},{"given":"G.","family":"Laurent","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Walter Reed Army Institute of Research,Washington, District of Columbia 20307-5100."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1993.265.3.F425","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:27:23Z","timestamp":1567974443000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1993.265.3.F425"}},"issued":{"date-parts":[[1993,9,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1993,9,1]]}},"alternative-id":["10.1152\/ajprenal.1993.265.3.F425"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1993.265.3.f425","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1993,9,1]]}},{"indexed":{"date-parts":[[2024,6,17]],"date-time":"2024-06-17T19:50:00Z","timestamp":1718653800238},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1993,1,1]]},"abstract":"<jats:p> H+\/OH- transport in the absence of bicarbonate was studied in the rabbit proximal convoluted tubule (PCT) perfused in vitro using measurements of membrane potential and intracellular pH (pHi). Blockade of apical Na\/H exchange led to a cell acidification of 0.64 +\/- 0.1 pH units from a control pHi of 7.27 +\/- 0.04. A bafilomycin-insensitive recovery of pHi of 0.05 +\/- 0.02 pH units occurred, but pHi did not exceed electrochemical equilibrium. A larger, sustained acidification of 0.87 +\/- 0.07 from an initial control pHi of 7.25 +\/- 0.05 induced by bilateral Na removal left pHi substantially below electrochemical equilibrium. These results suggest the absence of Na-independent active proton extrusion. We also examined the possibility that a passive electrogenic proton leak may exist. The removal of luminal glucose and alanine led to a basolateral membrane hyperpolarization of 31.3 +\/- 0.5 mV, which was associated with a cell acidification of 0.15 +\/- 0.02 pH units. These responses were reversed by addition of luminal glucose and alanine but not by depolarization by basolateral barium, suggesting that luminal glucose and alanine effects on pHi were due to changes other than cell potential. We conclude that, in the absence of bicarbonate, all active proton extrusion in the rabbit PCT is dependent on active Na transport and that a proton leak is negligible. <\/jats:p>","DOI":"10.1152\/ajprenal.1993.264.1.f175","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T04:34:43Z","timestamp":1514003683000},"page":"F175-F180","source":"Crossref","is-referenced-by-count":2,"title":["Evidence against a proton pump in rabbit proximal convoluted tubule"],"prefix":"10.1152","volume":"264","author":[{"given":"J.","family":"Beck","sequence":"first","affiliation":[{"name":"Membrane Transport Research Group, University of Montreal, Quebec,Canada."}]},{"given":"R.","family":"Laprade","sequence":"additional","affiliation":[{"name":"Membrane Transport Research Group, University of Montreal, Quebec,Canada."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1993.264.1.F175","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:22:52Z","timestamp":1567959772000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1993.264.1.F175"}},"issued":{"date-parts":[[1993,1,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1993,1,1]]}},"alternative-id":["10.1152\/ajprenal.1993.264.1.F175"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1993.264.1.f175","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1993,1,1]]}},{"indexed":{"date-parts":[[2024,9,4]],"date-time":"2024-09-04T10:16:43Z","timestamp":1725445003208},"reference-count":56,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2008,3]]},"abstract":"<jats:p>Nephrotic syndrome (NS) is a clinical state characterized by massive proteinuria and edema. It is believed that nephrin and podocin are involved in the development of proteinuria. The proteinuria and effects of eplerenone alone or combined with enalapril on nephrin\/podocin abundance in rats with NS have not yet been studied. Therefore, the present study was designed to examine the early (beginning 2 days before NS induction) and late (beginning 2 wk after NS induction) effects of eplerenone and enalapril, alone or combined, on proteinuria and nephrin\/podocin abundance in rats with adriamycin-induced NS. Adriamycin caused a significant increase in daily protein excretion (U<jats:sub>pr<\/jats:sub>V; from 26.96 \u00b1 3.43 to 958.57 \u00b1 56.7 mg\/day, P &lt; 0.001) and cumulative proteinuria [from 900.33 \u00b1 135.5 to 22,490.62 \u00b1 931.26 mg ( P &lt; 0.001)] during 6 wk. Early treatment with enalapril significantly decreased U<jats:sub>pr<\/jats:sub>V from 958.6 \u00b1 56.7 to 600.31 \u00b1 65.13 mg\/day ( P &lt; 0.001) and cumulative proteinuria to 12,842.37 \u00b1 1,798.17 mg\/6 wk ( P &lt; 0.001). Similarly, early treatment with eplerenone produced a profound antiproteinuric effect: U<jats:sub>pr<\/jats:sub>V decreased from 958.57 \u00b1 56.7 to 593.38 \u00b1 21.83 mg\/day, P &lt; 0.001, and cumulative proteinuria to 16,601.84 \u00b1 1,334.31 mg\/6 wk; P &lt; 0.001. An additive effect was obtained when enalapril and eplerenone were combined: U<jats:sub>pr<\/jats:sub>V decreased from 958.57 \u00b1 56.69 to 424.17 \u00b1 38.54 mg\/day, P &lt; 0.001, and cumulative protein excretion declined to 10,252.88 \u00b1 1,011.3 mg\/6 wk, P &lt; 0.001. These antiproteinuric effects were associated with substantial preservation of glomerular nephrin and podocin. In contrast, late treatment with either enalapril or eplerenone alone or combined mildly decreased U<jats:sub>pr<\/jats:sub>V and cumulative proteinuria. Thus pretreatment with eplerenone or enalapril is effective in reducing daily and cumulative protein excretion and preservation of nephrin\/podocin. More profound antiproteinuric effects were obtained when enalapril and eplerenone were combined.<\/jats:p>","DOI":"10.1152\/ajprenal.00524.2007","type":"journal-article","created":{"date-parts":[[2007,12,20]],"date-time":"2007-12-20T01:34:48Z","timestamp":1198114488000},"page":"F628-F637","source":"Crossref","is-referenced-by-count":21,"title":["Eplerenone potentiates the antiproteinuric effects of enalapril in experimental nephrotic syndrome"],"prefix":"10.1152","volume":"294","author":[{"given":"Farid","family":"Nakhoul","sequence":"first","affiliation":[]},{"given":"Eliyahu","family":"Khankin","sequence":"additional","affiliation":[]},{"given":"Afif","family":"Yaccob","sequence":"additional","affiliation":[]},{"given":"Hiroshi","family":"Kawachi","sequence":"additional","affiliation":[]},{"given":"Tony","family":"Karram","sequence":"additional","affiliation":[]},{"given":"Huda","family":"Awaad","sequence":"additional","affiliation":[]},{"given":"Nakhoul","family":"Nakhoul","sequence":"additional","affiliation":[]},{"given":"Aaron","family":"Hoffman","sequence":"additional","affiliation":[]},{"given":"Zaid","family":"Abassi","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1016\/S1262-3636(07)70122-2"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2003.11.005"},{"key":"R3","doi-asserted-by":"crossref","unstructured":"Benigni A, Tomasoni S, Gagliardini E, Zoja C, Grunkemeyer JA, Kalluri R, Remuzzi G.Blocking angiotensin II synthesis\/activity preserves glomerular nephrin in rats with severe nephrosis.J Am Soc Nephrol12: 941\u2013948, 2001.","DOI":"10.1681\/ASN.V125941"},{"key":"R4","unstructured":"Bertani T, Poggi A, Pozzoni R, Delaini F, Sacchi G, Thoua Y, Mecca G, Remuzzi G, Donati MB.Adriamycin-induced nephrotic syndrome in rats: sequence of pathologic events.Lab Invest46: 16\u201323, 1982."},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00929.x"},{"key":"R6","unstructured":"Blum S, Nakhoul F, Khankin E, Abassi Z.Renal slit diaphragm\u2013the open zipper and the failing heart.Isr Med Assoc J9: 107\u2013111, 2007."},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1007\/s001250100546"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000060578.79050.E0"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1053\/S0270-9295(03)00137-2"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1038\/ncpneph0362"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1517\/14656566.4.7.1185"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)64128-4"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1016\/j.amjmed.2006.03.038"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfg339"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00980.x"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-200205000-00034"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00913.x"},{"key":"R18","doi-asserted-by":"crossref","unstructured":"Guo C, Martinez-Vasquez D, Mendez GP, Toniolo MF, Yao TM, Oestreicher EM, Kikuchi T, Lapointe N, Pojoga L, Williams GH, Ricchiuti V, Adler GK.Mineralocorticoid receptor antagonist reduces renal injury in rodent models of types 1 and 2 diabetes mellitus.Endocrinology147: 5363\u20135373, 2007.","DOI":"10.1210\/en.2006-0944"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)65483-1"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/17.3.478"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-200301000-00011"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra052131"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00044.x"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/17.7.1327"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002075"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1007\/s00125-002-0946-y"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00312.2001"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1086\/302182"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199311113292004"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00308.x"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000222003.28517.99"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(03)12229-5"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00451.2004"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1254\/fpj.124.101"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00254.x"},{"key":"R36","doi-asserted-by":"crossref","unstructured":"Pitt B, Remme W, Zannad F, Neaton J, Martinez F, Roniker B, Bittman R, Hurley S, Kleiman J, Gatlin M; Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy, and Survival Study Investigators.Eplerenone, a selective aldosterone blocker, in patients with left ventricular dysfunction after myocardial infarctionN Engl J Med148: 1309\u20131321, 2003.","DOI":"10.1056\/NEJMoa030207"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/10.1.1"},{"key":"R38","unstructured":"Remuzzi A, Monaci N, Bonassi ME, Corna D, Zoja C, Mohammed EI, Remuzzi G.Angiotensin-converting enzyme inhibition prevents loss of glomerular hydraulic permeability in passive Heymann nephritis.Lab Invest79: 1501\u20131510, 1999."},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(96)11445-8"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.09911.x"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.31.1.451"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1210\/en.2002-220120"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.24.2.550-560.2004"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1016\/j.mce.2003.10.047"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1089\/ars.2005.7.1294"},{"key":"R46","doi-asserted-by":"crossref","unstructured":"Sato A, Hayashi K, Saruta T.Antiproteinuric effects of mineralocorticoid receptor blockade in patients with chronic renal disease.Am J Hypertens18: 44\u201349, 2005.","DOI":"10.1016\/j.amjhyper.2004.06.029"},{"key":"R47","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00756.x"},{"key":"R48","doi-asserted-by":"publisher","DOI":"10.1172\/JCI200112849"},{"key":"R49","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000255636.11931.a2"},{"key":"R50","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)63080-5"},{"key":"R51","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200207000-00001"},{"key":"R52","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00031.x"},{"key":"R53","doi-asserted-by":"publisher","DOI":"10.1086\/302182"},{"key":"R54","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(99)70360-4"},{"key":"R55","doi-asserted-by":"crossref","unstructured":"Yuan H, Takeuchi E, Taylor GA, McLaughlin M, Brown D, Salant DJ.Nephrin dissociates from actin, and its expression is reduced in early experimental membranous nephropathy.J Am Soc Nephrol13: 946\u2013956, 2002.","DOI":"10.1681\/ASN.V134946"},{"key":"R56","doi-asserted-by":"publisher","DOI":"10.1159\/000077396"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00524.2007","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,8,31]],"date-time":"2021-08-31T01:20:38Z","timestamp":1630372838000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00524.2007"}},"issued":{"date-parts":[[2008,3]]},"references-count":56,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2008,3]]}},"alternative-id":["10.1152\/ajprenal.00524.2007"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00524.2007","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2008,3]]}},{"indexed":{"date-parts":[[2024,5,12]],"date-time":"2024-05-12T17:58:24Z","timestamp":1715536704395},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1988,10,1]]},"abstract":"<jats:p> ACRIP is a competitive inhibitor of renin in which an analogue of statine, (3R,4S)-4-amino-3-hydroxy-6-methylheptanoic acid, is incorporated into analogues of porcine renin substrate. ACRIP inhibits the enzymatic activity of renin, thus blocking the initiation of the angiotensin cascade. We studied the intrarenal action of ACRIP in small quantities without measurable systemic effects on renal function. In the first experiment, ACRIP was administered intrarenally at 0.02, 0.2, and 2 micrograms.kg-1.min-1 to uninephrectomized conscious dogs (n = 6) in metabolic balance at sodium intake of 10 meq\/day. ACRIP, in doses of 0.02 and 0.2 micrograms.kg-1.min-1, markedly increased urine sodium excretion (UNaV) from 5.8 +\/- 1.4 to 15.1 +\/- 5.1 and 19.9 +\/- 3.2 mu eq\/min, respectively. Urinary flow rate (UV) underwent a similar increase and glomerular filtration rate (GFR) increased from 25.7 +\/- 2.5 to 35.6 +\/- 2.5 at 0.02 micrograms.kg-1.min-1 of ACRIP. Renal plasma flow (RPF), plasma renin activity (PRA), and plasma aldosterone concentration (PAC) were not affected. At 2 micrograms.kg-1.min-1, ACRIP traversed the kidney in quantities large enough to produce a reduction in systemic PRA and mean arterial pressure and caused natriuresis, diuresis, and increased GFR. In a second experiment, ACRIP was administered intrarenally at 0.2 micrograms.kg-1.min-1 in a separate group (n = 4) under identical conditions. ACRIP-induced increases in UV and UNaV were completely blocked by concurrent intrarenal administration of angiotensin II. The results indicate that intrarenal angiotensin II acts as a physiological regulator of renal sodium and fluid homeostasis. <\/jats:p>","DOI":"10.1152\/ajprenal.1988.255.4.f749","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T21:24:38Z","timestamp":1513977878000},"page":"F749-F754","source":"Crossref","is-referenced-by-count":0,"title":["Intrarenal renin inhibition increases renal function by an angiotensin II-dependent mechanism"],"prefix":"10.1152","volume":"255","author":[{"given":"H. M.","family":"Siragy","sequence":"first","affiliation":[{"name":"Department of Internal Medicine and Pharmacology, University ofVirginia School of Medicine, Charlottesville 22908."}]},{"given":"N. E.","family":"Lamb","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine and Pharmacology, University ofVirginia School of Medicine, Charlottesville 22908."}]},{"suffix":"Jr","given":"C. E.","family":"Rose","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine and Pharmacology, University ofVirginia School of Medicine, Charlottesville 22908."}]},{"given":"M. J.","family":"Peach","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine and Pharmacology, University ofVirginia School of Medicine, Charlottesville 22908."}]},{"given":"R. M.","family":"Carey","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine and Pharmacology, University ofVirginia School of Medicine, Charlottesville 22908."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1988.255.4.F749","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:10:59Z","timestamp":1567969859000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1988.255.4.F749"}},"issued":{"date-parts":[[1988,10,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1988,10,1]]}},"alternative-id":["10.1152\/ajprenal.1988.255.4.F749"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1988.255.4.f749","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1988,10,1]]}},{"indexed":{"date-parts":[[2024,5,12]],"date-time":"2024-05-12T17:29:14Z","timestamp":1715534954887},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1984,1,1]]},"abstract":"<jats:p> Nephron filtration rate (SNGFR), its determinants, and proximal tubular reabsorption were measured in hydropenic Munich-Wistar rats with sham-operated (sham) or denervated (DNx) kidneys before and during the administration of [Sar1, Ala8]angiotensin II or SQ 14225. The glomerular ultrafiltration coefficient (LpA) was significantly lower in DNx than in sham rats (P less than 0.025). However, SNGFR was not altered due to an offsetting increment in transcapillary glomerular hydrostatic pressure (delta P) in DNx (P less than 0.005). The marked increment of delta P in DNx was due to an increase in the glomerular capillary hydrostatic pressure, secondary to decreased afferent arteriolar resistance. The infusion of angiotensin II inhibitors to denervated kidneys completely normalized LpA but did not alter sham values. SQ 14225 but not [Sar1, Ala8]angiotensin II infusion provided a nephron plasma flow-dependent increase in SNGFR, secondary to a striking reduction in both glomerular vascular resistances. Endogenous angiotensin II activity may be enhanced by renal denervation, and angiotensin II acts to reduce LpA in this condition and may modulate the final level of renal vascular resistances after acute renal denervation. <\/jats:p>","DOI":"10.1152\/ajprenal.1984.246.1.f87","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T16:54:32Z","timestamp":1513961672000},"page":"F87-F95","source":"Crossref","is-referenced-by-count":2,"title":["Analysis of renal denervation in the hydropenic rat: interactions with angiotensin II"],"prefix":"10.1152","volume":"246","author":[{"given":"J. C.","family":"Pelayo","sequence":"first","affiliation":[]},{"given":"R. C.","family":"Blantz","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1984.246.1.F87","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:35:31Z","timestamp":1567967731000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1984.246.1.F87"}},"issued":{"date-parts":[[1984,1,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1984,1,1]]}},"alternative-id":["10.1152\/ajprenal.1984.246.1.F87"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1984.246.1.f87","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1984,1,1]]}},{"indexed":{"date-parts":[[2024,5,12]],"date-time":"2024-05-12T19:30:31Z","timestamp":1715542231618},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1982,9,1]]},"abstract":"<jats:p> The influence of thiopental anesthesia on renal tubular sodium reabsorption was investigated in the well-trained dog. After administration of the anesthetic, renal sodium reabsorption was depressed, leading to the enhanced excretion of sodium and water. Associated with this response was a decrease in the plasma levels of epinephrine and norepinephrine. Neither renal hemodynamic functions nor the humoral factors, prostaglandin E, plasma renin activity, or arginine vasopressin appeared to be the major determinants of the natriuresis. These observations suggest that the administration of thiopental depresses renal sympathetic nerve activity, thereby diminishing the renal tubular transport of sodium. <\/jats:p>","DOI":"10.1152\/ajprenal.1982.243.3.f265","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T13:42:44Z","timestamp":1513950164000},"page":"F265-F270","source":"Crossref","is-referenced-by-count":0,"title":["Influence of thiopental anesthesia on renal sodium and water excretion in the dog"],"prefix":"10.1152","volume":"243","author":[{"given":"J. A.","family":"Gagnon","sequence":"first","affiliation":[]},{"given":"I.","family":"Felipe","sequence":"additional","affiliation":[]},{"given":"L. D.","family":"Nelson","sequence":"additional","affiliation":[]},{"given":"D. E.","family":"Butkus","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1982.243.3.F265","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:20:31Z","timestamp":1567966831000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1982.243.3.F265"}},"issued":{"date-parts":[[1982,9,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1982,9,1]]}},"alternative-id":["10.1152\/ajprenal.1982.243.3.F265"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1982.243.3.f265","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1982,9,1]]}},{"indexed":{"date-parts":[[2024,5,12]],"date-time":"2024-05-12T22:32:28Z","timestamp":1715553148434},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1987,12,1]]},"abstract":"<jats:p> The purpose of this work was to investigate the effects of atrial peptides on the cytosolic Ca levels of cultured, adherent, mesangial cells. Resting Ca levels, measured by the use of fura-2, were dose-dependently decreased by up to 30%, by atriopeptin 23. The half-maximal effect was elicited by approximately 30 pM atriopeptin-23. Atriopeptin 21 also decreased resting Ca levels by up to 30%, but this peptide was approximately 30-fold less potent than atriopeptin 23. Atriopeptin 23 (100 nM) inhibited both the Ca transient and the peak Ca value elicited by 1 nM vasopressin, but the atrial peptide had no significant effect on the Ca transient elicited by higher vasopressin concentrations. At concentrations lower than 100 nM, atriopeptin 23 had no effect on the vasopressin-induced Ca transient. Atriopeptin 23 also decreased the Ca transient and the peak Ca value elicited by 100 nM angiotensin II. Similar to vasopressin, the angiotensin II-induced Ca transient was inhibited by 100 nM but not lower concentrations of atriopeptin 23. In contrast to the effect of atriopeptin 23, atriopeptin 21 (100 nM) had no effect on the Ca transient elicited by vasopressin. These results demonstrate that atriopeptins function as modulators of resting and, under certain conditions, of hormone-increased Ca levels in cultured mesangial cells. <\/jats:p>","DOI":"10.1152\/ajprenal.1987.253.6.f1077","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T03:25:22Z","timestamp":1513999522000},"page":"F1077-F1082","source":"Crossref","is-referenced-by-count":2,"title":["Atriopeptins decrease resting and hormone-elevated cytosolic Ca in cultured mesangial cells"],"prefix":"10.1152","volume":"253","author":[{"given":"A.","family":"Hassid","sequence":"first","affiliation":[{"name":"Department of Pharmacology, University of Tennessee, Memphis38163."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1987.253.6.F1077","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:51:09Z","timestamp":1567972269000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1987.253.6.F1077"}},"issued":{"date-parts":[[1987,12,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1987,12,1]]}},"alternative-id":["10.1152\/ajprenal.1987.253.6.F1077"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1987.253.6.f1077","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1987,12,1]]}},{"indexed":{"date-parts":[[2024,5,12]],"date-time":"2024-05-12T21:25:23Z","timestamp":1715549123519},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1988,7,1]]},"abstract":"<jats:p> Secretory granules swell during exocytosis. Swelling may follow fusion and assist in extrusion of the granular content, or swelling may cause granular fusion with the plasmalemma. A granular proton gradient has been suggested to be involved in such preexocytic granular swelling. Exocytosis of renin from juxtaglomerular cells of isolated preparations is very sensitive to changes in the extracellular osmolality. Extracellular hyposmolality causes swelling of secretory granules, fusions between peripherally located granules and plasmalemma, and an increased number of release episodes. Induction of granule swelling at constant extracellular osmolality also stimulates renin release. Newly recruited renin granules are osmosensitive, and a high extracellular osmolality blocks secretion induced by other means (low calcium). Dissipation of granular proton gradients inhibits renin release without affecting the osmosensitivity. Thus, in renin release in vitro, a granular swelling precedes fusion and exocytosis, and a granular proton gradient may contribute to preexocytic swelling when extracellular osmolality is constant. The osmosensitivity may be important for macula densamediated renin release. <\/jats:p>","DOI":"10.1152\/ajprenal.1988.255.1.f1","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T03:07:22Z","timestamp":1513998442000},"page":"F1-F10","source":"Crossref","is-referenced-by-count":8,"title":["Do osmotic forces play a role in renin secretion?"],"prefix":"10.1152","volume":"255","author":[{"given":"O.","family":"Skott","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, University of Michigan MedicalCenter, Ann Arbor 48109."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1988.255.1.F1","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:48:26Z","timestamp":1567972106000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1988.255.1.F1"}},"issued":{"date-parts":[[1988,7,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1988,7,1]]}},"alternative-id":["10.1152\/ajprenal.1988.255.1.F1"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1988.255.1.f1","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1988,7,1]]}},{"indexed":{"date-parts":[[2024,5,12]],"date-time":"2024-05-12T18:59:38Z","timestamp":1715540378524},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1977,1,1]]},"abstract":"<jats:p> A method for estimating glomerular filtration rate (GFR) has been developed that is based on an analysis of the total area under the plasma radioactivity-time curve after a single intravenous injection of [125I]iothalamate. Glomerular filtration rates obtained by this method (method A) and those obtained with two widely used single-injection techniques, the slope-intercept method (method B), and the two-compartment method (method C), were compared with GFRs obtained by standard inulin clearance techniques in 14 dogs. Method B consistently over. estimated inulin clearances more than 30%. Method C also overestimated inulin clearance considerably in dogs with an increased extracellular fluid volume, but was fairly reliable in normal dogs. Glomerular filtration rates obtained by the new method (method A) were in excellent agreement with inulin clearances in all dogs, regardless of the state of body hydration. The mean inulin clearance for all 14 experiments was 72.7+\/-6.0 SE ml\/min, while GFRs obtained by method A averaged 75.1+\/-6.0 ml\/min. The data from this study suggest that method A is a reliable means for estimating GFR that is especially useful in chronic experiments. <\/jats:p>","DOI":"10.1152\/ajprenal.1977.232.1.f72","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T15:20:34Z","timestamp":1513956034000},"page":"F72-F76","source":"Crossref","is-referenced-by-count":10,"title":["A single-injection method for measuring glomerular filtration rate"],"prefix":"10.1152","volume":"232","author":[{"given":"J. E.","family":"Hall","sequence":"first","affiliation":[]},{"given":"A. C.","family":"Guyton","sequence":"additional","affiliation":[]},{"given":"B. M.","family":"Farr","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1977.232.1.F72","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T14:58:04Z","timestamp":1567954684000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1977.232.1.F72"}},"issued":{"date-parts":[[1977,1,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1977,1,1]]}},"alternative-id":["10.1152\/ajprenal.1977.232.1.F72"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1977.232.1.f72","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1977,1,1]]}},{"indexed":{"date-parts":[[2024,5,12]],"date-time":"2024-05-12T18:59:46Z","timestamp":1715540386099},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1982,4,1]]},"DOI":"10.1152\/ajprenal.1982.242.4.f370","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T08:48:59Z","timestamp":1513932539000},"page":"F370-F378","source":"Crossref","is-referenced-by-count":1,"title":["Papillary plasma flow and tissue osmolality in chronic caval dogs"],"prefix":"10.1152","volume":"242","author":[{"given":"P. F.","family":"Faubert","sequence":"first","affiliation":[]},{"given":"S. Y.","family":"Chou","sequence":"additional","affiliation":[]},{"given":"J. G.","family":"Porush","sequence":"additional","affiliation":[]},{"given":"I. J.","family":"Belizon","sequence":"additional","affiliation":[]},{"given":"S.","family":"Spitalewitz","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1982.242.4.F370","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T14:18:51Z","timestamp":1567952331000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1982.242.4.F370"}},"issued":{"date-parts":[[1982,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1982,4,1]]}},"alternative-id":["10.1152\/ajprenal.1982.242.4.F370"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1982.242.4.f370","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1982,4,1]]}},{"indexed":{"date-parts":[[2024,5,12]],"date-time":"2024-05-12T23:17:31Z","timestamp":1715555851510},"reference-count":44,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2006,2]]},"abstract":"<jats:p>Recent investigations have revealed the importance of glomerular podocytes with its diaphragm as the major filtration barrier. Junctional adhesion molecule 4 (JAM4) has been identified as a protein that interacts with membrane-associated guanyl kinase inverted (MAGI)-1 and is reported to be expressed on podocytes. To elucidate the role of JAM4 on podocytes, we examined the expression of JAM4 and MAGI-1 in normal and two different proteinuric rat models: puromycin aminonucleoside (PAN) nephropathy and anti-nephrin antibody-induced (ANA) nephropathy, one model with and one without effacement of podocyte foot processes. JAM4 was detected by immunomicroscopy at the apical membrane of normal podocytes. JAM4 immunostaining was focally increased in the podocytes in PAN nephropathy but not in ANA nephropathy. In proteinuric podocytes, the expression of JAM4 was distinct from that of MAGI-1 or other slit diaphragm molecules such as nephrin and ZO-1. Close colocalization of JAM4 and ezrin was maintained in PAN nephropathy. By immunoelectron microscopy, the signals for JAM4 were detected at the free apical membrane of the podocytes with effaced foot processes. Studies with selective detergent extract revealed that the subcellular localization of JAM4 was altered in PAN nephropathy. Thus the altered expression of JAM4 appears to be associated with morphological changes in podocytes and can be a useful marker of injured podocytes. JAM4 may have a different role at the apical membrane besides the role as a junctional molecule and is likely associated with the unique structure of this epithelium.<\/jats:p>","DOI":"10.1152\/ajprenal.00253.2005","type":"journal-article","created":{"date-parts":[[2005,8,24]],"date-time":"2005-08-24T02:53:52Z","timestamp":1124852032000},"page":"F335-F344","source":"Crossref","is-referenced-by-count":8,"title":["Altered expression of junctional adhesion molecule 4 in injured podocytes"],"prefix":"10.1152","volume":"290","author":[{"given":"Yutaka","family":"Harita","sequence":"first","affiliation":[]},{"given":"Naoko","family":"Miyauchi","sequence":"additional","affiliation":[]},{"given":"Tamaki","family":"Karasawa","sequence":"additional","affiliation":[]},{"given":"Koichi","family":"Suzuki","sequence":"additional","affiliation":[]},{"given":"Gi Dong","family":"Han","sequence":"additional","affiliation":[]},{"given":"Hiroko","family":"Koike","sequence":"additional","affiliation":[]},{"given":"Takashi","family":"Igarashi","sequence":"additional","affiliation":[]},{"given":"Fujio","family":"Shimizu","sequence":"additional","affiliation":[]},{"given":"Hiroshi","family":"Kawachi","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000130167.30769.55"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.261452898"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1986.24"},{"key":"R4","unstructured":"Diamond JRand Karnovsky MJ.Focal and segmental glomerulosclerosis following a single intravenous dose of puromycin aminonucleoside.Am J Pathol122: 481\u2013487, 1986."},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.50.31589"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.00930"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.45.31903"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000097371.64671.65"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.23.12.4267-4282.2003"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M100630200"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1016\/S0300-9084(03)00056-7"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00195.x"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1203153"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2249.1992.tb06461.x"},{"key":"R15","unstructured":"Kawachi H, Abrahamson DR, St John PL, Goldstein DJ, Shia MA, Matsui K, Shimizu F, and Salant DJ.Developmental expression of the nephritogenic antigen of monoclonal antibody 5\u20131-6.Am J Pathol147: 823\u2013833, 1995."},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00044.x"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000037401.02391.76"},{"key":"R18","unstructured":"Kerjaschki D.Polycation-induced dislocation of slit diaphragms and formation of cell junctions in rat kidney glomeruli.Lab Invest39: 430\u2013440, 1978."},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.98.4.1591"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1172\/JCI200114629"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.47"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00044.x"},{"key":"R23","unstructured":"Kurihara H, Anderson JM, Kerjaschki D, and Farquhar MG.The altered glomerular filtration slits seen in puromycin aminonucleoside nephrosis and protamine sulfate-treated rats contain the tight junction protein ZO-1.Am J Pathol141: 805\u2013816, 1992."},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00131.2001"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1006\/excr.1997.3739"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000039661.06947.FD"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1097\/01.LAB.0000073307.82991.CC"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1016\/S0891-5849(96)00349-8"},{"key":"R29","doi-asserted-by":"crossref","unstructured":"Orikasa M, Matsui K, Oite T, and Shimizu F.Massive proteinuria induced in rats by a single intravenous injection of a monoclonal antibody.J Immunol141: 807\u2013814, 1988.","DOI":"10.4049\/jimmunol.141.3.807"},{"key":"R30","doi-asserted-by":"crossref","unstructured":"Orlando RA, Takeda T, Zak B, Shmieder S, Benoit VM, Mcquistan T, Furthmayr H, and Farquhar MG.The glomerular epithelial cell anti-adhesion podocalyxin associates with the actin cytoskeleton through interactions with ezrin.J Am Soc Nephrol12: 1589\u20131598, 2001.","DOI":"10.1681\/ASN.V1281589"},{"key":"R31","doi-asserted-by":"crossref","unstructured":"Patrie KM, Drescher AJ, Goyal M, Wiggins RC, and Margolis B.The membrane-associated guanylate kinase protein MAGI-1 binds megalin and is present in glomerular podocytes.J Am Soc Nephrol12: 667\u2013677, 2001.","DOI":"10.1681\/ASN.V124667"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00020.2002"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.60.2.423"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.14.7962"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.111.3.1255"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1998.8603"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1007\/s001090050206"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1038\/74139"},{"key":"R39","doi-asserted-by":"crossref","unstructured":"Sundberg Uand Obrink B.CEACAM1 isoforms with different cytoplasmic domains show different localization, organization and adhesive properties in polarized epithelial cells.J Cell Biol115: 1273\u20131284, 2002.","DOI":"10.1242\/jcs.115.6.1273"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2443.2003.00673.x"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.11.9.3219"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1172\/JCI12539"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1007\/s10157-003-0257-8"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1172\/JCI7728"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00253.2005","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,5,4]],"date-time":"2023-05-04T08:12:17Z","timestamp":1683187937000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00253.2005"}},"issued":{"date-parts":[[2006,2]]},"references-count":44,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2006,2]]}},"alternative-id":["10.1152\/ajprenal.00253.2005"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00253.2005","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2006,2]]}},{"indexed":{"date-parts":[[2024,8,6]],"date-time":"2024-08-06T21:40:01Z","timestamp":1722980401169},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1996,4,1]]},"abstract":"<jats:p> The renal Na(+)-dicarboxylate cotransporter reabsorbs Krebs cycle intermediates, such as succinate and citrate, from the glomerular filtrate. The present study describes the cloning and characterization of the human renal Na(+)-dicarboxylate cotransporter, hNaDC-1. The amino acid sequence of hNaDC-1 is 78% identical to the rabbit renal Na(+)-dicarboxylate cotransporter, NaDC-1, and 42% identical to the rat renal Na(+)-sulfate transporter, NaSi-1. The carboxy terminus of hNaDC-1 protein contains two N-glycosylation sites that appear to be utilized. Xenopus oocytes injected with hNaDC-1 cRNA expressed a low-affinity Na(+)-dependent dicarboxylate transporter with Michaelis constant (Km) for succinate around 0.4 mM. The transport of succinate by hNaDC-1 was insensitive to the pH of the medium, whereas the transporter of citrate was stimulated by acidic pH. Northern blot analysis indicates that hNaDC-1 mRNA is found in both kidney and intestine. The gene for hNaDC-1 was localized to chromosome 17. This study provides the first demonstration that the human kidney contains a low-affinity Na(+)-dicarboxylate cotransporter with properties that resemble those of the Na(+)-dicarboxylate cotransporter on the apical membrane of the rabbit renal proximal tubule. <\/jats:p>","DOI":"10.1152\/ajprenal.1996.270.4.f642","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T07:32:56Z","timestamp":1514014376000},"page":"F642-F648","source":"Crossref","is-referenced-by-count":18,"title":["Molecular cloning and functional expression of a sodium-dicarboxylate cotransporter from human kidney"],"prefix":"10.1152","volume":"270","author":[{"given":"A. M.","family":"Pajor","sequence":"first","affiliation":[{"name":"University of Arizona, Department of Physiology, College of Medicine,Tucson 85724, USA."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1996.270.4.F642","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:07:45Z","timestamp":1567973265000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1996.270.4.F642"}},"issued":{"date-parts":[[1996,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1996,4,1]]}},"alternative-id":["10.1152\/ajprenal.1996.270.4.F642"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1996.270.4.f642","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1996,4,1]]}},{"indexed":{"date-parts":[[2024,7,28]],"date-time":"2024-07-28T09:07:38Z","timestamp":1722157658432},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1987,4,1]]},"abstract":"<jats:p> Cultured rat mesangial cells were exposed to a reactive oxygen species (ROS) generating system (xanthine plus xanthine oxidase) to explore the effect of ROS on their metabolism of arachidonic acid (AA). Cell viability, as assessed by 51Cr release, was not affected by the concentrations of xanthine plus xanthine oxidase used. Prostaglandin E2 (PGE2) production following exposure to increasing quantities of xanthine plus xanthine oxidase was significantly decreased to 38.1 +\/- 9.7 or 30.8 +\/- 6.9% of control levels (P less than 0.05) when cells were stimulated with the calcium ionophore A23187 (1 microgram\/ml) or AA (10(-6) M), respectively. Maximum suppression of production was seen within 10 min of ROS exposure. Thromboxane B2 production was similarly decreased to 83.1 +\/- 7.6 (0.05 less than P less than 0.10) or 54.9 +\/- 2.5% (P less than 0.05). This effect was reversed by addition of catalase to the ROS generating system but not by superoxide dismutase or mannitol, which suggested that H2O2 was the responsible metabolite. High levels of H2O2 (5 x 10(-4) M) suppressed PGE2 production to 44.0 +\/- 4.1 or 17.4 +\/- 6.2% of A23187- or AA-stimulated production (P less than 0.05). Lower levels of H2O2 resulted in significant stimulation of base-line PGE2 production. Analysis of release of [3H]AA-labeled metabolites from A23187-stimulated cells showed no effect of H2O2 on phospholipase activity. Thus ROS can stimulate or inhibit AA metabolism in the glomerular mesangium, which may have important effects on glomerular hemodynamics during glomerular injury. <\/jats:p>","DOI":"10.1152\/ajprenal.1987.252.4.f743","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T02:13:31Z","timestamp":1513995211000},"page":"F743-F749","source":"Crossref","is-referenced-by-count":3,"title":["Biphasic effect of oxygen radicals on prostaglandin production by rat mesangial cells"],"prefix":"10.1152","volume":"252","author":[{"given":"S.","family":"Adler","sequence":"first","affiliation":[]},{"given":"R. A.","family":"Stahl","sequence":"additional","affiliation":[]},{"given":"P. J.","family":"Baker","sequence":"additional","affiliation":[]},{"given":"Y. P.","family":"Chen","sequence":"additional","affiliation":[]},{"given":"P. M.","family":"Pritzl","sequence":"additional","affiliation":[]},{"given":"W. G.","family":"Couser","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1987.252.4.F743","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:44:49Z","timestamp":1567971889000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1987.252.4.F743"}},"issued":{"date-parts":[[1987,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1987,4,1]]}},"alternative-id":["10.1152\/ajprenal.1987.252.4.F743"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1987.252.4.f743","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1987,4,1]]}},{"indexed":{"date-parts":[[2022,4,5]],"date-time":"2022-04-05T06:49:17Z","timestamp":1649141357355},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1991,1,1]]},"abstract":"<jats:p> An abnormal rightward shift of the pressure-natriuresis curve is a well known feature of the renal function in hypertension. The participation of intrinsic neural factors in the kidney in this phenomenon was investigated in anesthetized young and adult spontaneously hypertensive rats (SHR). At 7-8 wk of age, the renal pressure-diuresis curve and pressure-natriuresis curve were shifted to the left in denervated SHR compared with innervated animals. Fractional excretion of sodium was higher, and plasma renin activity was lower in denervated SHR. Glomerular filtration rate was not affected by renal denervation. In 13- to 15-wk-old SHR, renal denervation did not affect the pressure-diuresis and -natriuresis curves, although other parameters were changed compared with the results at 7-8 wk. In Wistar-Kyoto rats, the pressure-diuresis curve was shifted to the left by renal denervation at both ages. These results suggest that the renal nerves have an important effect on the renal pressure-diuresis and -natriuresis curves. However, renal innervation cannot be thought to cause an abnormal rightward shift of the pressure-diuresis and -natriuresis curves in SHR, especially in the established stage of hypertension. <\/jats:p>","DOI":"10.1152\/ajprenal.1991.260.1.f81","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T18:57:05Z","timestamp":1513969025000},"page":"F81-F85","source":"Crossref","is-referenced-by-count":2,"title":["Role of renal nerves on pressure natriuresis in spontaneously hypertensive rats"],"prefix":"10.1152","volume":"260","author":[{"given":"M.","family":"Yoshida","sequence":"first","affiliation":[{"name":"Department of Pharmacology, Tohoku University, Miyagi, Japan."}]},{"given":"S.","family":"Satoh","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Tohoku University, Miyagi, Japan."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1991.260.1.F81","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:26:24Z","timestamp":1567956384000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1991.260.1.F81"}},"issued":{"date-parts":[[1991,1,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1991,1,1]]}},"alternative-id":["10.1152\/ajprenal.1991.260.1.F81"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1991.260.1.f81","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1991,1,1]]}},{"indexed":{"date-parts":[[2022,4,1]],"date-time":"2022-04-01T21:10:50Z","timestamp":1648847450650},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1987,4,1]]},"abstract":"<jats:p> Cholera toxin (CT) irreversibly ADP-ribosylates and activates the nucleotide-stimulatory (Ns) subunit of adenylate cyclase in many tissues, thereby eliciting cyclase-dependent functions. Although earlier studies performed at room temperature could not demonstrate CT-stimulated water transport in toad urinary bladder, subsequent work in other tissues has emphasized the need for incubation at 35-37 degrees C to effect ribosylation and the subsequent physiological effects. We found that incubating tissues with amphibian culture media, rather than Ringer solution, maintained tissue viability at this higher temperature and permitted prolonged incubation with CT. At 37 degrees C, in the presence of 0.1 mM phosphodiesterase inhibitor (1-methyl-3-isobutylxanthine, MIX), 0.2-200 nM mucosal CT caused a dose-dependent but submaximal enhancement of water flux and urea transport. Elimination of MIX from the bath diminished subsequent CT-induced stimulation, supporting a role for adenosine 3',5'-cyclic monophosphate (cAMP) as mediator of the CT effect. The increased water flow was stable for greater than 1 h after removal of CT from the bath, consistent with irreversible stimulation of the cyclase. Mucosal CT stimulated transport to a greater degree than serosal CT, paralleling the pattern seen in the intestine, which is compatible with passage of the toxin's a subunit across the cell to the serosal membrane cyclase. Exposure of the tissue's mucosal surface to GM1 ganglioside, (the natural receptor for the CT b subunit) yielded maximal stimulation of water flow and near-maximal urea transport, presumably by increasing CT's binding to the cell membrane.(ABSTRACT TRUNCATED AT 250 WORDS) <\/jats:p>","DOI":"10.1152\/ajprenal.1987.252.4.f621","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T02:13:31Z","timestamp":1513995211000},"page":"F621-F626","source":"Crossref","is-referenced-by-count":0,"title":["Cholera toxin enhances adenylate cyclase-dependent transport in toad urinary bladder"],"prefix":"10.1152","volume":"252","author":[{"given":"B. S.","family":"Hoch","sequence":"first","affiliation":[]},{"given":"S. D.","family":"Levine","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1987.252.4.F621","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:44:41Z","timestamp":1567971881000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1987.252.4.F621"}},"issued":{"date-parts":[[1987,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1987,4,1]]}},"alternative-id":["10.1152\/ajprenal.1987.252.4.F621"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1987.252.4.f621","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1987,4,1]]}},{"indexed":{"date-parts":[[2024,7,27]],"date-time":"2024-07-27T09:56:25Z","timestamp":1722074185828},"reference-count":28,"publisher":"American Physiological Society","issue":"7","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2012,4,1]]},"abstract":"<jats:p> The extracellular matrix (ECM) acts as a scaffold for kidney cellular organization. Local secretion of the ECM allows kidney cells to readily adapt to changes occurring within the kidney. In addition to providing structural support for cells, the ECM also modulates cell survival, migration, proliferation, and differentiation. Although aberrant regulation of ECM proteins can play a causative role in many diseases, it is not known whether ECM production, cell adhesion, and migration are regulated in a similar manner in kidney epithelial and endothelial cells. Here, we demonstrate that lack of BIM expression differentially impacts kidney endothelial and epithelial cell ECM production, migration, and adhesion, further emphasizing the specialized role of these cell types in kidney function . Bim \u2212\/\u2212 kidney epithelial cells demonstrated decreased migration, increased adhesion, and sustained expression of osteopontin and thrombospondin-1 (TSP1). In contrast, bim \u2212\/\u2212 kidney endothelial cells demonstrated increased cell migration, and decreased expression of osteopontin and TSP1. We also observed a fivefold increase in VEGF expression in bim \u2212\/\u2212 kidney endothelial cells consistent with their increased migration and capillary morphogenesis. These cells also had decreased endothelial nitric oxide synthase activity and nitric oxide bioavailability. Thus kidney endothelial and epithelial cells make unique contributions to the regulation of their ECM composition, with specific impact on adhesive and migratory properties that are essential for their proper function. <\/jats:p>","DOI":"10.1152\/ajprenal.00498.2011","type":"journal-article","created":{"date-parts":[[2011,12,15]],"date-time":"2011-12-15T02:20:14Z","timestamp":1323915614000},"page":"F809-F819","source":"Crossref","is-referenced-by-count":11,"title":["BIM deficiency differentially impacts the function of kidney endothelial and epithelial cells through modulation of their local microenvironment"],"prefix":"10.1152","volume":"302","author":[{"given":"Nader","family":"Sheibani","sequence":"first","affiliation":[{"name":"Departments of 1Ophthalmology and Visual Sciences,"},{"name":"Pharmacology, and"}]},{"given":"Margaret E.","family":"Morrison","sequence":"additional","affiliation":[{"name":"Pediatrics, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin"}]},{"given":"Zafer","family":"Gurel","sequence":"additional","affiliation":[{"name":"Departments of 1Ophthalmology and Visual Sciences,"}]},{"given":"SunYoung","family":"Park","sequence":"additional","affiliation":[{"name":"Departments of 1Ophthalmology and Visual Sciences,"}]},{"given":"Christine M.","family":"Sorenson","sequence":"additional","affiliation":[{"name":"Pediatrics, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M609048200"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-291X(02)02708-0"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.006064"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.041359198"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1097-0029(19971101)39:3<254::AID-JEMT5>3.0.CO;2-K"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.87.17.6624"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajplung.00390.2009"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/nrc2561"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1080\/0897719041682863"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00489.2006"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.90633.2007"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.140.2.419"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1172\/JCI1684"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)64557-9"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)64649-4"},{"key":"B16","first-page":"364","volume":"129","author":"Raugi GJ","year":"1987","journal-title":"Am J Pathol"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1038\/ncb1026"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.20114"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.2337\/diab.45.4.522"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.20858"},{"key":"B22","first-page":"171","volume":"9","author":"Su X","year":"2003","journal-title":"Mol Vis"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)65281-9"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1016\/j.ydbio.2004.12.017"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1002\/dvdy.10412"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00821.x"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1042\/bj20031730"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00129.2004"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.120055097"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00498.2011","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T00:20:36Z","timestamp":1567988436000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00498.2011"}},"issued":{"date-parts":[[2012,4,1]]},"references-count":28,"journal-issue":{"issue":"7","published-print":{"date-parts":[[2012,4,1]]}},"alternative-id":["10.1152\/ajprenal.00498.2011"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00498.2011","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2012,4,1]]}},{"indexed":{"date-parts":[[2024,7,4]],"date-time":"2024-07-04T13:54:14Z","timestamp":1720101254108},"reference-count":35,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1998,4,1]]},"abstract":"<jats:p>The role of nitric oxide (NO) during cyclosporin renal vasoconstriction was evaluated by glomerular hemodynamic and histological changes produced by chronic NO synthesis inhibition and neuronal (nNOS), inducible (iNOS), and endothelial (eNOS) NO synthases mRNA expression in renal cortex and medulla. Uninephrectomized rats treated during 7 days with vehicle (Veh), cyclosporin A (CsA) 30 mg\/kg, CsA + nitro-l-arginine methyl ester (l-NAME), and Veh +l-NAME (10 mg\/dl) in the drinking water were studied. Increase in arterial pressure and afferent and efferent resistances, as well as decrease in glomerular plasma flow, ultrafiltration coefficient, and single-nephron glomerular filtration rate were significantly greater with CsA +l-NAME than with CsA alone. The increase in afferent resistance was higher with CsA +l-NAME than with Veh +l-NAME. In addition, glomerular thrombosis, proximal tubular vacuolization, and arteriolar thickening were more prominent. In renal cortex, eNOS mRNA expression exhibited a 2.7-fold increase in CsA, whereas, in medulla, nNOS and iNOS expression were lower in CsA than in Veh, while eNOS tended to increase. Our results support the hypothesis that NO synthesis is enhanced at cortical level during CsA nephrotoxicity, counterbalancing predominantly preglomerular vasoconstriction. Higher NO production could be the result of increased eNOS mRNA expression.<\/jats:p>","DOI":"10.1152\/ajprenal.1998.274.4.f791","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T15:43:32Z","timestamp":1514043812000},"page":"F791-F798","source":"Crossref","is-referenced-by-count":13,"title":["Role of NO in cyclosporin nephrotoxicity: effects of chronic NO inhibition and NO synthases gene expression"],"prefix":"10.1152","volume":"274","author":[{"given":"Norma A.","family":"Bobadilla","sequence":"first","affiliation":[{"name":"Departments of Nephrology and"}]},{"given":"Gerardo","family":"Gamba","sequence":"additional","affiliation":[{"name":"Molecular Physiology Unit, Department of Nephrology and Mineral Metabolism,Instituto Nacional de la Nutrici\u00f3n Salvador Zubir\u00e1n and Instituto de Investigaciones Biom\u00e9dicas, National University of Mexico, Mexico City CP 14080, Mexico"}]},{"given":"Edilia","family":"Tapia","sequence":"additional","affiliation":[{"name":"Departments of Nephrology and"}]},{"given":"Romeo","family":"Garc\u00eda-Torres","sequence":"additional","affiliation":[{"name":"Pathology, Instituto Nacional de Cardiolog\u0131\u0301a Ignacio Ch\u00e1vez; and"}]},{"given":"Alexis","family":"Bolio","sequence":"additional","affiliation":[{"name":"Departments of Nephrology and"}]},{"given":"Pedro","family":"L\u00f3pez-Zetina","sequence":"additional","affiliation":[{"name":"Departments of Nephrology and"}]},{"given":"Jaime","family":"Herrera-Acosta","sequence":"additional","affiliation":[{"name":"Departments of Nephrology and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.213"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajplegacy.1976.230.4.1148"},{"key":"B3","doi-asserted-by":"crossref","first-page":"875","DOI":"10.1681\/ASN.V16875","volume":"1","author":"Baylis C.","year":"1990","journal-title":"J. Am. Soc. Nephrol."},{"issue":"38","key":"B4","first-page":"F134","volume":"269","author":"Beierwaltes W. H.","year":"1995","journal-title":"Am. J. Physiol."},{"key":"B5","first-page":"55","volume":"1","author":"Bobadilla N. A.","year":"1997","journal-title":"Arch. Med. Res."},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.332"},{"key":"B8","first-page":"351","volume":"62","author":"Davidson W. D.","year":"1963","journal-title":"J. Lab. Clin. Med."},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.23.6.957"},{"key":"B10","doi-asserted-by":"crossref","first-page":"1291","DOI":"10.1681\/ASN.V281291","volume":"2","author":"Diederich D.","year":"1992","journal-title":"J. Am. Soc. Nephrol."},{"key":"B11","doi-asserted-by":"crossref","first-page":"1498","DOI":"10.1681\/ASN.V571498","volume":"5","author":"Fujihara C. K.","year":"1995","journal-title":"J. Am. Soc. Nephrol."},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1989.179"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1990.139"},{"issue":"41","key":"B16","first-page":"F561","volume":"272","author":"Kone B. C.","year":"1997","journal-title":"Am. J. Physiol."},{"issue":"40","key":"B17","first-page":"H1072","volume":"271","author":"L\u00f3pez-Ongil S.","year":"1996","journal-title":"Am. J. Physiol."},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.25.4.764"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.135"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1988.38"},{"key":"B21","first-page":"S83","volume":"25","author":"Perico N.","year":"1986","journal-title":"Clin. Nephrol."},{"issue":"20","key":"B22","first-page":"F581","volume":"251","author":"Perico N.","year":"1986","journal-title":"Am. J. Physiol."},{"issue":"31","key":"B23","first-page":"F679","volume":"262","author":"Rocco M. V.","year":"1992","journal-title":"Am. J. Physiol."},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.74.12.5463"},{"issue":"38","key":"B26","first-page":"F825","volume":"269","author":"Schricker K.","year":"1995","journal-title":"Am. J. Physiol."},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM198112033052306"},{"issue":"39","key":"B28","first-page":"F1027","volume":"270","author":"Singh I.","year":"1996","journal-title":"Am. J. Physiol."},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.29.2.570"},{"key":"B30","doi-asserted-by":"crossref","first-page":"42","DOI":"10.1681\/ASN.V3142","volume":"3","author":"Takenaka T.","year":"1992","journal-title":"J. Am. Soc. Nephrol."},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.62"},{"issue":"36","key":"B32","first-page":"F296","volume":"267","author":"Ujiie K.","year":"1994","journal-title":"Am. J. Physiol."},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1016\/0003-2697(78)90451-7"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1016\/0003-2697(66)90222-3"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.89.24.11993"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1989.107"},{"issue":"30","key":"B37","first-page":"F360","volume":"261","author":"Zatz R.","year":"1991","journal-title":"Am. J. Physiol."},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1161\/01.STR.24.12.2016"},{"key":"B39","first-page":"455","volume":"55","author":"Zoja C.","year":"1986","journal-title":"Lab. Invest."}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1998.274.4.F791","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:49:39Z","timestamp":1660189779000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1998.274.4.F791"}},"issued":{"date-parts":[[1998,4,1]]},"references-count":35,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1998,4,1]]}},"alternative-id":["10.1152\/ajprenal.1998.274.4.F791"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1998.274.4.f791","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1998,4,1]]}},{"indexed":{"date-parts":[[2024,8,8]],"date-time":"2024-08-08T08:33:44Z","timestamp":1723106024838},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1997,4,1]]},"abstract":"<jats:p> Epithelial cells go to great trouble to organize the subdomains of their plasma membranes. The apical and basolateral surfaces of polarized epithelia are equipped with markedly distinct populations of channels, carriers, and pumps. This anisotropy is an absolute prerequisite for vectorial solute and fluid transport. The physiological properties of an individual epithelial cell type are determined not only by its census of transport proteins but also by the manner in which these proteins are segregated between the apical and basolateral portions of the plasmalemma (Curr. Top. Membr. 39: 37-86, 1991). To achieve this asymmetry, an epithelial cell must be able to establish distinct surface domains, to target newly synthesized transport proteins to their appropriate sites of functional residence, and to retain them there following their delivery. Studies of the cellular pathways involved in generating and maintaining the polarized state have begun to illuminate an elegant network of cell biological specializations that may be involved not only in establishing the distributions of transport proteins but in dynamically regulating their function as well. <\/jats:p>","DOI":"10.1152\/ajprenal.1997.272.4.f425","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T03:11:57Z","timestamp":1513998717000},"page":"F425-F429","source":"Crossref","is-referenced-by-count":16,"title":["Membrane polarity in epithelial cells: protein sorting and establishment of polarized domains"],"prefix":"10.1152","volume":"272","author":[{"given":"M. J.","family":"Caplan","sequence":"first","affiliation":[{"name":"Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1997.272.4.F425","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:15:16Z","timestamp":1567959316000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1997.272.4.F425"}},"issued":{"date-parts":[[1997,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1997,4,1]]}},"alternative-id":["10.1152\/ajprenal.1997.272.4.F425"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1997.272.4.f425","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1997,4,1]]}},{"indexed":{"date-parts":[[2025,2,26]],"date-time":"2025-02-26T05:34:22Z","timestamp":1740548062968,"version":"3.38.0"},"reference-count":37,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2010,12]]},"abstract":"<jats:p>Acute intramedullary infusion of hyperosmotic NaCl, used to simulate a high-salt diet-induced increase of medullary osmolality, increases urine production and endothelin release from the kidney. To determine whether endothelin mediates this diuretic and natriuretic response, urine flow and Na<jats:sup>+<\/jats:sup>excretion rate were measured during acute intramedullary infusion of hyperosmotic NaCl in anesthetized rats, with or without endothelin receptor antagonism. Isosmotic NaCl was infused into the left renal medulla during an equilibration period and 30-min baseline period, followed by hyperosmotic NaCl for two additional 30-min periods. Hyperosmotic NaCl infusion significantly increased urine flow of vehicle-treated rats (from 5.9 \u00b1 0.9 to 11.1 \u00b1 1.8 \u03bcl\/min). Systemic ET<jats:sub>B<\/jats:sub>receptor blockade enhanced this effect (A-192621; from 7.7 \u00b1 1.1 to 18.7 \u00b1 2.9 \u03bcl\/min; P &lt; 0.05), ET<jats:sub>A<\/jats:sub>receptor blockade (ABT-627) had no significant effect alone, but the diuresis was markedly attenuated by combined ABT-627 and A-192621 administration (from 4.4 \u00b1 0.7 to 5.4 \u00b1 0.9 \u03bcl\/min). Mean arterial pressures overall were not significantly different between groups. Surprisingly, the natriuretic response to hyperosmotic NaCl infusion was not significantly altered by systemic endothelin receptor blockade, and furthermore, intramedullary ET<jats:sub>B<\/jats:sub>receptor blockade enhanced the diuretic and natriuretic response to hyperosmotic NaCl infusion. ET<jats:sub>A<\/jats:sub>receptor blockade significantly attenuated both the diuretic and natriuretic responses to hyperosmotic NaCl infusion in ET<jats:sub>B<\/jats:sub>receptor-deficient sl\/sl rats. These results demonstrate an important role of endothelin in mediating diuretic responses to intramedullary infusion of hyperosmotic NaCl. Moreover, these data suggest ET<jats:sub>A<\/jats:sub>and ET<jats:sub>B<\/jats:sub>receptors are both required for the full diuretic and natriuretic actions of endothelin.<\/jats:p>","DOI":"10.1152\/ajprenal.00015.2010","type":"journal-article","created":{"date-parts":[[2010,9,16]],"date-time":"2010-09-16T01:48:23Z","timestamp":1284601703000},"page":"F1424-F1432","source":"Crossref","is-referenced-by-count":16,"title":["Cooperative role of ET<sub>A<\/sub>and ET<sub>B<\/sub>receptors in mediating the diuretic response to intramedullary hyperosmotic NaCl infusion"],"prefix":"10.1152","volume":"299","author":[{"given":"Erika I.","family":"Boesen","sequence":"first","affiliation":[{"name":"Vascular Biology Center, Medical College of Georgia, Augusta, Georgia"}]},{"given":"David M.","family":"Pollock","sequence":"additional","affiliation":[{"name":"Vascular Biology Center, Medical College of Georgia, Augusta, Georgia"}]}],"member":"24","reference":[{"key":"B1","first-page":"152","volume":"16","author":"Abassi ZA","year":"2001","journal-title":"News Physiol Sci"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.20.1.89"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1172\/JCI200421064"},{"key":"B4","doi-asserted-by":"crossref","first-page":"345","DOI":"10.1016\/S0022-3565(24)38745-2","volume":"296","author":"Ballew JR","year":"2001","journal-title":"J Pharmacol Exp Ther"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00021.2006"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90321.2008"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1997.273.1.R1"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.1997.749ba.x"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1994.1395"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1172\/JCI8609"},{"key":"B11","doi-asserted-by":"crossref","first-page":"976","DOI":"10.1681\/ASN.V25976","volume":"2","author":"Garvin J","year":"1991","journal-title":"J Am Soc Nephrol"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00190.2006"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90279.2008"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00100.2005"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.6.F1166"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00209.2004"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/S0895-7061(01)02169-0"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00368.2003"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1097\/01.mnh.0000186852.15889.1a"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1172\/JCI116286"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.265.5.F670"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00878.2005"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.108.123687"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.261.6.F951"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.2.F326"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.281.1.F144"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00085.2007"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.2007.01754.x"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00589.2002"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1172\/JCI114667"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.264.4.F690"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000070958.39174.7E"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1021\/jm990170q"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1369\/jhc.5A6888.2006"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.260.4.F579"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.264.4.F684"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1989.257.6.C1101"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00015.2010","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,2,25]],"date-time":"2025-02-25T21:32:23Z","timestamp":1740519143000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00015.2010"}},"issued":{"date-parts":[[2010,12]]},"references-count":37,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2010,12]]}},"alternative-id":["10.1152\/ajprenal.00015.2010"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00015.2010","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2010,12]]}},{"indexed":{"date-parts":[[2025,7,30]],"date-time":"2025-07-30T13:11:32Z","timestamp":1753881092235,"version":"3.41.2"},"reference-count":0,"publisher":"American Physiological Society","funder":[{"DOI":"10.13039\/100017540","name":"HHS | NIH | NHLBI | Division of Intramural Research","doi-asserted-by":"publisher","award":["ZIA-HL001285","ZIA-HL006129"],"award-info":[{"award-number":["ZIA-HL001285","ZIA-HL006129"]}],"id":[{"id":"10.13039\/100017540","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"abstract":"<jats:p> We have devised a user-friendly downloadable, standalone application that solves a set of ordinary differential equations describing steady-state mass balance for salt (NaCl), urea and water in a single renal tubule with axial flow. The model was programmed in Python using an explicit ordinary differential equation solver. The standalone version allows users to interact with a GUI to insert parameter values and initiate the calculations. It outputs volume flow rate and solute concentrations as a function of position along the tubule. We illustrate the use of the model to address questions about the roles of the mammalian distal convoluted tubule (DCT) in water balance. The simulations suggest an important role for the DCT as a second diluting segment beyond the cortical thick ascending limb (CTAL), consistent with a critical function in excretion of water loads. Simulation of the effect of thiazide diuretics, which inhibit active salt absorption in the DCT, provides an explanation for the observation that these agents can produce hyponatremia when used clinically. The simulations also indicate that the DCT may transport salt in either direction (in accord with micropuncture findings), depending on the salt concentration in the fluid entering from the CTAL. Salt reabsorption by active transport is balanced by passive salt secretion as the luminal salt concentration approaches an asymptotic \u2018static head\u2019 level. The tool will allow users with no mathematical modeling experience to simulate transport in renal tubules, working toward the goal of expanding the use of mathematical modeling in physiology. <\/jats:p>","DOI":"10.1152\/ajprenal.00285.2024","type":"journal-article","created":{"date-parts":[[2025,3,19]],"date-time":"2025-03-19T17:10:07Z","timestamp":1742404207000},"update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Downloadable Tool for Modeling of Salt, Urea and Water Transport in a Renal Tubule Segment: Application to the DCT"],"prefix":"10.1152","author":[{"given":"Nipun U.","family":"Jayatissa","sequence":"first","affiliation":[{"name":"NIH"}]},{"given":"Shahzad","family":"Sohail","sequence":"additional","affiliation":[{"name":"NIH"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6237-5893","authenticated-orcid":false,"given":"Ray","family":"Mejia","sequence":"additional","affiliation":[{"name":"NIH"}]},{"given":"Adri\u00e1n R.","family":"Murillo-de-Ozores","sequence":"additional","affiliation":[{"name":"NIH"}]},{"given":"Shaza","family":"Khan","sequence":"additional","affiliation":[{"name":"NIH"}]},{"given":"Viswanathan","family":"Raghuram","sequence":"additional","affiliation":[{"name":"NIH"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4878-9501","authenticated-orcid":false,"given":"Chung-Lin","family":"Chou","sequence":"additional","affiliation":[{"name":"NIH"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3445-9819","authenticated-orcid":false,"given":"Chin-Rang","family":"Yang","sequence":"additional","affiliation":[{"name":"NIH"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2276-8091","authenticated-orcid":false,"given":"Mark A.","family":"Knepper","sequence":"additional","affiliation":[{"name":"NIH"}]}],"member":"24","published-online":{"date-parts":[[2025,3,19]]},"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00285.2024","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,3,19]],"date-time":"2025-03-19T17:10:09Z","timestamp":1742404209000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00285.2024"}},"issued":{"date-parts":[[2025,3,19]]},"references-count":0,"alternative-id":["10.1152\/ajprenal.00285.2024"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00285.2024","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2025,3,19]]},"assertion":[{"value":"2024-10-07","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2025-03-14","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2025-03-19","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}],"article-number":"ajprenal.00285.2024"},{"indexed":{"date-parts":[[2025,7,30]],"date-time":"2025-07-30T13:11:33Z","timestamp":1753881093018,"version":"3.41.2"},"reference-count":0,"publisher":"American Physiological Society","content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"DOI":"10.1152\/ajprenal.00387.2023","type":"journal-article","created":{"date-parts":[[2023,12,22]],"date-time":"2023-12-22T19:00:14Z","timestamp":1703271614000},"update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["The kidney in health and disease in 2022: Gaps in and opportunities for new knowledge"],"prefix":"10.1152","author":[{"given":"Kate M.","family":"Denton","sequence":"first","affiliation":[{"name":"Department of Physiology, Monash University, Clayton, VIC, Australia"}]}],"member":"24","published-online":{"date-parts":[[2023,12,22]]},"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00387.2023","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,12,20]],"date-time":"2024-12-20T16:43:36Z","timestamp":1734713016000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00387.2023"}},"issued":{"date-parts":[[2023,12,22]]},"references-count":0,"alternative-id":["10.1152\/ajprenal.00387.2023"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00387.2023","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2023,12,22]]},"assertion":[{"value":"2023-12-05","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2023-12-18","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2023-12-22","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}],"article-number":"ajprenal.00387.2023"},{"indexed":{"date-parts":[[2025,2,21]],"date-time":"2025-02-21T11:59:31Z","timestamp":1740139171815,"version":"3.37.3"},"reference-count":10,"publisher":"American Physiological Society","issue":"2","funder":[{"DOI":"10.13039\/501100000291","name":"Kidney Research UK","doi-asserted-by":"publisher","award":["PD6\/2012"],"award-info":[{"award-number":["PD6\/2012"]}],"id":[{"id":"10.13039\/501100000291","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000360","name":"Scottish Funding Council (SFC)","doi-asserted-by":"publisher","award":["SSCF"],"award-info":[{"award-number":["SSCF"]}],"id":[{"id":"10.13039\/501100000360","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2016,8,1]]},"DOI":"10.1152\/ajprenal.00296.2016","type":"journal-article","created":{"date-parts":[[2016,6,8]],"date-time":"2016-06-08T23:34:31Z","timestamp":1465428871000},"page":"F404-F405","source":"Crossref","is-referenced-by-count":1,"title":["Wnt6: another player in the yin and yang of renal Wnt signaling"],"prefix":"10.1152","volume":"311","author":[{"given":"Laura","family":"Denby","sequence":"first","affiliation":[{"name":"Centre for Cardiovascular Science, Queens Medical Research Institute, University of Edinburgh, United Kingdom"}]},{"given":"Bryan R.","family":"Conway","sequence":"additional","affiliation":[{"name":"Centre for Cardiovascular Science, Queens Medical Research Institute, University of Edinburgh, United Kingdom"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00136.2016"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/382638a0"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M111.223164"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005121355"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0912228107"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014121188"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/j.ydbio.2011.02.019"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1211179110"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.322"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2012.173"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00296.2016","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:43:49Z","timestamp":1567975429000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00296.2016"}},"issued":{"date-parts":[[2016,8,1]]},"references-count":10,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2016,8,1]]}},"alternative-id":["10.1152\/ajprenal.00296.2016"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00296.2016","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2016,8,1]]}},{"indexed":{"date-parts":[[2025,2,21]],"date-time":"2025-02-21T11:59:36Z","timestamp":1740139176398,"version":"3.37.3"},"reference-count":44,"publisher":"American Physiological Society","issue":"5","funder":[{"DOI":"10.13039\/100006108","name":"HHS | NIH | National Center for Advancing Translational Sciences","doi-asserted-by":"publisher","award":["TL1TR002344"],"award-info":[{"award-number":["TL1TR002344"]}],"id":[{"id":"10.13039\/100006108","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK11186102"],"award-info":[{"award-number":["DK11186102"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK11062204"],"award-info":[{"award-number":["DK11062204"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100008457","name":"School of Medicine, University of Virginia","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100008457","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2022,11,1]]},"abstract":"<jats:p> We report MRI tools to measure and map single-nephron function in the isolated, perfused rat kidney. We used imaging tracers to identify nephrons throughout the kidney and to measure the delivery and filtration of the tracers at the location of the glomeruli. With this technique, we directly measured physiological parameters including estimated single-nephron glomerular filtration rate throughout the kidney. This work provides a foundation for new studies to simultaneously map the function of large numbers of nephrons. <\/jats:p>","DOI":"10.1152\/ajprenal.00103.2022","type":"journal-article","created":{"date-parts":[[2022,9,1]],"date-time":"2022-09-01T18:47:00Z","timestamp":1662058020000},"page":"F602-F611","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":2,"title":["Mapping single-nephron filtration in the isolated, perfused rat kidney using magnetic resonance imaging"],"prefix":"10.1152","volume":"323","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3482-373X","authenticated-orcid":false,"given":"Edwin J.","family":"Baldelomar","sequence":"first","affiliation":[{"name":"Mallinckrodt Institute of Radiology, Washington University in St. Louis, St. Louis, Missouri"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2225-535X","authenticated-orcid":false,"given":"Jennifer R.","family":"Charlton","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Pediatrics, University of Virginia, Charlottesville, Virginia"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1706-4660","authenticated-orcid":false,"given":"Kevin M.","family":"Bennett","sequence":"additional","affiliation":[{"name":"Mallinckrodt Institute of Radiology, Washington University in St. Louis, St. Louis, Missouri"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-013-2494\u20138"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-008-0581-7"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1007\/bf00362733"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00521.2005"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00159.2002"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/physiol.00001.2009"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00417.2010"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1681\/asn.2020040423"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1056\/nejmoa1614329"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1681\/asn.2009121248"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2016020154"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00044.2011"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1002\/mrm.21684"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00092.2014"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1038\/s41390-019-0684-1"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2015.316"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2020.08.021"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00078.2019"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00399.2017"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1975.1"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1042\/cs0550513"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.3791\/54712"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1053\/j.semnuclmed.2007.09.004"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1053\/j.semnuclmed.2010.09.001"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00326.2014"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1148\/radiol.13121352"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1002\/ar.24419"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1002\/nbm.1149"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/j.jss.2010.08.033"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1982.243.3.F284"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1172\/jci111189"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000395"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1991.180"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0079992"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00218.2006"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0730776100"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1681\/asn.2018050490"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1681\/asn.2010101054"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1159\/000070813"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.1.F223"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.2174\/1874418401105010015"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/ajplegacy.1976.231.6.1699"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1980.238.2.F71"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.7554\/elife.75284"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00103.2022","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,10,19]],"date-time":"2022-10-19T17:47:34Z","timestamp":1666201654000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00103.2022"}},"issued":{"date-parts":[[2022,11,1]]},"references-count":44,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2022,11,1]]}},"alternative-id":["10.1152\/ajprenal.00103.2022"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00103.2022","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2022,11,1]]},"assertion":[{"value":"2022-04-13","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2022-08-16","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2022-08-25","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2022-10-19","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2025,9,20]],"date-time":"2025-09-20T19:10:41Z","timestamp":1758395441226,"version":"3.41.0"},"reference-count":33,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1998,1,1]]},"abstract":"<jats:p>In recent years, both molecular biological and immunohistochemical techniques, utilizing receptor subtype-specific probes and antibodies to cloned central nervous system dopamine receptors, have revealed their presence in a number of peripheral organs and tissues. Molecular techniques have been hindered by the low abundance of receptor mRNA in these sites, and reverse transcription-polymerase chain reaction (RT-PCR) has been utilized to address this problem. However, RT-PCR is most often employed on either isolated mRNA or microdissected tissue samples, thereby limiting interpretation of whole tissue distribution. The present paper describes the use of a novel self-sustained sequence replication system (3SR) to amplify a target mRNA sequence in situ within the tissue or cell of interest that is then detected with the use of an internal labeled probe, using standard nonisotopic in situ hybridization. Specifically, D<jats:sub>1A<\/jats:sub>receptor mRNA was amplified and detected in kidney sections of Wistar-Kyoto rats (WKY). The amplified D<jats:sub>1A<\/jats:sub>receptor mRNA was localized to renal arterioles, juxtaglomerular apparatus, and both proximal and distal tubules. mRNA was colocalized to regions shown also to contain D<jats:sub>1A<\/jats:sub>receptor protein. D<jats:sub>1A<\/jats:sub>receptor mRNA was predominantly localized in the cortex. Specificity of D<jats:sub>1A<\/jats:sub>receptor mRNA detection was confirmed by appropriate localization in rat brain sections known to express D<jats:sub>1A<\/jats:sub>receptor mRNA. In addition, we confirmed the presence of renal D<jats:sub>1A<\/jats:sub>receptor mRNA by RT-PCR. We conclude that D<jats:sub>1A<\/jats:sub>receptor mRNA is expressed in a site-specific manner in the WKY kidney. The use of 3SR in situ permits elucidation of site specific mRNA localization in a manner not reported previously.<\/jats:p>","DOI":"10.1152\/ajprenal.1998.274.1.f232","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T14:24:43Z","timestamp":1514039083000},"page":"F232-F241","source":"Crossref","is-referenced-by-count":11,"title":["Detection of dopamine receptor D<sub>1A<\/sub>subtype-specific mRNA in rat kidney by in situ amplification"],"prefix":"10.1152","volume":"274","author":[{"given":"Damian P.","family":"O\u2019Connell","sequence":"first","affiliation":[{"name":"Department of Pharmacology and Therapeutics, University College Cork, Cork, Ireland; and the"}]},{"given":"Anna M.","family":"Aherne","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Therapeutics, University College Cork, Cork, Ireland; and the"}]},{"given":"Eamon","family":"Lane","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Therapeutics, University College Cork, Cork, Ireland; and the"}]},{"given":"Robin A.","family":"Felder","sequence":"additional","affiliation":[{"name":"Departments of Medicine and Pathology, University of Virginia Health Sciences Center, Charlottesville, Virginia 22908"}]},{"given":"Robert M.","family":"Carey","sequence":"additional","affiliation":[{"name":"Departments of Medicine and Pathology, University of Virginia Health Sciences Center, Charlottesville, Virginia 22908"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-199401000-00005"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/336783a0"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/347072a0"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.8.4005"},{"issue":"15","key":"B6","first-page":"F557","volume":"246","author":"Felder R. A.","year":"1984","journal-title":"Am. J. Physiol."},{"issue":"26","key":"B8","first-page":"F315","volume":"257","author":"Felder R. A.","year":"1989","journal-title":"Am. J. Physiol."},{"issue":"33","key":"B9","first-page":"R726","volume":"264","author":"Felder R. A.","year":"1993","journal-title":"Am. J. Physiol."},{"issue":"4","key":"B10","first-page":"F646","volume":"35","author":"Gao D.-Q.","year":"1994","journal-title":"Am. J. Physiol."},{"issue":"37","key":"B12","first-page":"F423","volume":"268","author":"Grenader A. C.","year":"1995","journal-title":"Am. J. Physiol."},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.87.5.1874"},{"key":"B14","first-page":"577","volume":"73","author":"Hofler H.","year":"1995","journal-title":"Lab. Invest."},{"key":"B15","doi-asserted-by":"crossref","first-page":"1265","DOI":"10.1681\/ASN.V281265","volume":"2","author":"Jose P. A.","year":"1992","journal-title":"J. Am. Soc. Nephrol."},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1038\/277093a0"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/0922-4106(94)90212-7"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1006\/jsre.1993.1094"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.93.19.10377"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.87.17.6723"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/342926a0"},{"key":"B23","doi-asserted-by":"crossref","first-page":"918","DOI":"10.1016\/S0026-895X(25)13284-7","volume":"44","author":"Nash S. R.","year":"1993","journal-title":"Mol. Pharmacol."},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1101\/gr.2.4.305"},{"issue":"37","key":"B25","first-page":"F1185","volume":"268","author":"O\u2019Connell D. P.","year":"1995","journal-title":"Am. J. Physiol."},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/0922-4106(94)90228-3"},{"issue":"26","key":"B27","first-page":"F469","volume":"257","author":"Siragy H. M.","year":"1989","journal-title":"Am. J. Physiol."},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1038\/347146a0"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.91.22.10536"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1038\/350614a0"},{"key":"B31","doi-asserted-by":"crossref","first-page":"495","DOI":"10.1016\/S0022-3565(25)38500-9","volume":"268","author":"Tang L.","year":"1994","journal-title":"J. Pharmacol. Exp. Ther."},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.88.17.7491"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1038\/350610a0"},{"key":"B34","doi-asserted-by":"crossref","first-page":"22427","DOI":"10.1016\/S0021-9258(18)54590-7","volume":"266","author":"Weinshank R. L.","year":"1991","journal-title":"J. Biol. Chem."},{"issue":"33","key":"B36","first-page":"F280","volume":"264","author":"Yamaguchi I.","year":"1993","journal-title":"Am. J. Physiol."},{"key":"B37","first-page":"20","volume":"1","author":"Zehbe I.","year":"1994","journal-title":"Cell Vision"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1038\/347076a0"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1998.274.1.F232","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,6,29]],"date-time":"2025-06-29T04:38:20Z","timestamp":1751171900000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1998.274.1.F232"}},"issued":{"date-parts":[[1998,1,1]]},"references-count":33,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1998,1,1]]}},"alternative-id":["10.1152\/ajprenal.1998.274.1.F232"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1998.274.1.f232","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[1998,1,1]]}},{"indexed":{"date-parts":[[2025,9,25]],"date-time":"2025-09-25T16:18:51Z","timestamp":1758817131676},"reference-count":31,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2003,4,1]]},"abstract":"<jats:p>Hypophosphatemia leads to an increase in Na<jats:sup>+<\/jats:sup>-P<jats:sub>i<\/jats:sub>cotransporter (NaPi-2) mRNA levels. This increase is posttranscriptional and correlates with a more stable transcript mediated by the terminal 698 nt of the NaPi-2 mRNA. A 71-nt binding element was identified with renal proteins from rats fed control and low-P<jats:sub>i<\/jats:sub>(\u2212P<jats:sub>i<\/jats:sub>) diet. The binding of \u2212P<jats:sub>i<\/jats:sub>renal proteins to this transcript was increased compared with control proteins. The functionality of the ciselement was demonstrated by an in vitro degradation assay. \u2212P<jats:sub>i<\/jats:sub>renal proteins stabilized transcripts that included the cis element compared with control renal extracts. The full-length NaPi-2 transcript, but not control transcripts, was stabilized by \u2212P<jats:sub>i<\/jats:sub>extracts. Insertion of the binding element into green fluorescent protein (GFP) as a reporter gene decreased chimeric GFP mRNA levels in transfection experiments. Our results suggest that the protein-binding region of the NaPi-2 mRNA functions as a cis-acting instability element. In hypophosphatemia there is increased binding to the cis-acting element and subsequent stabilization of NaPi-2 mRNA.<\/jats:p>","DOI":"10.1152\/ajprenal.00332.2002","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:37:40Z","timestamp":1425415060000},"page":"F663-F670","source":"Crossref","is-referenced-by-count":11,"title":["Characterization of<i>cis<\/i>-acting element in renal NaPi-2 cotransporter mRNA that determines mRNA stability"],"prefix":"10.1152","volume":"284","author":[{"given":"Yulia","family":"Moz","sequence":"first","affiliation":[{"name":"Minerva Center for Calcium and Bone Metabolism, Nephrology Services, Hadassah University Hospital, Jerusalem, Israel 91120"}]},{"given":"Justin","family":"Silver","sequence":"additional","affiliation":[{"name":"Minerva Center for Calcium and Bone Metabolism, Nephrology Services, Hadassah University Hospital, Jerusalem, Israel 91120"}]},{"given":"Tally","family":"Naveh-Many","sequence":"additional","affiliation":[{"name":"Minerva Center for Calcium and Bone Metabolism, Nephrology Services, Hadassah University Hospital, Jerusalem, Israel 91120"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.9.5372"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1988.255.2.C155"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/S0378-1119(01)00350-X"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.24.14564"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.97.6.2916"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.268.4.F784"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00115.x"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.40.28256"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.268.6.F1017"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118038"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M005471200"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(93)90046-S"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119289"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.267.5.F900"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118022"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.90.13.5979"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1007\/BF00373881"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.9.5253"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.36.25266"},{"key":"B20","doi-asserted-by":"crossref","first-page":"1649","DOI":"10.1681\/ASN.V2121649","volume":"2","author":"Murer H.","year":"1992","journal-title":"J Am Soc Nephrol"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.5.F676"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1080\/09687680010019357"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.32.20125"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.4.1909"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.275.10.7424"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.0092.2001"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/S0167-4781(97)00231-5"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.23.14575"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.R000019200"},{"key":"B30","doi-asserted-by":"crossref","first-page":"6637","DOI":"10.1016\/S0021-9258(17)37420-3","volume":"269","author":"Werner A","year":"1994","journal-title":"J Biol Chem"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.2001.280.2.R301"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00332.2002","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,5,1]],"date-time":"2022-05-01T09:36:45Z","timestamp":1651397805000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00332.2002"}},"issued":{"date-parts":[[2003,4,1]]},"references-count":31,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2003,4,1]]}},"alternative-id":["10.1152\/ajprenal.00332.2002"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00332.2002","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2003,4,1]]}},{"indexed":{"date-parts":[[2025,10,8]],"date-time":"2025-10-08T22:41:26Z","timestamp":1759963286002},"reference-count":56,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2007,6]]},"abstract":"<jats:p>Obstruction-induced fibrosis is a leading cause of end-stage renal failure in children. The pathophysiological mechanisms may involve apoptosis and the renin-angiotensin system. We studied apoptosis and fibrosis in a well-established neonatal pig model with unilateral partial ureteral obstruction (PUUO) induced during ongoing nephrogenesis in 2-day-old piglets. The role of angiotensin II (ANG II) was studied using the AT<jats:sub>1<\/jats:sub>receptor blocker CV-11974 (0.12 mg\/h candesartan from age 23 to 30 days). At day 30 the kidneys were perfusion fixed and fibrosis, apoptosis, and tubular lengths were quantitated using stereological methods, picro Sirius red staining, and immunohistochemical techniques identifying activated caspase 3, aquaporin-2 (AQP2), and von Willebrand factor. The collagen content was assessed by hydroxyproline density. Neonatal induced PUUO increased interstitial and glomerular cell apoptosis and fibrosis. At this stage, PUUO did not increase tubular cell apoptosis or decrease tubular length and cell number. AT<jats:sub>1<\/jats:sub>receptor blockade prevented the PUUO-induced interstitial and glomerular cell apoptosis but did not attenuate fibrosis. In conclusion, AT<jats:sub>1<\/jats:sub>receptor blockade after the end of nephrogenesis may prevent interstitial and glomerular cell apoptosis but not fibrosis, suggesting that pathways not involving AT<jats:sub>1<\/jats:sub>receptor stimulation contribute to neonatal obstruction-induced fibrosis or that prevention of interstitial cell apoptosis counteracts a potential antifibrotic effect of AT<jats:sub>1<\/jats:sub>receptor blockade in this pig model of congenital obstructive nephropathy. Our results demonstrate that ANG II plays a role in PUUO-induced glomerular cell apoptosis.<\/jats:p>","DOI":"10.1152\/ajprenal.00479.2006","type":"journal-article","created":{"date-parts":[[2007,3,14]],"date-time":"2007-03-14T00:50:23Z","timestamp":1173833423000},"page":"F1771-F1781","source":"Crossref","is-referenced-by-count":12,"title":["AT<sub>1<\/sub>receptor blockade prevents interstitial and glomerular apoptosis but not fibrosis in pigs with neonatal induced partial unilateral ureteral obstruction"],"prefix":"10.1152","volume":"292","author":[{"given":"Anni","family":"Eskild-Jensen","sequence":"first","affiliation":[]},{"given":"Lene Fogt","family":"Paulsen","sequence":"additional","affiliation":[]},{"given":"Lise","family":"Wogensen","sequence":"additional","affiliation":[]},{"given":"Ping","family":"Olesen","sequence":"additional","affiliation":[]},{"given":"Lea","family":"Pedersen","sequence":"additional","affiliation":[]},{"given":"J\u00f8rgen","family":"Fr\u00f8ki\u00e6r","sequence":"additional","affiliation":[]},{"given":"Jens Randel","family":"Nyengaard","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00486.x"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00488.x"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1034\/j.1399-3046.2003.00029.x"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00246.2002"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00775.x"},{"key":"R6","doi-asserted-by":"crossref","unstructured":"Cervenka L, Wang CT, Navar LG.Effects of acute AT1 receptor blockade by candesartan on arterial pressure and renal function in rats.Am J Physiol Renal Physiol274: F940\u2013F945, 1998.","DOI":"10.1152\/ajprenal.1998.274.5.F940"},{"key":"R7","doi-asserted-by":"crossref","unstructured":"Chen CO, Park MH, Forbes MS, Thornhill BA, Kiley S, Yoo KH, Chevalier RL.Angiotensin-converting enzyme inhibition aggravates renal interstitial injury resulting from partial unilateral ureteral obstruction in the neonatal rat.Am J Physiol Renal Physiol292: F946\u2013F955, 2007.","DOI":"10.1152\/ajprenal.00287.2006"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1097\/01.mop.0000193287.56528.a4"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(01)65633-7"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.057003882.x"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00966.x"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1159\/000020657"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2000.00371.x"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.1.F41"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00310.x"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.268.6.F1117"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004090771"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00240.2001"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1990.259.3.R637"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00045.2005"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2818.2001.00958.x"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00362.x"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(05)67591-X"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(05)65338-4"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00019.2006"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1172\/JCI4236"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.06703.x"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-200018020-00001"},{"key":"R29","doi-asserted-by":"crossref","unstructured":"Hayashi M, Araki T.Caspase in renal development.Nephrol Dial Transplant17,Suppl9: 8\u201310, 2002.","DOI":"10.1093\/ndt\/17.suppl_9.8"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.161"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.183"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200405000-00003"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1016\/j.juro.2006.03.076"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00428.x"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1016\/0272-6386(95)90167-1"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.00150.2002"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1097\/01.ju.0000067385.26560.7c"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00643.x"},{"key":"R39","unstructured":"Morrissey JJ, Ishidoya S, McCracken R, Klahr S.The effect of ACE inhibitors on the expression of matrix genes and the role of p53 and p21 (WAF1) in experimental renal fibrosis.Kidney Int Suppl54: S83\u2013S87, 1996."},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005070757"},{"key":"R41","unstructured":"Nielsen TW, Maaske CA, Booth NH.Some comparative aspects of porcine renal function. In:Swine in Biomedical Research, edited by Bukstad LK and McClellan RO. Seattle, WA: Frayn, 1965, p. 529\u2013537."},{"key":"R42","doi-asserted-by":"crossref","unstructured":"Nyengaard JR.Stereologic methods and their application in kidney research.J Am Soc Nephrol10: 1100\u20131123, 1999.","DOI":"10.1681\/ASN.V1051100"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1111\/j.1582-4934.2004.tb00468.x"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1097\/01.ju.0000091106.61065.e3"},{"key":"R45","doi-asserted-by":"crossref","unstructured":"Satoh M, Kashihara N, Yamasaki Y, Maruyama K, Okamoto K, Maeshima Y, Sugiyama H, Sugaya T, Murakami K, Makino H.Renal interstitial fibrosis is reduced in angiotensin II type 1a receptor-deficient mice.J Am Soc Nephrol12: 317\u2013325, 2001.","DOI":"10.1681\/ASN.V122317"},{"key":"R46","unstructured":"Sweat F, Puchtler H, Rosenthal SI.Sirius red F3BA as a stain for connective tissue.Arch Pathol78: 69\u201372, 1964."},{"key":"R47","unstructured":"Terris JM.Swine as a model in renal physiology and nephrology: an overview. In:Swine in Biomedical Research, edited by Tumbleson M. New York: Plenum, 1986, p. 1673\u20131709."},{"key":"R48","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00052.x"},{"key":"R49","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.060003924.x"},{"key":"R50","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.303"},{"key":"R51","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(17)64796-7"},{"key":"R52","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00452.2003"},{"key":"R53","unstructured":"Woessner JF.Determination of hydroxyproline in connective tissue research. In:The Methodology of Connective Tissue Research, edited by Hall DA. Oxford, UK: Joynson-Bruvers, 1976, p. 227\u2013233."},{"key":"R54","doi-asserted-by":"crossref","unstructured":"Wolf G.Angiotensin II and tubular development.Nephrol Dial Transplant17,Suppl9: 48\u201351, 2002.","DOI":"10.1093\/ndt\/17.suppl_9.48"},{"key":"R55","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00013.x"},{"key":"R56","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.2000.278.3.R640"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00479.2006","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,5,11]],"date-time":"2023-05-11T00:15:17Z","timestamp":1683764117000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00479.2006"}},"issued":{"date-parts":[[2007,6]]},"references-count":56,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2007,6]]}},"alternative-id":["10.1152\/ajprenal.00479.2006"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00479.2006","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2007,6]]}},{"indexed":{"date-parts":[[2025,10,19]],"date-time":"2025-10-19T05:57:13Z","timestamp":1760853433286},"reference-count":51,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2009,11]]},"abstract":"<jats:p>Our recent studies showed that transglutaminase-1 (TGase-1) is uniquely expressed in mouse renal proximal tubular cells (RPTC) and mediates cell proliferation. In this study, we investigated the role of TGase-1 in cell survival and the survival signaling pathways regulated by TGase-1 in RPTC following oxidant injury. Exposure of RPTC to hydrogen peroxide (H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>) resulted in apoptosis and an increase in TGase activity. Inhibition of TGase activity with monodansylcadervine (MDC), a TGase inhibitor, or knockdown of TGase-1 with small interference (si)RNA enhanced apoptosis and decreased cell survival in H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>-treated RPTC. Conversely, overexpression of TGase-1 rendered RPTC more resistant to H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>toxicity and MDC treatment blocked this response. Concurrent with RPTC apoptosis, phosphorylation of AKT, signal transducer and activator of transcription-3 (STAT3), and glucogen synthase kinase-3\u03b2 (GSK-3\u03b2) were observed. Pretreatment of cells with MDC or TGase-1 siRNA inhibited phosphorylation of all these molecules. Inhibition of either the AKT or STAT3 pathway potentiated H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>-induced cell death and increased GSK-3\u03b2 activity by dephosphorylation at serine 9. Furthermore, treatment with GSK-3\u03b2 inhibitors reduced H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>-induced apoptosis and abolished the death-promoting effect of AKT and STAT3 inhibition. Therefore, we have identified TGase-1 as a novel survival factor in renal epithelial cells and it contributes to cell survival through activation of the AKT and STAT3 signaling pathways following oxidant injury.<\/jats:p>","DOI":"10.1152\/ajprenal.00251.2009","type":"journal-article","created":{"date-parts":[[2009,8,27]],"date-time":"2009-08-27T01:41:14Z","timestamp":1251337274000},"page":"F1361-F1370","source":"Crossref","is-referenced-by-count":27,"title":["Transglutaminase-1 protects renal epithelial cells from hydrogen peroxide-induced apoptosis through activation of STAT3 and AKT signaling pathways"],"prefix":"10.1152","volume":"297","author":[{"given":"Murugavel","family":"Ponnusamy","sequence":"first","affiliation":[{"name":"Departments of 1 Medicine and"}]},{"given":"Maoyin","family":"Pang","sequence":"additional","affiliation":[{"name":"Departments of 1 Medicine and"}]},{"given":"Pavan Kumar","family":"Annamaraju","sequence":"additional","affiliation":[{"name":"Departments of 1 Medicine and"}]},{"given":"Zhu","family":"Zhang","sequence":"additional","affiliation":[{"name":"Departments of 1 Medicine and"}]},{"given":"Rujun","family":"Gong","sequence":"additional","affiliation":[{"name":"Departments of 1 Medicine and"}]},{"given":"Y. Eugene","family":"Chin","sequence":"additional","affiliation":[{"name":"Surgery, Brown University School of Medicine, Rhode Island Hospital, Providence, Rhode Island"}]},{"given":"Shougang","family":"Zhuang","sequence":"additional","affiliation":[{"name":"Departments of 1 Medicine and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.9.5333"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/cr.2008.18"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M404976200"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M105318200"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00152.x"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1007\/s10529-006-9079-6"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1089\/152308602762197452"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.2174\/1566524023362456"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M802481200"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/j.pneurobio.2006.07.006"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.C200147200"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1093\/carcin\/bgn158"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1021\/bi0606795"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1995.269.2.C323"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1089\/hum.2008.016"},{"key":"B16","doi-asserted-by":"crossref","first-page":"41","DOI":"10.1124\/mol.104.005421","volume":"68","author":"Haider UG","year":"2005","journal-title":"Mol Pharmacol"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1080\/1521654031000115951"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.48.34148"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1007\/s00726-007-0517-0"},{"key":"B20","first-page":"4","volume":"20","author":"Kelly KJ","year":"2000","journal-title":"Semin Nephrol"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/j.brainres.2007.10.018"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1159\/000142935"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1206598"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.03473"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1159\/000129389"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1161\/01.ATV.21.3.321"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1186\/1741-7007-2-24"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M607413200"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2005.11.071"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M311919200"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1080\/08941930701366471"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M707238200"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1016\/j.mce.2008.08.004"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1016\/j.freeradbiomed.2009.03.026"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1016\/0306-4522(94)00556-K"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1023\/A:1009680229931"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1016\/j.biochi.2009.01.010"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200107009"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200007000-00015"},{"key":"B39a","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M308734200"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0609757104"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1998.275.6.C1640"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1016\/S0960-9822(02)70790-2"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1158\/1078-0432.CCR-07-1533"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1158\/0008-5472.CAN-06-2387"},{"key":"B45","doi-asserted-by":"crossref","first-page":"5241","DOI":"10.1016\/S0021-9258(17)37680-9","volume":"269","author":"Vlahos CJ","year":"1994","journal-title":"J Biol Chem"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.26.2.569-579.2006"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.25.15719"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.22.12.4062-4072.2002"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M808396200"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00282.2003"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00251.2009","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,10,10]],"date-time":"2021-10-10T03:04:56Z","timestamp":1633835096000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00251.2009"}},"issued":{"date-parts":[[2009,11]]},"references-count":51,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2009,11]]}},"alternative-id":["10.1152\/ajprenal.00251.2009"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00251.2009","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2009,11]]}},{"indexed":{"date-parts":[[2025,10,22]],"date-time":"2025-10-22T03:04:53Z","timestamp":1761102293337,"version":"3.37.3"},"reference-count":37,"publisher":"American Physiological Society","issue":"1","funder":[{"DOI":"10.13039\/100000062","name":"NIDDK","doi-asserted-by":"crossref","award":["DK 110375","DK 104125"],"award-info":[{"award-number":["DK 110375","DK 104125"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2018,7,1]]},"abstract":"<jats:p> \u03b1-Ketoglutarate (\u03b1-KG) is a citric acid cycle intermediate and a glutamine catabolism product. It is also the natural ligand of 2-oxoglutarate receptor 1 (OXGR1), a G<jats:sub>q<\/jats:sub> protein-coupled receptor expressed on the apical membrane of intercalated cells. In the cortical collecting duct (CCD), Cl<jats:sup>\u2212<\/jats:sup>\/[Formula: see text] exchange increases upon \u03b1-KG binding to the OXGR1. To determine the signaling pathway(s) by which \u03b1-KG stimulates Cl<jats:sup>\u2212<\/jats:sup> absorption, we examined \u03b1-KG-stimulated Cl<jats:sup>\u2212<\/jats:sup> absorption in isolated perfused mouse CCDs. \u03b1-KG increased electroneutral Cl<jats:sup>\u2212<\/jats:sup> absorption in CCDs from wild-type mice but had no effect on Cl<jats:sup>\u2212<\/jats:sup> absorption in pendrin knockout mice. Because G<jats:sub>q<\/jats:sub> protein-coupled receptors activate PKC, we hypothesized that \u03b1-KG stimulates Cl<jats:sup>\u2212<\/jats:sup> absorption through PKC. If so, PKC agonists should mimic, whereas PKC inhibitors should abolish, \u03b1-KG-stimulated Cl<jats:sup>\u2212<\/jats:sup> absorption. Like \u03b1-KG, PKC agonist (phorbol-12,13-dibutyrate, 500 nM) application increased Cl<jats:sup>\u2212<\/jats:sup> absorption in wild-type but not in pendrin null CCDs. Moreover, PKC inhibitors (2.5 mM GF109203X and 20 nM calphostin C), Ca<jats:sup>2+<\/jats:sup> chelators (BAPTA, 10\u201320 \u03bcM), or PKC-\u03b1 or -\u03b4 gene ablation eliminated \u03b1-KG-stimulated Cl<jats:sup>\u2212<\/jats:sup> absorption. We have shown that STE20\/SPS-1-related proline-alanine-rich protein kinase (SPAK) gene ablation increases urinary \u03b1-KG excretion, renal pendrin abundance, and CCD Cl<jats:sup>\u2212<\/jats:sup> absorption. However, in SPAK null CCDs, Cl<jats:sup>\u2212<\/jats:sup> absorption was not activated further by luminal \u03b1-KG application nor was Cl<jats:sup>\u2212<\/jats:sup> absorption reduced with the PKC inhibitor GF109203 . Thus SPAK gene ablation likely acts through a PKC-independent pathway to produce a chronic adaptive increase in pendrin function. In conclusion, \u03b1-KG stimulates pendrin-dependent Cl<jats:sup>\u2212<\/jats:sup>\/[Formula: see text] exchange through a mechanism dependent on PKC and Ca<jats:sup>2+<\/jats:sup> that involves PKC-\u03b1 and PKC-\u03b4. <\/jats:p>","DOI":"10.1152\/ajprenal.00576.2017","type":"journal-article","created":{"date-parts":[[2018,2,7]],"date-time":"2018-02-07T13:19:51Z","timestamp":1518009591000},"page":"F7-F15","source":"Crossref","is-referenced-by-count":11,"title":["\u03b1-Ketoglutarate stimulates pendrin-dependent Cl<sup>\u2212<\/sup> absorption in the mouse CCD through protein kinase C"],"prefix":"10.1152","volume":"315","author":[{"given":"Yoskaly","family":"Lazo-Fernandez","sequence":"first","affiliation":[{"name":"Department of Medicine, Emory University School of Medicine, Atlanta, Georgia"}]},{"given":"Paul A.","family":"Welling","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland"}]},{"given":"Susan M.","family":"Wall","sequence":"additional","affiliation":[{"name":"Department of Medicine, Emory University School of Medicine, Atlanta, Georgia"},{"name":"Department of Physiology, Emory University School of Medicine, Atlanta, Georgia"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1038\/nm1000"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.3390\/ijms151119700"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1221496110"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.3390\/cancers7030836"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajplung.00040.2014"},{"volume-title":"Vander\u2019s Renal Physiology","year":"2004","author":"Eaton DC","key":"B6"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00239.x"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M900142200"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.110.217117"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1172\/JCI78558"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M112.402800"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1038\/nature02488"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2016010085"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1002\/jcb.25314"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00016.2006"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1985.249.6.F870"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1984.247.5.F729"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1172\/JCI40145"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.109.195313"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2011.07.009"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/j.cccn.2003.10.023"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00471.2013"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.201611623"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1002\/emmm.200900058"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00273.2003"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.071516798"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115662"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90300.2008"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.259.3.F519"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1172\/JCI67562"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1002\/bdd.2089"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000088321.67254.B7"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.270.3.F432"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000145863.96091.89"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00022.2013"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1155\/2015\/817604"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009121295"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00576.2017","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T21:36:34Z","timestamp":1567978594000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00576.2017"}},"issued":{"date-parts":[[2018,7,1]]},"references-count":37,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2018,7,1]]}},"alternative-id":["10.1152\/ajprenal.00576.2017"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00576.2017","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2018,7,1]]}},{"indexed":{"date-parts":[[2025,10,21]],"date-time":"2025-10-21T15:04:13Z","timestamp":1761059053128},"reference-count":52,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2010,9]]},"abstract":"<jats:p>Large-conductance, calcium-activated potassium channels (BK) are expressed in principal cells (PC) and intercalated cells (IC) in mammalian nephrons as BK-\u03b1\/\u03b21 and BK-\u03b1\/\u03b24, respectively. IC, which protrude into the lumens of tubules, express substantially more BK than PC despite lacking sufficient Na-K-ATPase to support K secretion. We previously showed in mice that IC exhibit size reduction when experiencing high distal flows induced by a high-K diet. We therefore tested the hypothesis that BK-\u03b1\/\u03b24 are regulators of IC volume via a shear stress (\u03c4)-induced, calcium-dependent mechanism, resulting in a reduction in intracellular K content. We determined by Western blot and immunocytochemical analysis that C11-Madin-Darby canine kidney cells contained a predominance of BK-\u03b1\/\u03b24. To determine the role of BK-\u03b1\/\u03b24 in \u03c4-induced volume reduction, we exposed C11 cells to \u03c4 and measured K efflux by flame photometry and cell volume by calcein staining, which changes inversely to cell volume. With 10 dynes\/cm<jats:sup>2<\/jats:sup>, calcein intensity significantly increased 39% and monovalent cationic content decreased significantly by 37% compared with static conditions. Furthermore, the shear-induced K loss from C11 was abolished by the reduction of extracellular calcium, addition of 5 mM TEA, or BK-\u03b24 small interfering (si) RNA, but not by addition of nontarget siRNA. These results show that BK-\u03b1\/\u03b24 plays a role in shear-induced K loss from IC, suggesting that BK-\u03b1\/\u03b24 regulate IC volume during high-flow conditions. Furthermore, these results support the use of C11 cells as in vitro models for studying BK-related functions in IC of the kidney.<\/jats:p>","DOI":"10.1152\/ajprenal.00222.2010","type":"journal-article","created":{"date-parts":[[2010,6,25]],"date-time":"2010-06-25T03:09:37Z","timestamp":1277435377000},"page":"F507-F516","source":"Crossref","is-referenced-by-count":25,"title":["Shear stress-induced volume decrease in C11-MDCK cells by BK-\u03b1\/\u03b24"],"prefix":"10.1152","volume":"299","author":[{"given":"J. David","family":"Holtzclaw","sequence":"first","affiliation":[{"name":"Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska"}]},{"given":"Liping","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska"}]},{"given":"P. Richard","family":"Grimm","sequence":"additional","affiliation":[{"name":"Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska"}]},{"given":"Steven C.","family":"Sansom","sequence":"additional","affiliation":[{"name":"Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000388"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1007\/BF01869613"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1038\/nn1573"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.2.F270"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.265.5.F677"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000194321.60300.d6"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.261.1.F91"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90528.2008"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.256.1.F143"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1007\/BF00374853"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M003941200"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00471.2004"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00191.2009"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0904635106"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00018.2007"},{"key":"B16","doi-asserted-by":"crossref","first-page":"3440","DOI":"10.1016\/S0021-9258(19)83641-4","volume":"260","author":"Grynkiewicz G","year":"1985","journal-title":"J Biol Chem"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.4.F673"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2008.163550"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1987.253.2.C323"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009080817"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00277.2003"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5001633"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200805124"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00057.2007"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00067.2003"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M206644200"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.6.F954"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1977.57.3.510"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.256.5.F932"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.253.4.F742"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.261.4.F696"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00191.2006"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00340.2004"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1007\/s00232-002-1055-z"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1007\/s00232-001-0075-4"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.67.040403.101353"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1988.230"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002369"},{"key":"B39","doi-asserted-by":"crossref","first-page":"913","DOI":"10.1681\/ASN.V105913","volume":"10","author":"Sabolic I","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.258.3.F732"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1007\/s002329900391"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00458.2005"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-002-0926-6"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.200509436"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00365.2007"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.5.F786"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00316.2001"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00462.2006"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.1041640121"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00285.2006"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90542.2008"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00379.2006"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00222.2010","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,10,30]],"date-time":"2021-10-30T03:49:40Z","timestamp":1635565780000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00222.2010"}},"issued":{"date-parts":[[2010,9]]},"references-count":52,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2010,9]]}},"alternative-id":["10.1152\/ajprenal.00222.2010"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00222.2010","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2010,9]]}},{"indexed":{"date-parts":[[2025,10,21]],"date-time":"2025-10-21T15:28:05Z","timestamp":1761060485074,"version":"3.41.0"},"reference-count":45,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1998,6,1]]},"abstract":"<jats:p>Extracellular ATP affects a wide variety of cells via purinergic membrane receptors. One class of purinergic receptors, P2X, consists of ATP-gated, calcium-permeable, cation-selective channels. We performed whole cell patch-clamp studies, intracellular calcium concentration ([Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>) measurements, and reverse transcription-polymerase chain reaction (RT-PCR) to determine whether P2X receptors are expressed in LLC-PK<jats:sub>1<\/jats:sub>cells. First, in patch-clamp studies, 100 \u03bcM ATP depolarized the cell membrane and increased the whole cell conductance of LLC-PK<jats:sub>1<\/jats:sub>cells. This response was dose dependent and inhibited by 100 \u03bcM suramin, a P2 receptor antagonist. The ATP-induced conductance was cation selective but did not discriminate between Na<jats:sup>+<\/jats:sup>and K<jats:sup>+<\/jats:sup>. ADP, \u03b1,\u03b2-methylene-ATP, and \u03b2,\u03b3-methylene-ATP had no effect on the whole cell conductance. Next, 10 \u03bcM ATP caused a rapid rise in [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>in LLC-PK<jats:sub>1<\/jats:sub>cells. This effect of ATP was inhibited by the absence of extracellular calcium and by suramin but not by pretreatment with pertussis toxin. ADP and \u03b2,\u03b3-methylene- ATP had little or no effect on [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>. Finally, RT-PCR produced a 330-bp fragment from LLC-PK<jats:sub>1<\/jats:sub>cell RNA, whose sequence was 80% identical to the rat P2X<jats:sub>1<\/jats:sub>receptor. We conclude that LLC-PK<jats:sub>1<\/jats:sub>cells express purinergic receptors of the P2X class, which mediate depolarization and calcium entry when activated.<\/jats:p>","DOI":"10.1152\/ajprenal.1998.274.6.f1070","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T15:24:19Z","timestamp":1514042659000},"page":"F1070-F1077","source":"Crossref","is-referenced-by-count":13,"title":["Functional and molecular evidence for P2X receptors in LLC-PK<sub>1<\/sub>cells"],"prefix":"10.1152","volume":"274","author":[{"given":"Dragana M.","family":"Filipovic","sequence":"first","affiliation":[{"name":"Division of Nephrology and"}]},{"given":"Olugbenga A.","family":"Adebanjo","sequence":"additional","affiliation":[{"name":"Division of Endocrinology, University of Arkansas for Medical Sciences and John. L. McClellan Veterans Affairs Hospital, Little Rock, Arkansas 72205"}]},{"given":"Mone","family":"Zaidi","sequence":"additional","affiliation":[{"name":"Division of Endocrinology, University of Arkansas for Medical Sciences and John. L. McClellan Veterans Affairs Hospital, Little Rock, Arkansas 72205"}]},{"given":"W. Brian","family":"Reeves","sequence":"additional","affiliation":[{"name":"Division of Nephrology and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.10-01-00001.1990"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/0165-6147(92)90032-2"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(95)01203-Q"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/371519a0"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1002\/j.1460-2075.1996.tb00333.x"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1991.260.1.C143"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(95)90408-5"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.16-08-02495.1996"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.88.20.9262"},{"key":"B10","doi-asserted-by":"crossref","first-page":"449","DOI":"10.1016\/S0031-6997(25)06812-7","volume":"46","author":"Dalziel H. H.","year":"1994","journal-title":"Pharmacol. Rev."},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1993.265.3.C577"},{"issue":"36","key":"B12","first-page":"F998","volume":"267","author":"Ecelbarger C. A.","year":"1994","journal-title":"Am. J. Physiol."},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1038\/359144a0"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1038\/357503a0"},{"key":"B15","doi-asserted-by":"crossref","first-page":"178","DOI":"10.1016\/S0026-895X(25)10232-0","volume":"48","author":"Evans R. J.","year":"1995","journal-title":"Mol. Pharmacol."},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1996.sp021777"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1997.272.2.C737"},{"issue":"40","key":"B18","first-page":"F610","volume":"271","author":"Firstein B. L.","year":"1996","journal-title":"Am. J. Physiol."},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.212"},{"key":"B20","doi-asserted-by":"crossref","first-page":"3440","DOI":"10.1016\/S0021-9258(19)83641-4","volume":"260","author":"Grynkiewicz G.","year":"1985","journal-title":"J. Biol. Chem."},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/0006-2952(91)90465-H"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1993.264.4.C956"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.pa.35.040195.002545"},{"key":"B24","first-page":"253","volume":"14","author":"Humes H.","year":"1991","journal-title":"Renal Physiol. Biochem."},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1038\/377432a0"},{"issue":"33","key":"B26","first-page":"F867","volume":"264","author":"Middleton J. P.","year":"1993","journal-title":"Am. J. Physiol."},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1996.76.2.425"},{"key":"B28","first-page":"137","volume":"12","author":"O\u2019Conner S. E.","year":"1991","journal-title":"Trends Biochem. Sci."},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1038\/359241a0"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-291X(88)80751-4"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1126\/science.271.5257.1876"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1992.262.4.C934"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1007\/s002329900298"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1016\/0166-2236(87)90091-9"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1126\/science.272.5262.735"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1986.251.1.C120"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.84.21.7735"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1016\/0167-4889(96)00086-9"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1038\/371516a0"},{"issue":"23","key":"B40","first-page":"F311","volume":"254","author":"Weinberg J. M.","year":"1988","journal-title":"Am. J. Physiol."},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1989.256.5.C967"},{"issue":"19","key":"B42","first-page":"F720","volume":"250","author":"Weinberg J. M.","year":"1986","journal-title":"Am. J. Physiol."},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1996.270.4.C1096"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1016\/0896-6273(95)90021-7"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.24.14445"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1998.274.6.F1070","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,6,29]],"date-time":"2025-06-29T04:39:11Z","timestamp":1751171951000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1998.274.6.F1070"}},"issued":{"date-parts":[[1998,6,1]]},"references-count":45,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1998,6,1]]}},"alternative-id":["10.1152\/ajprenal.1998.274.6.F1070"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1998.274.6.f1070","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[1998,6,1]]}},{"indexed":{"date-parts":[[2025,10,21]],"date-time":"2025-10-21T03:21:54Z","timestamp":1761016914439},"reference-count":39,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2012,1,1]]},"abstract":"<jats:p>The N<jats:sup>\u03c9<\/jats:sup>-nitro-l-arginine methyl ester (l-NAME) model is widely employed to investigate the role of nitric oxide (NO) in renal injury. The present studies show that Sprague-Dawley rats from Harlan (H) and Charles River (CR) exhibit strikingly large differences in susceptibility to l-NAME nephropathy. After 4 wk of l-NAME (\u223c50 mg\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7day<jats:sup>\u22121<\/jats:sup>in drinking water), H rats ( n = 13) exhibited the expected hypertension [average radiotelemetric systolic blood pressure (BP), 180 \u00b1 3 mmHg], proteinuria (136 \u00b1 17 mg\/24 h), and glomerular injury (GI) (12 \u00b1 2%). By contrast, CR rats developed less hypertension (142 \u00b1 4), but surprisingly no proteinuria or GI, indicating a lack of glomerular hypertension. Additional studies showed that conscious H, but not CR, rats exhibit dose-dependent renal vasoconstriction after l-NAME. To further investigate these susceptibility differences, l-NAME was given 2 wk after 3\/4 normotensive nephrectomy (NX) and comparably impaired renal autoregulation in CR-NX and H-NX rats. CR-NX rats, nevertheless, still failed to develop proteinuria and GI despite moderate hypertension (144 \u00b1 2 mmHg, n = 29). By contrast, despite an 80\u201390% l-NAME dose reduction and lesser BP increases (169 \u00b1 4 mmHg), H-NX rats ( n = 20) developed greater GI (26 \u00b1 3%) compared with intact H rats. Linear regression analysis showed significant ( P &lt; 0.01) differences in the slope of the relationship between BP and GI between H-NX (slope 0.56 \u00b1 0.14; r = 0.69; P &lt; 0.008) and CR-NX (slope 0.09 \u00b1 0.06; r = 0.29; P = 0.12) rats. These data indicate that blunted BP responses to l-NAME in the CR rats are associated with BP-independent resistance to nephropathy, possibly mediated by a resistance to the renal (efferent arteriolar) vasoconstrictive effects of NO inhibition.<\/jats:p>","DOI":"10.1152\/ajprenal.00070.2011","type":"journal-article","created":{"date-parts":[[2011,9,22]],"date-time":"2011-09-22T02:23:19Z","timestamp":1316658199000},"page":"F173-F182","source":"Crossref","is-referenced-by-count":20,"title":["Large BP-dependent and -independent differences in susceptibility to nephropathy after nitric oxide inhibition in Sprague-Dawley rats from two major suppliers"],"prefix":"10.1152","volume":"302","author":[{"given":"Karen","family":"Griffin","sequence":"first","affiliation":[{"name":"Departments of 1Medicine and"}]},{"given":"Aaron","family":"Polichnowski","sequence":"additional","affiliation":[{"name":"Departments of 1Medicine and"}]},{"given":"Hector","family":"Licea-Vargas","sequence":"additional","affiliation":[{"name":"Departments of 1Medicine and"}]},{"given":"Maria","family":"Picken","sequence":"additional","affiliation":[{"name":"Department of Electrical and Computer Engineering, Illinois Institute of Technology, Chicago, Illinois"}]},{"given":"Jianrui","family":"Long","sequence":"additional","affiliation":[{"name":"Department of Electrical and Computer Engineering, Illinois Institute of Technology, Chicago, Illinois"}]},{"given":"Geoffrey","family":"Williamson","sequence":"additional","affiliation":[{"name":"Department of Electrical and Computer Engineering, Illinois Institute of Technology, Chicago, Illinois"}]},{"given":"Anil","family":"Bidani","sequence":"additional","affiliation":[{"name":"Departments of 1Medicine and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00349.2004"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.268.5.F885"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00424.2007"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115849"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.256"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.109.133777"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00012.2003"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000060574.38107.3B"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1067\/mob.2001.110448"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1007\/978-3-642-80449-6_1"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00444.2005"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000086476.48686.7D"},{"key":"B13","doi-asserted-by":"crossref","first-page":"1498","DOI":"10.1681\/ASN.V571498","volume":"5","author":"Fujihara CK","year":"1995","journal-title":"J Am Soc Nephrol"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00407.2006"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000049881.25304.73"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1993.264.6.R1254"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00401.2003"},{"key":"B18","doi-asserted-by":"crossref","first-page":"2023","DOI":"10.1681\/ASN.V4122023","volume":"4","author":"Griffin KA","year":"1994","journal-title":"J Am Soc Nephrol"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118125"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000036865.22253.D4"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0b013e3282f88a1f"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2005.094888"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)64175-2"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.272.5.F561"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1161\/01.ATV.0000153088.15433.8f"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00374.2004"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006050459"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90450.2008"},{"key":"B29","volume-title":"Renal Disease Caused by Hypertension","author":"Olson JL","year":"2005"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.109.139287"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1998.275.5.R1719"},{"key":"B32","first-page":"296","volume":"19","author":"Raij L","year":"1999","journal-title":"Semin Nephrol"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.20.3.298"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00346.2005"},{"key":"B35","doi-asserted-by":"crossref","first-page":"363","DOI":"10.1681\/ASN.V93363","volume":"9","author":"Van Dokkum RP","year":"1998","journal-title":"J Am Soc Nephrol"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1139\/y00-129"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.61.4.531"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.32.6.958"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006070798"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00070.2011","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,12,6]],"date-time":"2021-12-06T01:38:52Z","timestamp":1638754732000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00070.2011"}},"issued":{"date-parts":[[2012,1,1]]},"references-count":39,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2012,1,1]]}},"alternative-id":["10.1152\/ajprenal.00070.2011"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00070.2011","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2012,1,1]]}},{"indexed":{"date-parts":[[2025,11,2]],"date-time":"2025-11-02T16:17:24Z","timestamp":1762100244223},"reference-count":42,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2004,11]]},"abstract":"<jats:p> Oxidant stress is an important contributor to renal dysfunction and hypertension. We have previously demonstrated that regulation of renal oxygen consumption by nitric oxide (NO) is impaired in the kidney of spontaneously hypertensive rats (SHR) due to increased superoxide production. We further explored the mechanisms of enhanced oxidant stress in the kidney of SHR. Suppression of cortical oxygen consumption by bradykinin (BK) or enalaprilat (Enal), which act through stimulation of endogenous NO, was impaired in SHR (BK: \u221214.1 \u00b1 1.2%; Enal: \u221215.5 \u00b1 1.2%) and was restored by addition of apocynin, an inhibitor of assembly of the NAD(P)H oxidase complex (BK: \u221221.0 \u00b1 0.6%; Enal: \u221225.3 \u00b1 1.4%), suggesting this as the source of enhanced superoxide production. Addition of an angiotensin type 1 receptor blocker, losartan, also restored responsiveness to control levels (BK: \u221222.0 \u00b1 1.1%; Enal: \u221223.6 \u00b1 1.3%), suggesting that ANG II is responsible for enhanced oxidase activity. A similar defect in responsiveness to BK and Enal could be induced in Wistar-Kyoto kidneys by ANG II and was reversed by a superoxide scavenger (tempol), apocynin or losartan. Immunoblotting of cortical samples demonstrated enhanced expression of endothelial NO synthase (eNOS 1.9\u00d7) and NAD(P)H oxidase components (gp91<jats:sup> phox<\/jats:sup> 1.6\u00d7 and Rac-1 4.5\u00d7). Expression of SOD-1 and -2 were unchanged, but SOD-3 was significantly decreased in SHR (0.5\u00d7). Thus NO bioavailability is impaired in SHR owing to an ANG II-mediated increase in superoxide production in association with enhanced expression of NAD(P)H oxidase components, despite increased expression of eNOS. Loss of SOD-3, an important superoxide scavenger, may also contribute to enhanced oxidant stress. <\/jats:p>","DOI":"10.1152\/ajprenal.00060.2004","type":"journal-article","created":{"date-parts":[[2004,10,8]],"date-time":"2004-10-08T22:52:57Z","timestamp":1097275977000},"page":"F907-F913","source":"Crossref","is-referenced-by-count":87,"title":["Oxidant stress in kidneys of spontaneously hypertensive rats involves both oxidase overexpression and loss of extracellular superoxide dismutase"],"prefix":"10.1152","volume":"287","author":[{"given":"S.","family":"Adler","sequence":"first","affiliation":[]},{"given":"H.","family":"Huang","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.5.F838"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000019781.90630.0F"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1161\/hy0202.103264"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000057755.02845.F9"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1172\/JCI650"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000043280.65241.04"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1172\/JCI9551"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.130135897"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.86.5.494"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1038\/320454a0"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000018041.48432.B5"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000037063.90643.0B"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1089\/152308602762197443"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00166.x"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa013591"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1161\/hy1101.095331"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000092140.81594.A8"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000092145.90389.65"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00550.2002"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.34.4.539"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000070028.99408.E8"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000039528.49161.E9"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00387.2002"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1161\/hh1701.096037"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1986.250.5.H822"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00605.2001"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.32.1.59"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.33.1.424"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M007597200"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1016\/S0008-6363(03)00424-3"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000079165.84309.4D"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.16.9220"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.31.6.1248"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00702.x"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00670.x"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00711.x"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.36.6.957"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00483.x"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00729.x"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.1.F130"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.40.25804"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00372.x"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00060.2004","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T17:52:57Z","timestamp":1567965177000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00060.2004"}},"issued":{"date-parts":[[2004,11]]},"references-count":42,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2004,11]]}},"alternative-id":["10.1152\/ajprenal.00060.2004"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00060.2004","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2004,11]]}},{"indexed":{"date-parts":[[2025,11,2]],"date-time":"2025-11-02T19:59:06Z","timestamp":1762113546107},"reference-count":75,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2016,3,15]]},"DOI":"10.1152\/ajprenal.00312.2015","type":"journal-article","created":{"date-parts":[[2016,1,20]],"date-time":"2016-01-20T22:09:04Z","timestamp":1453327744000},"page":"F446-F453","source":"Crossref","is-referenced-by-count":7,"title":["Recent advances in immunosuppression and acquired immune tolerance in renal transplants"],"prefix":"10.1152","volume":"310","author":[{"given":"Federica","family":"Casiraghi","sequence":"first","affiliation":[{"name":"IRCCS-Istituto di Ricerche Farmacologiche \u201cMario Negri,\u201d Transplant Research Center \u201cChiara Cucchi de Alessandri e Gilberto Crespi,\u201d Ranica, Bergamo, Italy;"},{"name":"IRCCS-Istituto di Ricerche Farmacologiche \u201cMario Negri,\u201d Clinical Research Center for Rare Diseases \u201cAldo e Cele Dacc\u00f2,\u201d Ranica, Bergamo, Italy;"}]},{"given":"Monica","family":"Cortinovis","sequence":"additional","affiliation":[{"name":"IRCCS-Istituto di Ricerche Farmacologiche \u201cMario Negri,\u201d Transplant Research Center \u201cChiara Cucchi de Alessandri e Gilberto Crespi,\u201d Ranica, Bergamo, Italy;"},{"name":"IRCCS-Istituto di Ricerche Farmacologiche \u201cMario Negri,\u201d Clinical Research Center for Rare Diseases \u201cAldo e Cele Dacc\u00f2,\u201d Ranica, Bergamo, Italy;"}]},{"given":"Norberto","family":"Perico","sequence":"additional","affiliation":[{"name":"IRCCS-Istituto di Ricerche Farmacologiche \u201cMario Negri,\u201d Clinical Research Center for Rare Diseases \u201cAldo e Cele Dacc\u00f2,\u201d Ranica, Bergamo, Italy;"}]},{"given":"Giuseppe","family":"Remuzzi","sequence":"additional","affiliation":[{"name":"IRCCS-Istituto di Ricerche Farmacologiche \u201cMario Negri,\u201d Transplant Research Center \u201cChiara Cucchi de Alessandri e Gilberto Crespi,\u201d Ranica, Bergamo, Italy;"},{"name":"IRCCS-Istituto di Ricerche Farmacologiche \u201cMario Negri,\u201d Clinical Research Center for Rare Diseases \u201cAldo e Cele Dacc\u00f2,\u201d Ranica, Bergamo, Italy;"},{"name":"Unit of Nephrology and Dialysis, Azienda Ospedaliera Papa Giovanni XXIII, Bergamo, Italy; and"},{"name":"Department of Biomedical and Clinical Sciences, University of Milan, Milan, Italy"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2004-04-1559"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-6143.2011.03566.x"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014050480"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0705834104"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-6143.2012.04249.x"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-6143.2012.04115.x"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1097\/MOT.0000000000000035"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1111\/ajt.12459"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014040404"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1111\/ajt.12508"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1101\/cshperspect.a015545"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2011060543"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2010-10-311894"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1111\/ajt.12589"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1186\/scrt75"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-6143.2010.03016.x"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1097\/TP.0000000000000243"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2249.2009.03874.x"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-6143.2011.03572.x"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2013.183"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra033540"},{"key":"B22","volume":"15","author":"Harland R","year":"2015","journal-title":"Am J Transplant"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-6143.2011.03869.x"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1038\/307168a0"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1111\/ajt.12647"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa071074"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1111\/ajt.12731"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMc1213779"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-6143.2011.03762.x"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004121113"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2002-07-2104"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-6143.2010.03283.x"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-6143.2005.00749.x"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1126\/scitranslmed.3003509"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1097\/TP.0000000000000605"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-6143.2011.03961.x"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1097\/TP.0b013e3181ffbaff"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1097\/01.tp.0000203166.44968.86"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.2337\/dc12-0038"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1097\/00007890-200205150-00005"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1016\/j.molimm.2006.06.026"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1126\/scitranslmed.3010760"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1097\/00000658-195809000-00004"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa020009"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1172\/JCI39933"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1111\/ajt.13480"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1097\/SLA.0b013e3181f3efb0"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2010.162"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1111\/tri.12132"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.04950610"},{"key":"B51","doi-asserted-by":"crossref","first-page":"4542","DOI":"10.4049\/jimmunol.1202710","volume":"190","author":"Reading JL","year":"2013","journal-title":"J Immunol"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1111\/ajt.13132"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1111\/ajt.12460"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-6143.2006.01280.x"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1101\/cshperspect.a015529"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1172\/JCI39922"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa074191"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-6143.2012.03992.x"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMc1107841"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1111\/ajt.13091"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010111160"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1111\/tri.12570"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1097\/00007890-199908270-00006"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1097\/TP.0b013e31820a3068"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1101\/cshperspect.a015552"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.1203261"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1126\/scitranslmed.aaa7721"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.1016\/j.clim.2009.06.001"},{"key":"B69","doi-asserted-by":"publisher","DOI":"10.1097\/TP.0b013e31820c10eb"},{"key":"B70","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-6143.2009.03005.x"},{"key":"B71","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-6143.2011.03785.x"},{"key":"B72","doi-asserted-by":"publisher","DOI":"10.1097\/MOT.0b013e32835a4c0d"},{"key":"B73","doi-asserted-by":"publisher","DOI":"10.1038\/nri3227"},{"key":"B74","doi-asserted-by":"crossref","first-page":"552","DOI":"10.1111\/ajt.12091","volume":"13","author":"Yamashita K","year":"2013","journal-title":"Am J Transplant"},{"key":"B75","doi-asserted-by":"publisher","DOI":"10.1097\/MOT.0000000000000156"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00312.2015","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:32:32Z","timestamp":1567974752000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00312.2015"}},"issued":{"date-parts":[[2016,3,15]]},"references-count":75,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2016,3,15]]}},"alternative-id":["10.1152\/ajprenal.00312.2015"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00312.2015","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2016,3,15]]}},{"indexed":{"date-parts":[[2025,11,1]],"date-time":"2025-11-01T09:13:36Z","timestamp":1761988416648},"reference-count":30,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2012,3,1]]},"abstract":"<jats:p> Salt-sensitive hypertension and chronic kidney disease (CKD) following recovery from acute kidney injury (AKI) may occur secondary to incomplete repair, or by activation of circulating factors stimulated by injury. We created two types of renal injury induced by unilateral ischemia-reperfusion (I\/R); in a direct\/ipsilateral AKI group, rats were subjected to unilateral I\/R and the untouched contralateral kidney was removed by unilateral nephrectomy after 5 wk to isolate effects on the injured kidney. In the remote\/contralateral AKI group, the injured kidney was removed after 5 wk to isolate effects on the untouched kidney. When these animals were subsequently challenged with elevated dietary sodium for an additional 4 wk (0.4 to 4%), both remote\/contralateral and direct\/ipsilateral AKI rats manifested a significant increase in blood pressure relative to sham-operated controls. Similarly, in acute studies, both ipsilateral and contralateral kidneys had impaired pressure natriuresis and hemodynamic responses. Reductions in vascular density were observed following direct\/ipsilateral injury, but were not observed in the remote\/contralateral kidney. However, both remote\/contralateral and direct\/ipsilateral kidneys contained interstitial cells, some of which were identified as activated (low CD62L\/CD4+) T lymphocytes. In contrast, only the direct\/ipsilateral AKI group demonstrated significant CKD following exposure to elevated salt. This was characterized by a significant reduction in creatinine clearance, an increase in albuminuria, and a dramatic expansion of interstitial inflammation. Taken together, these data suggest that the salt-sensitive features of AKI on hypertension and CKD are segregable such that effects on hemodynamics and hypertension occur independent of direct renal damage. However, prior direct injury to the kidney is required to elicit the full manifestation of CKD induced by elevated sodium intake. <\/jats:p>","DOI":"10.1152\/ajprenal.00562.2011","type":"journal-article","created":{"date-parts":[[2011,11,24]],"date-time":"2011-11-24T04:08:52Z","timestamp":1322107732000},"page":"F625-F635","source":"Crossref","is-referenced-by-count":43,"title":["Distinct effects on long-term function of injured and contralateral kidneys following unilateral renal ischemia-reperfusion"],"prefix":"10.1152","volume":"302","author":[{"given":"David P.","family":"Basile","sequence":"first","affiliation":[{"name":"Department of Cellular and Integrative Physiology,"}]},{"given":"Ellen C.","family":"Leonard","sequence":"additional","affiliation":[{"name":"Department of Cellular and Integrative Physiology,"}]},{"given":"Deoye","family":"Tonade","sequence":"additional","affiliation":[]},{"given":"Jessica L.","family":"Friedrich","sequence":"additional","affiliation":[{"name":"Department of Cellular and Integrative Physiology,"}]},{"given":"Shreevrat","family":"Goenka","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Indiana University, Indianapolis, Indiana"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010030233"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00269.2005"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00169.2002"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00050.2001"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00596.2007"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00546.2010"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.761_2.x"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00229.2005"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00163.x"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00298.2009"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00454.2010"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2009.080295"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-010-1653-4"},{"key":"B14","author":"Grams ME","journal-title":"Kidney Int"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00023.2007"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007080837"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1038\/labinvest.2008.124"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00099.2008"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00321.2002"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1991.260.6.R1200"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00821.2007"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.91022.2008"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00448.2009"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.12.2.168"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00279.2006"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119632"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1973.134"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00017.2010"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1038\/nm.2144"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00061.2009"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00562.2011","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T00:20:53Z","timestamp":1567988453000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00562.2011"}},"issued":{"date-parts":[[2012,3,1]]},"references-count":30,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2012,3,1]]}},"alternative-id":["10.1152\/ajprenal.00562.2011"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00562.2011","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2012,3,1]]}},{"indexed":{"date-parts":[[2025,11,2]],"date-time":"2025-11-02T16:33:23Z","timestamp":1762101203045},"reference-count":33,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2011,10]]},"abstract":"<jats:p>We hypothesized that the calcineurin-nuclear factor of activated T-cells (NFAT) pathway is activated following partial bladder outlet obstruction (pBOO), which would allow for pharmacologic treatment to prevent the ensuing bladder wall hypertrophy. Using a model of pBOO in male mice, we were able to demonstrate increased nuclear importation of the transcription factors NFAT and myocyte enhanching factor 2 both of which are under control of calcineurin in both the whole bladder wall as well as the urothelium. We further confirmed that this pathway was activated using transgenic mice containing an NFAT-luciferase reporter construct. Mice were randomized following pBOO to treatment with or without cyclosporine A (CsA), a known inhibitor of calcineurin. The bladder-to-body mass ratio (mg bladder wt\/g body wt) of 0.95 \u00b1 0.03 in shams increased to 3.1 \u00b1 0.35 following pBOO, and it dropped back to 1.7 \u00b1 0.22 in the CsA+ group ( P &lt; 0.001). Luciferase values (RLU) of 1,130 \u00b1 133 in shams increased to 2,010 \u00b1 474 following pBOO and were suppressed to 562 \u00b1 177 in the CsA+ group ( P &lt; 0.05). The myosin heavy chain mRNA (A\/B) isoform ratio of 0.07 \u00b1 0.03 in shams increased to 1.04 \u00b1 0.19 following pBOO but it diminished to 0.24 \u00b1 0.1 in the CsA+ group ( P &lt; 0.001). In vitro whole organ physiology studies demonstrated improved responses in those bladders from mice treated with CsA. The mRNAs for all four known calcineurin-responsive NFAT isoforms are expressed in the bladder wall, although NFATc<jats:sub>3<\/jats:sub>and NFATc<jats:sub>4<\/jats:sub>predominate. Both NFATc3 and NFATc4 are expressed in urothelial as well as smooth muscle cells. We conclude that pBOO activates the calcineurin-NFAT pathway and that CsA treatment decreased bladder hypertrophy, shifted the pattern of myosin isoform mRNA expression back toward that seen in normal controls, and resulted in improved in vitro whole organ performance.<\/jats:p>","DOI":"10.1152\/ajprenal.00586.2010","type":"journal-article","created":{"date-parts":[[2011,7,21]],"date-time":"2011-07-21T02:24:52Z","timestamp":1311215092000},"page":"F813-F822","source":"Crossref","is-referenced-by-count":9,"title":["Calcineurin mediates bladder wall remodeling secondary to partial outlet obstruction"],"prefix":"10.1152","volume":"301","author":[{"given":"Andy Y.","family":"Chang","sequence":"first","affiliation":[{"name":"John W. Duckett Jr. Center for Pediatric Urology at The Children's Hospital of Philadelphia and"}]},{"given":"Joanna","family":"Sliwoski","sequence":"additional","affiliation":[{"name":"John W. Duckett Jr. Center for Pediatric Urology at The Children's Hospital of Philadelphia and"}]},{"given":"Stephan","family":"Butler","sequence":"additional","affiliation":[{"name":"John W. Duckett Jr. Center for Pediatric Urology at The Children's Hospital of Philadelphia and"}]},{"given":"George","family":"Hearn","sequence":"additional","affiliation":[{"name":"John W. Duckett Jr. Center for Pediatric Urology at The Children's Hospital of Philadelphia and"}]},{"given":"Jenny","family":"Lassmann","sequence":"additional","affiliation":[{"name":"John W. Duckett Jr. Center for Pediatric Urology at The Children's Hospital of Philadelphia and"}]},{"given":"Samuel","family":"Chacko","sequence":"additional","affiliation":[{"name":"The University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania"}]},{"given":"Douglas A.","family":"Canning","sequence":"additional","affiliation":[{"name":"John W. Duckett Jr. Center for Pediatric Urology at The Children's Hospital of Philadelphia and"}]},{"given":"Stephen A.","family":"Zderic","sequence":"additional","affiliation":[{"name":"John W. Duckett Jr. Center for Pediatric Urology at The Children's Hospital of Philadelphia and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1097\/01.ju.0000138045.61378.96"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/ncb1101-1025"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00029.2004"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1203\/PDR.0b013e318180e4c9"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90749.2008"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M600214200"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1172\/JCI10079"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1016\/j.juro.2006.04.027"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(02)00699-2"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00513.2002"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(17)36650-8"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1999.277.2.C343"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(01)00396-8"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1101\/gad.1102703"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0601180103"},{"key":"B16","first-page":"195","volume":"539","author":"Kirsch AJ","year":"2003","journal-title":"Adv Exp Med Biol"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1097\/00005392-199707000-00024"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00477.2007"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00435.2007"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0308703100"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1242\/dev.01576"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.44.27788"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0800969105"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.90.11.4986"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1994.266.1.R20"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(05)67242-4"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00274.2002"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(01)66073-7"},{"key":"B29","doi-asserted-by":"crossref","first-page":"11927","DOI":"10.1016\/S0021-9258(17)32661-3","volume":"269","author":"Waldron RT","year":"1994","journal-title":"J Biol Chem"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000109415.17511.18"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/20.22.6414"},{"key":"B32","first-page":"1061","volume-title":"Adult and Pediatric Urology","author":"Zderic SA","year":"2002"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1038\/gene.2009.66"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00586.2010","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,11,28]],"date-time":"2021-11-28T12:24:23Z","timestamp":1638102263000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00586.2010"}},"issued":{"date-parts":[[2011,10]]},"references-count":33,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2011,10]]}},"alternative-id":["10.1152\/ajprenal.00586.2010"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00586.2010","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2011,10]]}},{"indexed":{"date-parts":[[2025,11,3]],"date-time":"2025-11-03T13:21:30Z","timestamp":1762176090906},"reference-count":58,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2007,5]]},"abstract":"<jats:p>Following a blood meal, the mosquito Aedes aegypti will have acquired an enormous sodium load that must be rapidly excreted to restore ion homeostasis. It is a process that demands robust sodium and fluid transport capabilities. Even though the identities of the components involved in this ion transport across the mosquito Malpighian tubule epithelia have not been completely determined, electrophysiological studies suggest the contribution of a Na<jats:sup>+<\/jats:sup>\/H<jats:sup>+<\/jats:sup>exchanger extruding cations into the lumen driven secondarily by the proton gradient created by the V-type H<jats:sup>+<\/jats:sup>-ATPase in the tubules' apical membrane. We have identified the putative exchanger and designated it AeNHE8. Immunolocalization studies demonstrated that AeNHE8 is expressed in the apical membranes of Malpighian tubules, gastric caecae, and rectum. When heterologously expressed in salt-sensitive yeast cells lacking Na<jats:sup>+<\/jats:sup>extrusion and Na<jats:sup>+<\/jats:sup>\/H<jats:sup>+<\/jats:sup>exchange proteins, AeNHE8 rescues the salt-sensitive phenotype and restores the cells' ability to grow in high NaCl media. Furthermore, heterologous expression of AeNHE8 in NHE-deficient fibroblast cells results in an amiloride-sensitive<jats:sup>22<\/jats:sup>Na<jats:sup>+<\/jats:sup>uptake. To determine the exchanger's kinetic properties, we reconstituted membranes from yeast cells expressing the protein into lipid proteoliposomes and assayed for cation-dependent H<jats:sup>+<\/jats:sup>exchange by fluorimetric methods. Our results indicate that AeNHE8 mediates saturable exchange of Na<jats:sup>+<\/jats:sup>and K<jats:sup>+<\/jats:sup>for H<jats:sup>+<\/jats:sup>. We propose that AeNHE8 may be coupled to the inward H<jats:sup>+<\/jats:sup>gradient across the Malpighian tubules and plays a role in the extrusion of excess sodium and potassium while maintaining steady intracellular pH in the principal cells.<\/jats:p>","DOI":"10.1152\/ajprenal.00487.2005","type":"journal-article","created":{"date-parts":[[2007,2,8]],"date-time":"2007-02-08T01:07:54Z","timestamp":1170896874000},"page":"F1501-F1512","source":"Crossref","is-referenced-by-count":45,"title":["NHE8 mediates amiloride-sensitive Na<sup>+<\/sup>\/H<sup>+<\/sup>exchange across mosquito Malpighian tubules and catalyzes Na<sup>+<\/sup>and K<sup>+<\/sup>transport in reconstituted proteoliposomes"],"prefix":"10.1152","volume":"292","author":[{"given":"Wanyoike","family":"Kang'ethe","sequence":"first","affiliation":[]},{"given":"Karlygash G.","family":"Aimanova","sequence":"additional","affiliation":[]},{"given":"Ashok K.","family":"Pullikuth","sequence":"additional","affiliation":[]},{"given":"Sarjeet S.","family":"Gill","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1002\/1097-010X(20010401\/30)289:4<232::AID-JEZ4>3.0.CO;2-T"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.ph.47.030185.002553"},{"key":"R3","doi-asserted-by":"crossref","unstructured":"Beyenbach KW.Energizing epithelial transport with the vacuolar H+-ATPase.News Physiol Sci16: 145\u2013151, 2001.","DOI":"10.1152\/physiologyonline.2001.16.4.145"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1242\/jeb.00639"},{"key":"R5","doi-asserted-by":"crossref","unstructured":"Beyenbach KW, Pannabecker TL, Nagel W.Central role of the apical membrane H+-ATPase in electrogenesis and epithelial transport in Malpighian tubules.J Exp Biol203: 1459\u20131468, 2000.","DOI":"10.1242\/jeb.203.9.1459"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00360.2004"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1104\/pp.95.1.242"},{"key":"R8","unstructured":"Burckhardt G, Di Sole F, Helmle-Kolb C.The Na+\/H+exchanger gene family.J Nephrol15,Suppl5: S3\u2013S21, 2002."},{"key":"R9","unstructured":"Clements AN.The Biology of Mosquitoes. London: Chapman and Hill, 1992."},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1016\/S0065-2806(02)29004-9"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.90.10.4508"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.275.1.1"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1042\/bj3510241"},{"key":"R14","doi-asserted-by":"crossref","unstructured":"Gan BS, Krump E, Shrode LD, Grinstein S.Loading pyranine via purinergic receptors or hypotonic stress for measurement of cytosolic pH by imaging.Am J Physiol Cell Physiol275: C1158\u2013C1166, 1998.","DOI":"10.1152\/ajpcell.1998.275.4.C1158"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.4.1480"},{"key":"R16","doi-asserted-by":"crossref","unstructured":"Giannakou ME, Dow JA.Characterization of theDrosophila melanogasteralkali-metal\/proton exchanger (NHE) gene family.J Exp Biol204: 3703\u20133716, 2001.","DOI":"10.1242\/jeb.204.21.3703"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00229.2004"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00352.2002"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1002\/arch.10057"},{"key":"R20","doi-asserted-by":"crossref","unstructured":"Harvey WR, Wieczorek H.Animal plasma membrane energization by chemiosmotic H+V-ATPases.J Exp Biol200: 203\u2013216, 1997.","DOI":"10.1242\/jeb.200.2.203"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.2002.tb04747.x"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1242\/jeb.02210"},{"key":"R23","doi-asserted-by":"crossref","unstructured":"Kasahara M, Hinkle PC.Reconstitution and purification of thed-glucose transporter from human erythrocytes.J Biol Chem252: 7384\u20137390, 1977.","DOI":"10.1016\/S0021-9258(19)66976-0"},{"key":"R24","unstructured":"Klowden MJ.Physiological Systems in Insects. San Diego, CA: Academic, 2002."},{"key":"R25","unstructured":"Lepier A, Azuma M, Harvey WR, Wieczorek H.K+\/H+antiport in the tobacco hornworm midgut: the K+-transporting component of the K+pump.J Exp Biol196: 361\u2013373, 1994."},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.24.14838"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1016\/S0223-5234(03)00100-4"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M410041200"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.33.21054"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M203200200"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbamem.2003.07.003"},{"key":"R32","doi-asserted-by":"crossref","unstructured":"Orlowski J.Heterologous expression and functional properties of amiloride high affinity (NHE-1) and low affinity (NHE-3) isoforms of the rat Na\/H exchanger.J Biol Chem268: 16369\u201316377, 1993.","DOI":"10.1016\/S0021-9258(19)85430-3"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-003-1110-3"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.en.40.010195.002425"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.2000.279.6.R1996"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1987.253.5.R701"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-1910(99)00076-1"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.81.15.4833"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(96)00470-X"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1242\/jeb.02419"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1242\/jeb.00641"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-5793(00)01412-5"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.132092099"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1016\/S0005-2736(96)00153-8"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2728(94)90111-2"},{"key":"R46","doi-asserted-by":"crossref","unstructured":"Rodriguez-Navarro A, Ramos J.Dual system for potassium transport inSaccharomyces cerevisiae.J Bacteriol159: 940\u2013945, 1984.","DOI":"10.1128\/JB.159.3.940-945.1984"},{"key":"R47","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1981.61.2.296"},{"key":"R48","doi-asserted-by":"publisher","DOI":"10.2144\/96213bm08"},{"key":"R49","doi-asserted-by":"publisher","DOI":"10.1021\/bi00578a012"},{"key":"R50","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/25.24.4876"},{"key":"R51","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0403087101"},{"key":"R52","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2736(93)90342-W"},{"key":"R53","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M105043200"},{"key":"R54","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M306690200"},{"key":"R55","doi-asserted-by":"publisher","DOI":"10.1242\/jeb.00385"},{"key":"R56","doi-asserted-by":"publisher","DOI":"10.1002\/arch.940070202"},{"key":"R57","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1521-1878(199908)21:8<637::AID-BIES3>3.0.CO;2-W"},{"key":"R58","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.00552.2004"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00487.2005","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,8,8]],"date-time":"2021-08-08T14:05:30Z","timestamp":1628431530000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00487.2005"}},"issued":{"date-parts":[[2007,5]]},"references-count":58,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2007,5]]}},"alternative-id":["10.1152\/ajprenal.00487.2005"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00487.2005","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2007,5]]}},{"indexed":{"date-parts":[[2025,11,13]],"date-time":"2025-11-13T12:28:00Z","timestamp":1763036880007},"reference-count":28,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2003,2,1]]},"abstract":"<jats:p>A<jats:sub>3<\/jats:sub>adenosine receptor (AR) activation and inhibition worsen and improve, respectively, renal function after ischemia-reperfusion (I\/R) injury in rats. We sought to further characterize the role of A<jats:sub>3<\/jats:sub>ARs in modulating renal function after either I\/R or myoglobinuric renal injury. A<jats:sub>3<\/jats:sub>knockout mice had significantly lower plasma creatinines compared with C57 controls 24 h after I\/R or myoglobinuric renal injury. C57 control mice pretreated with the A<jats:sub>3<\/jats:sub>AR antagonist [3-ethyl-5-benzyl-2-methyl-4-phenylethynyl-6-phenyl-1,4-(\u00b1)-dihydropyridine-3,5 dicarboxylate] or agonist [0.125 mg\/kg N<jats:sup>6<\/jats:sup>-(3-iodobenzyl)- N-methyl-5\u2032-carbamoyladenosine (IB-MECA)] demonstrated improved or worsened renal function, respectively, after I\/R or myoglobinuric renal injury. Higher doses of IB-MECA were lethal in C57 mice subjected to renal ischemia. H<jats:sub>1<\/jats:sub>but not H<jats:sub>2<\/jats:sub>histamine receptor antagonist prevented death in mice pretreated with IB-MECA before renal ischemia. Improvement in renal function was associated with significantly improved renal histology. In conclusion, preischemic A<jats:sub>3<\/jats:sub>AR activation (0.125 mg\/kg IB-MECA) exacerbated renal I\/R injury in mice. Mice lacking A<jats:sub>3<\/jats:sub>ARs or blocking A<jats:sub>3<\/jats:sub>ARs in wild-type mice resulted in significant renal protection from ischemic or myoglobinuric renal failure.<\/jats:p>","DOI":"10.1152\/ajprenal.00271.2002","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:37:06Z","timestamp":1425415026000},"page":"F267-F273","source":"Crossref","is-referenced-by-count":78,"title":["A<sub>3<\/sub>adenosine receptor knockout mice are protected against ischemia- and myoglobinuria-induced renal failure"],"prefix":"10.1152","volume":"284","author":[{"given":"H. Thomas","family":"Lee","sequence":"first","affiliation":[{"name":"Department of Anesthesiology and"}]},{"given":"Ayuko","family":"Ota-Setlik","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology and"}]},{"given":"Hua","family":"Xu","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology and"}]},{"given":"Vivette D.","family":"D'Agati","sequence":"additional","affiliation":[{"name":"Department of Pathology, College of Physicians and Surgeons of Columbia University, New York, New York 10032; and"}]},{"given":"Marlene A.","family":"Jacobson","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Merck Research Laboratories, West Point, Pennsylvania 19486"}]},{"given":"Charles W.","family":"Emala","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology and"}]}],"member":"24","reference":[{"key":"B1","first-page":"117","volume":"17","author":"Aronson S","year":"1998","journal-title":"J Cardiothorac Vasc Anesth"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1097\/00007890-200003150-00065"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.2001.281.4.H1751"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1994.266.5.H2042"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1006\/pupt.1999.0191"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/0014-2999(95)00822-5"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1007\/BF02001009"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1006\/jmcc.2001.1338"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/S0008-6363(01)00424-2"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1097\/00007890-198303000-00002"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1016\/S0165-6147(98)01203-6"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/S0028-3908(97)00104-4"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1021\/jm970091j"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.3.F380"},{"key":"B15","first-page":"A407","volume":"95","author":"Lee HT","year":"2001","journal-title":"Anesthesiology"},{"key":"B16","doi-asserted-by":"crossref","first-page":"233","DOI":"10.1681\/ASN.V122233","volume":"12","author":"Lee HT","year":"2001","journal-title":"J Am Soc Nephrol"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1053\/ajkd.2001.26888"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1159\/000065306"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1093\/cvr\/28.7.1057"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.4065\/71.2.117"},{"key":"B21","first-page":"175","volume":"148","author":"McComs PR","year":"1979","journal-title":"Surg Gynecol Obstet"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1007\/s000110050169"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.275.6.4429"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1006\/excr.1998.4134"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0704218"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1172\/JCI8253"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1006\/mvre.2001.2366"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.33.1.511"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00271.2002","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,5,1]],"date-time":"2022-05-01T09:36:13Z","timestamp":1651397773000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00271.2002"}},"issued":{"date-parts":[[2003,2,1]]},"references-count":28,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2003,2,1]]}},"alternative-id":["10.1152\/ajprenal.00271.2002"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00271.2002","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2003,2,1]]}},{"indexed":{"date-parts":[[2025,11,18]],"date-time":"2025-11-18T20:50:10Z","timestamp":1763499010064},"reference-count":26,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2010,12]]},"abstract":"<jats:p>The renal outer medullary K<jats:sup>+<\/jats:sup>(ROMK) channel plays a critical role in renal sodium handling. Recent genome sequencing efforts in the Framingham Heart Study offspring cohort (Ji W, Foo JN, O'Roak BJ, Zhao H, Larson MG, Simon DB, Newton-Cheh C, State MW, Levy D, and Lifton RP. Nat Genet 40: 592\u2013599, 2008) recently revealed an association between suspected loss-of-function polymorphisms in the ROMK channel and resistance to hypertension, suggesting that ROMK activity may also be a determinant of blood pressure control in the general population. Here we examine whether these sequence variants do, in fact, alter ROMK channel function and explore the mechanisms. As assessed by two-microelectrode voltage clamp in Xenopus oocytes, 3\/5 of the variants (R193P, H251Y, and T313FS) displayed an almost complete attenuation of whole cell ROMK channel activity. Surface antibody binding measurements of external epitope-tagged channels and analysis of glycosylation-state maturation revealed that these variants prevent channel expression at the plasmalemma, likely as a consequence of retention in the endoplasmic reticulum. The other variants (P166S, R169H) had no obvious effects on the basal channel activity or surface expression but, instead, conferred a gain in regulated-inhibitory gating. As assessed in giant excised patch-clamp studies, apparent phosphotidylinositol 4,5-bisphosphate (PIP<jats:sub>2<\/jats:sub>) binding affinity of the variants was reduced, causing channels to be more susceptible to inhibition upon PIP<jats:sub>2<\/jats:sub>depletion. Unlike the protein product of the major ROMK allele, these two variants are sensitive to the inhibitory affects of a G protein-coupled receptor, which stimulates PIP<jats:sub>2<\/jats:sub>hydrolysis. In summary, we have found that hypertension resistance sequence variants inhibit ROMK channel function by different mechanisms, providing new insights into the role of the channel in the maintenance of blood pressure.<\/jats:p>","DOI":"10.1152\/ajprenal.00257.2010","type":"journal-article","created":{"date-parts":[[2010,10,7]],"date-time":"2010-10-07T02:33:59Z","timestamp":1286418839000},"page":"F1359-F1364","source":"Crossref","is-referenced-by-count":32,"title":["Hypertension resistance polymorphisms in ROMK (Kir1.1) alter channel function by different mechanisms"],"prefix":"10.1152","volume":"299","author":[{"given":"Liang","family":"Fang","sequence":"first","affiliation":[{"name":"Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland"}]},{"given":"Dimin","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland"}]},{"given":"Paul A.","family":"Welling","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M403413200"},{"key":"B2","doi-asserted-by":"crossref","first-page":"10","DOI":"10.1681\/ASN.V12110","volume":"12","author":"Ecelbarger CA","year":"2001","journal-title":"J Am Soc Nephrol"},{"key":"B3","first-page":"3278","volume":"119","author":"Fang L","year":"2009","journal-title":"J Clin Invest"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.114.5.685"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2002.027581"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1007\/BF00584588"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.09105.x"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/35882"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1038\/ng.118"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1359\/jbmr.1997.12.5.715"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.275.14.10182"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/S0896-6273(02)00725-0"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M206644200"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M608776200"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0504332102"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00608.2009"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.51.36065"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/7.6.975"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.25.15336"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1038\/ng1096-152"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.273.3.F421"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1996.271.1.C103"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00181.2009"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M504836200"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M311599200"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M212301200"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00257.2010","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,11,11]],"date-time":"2021-11-11T11:43:10Z","timestamp":1636630990000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00257.2010"}},"issued":{"date-parts":[[2010,12]]},"references-count":26,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2010,12]]}},"alternative-id":["10.1152\/ajprenal.00257.2010"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00257.2010","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2010,12]]}},{"indexed":{"date-parts":[[2025,12,19]],"date-time":"2025-12-19T21:38:19Z","timestamp":1766180299090,"version":"3.37.3"},"reference-count":36,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2010,8]]},"abstract":"<jats:p>The retina expresses a local renin-angiotensin system (RAS). This study aimed to investigate the influence of systemic modulation of renin synthesis on the expression of renin in the retinal pigment epithelium (RPE), which forms part of the blood\/retina barrier. Freshly isolated RPE cells showed expression of renin 1A, which is the secreted isoform of renin. Systemic administration of the angiotensin-converting enzyme inhibitor enalapril in mice increased the renin expression in both the kidney and the retina. Systemic infusion of ANG II led to a decrease in the renin expression in the kidney and in the retina and RPE. The ANG II-dependent down-regulation of renin expression in the RPE was prevented by systemic application of the AT<jats:sub>1<\/jats:sub>receptor blocker losartan. However, water deprivation lead to an increase of the renin expression in the kidney but unexpectedly to a decrease of the renin expression in the retina. In sections of the mouse retina, the ANG II receptor AT<jats:sub>1<\/jats:sub>was found in the RPE and localized at the blood side of the epithelium. Short-time cultured RPE cells showed increases in intracellular free Ca<jats:sup>2+<\/jats:sup>in response to stimulation by ANG II that were sensitive to losartan. In summary, we conclude that the renin expression in cells of the blood\/retina barrier is influenced by the systemic RAS. ANG II circulating in the plasma is likely a mediator of this influence.<\/jats:p>","DOI":"10.1152\/ajprenal.00576.2009","type":"journal-article","created":{"date-parts":[[2010,6,3]],"date-time":"2010-06-03T02:28:49Z","timestamp":1275532129000},"page":"F396-F403","source":"Crossref","is-referenced-by-count":29,"title":["Regulation of the renin expression in the retinal pigment epithelium by systemic stimuli"],"prefix":"10.1152","volume":"299","author":[{"given":"Vladimir M.","family":"Milenkovic","sequence":"first","affiliation":[{"name":"Experimental Ophthalmology, Eye Hospital, University Medical Center Regensburg, and"}]},{"given":"Marisa","family":"Brockmann","sequence":"additional","affiliation":[{"name":"Experimental Ophthalmology, Eye Hospital, University Medical Center Regensburg, and"}]},{"given":"Christian","family":"Meyer","sequence":"additional","affiliation":[{"name":"Experimental Ophthalmology, Eye Hospital, University Medical Center Regensburg, and"}]},{"given":"Michael","family":"Desch","sequence":"additional","affiliation":[{"name":"Institut f\u00fcr Physiologie, Universit\u00e4t Regensburg, Regensburg, Germany"}]},{"given":"Frank","family":"Schweda","sequence":"additional","affiliation":[{"name":"Institut f\u00fcr Physiologie, Universit\u00e4t Regensburg, Regensburg, Germany"}]},{"given":"Armin","family":"Kurtz","sequence":"additional","affiliation":[{"name":"Institut f\u00fcr Physiologie, Universit\u00e4t Regensburg, Regensburg, Germany"}]},{"given":"Vladimir","family":"Todorov","sequence":"additional","affiliation":[{"name":"Institut f\u00fcr Physiologie, Universit\u00e4t Regensburg, Regensburg, Germany"}]},{"given":"Olaf","family":"Strauss","sequence":"additional","affiliation":[{"name":"Experimental Ophthalmology, Eye Hospital, University Medical Center Regensburg, and"}]}],"member":"24","reference":[{"key":"B1","first-page":"1450","volume":"36","author":"Berka JL","year":"1995","journal-title":"Invest Ophthalmol Vis Sci"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.1993.Supplement_17.27"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.3109\/02713689409047011"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.37.3.967"},{"key":"B5","first-page":"1008","volume":"35","author":"Danser AH","year":"1994","journal-title":"Invest Ophthalmol Vis Sci"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-198900076-00104"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1210\/endo-126-3-1673"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuroscience.2009.02.084"},{"key":"B9","first-page":"876","volume":"29","author":"Ferrari-Dileo G","year":"1988","journal-title":"Invest Ophthalmol Vis Sci"},{"key":"B10","doi-asserted-by":"crossref","first-page":"3440","DOI":"10.1016\/S0021-9258(19)83641-4","volume":"260","author":"Grynkiewicz G","year":"1985","journal-title":"J Biol Chem"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1016\/S0304-3940(97)00520-X"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(96)00077-7"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006060633"},{"key":"B14","first-page":"973","volume":"35","author":"Jacobi PC","year":"1994","journal-title":"Invest Ophthalmol Vis Sci"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1016\/0042-6989(96)00096-X"},{"key":"B16","first-page":"144","volume":"4","author":"Jurklies B","year":"1995","journal-title":"Ger J Ophthalmol"},{"key":"B17","doi-asserted-by":"crossref","first-page":"81","DOI":"10.1016\/S0031-6997(25)06838-3","volume":"32","author":"Keeton TK","year":"1980","journal-title":"Pharmacol Rev"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1017\/S0952523800008762"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.25.5.1111"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1994.267.3.R786"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.33.1.482"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.3181\/00379727-142-37011"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.26.15496"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.3181\/00379727-206-43776"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1007\/s00109-008-0328-0"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002571"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00280.2002"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1167\/iovs.06-1024"},{"key":"B29","doi-asserted-by":"crossref","first-page":"926","DOI":"10.1152\/ajplegacy.1973.224.4.926","volume":"224","author":"Shade RE","year":"1973","journal-title":"Am J Physiol"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1007\/s004240050379"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1007\/BF00158922"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00021.2004"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1080\/02713680490517944"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1186\/gb-2002-3-7-research0034"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000258856.19922.45"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1136\/bjo.80.2.159"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00576.2009","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,2,21]],"date-time":"2025-02-21T15:56:56Z","timestamp":1740153416000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00576.2009"}},"issued":{"date-parts":[[2010,8]]},"references-count":36,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2010,8]]}},"alternative-id":["10.1152\/ajprenal.00576.2009"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00576.2009","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2010,8]]}},{"indexed":{"date-parts":[[2026,1,2]],"date-time":"2026-01-02T14:24:45Z","timestamp":1767363885635,"version":"3.48.0"},"reference-count":110,"publisher":"American Physiological Society","issue":"1","funder":[{"DOI":"10.13039\/100000125","name":"HHS | CDC | National Institute for Occupational Safety and Health","doi-asserted-by":"publisher","award":["R01OH011528"],"award-info":[{"award-number":["R01OH011528"]}],"id":[{"id":"10.13039\/100000125","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2026,1,1]]},"abstract":"<jats:p>Ad libitum fluid intake, consistent with occupational hydration recommendations, does not attenuate renal oxidative stress, inflammation, or acute kidney injury risk during simulated heat stress. These findings challenge the assumption that current hydration recommendations are protective, suggesting that additional strategies are needed to mitigate heat-induced kidney injury in occupational settings.<\/jats:p>","DOI":"10.1152\/ajprenal.00234.2025","type":"journal-article","created":{"date-parts":[[2025,11,14]],"date-time":"2025-11-14T17:30:31Z","timestamp":1763141431000},"page":"F71-F88","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Ad libitum drinking does not mitigate acute kidney injury risk nor elevations in markers of oxidative stress and inflammation during simulated occupational heat stress"],"prefix":"10.1152","volume":"330","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2937-7912","authenticated-orcid":false,"given":"Erica","family":"Tourula","sequence":"first","affiliation":[{"name":"Indiana University School of Public Health-Bloomington","place":["United States"]}]},{"given":"M. Jo","family":"Hite","sequence":"additional","affiliation":[{"name":"Indiana University School of Public Health-Bloomington","place":["United States"]}]},{"given":"Molly E.","family":"Heikkinen","sequence":"additional","affiliation":[{"name":"Indiana University School of Public Health-Bloomington","place":["United States"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8432-7208","authenticated-orcid":false,"given":"Hayden W.","family":"Hess","sequence":"additional","affiliation":[{"name":"Indiana University School of Public Health-Bloomington","place":["United States"]},{"name":"University at Buffalo","place":["United States"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2936-4484","authenticated-orcid":false,"given":"Fabiano T.","family":"Amorim","sequence":"additional","affiliation":[{"name":"University of New Mexico","place":["United States"]}]},{"given":"Timothy D.","family":"Mickleborough","sequence":"additional","affiliation":[{"name":"Indiana University School of Public Health-Bloomington","place":["United States"]},{"name":"Chulalongkorn University","place":["Thailand"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1731-4415","authenticated-orcid":false,"given":"Blair D.","family":"Johnson","sequence":"additional","affiliation":[{"name":"Indiana University School of Public Health-Bloomington","place":["United States"]}]},{"given":"David","family":"Hostler","sequence":"additional","affiliation":[{"name":"University at Buffalo","place":["United States"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3590-3958","authenticated-orcid":false,"given":"Zachary J.","family":"Schlader","sequence":"additional","affiliation":[{"name":"Indiana University School of Public Health-Bloomington","place":["United States"]}]}],"member":"24","reference":[{"key":"B1","unstructured":"International Labour Organization. Heat at Work: Implications for Safety and Health (Online). International Labour Organization. https:\/\/www.ilo.org\/publications\/heat-work-implications-safety-and-health [2024 Oct 16]."},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/j.ekir.2017.08.012"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.13841215"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1136\/oemed-2020-106406"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1136\/oemed-2021-107933"},{"key":"B6","doi-asserted-by":"publisher","unstructured":"Strasma A, Sinclair MR, Park LP, Zhang HH, Mandayam SA, Shah MK, Wyatt CM, Fischer RSB. Chronic kidney disease of unknown etiology (CKDu) as an underappreciated cause of emergent hemodialysis utilization in the United States (Preprint). medRxiv 2025.02.28.25323090, 2025. doi:10.1101\/2025.02.28.25323090.","DOI":"10.1101\/2025.02.28.25323090"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.00787.2019"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.00601.2021"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.34067\/KID.0000000000000288"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00374.2019"},{"key":"B11","unstructured":"Rowell L. Human Circulation: Regulation During Physical Stress (Online). Oxford University Press. https:\/\/www.semanticscholar.org\/paper\/Human-Circulation%3A-Regulation-During-Physical-Rowell\/3194b81bc95a0bf684d63b7881d991cc3cc7835e [2023 Mar 20]."},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/jappl.1949.2.4.185"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1111\/1440-1681.12031"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006010017"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.3390\/nu12061639"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0000000000001050"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.00590.2024"},{"key":"B18","unstructured":"Jacklitsch BL, Williams WJ, Musolin K, Coca A, Kim JH, Turner N. Occupational Exposure to Heat and Hot Environments: Revised Criteria 2016 (Online). CDC. https:\/\/stacks.cdc.gov\/view\/cdc\/37911 [2025 Mar 19]."},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1002\/ajim.70022"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1080\/23328940.2022.2094160"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1096\/fasebj.2022.36.S1.R5231"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1249\/01.MSS.0000078924.61453.FB"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1186\/1479-5868-8-115"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2012.240739"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/jappl.1964.19.3.531"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/S0735-1097(00)01054-8"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1249\/00005768-198205000-00012"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1249\/00149619-200308000-00006"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1002\/cphy.c130017"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.2165\/00007256-200131100-00001"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1016\/S2542-5196(18)30237-7"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0205321"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1016\/0013-9351(67)90002-3"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/jappl.1974.37.2.247"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.2147\/IJNRD.S198222"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1186\/cc12503"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1515\/cclm-2016-0973"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1089\/jir.2008.0027"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.3389\/fimmu.2023.1303076"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1016\/j.jtherbio.2022.103433"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.3390\/ijms241914725"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1016\/j.intimp.2021.107598"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0265619"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2020040487"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.3390\/biomedicines10071757"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00381.2013"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.3389\/fonc.2023.1080237"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1186\/s12885-021-09055-1"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1007\/s00345-021-03900-5"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1016\/j.jjcc.2014.02.016"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1007\/BF01296004"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1186\/s12986-016-0089-7"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.3390\/biology12081088"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1007\/s00421-021-04603-w"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1007\/s00421-017-3781-z"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1080\/02640414.2018.1478612"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.3390\/nu15010216"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1139\/apnm-2018-0057"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1016\/j.jsams.2017.12.014"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1007\/s00421-017-3582-4"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1002\/1873-3468.14328"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1113\/EP092204"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1123\/ijspp.2019-0973"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1123\/ijsnem.2020-0367"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00034.2024"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1016\/j.jacc.2005.08.071"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1016\/S0008-6363(96)00128-9"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.3389\/fphys.2018.01928"},{"key":"B69","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.00328.2024"},{"key":"B70","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-8986.1993.tb02058.x"},{"key":"B71","doi-asserted-by":"publisher","DOI":"10.1038\/s41393-017-0037-z"},{"key":"B72","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.00314.2017"},{"key":"B73","doi-asserted-by":"publisher","DOI":"10.1249\/01.mss.0000222848.35004.41"},{"key":"B74","doi-asserted-by":"publisher","DOI":"10.1007\/s42978-024-00302-y"},{"key":"B75","doi-asserted-by":"publisher","DOI":"10.1249\/mss.0b013e31802ca597"},{"key":"B76","doi-asserted-by":"publisher","DOI":"10.1152\/jappl.1978.45.3.414"},{"key":"B77","doi-asserted-by":"publisher","DOI":"10.15585\/mmwr.mm6726a1"},{"key":"B78","unstructured":"National Institute for Occupational Safety and Health (NIOSH). Work Practices Guide for Manual Lifting (DHHS (NIOSH) Publication No. 81-122). U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control, 1981."},{"key":"B79","doi-asserted-by":"publisher","DOI":"10.1093\/annweh\/wxae097"},{"key":"B80","doi-asserted-by":"publisher","DOI":"10.1299\/jsmec.45.1073"},{"key":"B81","unstructured":"CDC. Heat Stress \u2013 Recommendations (Online). CDC. https:\/\/www.cdc.gov\/niosh\/topics\/heatstress\/recommendations.html [2023 Aug 4]."},{"key":"B82","doi-asserted-by":"publisher","DOI":"10.1093\/jat\/33.1.1"},{"key":"B83","doi-asserted-by":"publisher","DOI":"10.1016\/j.envres.2015.07.007"},{"key":"B84","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.00555.2023"},{"key":"B85","doi-asserted-by":"publisher","DOI":"10.1007\/s00421-021-04804-3"},{"key":"B86","doi-asserted-by":"publisher","DOI":"10.1080\/23328940.2020.1826841"},{"key":"B87","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00271.2016"},{"key":"B88","doi-asserted-by":"publisher","DOI":"10.1080\/15459624.2024.2315161"},{"key":"B89","doi-asserted-by":"publisher","DOI":"10.1007\/s10157-018-1559-1"},{"key":"B90","doi-asserted-by":"publisher","DOI":"10.1249\/00005768-198910001-00003"},{"key":"B91","doi-asserted-by":"publisher","DOI":"10.23736\/S0022-4707.23.15306-0"},{"key":"B92","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.00739.2019"},{"key":"B93","doi-asserted-by":"publisher","DOI":"10.1007\/s11255-013-0528-6"},{"key":"B94","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.00403.2019"},{"key":"B95","doi-asserted-by":"publisher","DOI":"10.1007\/978-94-007-7699-9_28"},{"key":"B96","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.00728.2023"},{"key":"B97","doi-asserted-by":"publisher","DOI":"10.1113\/EP088637"},{"key":"B98","doi-asserted-by":"publisher","DOI":"10.3390\/antiox12030642"},{"key":"B99","doi-asserted-by":"publisher","DOI":"10.1038\/s41420-024-02210-0"},{"key":"B100","doi-asserted-by":"publisher","DOI":"10.1055\/s-2007-965163"},{"key":"B101","doi-asserted-by":"publisher","DOI":"10.1007\/s40279-016-0654-2"},{"key":"B102","doi-asserted-by":"publisher","DOI":"10.1016\/j.ekir.2025.05.044"},{"key":"B103","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2015.12.033"},{"key":"B104","doi-asserted-by":"publisher","DOI":"10.1016\/j.ekir.2025.06.011"},{"key":"B105","doi-asserted-by":"publisher","DOI":"10.1097\/JOM.0000000000001261"},{"key":"B106","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00103.2021"},{"key":"B107","doi-asserted-by":"publisher","DOI":"10.1097\/JOM.0000000000002531"},{"key":"B108","doi-asserted-by":"publisher","unstructured":"Schlader ZJ, Boswell T, Prince H, Wesseling C, Amorim FA, Neupane D, Arias E, Poveda S, Hansson E, Lucas RAI, Jakobsson K, Wegman DH, Glaser J. A rest-shade-hydration-hygiene program reduces acute kidney injury and increases production at a sugar mill in Nicaragua, an economic analysis (Preprint). medRxiv 2025.02.19.25322486, 2025. doi:10.1101\/2025.02.19.25322486. 40034750","DOI":"10.1101\/2025.02.19.25322486"},{"key":"B109","unstructured":"CDC. Workplace Recommendations. (Online). CDC. https:\/\/www.cdc.gov\/niosh\/heat-stress\/recommendations\/index.html [2025 Apr 19]."},{"key":"B110","unstructured":"U.S. Department of Labor. Heat - Water. Rest. Shade | Occupational Safety and Health Administration (Online). U.S. Department of Labor. https:\/\/www.osha.gov\/heat-exposure\/water-rest-shade [2025 Apr 19]."}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00234.2025","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,1,2]],"date-time":"2026-01-02T14:23:57Z","timestamp":1767363837000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00234.2025"}},"issued":{"date-parts":[[2026,1,1]]},"references-count":110,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2026,1,1]]}},"alternative-id":["10.1152\/ajprenal.00234.2025"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00234.2025","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2026,1,1]]},"assertion":[{"value":"2025-06-13","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2025-08-04","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2025-11-12","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2026-01-02","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,1,2]],"date-time":"2026-01-02T07:36:48Z","timestamp":1767339408181,"version":"3.41.0"},"reference-count":45,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2000,4,1]]},"abstract":"<jats:p>Unique barrier properties of the urothelial surface membrane permit urine storage. Interstitial cystitis causes disabling dysuria, and frequency. Similarly, feline interstitial cystitis (FIC) occurs in cats. These studies define the permeability and structural properties of normal and FIC urothelium. To determine the effects of bladder filling, groups were studied before and after hydrodistention. Normal urothelium with or without hydrodistention exhibited high transepithelial resistances (TER) and low water and urea permeabilities, resembling other species. Fluorescence confocal microscopy revealed localization of the marker AE-31 to the apical surface of all umbrella cells in normal urothelium, with the tight junction protein ZO-1 localized to tight junctions. Scanning and transmission electron microscopy revealed uniform distribution of luminal cells with characteristic apical membrane and tight junction morphology. Urothelium in FIC animals displayed reduced TER and increased water and urea permeability following hydrodistention. Structural studies in FIC revealed denuded urothelium, with appearance of AE-31 in underlying epithelial cells. The results demonstrate severe epithelial damage and dysfunction in FIC and suggest novel approaches toward examining the etiology and therapy of IC.<\/jats:p>","DOI":"10.1152\/ajprenal.2000.278.4.f540","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T13:15:04Z","timestamp":1514034904000},"page":"F540-F553","source":"Crossref","is-referenced-by-count":121,"title":["Urothelial pathophysiological changes in feline interstitial cystitis: a human model"],"prefix":"10.1152","volume":"278","author":[{"given":"John P.","family":"Lavelle","sequence":"first","affiliation":[{"name":"Department of Urology, and"}]},{"given":"Susan A.","family":"Meyers","sequence":"additional","affiliation":[{"name":"Laboratory of Epithelial Cell Biology, Renal-Electrolyte Division, Department of Medicine, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania 15213; and"}]},{"given":"W. Giovani","family":"Ruiz","sequence":"additional","affiliation":[{"name":"Laboratory of Epithelial Cell Biology, Renal-Electrolyte Division, Department of Medicine, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania 15213; and"}]},{"given":"C. A. Tony","family":"Buffington","sequence":"additional","affiliation":[{"name":"Ohio State University Veterinary Hospital, Columbus, Ohio 43210-1089"}]},{"given":"Mark L.","family":"Zeidel","sequence":"additional","affiliation":[{"name":"Laboratory of Epithelial Cell Biology, Renal-Electrolyte Division, Department of Medicine, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania 15213; and"}]},{"given":"Gerard","family":"Apodaca","sequence":"additional","affiliation":[{"name":"Laboratory of Epithelial Cell Biology, Renal-Electrolyte Division, Department of Medicine, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania 15213; and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.125.1.67"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(01)64018-7"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.12-12-04878.1992"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1993.265.2.R326"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.109.6.3243"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1093\/jn\/124.suppl_12.2643S"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(01)66201-3"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1016\/S0195-5616(96)50212-3"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1994.267.5.C1483"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(17)45763-6"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1016\/S0090-4295(99)80329-X"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1159\/000282832"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(17)43863-8"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.103.5.1767"},{"key":"B15","doi-asserted-by":"crossref","first-page":"818","DOI":"10.1016\/S0022-3565(25)23839-3","volume":"271","author":"Gao X","year":"1994","journal-title":"J Pharmacol Exp Ther"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1988.255.2.F324"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.28.1.21"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-185X.1975.tb01057.x"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1098\/rstb.1974.0013"},{"key":"B20","first-page":"103","volume":"167","author":"Jost SP","year":"1989","journal-title":"J Anat"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1038\/339478a0"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.99.3.435"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.1.F205"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(17)41173-6"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1995.75.3.561"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1038\/297685a0"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/0076-6879(90)92100-R"},{"key":"B28","first-page":"77","volume":"151","author":"Maggi A.","year":"1990","journal-title":"Ciba Found Symp"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.77.3.685"},{"key":"B30","doi-asserted-by":"crossref","first-page":"2253","DOI":"10.1128\/JCM.25.12.2253-2257.1987","volume":"25","author":"Mobley HL","year":"1987","journal-title":"J Clin Microbiol"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(01)65933-0"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.4.F886"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1111\/1523-1747.ep12494172"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1016\/S0090-4295(97)00181-7"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1016\/S0090-4295(97)00180-5"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(17)39897-X"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(17)38437-9"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1002\/nau.1930130503"},{"key":"B39","first-page":"17","volume":"29","author":"Sant GR.","year":"1987","journal-title":"Urology"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1016\/S0090-4295(94)80074-X"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.53.1.73"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.125.1.171"},{"key":"B43","first-page":"4","volume":"1","author":"Yu J","year":"1992","journal-title":"Epithelial Cell Biol"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.111.3.1207"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.2.F243"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.2000.278.4.F540","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,6,29]],"date-time":"2025-06-29T04:37:21Z","timestamp":1751171841000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.2000.278.4.F540"}},"issued":{"date-parts":[[2000,4,1]]},"references-count":45,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2000,4,1]]}},"alternative-id":["10.1152\/ajprenal.2000.278.4.F540"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.2000.278.4.f540","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2000,4,1]]}},{"indexed":{"date-parts":[[2026,1,3]],"date-time":"2026-01-03T15:08:52Z","timestamp":1767452932575},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1990,2,1]]},"abstract":"<jats:p> Brush-border membrane vesicles (BBMV) were prepared from rat and human renal cortical tissue by magnesium aggregation and differential centrifugation, and the uptake of L-cystine, L-cysteine, and L-cysteine-D-penicillamine were assessed by a rapid-filtration technique. L-Cystine uptake was relatively sodium independent and associated with membrane binding. Sodium-stimulated uptake was sensitive to a cation but not anion diffusion potential. Both sodium-independent and sodium-stimulated uptake rates were inhibited by the cationic L-amino acids and by some neutral L-amino acids. The uptake rates of L-cysteine and L-cysteine-D-penicillamine were more sodium dependent, and sodium-stimulated uptake rates were more sensitive to cation and anion diffusion potentials. Neither the sodium-independent nor the sodium-stimulated uptake rates of L-cysteine or L-cysteine-D-penicillamine were inhibited by the cationic L-amino acids. L-Cysteine-D-penicillamine showed relatively little membrane binding. It is concluded that L-cystine is transported into renal cortical BBMV by pathways distinct from those concerned with the transport of L-cysteine and L-cysteine-D-penicillamine, and it is postulated that these differences may account for some of the effects of D-penicillamine in cystinuria. <\/jats:p>","DOI":"10.1152\/ajprenal.1990.258.2.f321","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T21:33:17Z","timestamp":1513978397000},"page":"F321-F327","source":"Crossref","is-referenced-by-count":2,"title":["D-penicillamine and the transport of L-cystine by rat and human renal cortical brush-border membrane vesicles"],"prefix":"10.1152","volume":"258","author":[{"given":"T. J.","family":"Furlong","sequence":"first","affiliation":[{"name":"Department of Medicine, Royal North Shore Hospital, St. Leonards, NewSouth Wales, Australia."}]},{"given":"S.","family":"Posen","sequence":"additional","affiliation":[{"name":"Department of Medicine, Royal North Shore Hospital, St. Leonards, NewSouth Wales, Australia."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1990.258.2.F321","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:11:50Z","timestamp":1567969910000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1990.258.2.F321"}},"issued":{"date-parts":[[1990,2,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1990,2,1]]}},"alternative-id":["10.1152\/ajprenal.1990.258.2.F321"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1990.258.2.f321","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1990,2,1]]}},{"indexed":{"date-parts":[[2025,12,31]],"date-time":"2025-12-31T07:58:51Z","timestamp":1767167931046,"version":"build-2238731810"},"update-to":[{"DOI":"10.1152\/ajprenal.00620.2016","type":"retraction","label":"Retraction","source":"retraction-watch","updated":{"date-parts":[[2017,10,1]],"date-time":"2017-10-01T00:00:00Z","timestamp":1506816000000},"record-id":"13406"}],"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2017,10,1]]},"DOI":"10.1152\/ajprenal.zh2-8358.retr-2017","type":"journal-article","created":{"date-parts":[[2017,10,9]],"date-time":"2017-10-09T20:25:30Z","timestamp":1507580730000},"page":"F1060-F1060","source":"Crossref","is-referenced-by-count":0,"title":["Retraction"],"prefix":"10.1152","volume":"313","member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.zh2-8358.retr-2017","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T21:17:22Z","timestamp":1567977442000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.zh2-8358.retr-2017"}},"issued":{"date-parts":[[2017,10,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2017,10,1]]}},"alternative-id":["10.1152\/ajprenal.zh2-8358.retr-2017"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.zh2-8358.retr-2017","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2017,10,1]]}},{"indexed":{"date-parts":[[2026,2,20]],"date-time":"2026-02-20T22:36:45Z","timestamp":1771627005972,"version":"3.50.1"},"reference-count":58,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2007,11]]},"abstract":"<jats:p>Autoregulation of renal blood flow (RBF) is mediated by a fast myogenic response (MR; \u223c5 s), a slower tubuloglomerular feedback (TGF; \u223c25 s), and potentially additional mechanisms. A<jats:sub>1<\/jats:sub>adenosine receptors (A1AR) mediate TGF in superficial nephrons and contribute to overall autoregulation, but the impact on the other autoregulatory mechanisms is unknown. We studied dynamic autoregulatory responses of RBF to rapid step increases of renal artery pressure in mice. MR was estimated from autoregulation within the first 5 s, TGF from that at 5\u201325 s, and a third mechanism from 25\u2013100 s. Genetic deficiency of A1AR (A1AR\u2212\/\u2212) reduced autoregulation at 5\u201325 s by 50%, indicating a residual fourth mechanism resembling TGF kinetics but independent of A1AR. MR and third mechanism were unaltered in A1AR\u2212\/\u2212. Autoregulation in A1AR\u2212\/\u2212 was faster at 5\u201325 than at 25\u2013100 s suggesting two separate mechanisms. Furosemide in wild-type mice (WT) eliminated the third mechanism and enhanced MR, indicating TGF-MR interaction. In A1AR\u2212\/\u2212, furosemide did not further impair autoregulation at 5\u201325 s, but eliminated the third mechanism and enhanced MR. The resulting time course was the same as during furosemide in WT, indicating that A1AR do not affect autoregulation during furosemide inhibition of TGF. We conclude that at least one novel mechanism complements MR and TGF in RBF autoregulation, that is slower than MR and TGF and sensitive to furosemide, but not mediated by A1AR. A fourth mechanism with kinetics similar to TGF but independent of A1AR and furosemide might also contribute. A1AR mediate classical TGF but not TGF-MR interaction.<\/jats:p>","DOI":"10.1152\/ajprenal.00256.2007","type":"journal-article","created":{"date-parts":[[2007,8,30]],"date-time":"2007-08-30T00:59:32Z","timestamp":1188435572000},"page":"F1489-F1500","source":"Crossref","is-referenced-by-count":35,"title":["A novel mechanism of renal blood flow autoregulation and the autoregulatory role of A<sub>1<\/sub>adenosine receptors in mice"],"prefix":"10.1152","volume":"293","author":[{"given":"Armin","family":"Just","sequence":"first","affiliation":[]},{"given":"William J.","family":"Arendshorst","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","unstructured":"Arendshorst WJ, Brannstrom K, Ruan X.Actions of angiotensin II on the renal microvasculature.J Am Soc Nephrol10,Suppl11: S149\u2013S161, 1999."},{"key":"R2","unstructured":"Arendshorst WJ, Navar LG.Renal circulation and glomerular hemodynamics. In:Diseases of the Kidney and Urinary Tract, edited by Schrier RW. Philadelphia, PA: Lippincott Williams & Wilkins, 2006, p. 59\u2013107."},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1978.234.2.F154"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.2001.281.5.R1362"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.267.1.F160"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1988.254.4.F601"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1992.tb09297.x"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.264.3.F515"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.270.1.F82"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.259.3.F529"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.258.6.F1479"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1990.259.6.H1890"},{"key":"R13","unstructured":"Grande PO.Dynamic and static components in the myogenic control of vascular tone in cat skeletal muscle.Acta Physiol Scand Suppl476: 1\u201344, 1979."},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00381.2005"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.256.6.F1007"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.260.1.F53"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-201X.2004.01317.x"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1172\/JCI18499"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.36.1.76"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00766.2002"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2005.094888"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.6.F1062"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2001.012593"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.1998.275bx.x"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.00359.2005"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1998.275.2.H467"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-201X.2004.01319.x"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1983.tb00015.x"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00515.2006"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000024262.11534.18"},{"key":"R31","doi-asserted-by":"crossref","unstructured":"Majid DS, Inscho EW, Navar LG.P2 purinoceptor saturation by adenosine triphosphate impairs renal autoregulation in dogs.J Am Soc Nephrol10: 492\u2013498, 1999.","DOI":"10.1681\/ASN.V103492"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00539.2004"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1998.274.2.R564"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.2003.tb07281.x"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.264.3.F458"},{"key":"R36","unstructured":"Moore LC.Interaction of tubuloglomerular feedback and proximal nephron reabsorption in autoregulation.Kidney Int Suppl12: S173\u2013S178, 1982."},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1007\/BF02460464"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1993.tb09532.x"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1996.76.2.425"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00242.2005"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00073.2007"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00205.2005"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00911.x"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002190"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.256.3.F421"},{"key":"R46","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.65.050102.085738"},{"key":"R47","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.258.3.F553"},{"key":"R48","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000183963.07801.65"},{"key":"R49","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00346.2005"},{"key":"R50","doi-asserted-by":"crossref","unstructured":"Siu KL, Chon KH, Sung B, Birzgalis A, Moore LC.Modulation of autoregulatory mechanisms by very-low frequency (VLF) rhythms in RBF (Abstract).FASEB J20: A761, 2006.","DOI":"10.1096\/fasebj.20.4.A761"},{"key":"R51","doi-asserted-by":"publisher","DOI":"10.1088\/0967-3334\/26\/4\/002"},{"key":"R52","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.171317998"},{"key":"R53","doi-asserted-by":"publisher","DOI":"10.1172\/JCI8761"},{"key":"R54","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1967.47.3.359"},{"key":"R55","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.5.F858"},{"key":"R56","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00343.2006"},{"key":"R57","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00420.2002"},{"key":"R58","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1981.240.5.F446"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00256.2007","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,8,22]],"date-time":"2021-08-22T14:43:32Z","timestamp":1629643412000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00256.2007"}},"issued":{"date-parts":[[2007,11]]},"references-count":58,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2007,11]]}},"alternative-id":["10.1152\/ajprenal.00256.2007"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00256.2007","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2007,11]]}},{"indexed":{"date-parts":[[2026,2,20]],"date-time":"2026-02-20T22:35:53Z","timestamp":1771626953840,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1985,5,1]]},"abstract":"<jats:p> Angiotensin II (ANG II) is a powerful effector agent in the regulation of extracellular volume and exerts an important influence on renal sodium excretion. In addition to its effects on aldosterone secretion, ANG II acts directly on the kidney causing retention of sodium at low (physiological) doses and enhanced sodium excretion at high doses. The mechanism for these responses involves vasoconstrictor actions of ANG II on the renal vasculature and a direct action of the peptide on tubular reabsorption. Micropuncture and microperfusion studies have demonstrated that proximal tubular sodium and water transport are stimulated by physiological concentrations (10(-12) to 10(-10) M) of ANG II on the peritubular side, whereas higher doses (10(-7) M) cause inhibition. A luminal site of action in the proximal tubule has also been reported and additional more distal sites are indicated. [125I]ANG II binding sites on the brush border and basolateral membranes of proximal tubule cells have high affinity (Kd in the nanomolar range) for ANG II and lower affinity for ANG III. The biphasic action of ANG II is exerted directly on the epithelial cells and appears to be electroneutral. The data indicate that ANG II binds to receptors on the basolateral cell membrane and alters the rate of entry of sodium through the luminal membrane to increase or decrease, depending on the concentration of peptide. Several possible cellular mechanisms that could mediate these responses are discussed. <\/jats:p>","DOI":"10.1152\/ajprenal.1985.248.5.f621","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T00:32:13Z","timestamp":1513989133000},"page":"F621-F630","source":"Crossref","is-referenced-by-count":46,"title":["Tubular transport responses to angiotensin"],"prefix":"10.1152","volume":"248","author":[{"given":"P. J.","family":"Harris","sequence":"first","affiliation":[]},{"given":"L. G.","family":"Navar","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1985.248.5.F621","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:32:02Z","timestamp":1567971122000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1985.248.5.F621"}},"issued":{"date-parts":[[1985,5,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1985,5,1]]}},"alternative-id":["10.1152\/ajprenal.1985.248.5.F621"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1985.248.5.f621","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1985,5,1]]}},{"indexed":{"date-parts":[[2026,2,20]],"date-time":"2026-02-20T22:35:55Z","timestamp":1771626955890,"version":"3.50.1"},"reference-count":51,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2003,7]]},"abstract":"<jats:p>Prostanoids derived from endogenous cylooxygenase (COX)-mediated arachidonic acid metabolism play important roles in the maintenance of renal blood flow and salt and water homeostasis. The relative importance of COX-1 and COX-2 isoforms is under active investigation. We have performed a comprehensive histochemical analysis by comparing rat and mouse kidneys for cellular and subcellular localization of COX-1 and -2 and microsomal-type PGE synthase (PGES), the rate-limiting biosynthetic enzyme in PGE<jats:sub>2<\/jats:sub>synthesis. A choice of different sera was compared, and the results were confirmed by antigen-retrieval techniques, in situ hybridization, RT-PCR, and the use of COX knockout mice. In the glomerulus, significant COX-1 expression was detected in a subset of mesangial cells. Along the renal tubule, the known COX-2 expression in cTAL and macula densa was paralleled by PGES staining. In the terminal distal convoluted tubule, connecting tubule, and cortical and medullary collecting ducts, a significant COX-1 signal was colocalized with PGES; COX-2 was not found in these sites. Intercalated cells were generally negative. Cortical fibroblasts were COX-1 and PGES positive in mice, whereas in rats only PGES could be reliably detected. Lipid-laden interstitial cells of the inner medulla were COX-1, -2, and PGES positive. Vascular smooth muscle cells were not stained. The present data support prominent functions of renal prostanoids, predominantly PGE<jats:sub>2<\/jats:sub>, by defining expression sites of the key enzymes for their biosynthesis in the rat and mouse. Results define the renal cell types involved in prostaglandin autacoid functions within spatially restricted sites such as the juxtaglomerular apparatus, mesangium, distal convolutions and collecting duct, and in compartments of the renal interstitium.<\/jats:p>","DOI":"10.1152\/ajprenal.00443.2002","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:38:32Z","timestamp":1425415112000},"page":"F19-F32","source":"Crossref","is-referenced-by-count":95,"title":["Key enzymes for renal prostaglandin synthesis: site-specific expression in rodent kidney (rat, mouse)"],"prefix":"10.1152","volume":"285","author":[{"given":"Valentina","family":"C\u00e2mpean","sequence":"first","affiliation":[]},{"given":"Franziska","family":"Theilig","sequence":"additional","affiliation":[]},{"given":"Alex","family":"Paliege","sequence":"additional","affiliation":[]},{"given":"Matthew","family":"Breyer","sequence":"additional","affiliation":[]},{"given":"Sebastian","family":"Bachmann","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"REF1","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00072.x"},{"key":"REF2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.268.5.F885"},{"key":"REF3","doi-asserted-by":"publisher","DOI":"10.1007\/s004290050294"},{"key":"REF4","doi-asserted-by":"crossref","unstructured":"Bek M, N\u00fcsing R, Kowark P, Henger A, Mundel P, and Pavenst\u00e4dt H.Characterization of prostanoid receptors in podocytes.J Am Soc Nephrol10: 2084-2093, 1999.","DOI":"10.1681\/ASN.V10102084"},{"key":"REF5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.1.F12"},{"key":"REF6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.0148.2001"},{"key":"REF7","doi-asserted-by":"publisher","DOI":"10.1172\/JCI10318"},{"key":"REF8","doi-asserted-by":"publisher","DOI":"10.1172\/JCI5505"},{"key":"REF9","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.85.5.1412"},{"key":"REF10","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00334.x"},{"key":"REF11","doi-asserted-by":"crossref","unstructured":"Ferguson S, H\u00e9bert RL, and Laneuville O.NS-398 upregulates constitutive cyclooxygenase-2 expression in the M-1 cortical collecting duct cell line.J Am Soc Nephrol10: 2261-2271, 1999.","DOI":"10.1681\/ASN.V10112261"},{"key":"REF12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.3.F360"},{"key":"REF13","doi-asserted-by":"publisher","DOI":"10.1172\/JCI13241"},{"key":"REF14","doi-asserted-by":"publisher","DOI":"10.1172\/JCI2872"},{"key":"REF15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.0116.2001"},{"key":"REF16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.3.F352"},{"key":"REF17","doi-asserted-by":"crossref","unstructured":"Harris RC.Cyclooxygenase-2 in the kidney.J Am Soc Nephrol11: 2387-2394, 2000.","DOI":"10.1681\/ASN.V11122387"},{"key":"REF18","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9149(02)02404-9"},{"key":"REF19","doi-asserted-by":"crossref","unstructured":"Harris RCand Breyer MD.Physiological regulation of cyclooxygenase-2 in the kidney.Am J Physiol Renal Physiol281: F1-F11, 2001.","DOI":"10.1152\/ajprenal.2001.281.1.F1"},{"key":"REF20","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117620"},{"key":"REF21","doi-asserted-by":"publisher","DOI":"10.1007\/PL00000215"},{"key":"REF22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.265.5.F643"},{"key":"REF23","doi-asserted-by":"publisher","DOI":"10.1007\/s004410000296"},{"key":"REF24","unstructured":"Jakobsson PJ, Thor\u00e9n S, Morgenstern R, and Samuelsson B.Identification of human prostaglandin E synthase: a microsomal, glutathione-dependent, inducible enzyme, constituting a potential novel drug target.Proc Natl Acad Sci USA96: 7720-7225, 1999."},{"key":"REF25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.6.F1001"},{"key":"REF26","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1996.271.1.C354"},{"key":"REF27","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00988.x"},{"key":"REF28","doi-asserted-by":"publisher","DOI":"10.1038\/5583"},{"key":"REF29","doi-asserted-by":"publisher","DOI":"10.1177\/019262339802600504"},{"key":"REF30","doi-asserted-by":"crossref","unstructured":"Kitahara M, Eitner F, Ostendorf T, Kunter U, Janssen U, Westenfeld R, Matsui K, Kerjaschki D, and Floege J.Selective cyclooxygenase-2 inhibition impairs glomerular capillary healing in experimental glomerulonephritis.J Am Soc Nephrol13: 1261-1270, 2002.","DOI":"10.1681\/ASN.V1351261"},{"key":"REF31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.272.4.F460"},{"key":"REF32","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1978.86"},{"key":"REF33","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(95)90125-6"},{"key":"REF34","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-5793(99)01088-1"},{"key":"REF35","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00435.x"},{"key":"REF36","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.37.1.129"},{"key":"REF37","doi-asserted-by":"publisher","DOI":"10.1172\/JCI0214752"},{"key":"REF38","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.3.F367"},{"key":"atypb1","unstructured":"Schneider Aand Stahl R.Cyclooxygenase-2 (COX-2) and the kidney: current status and potential perspectives.Nephrol Dial Transplant13: 10-12, 1998."},{"key":"REF40","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/16.9.1735"},{"key":"REF41","doi-asserted-by":"publisher","DOI":"10.1159\/000063782"},{"key":"REF42","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1978.235.5.F451"},{"key":"REF43","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.biochem.69.1.145"},{"key":"REF44","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.0590041283.x"},{"key":"REF45","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000013082.99285.35"},{"key":"REF46","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.30.3.687"},{"key":"REF47","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00615.x"},{"key":"REF48","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M006218200"},{"key":"REF49","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1999.277.4.Ha1"},{"key":"REF50","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00236.2001"},{"key":"REF51","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.273.6.F994"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00443.2002","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,5,1]],"date-time":"2022-05-01T09:38:00Z","timestamp":1651397880000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00443.2002"}},"issued":{"date-parts":[[2003,7]]},"references-count":51,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2003,7]]}},"alternative-id":["10.1152\/ajprenal.00443.2002"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00443.2002","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2003,7]]}},{"indexed":{"date-parts":[[2026,2,20]],"date-time":"2026-02-20T22:31:27Z","timestamp":1771626687286,"version":"3.50.1"},"reference-count":64,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2001,6,1]]},"abstract":"<jats:p> Na<jats:sup>+<\/jats:sup> absorption in the renal cortical collecting duct (CCD) is mediated by apical epithelial Na<jats:sup>+<\/jats:sup> channels (ENaCs). The CCD is subject to continuous variations in intraluminal flow rate that we speculate alters hydrostatic pressure, membrane stretch, and shear stress. Although ENaCs share limited sequence homology with putative mechanosensitive ion channels in Caenorhabditis elegans,controversy exists as to whether ENaCs are regulated by biomechanical forces. We examined the effect of varying the rate of fluid flow on whole cell Na<jats:sup>+<\/jats:sup> currents ( I <jats:sub>Na<\/jats:sub>) in oocytes expressing mouse \u03b1,\u03b2,\u03b3-ENaC (mENaC) and on net Na<jats:sup>+<\/jats:sup> absorption in microperfused rabbit CCDs. Oocytes injected with mENaC but not water responded to the initiation of superfusate flow (to 4\u20136 ml\/min) with a reversible threefold stimulation of I <jats:sub>Na<\/jats:sub>without a change in reversal potential. The increase in I <jats:sub>Na<\/jats:sub> was variable among oocytes. CCDs responded to a threefold increase in rate of luminal flow with a twofold increase in the rate of net Na<jats:sup>+<\/jats:sup> absorption. An increase in luminal viscosity achieved by addition of 5% dextran to the luminal perfusate did not alter the rate of net Na<jats:sup>+<\/jats:sup> absorption, suggesting that shear stress does not influence Na<jats:sup>+<\/jats:sup> transport in the CCD. In sum, our data suggest that flow stimulation of ENaC activity and Na<jats:sup>+<\/jats:sup> absorption is mediated by an increase in hydrostatic pressure and\/or membrane stretch. We propose that intraluminal flow rate may be an important regulator of channel activity in the CCD. <\/jats:p>","DOI":"10.1152\/ajprenal.2001.280.6.f1010","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T14:14:11Z","timestamp":1514038451000},"page":"F1010-F1018","source":"Crossref","is-referenced-by-count":183,"title":["Epithelial Na<sup>+<\/sup> channels are regulated by flow"],"prefix":"10.1152","volume":"280","author":[{"given":"Lisa M.","family":"Satlin","sequence":"first","affiliation":[{"name":"Department of Pediatrics, Mount Sinai School of Medicine, New York, New York 10029-6574; and"}]},{"given":"Shaohu","family":"Sheng","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania 15261"}]},{"given":"Craig B.","family":"Woda","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Mount Sinai School of Medicine, New York, New York 10029-6574; and"}]},{"given":"Thomas R.","family":"Kleyman","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania 15261"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1996.270.1.C224"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.1.F121"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.53.37834"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1999.277.2.C216"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.112.2.97"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-4899-1775-1_4"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.268.6.F1132"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/367463a0"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1999.276.2.C477"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.4.F861"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.5.2514"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1172\/JCI108073"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1995.75.3.519"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.59.1.527"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.253.5.F896"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.252.3.F458"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.256.1.F143"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/S0960-9822(95)00085-6"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1007\/BF00374984"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.5.F817"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.45.30012"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1172\/JCI106399"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1038\/362031a0"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1038\/367470a0"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1038\/367467a0"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.2.807"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.400"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1007\/BF00374386"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1998.275.5.C1182"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.114.1.13"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1992.263.4.C825"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.94.3.1013"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.266.3.F506"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.270.2.F344"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.256.5.F932"},{"key":"B36","doi-asserted-by":"crossref","first-page":"529","DOI":"10.1152\/ajplegacy.1966.211.3.529","volume":"211","author":"Malnic G","year":"1966","journal-title":"Am J Physiol"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.263.3.F392"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1977.233.6.F544"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.261.4.F696"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.83.8.2767"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.253.2.F333"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.107.1.35"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.262.1.F47"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1038\/46297"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-199409000-00003"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.266.1.F57"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.270.3.F391"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1978.235.6.F576"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1978.235.4.F367"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.275.12.8572"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00919.x"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1981.241.4.F395"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1990.259"},{"key":"B54","doi-asserted-by":"crossref","first-page":"453","DOI":"10.1152\/ajplegacy.1974.227.2.453","volume":"227","author":"Stoner LC","year":"1974","journal-title":"Am J Physiol"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1126\/science.7543698"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.59.1.659"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1161\/01.ATV.18.5.677"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.29.20144"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1038\/39329"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.259.3.F494"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1988.255.4.F720"},{"key":"B63","first-page":"40A","volume":"11","author":"Woda C","year":"2000","journal-title":"J Am Soc Nephrol"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1994.266.3.C809"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.6.F825"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.2001.280.6.F1010","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:57:06Z","timestamp":1567976226000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.2001.280.6.F1010"}},"issued":{"date-parts":[[2001,6,1]]},"references-count":64,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2001,6,1]]}},"alternative-id":["10.1152\/ajprenal.2001.280.6.F1010"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.2001.280.6.f1010","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2001,6,1]]}},{"indexed":{"date-parts":[[2026,2,21]],"date-time":"2026-02-21T03:23:20Z","timestamp":1771644200534,"version":"3.50.1"},"reference-count":44,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1997,10,1]]},"abstract":"<jats:p>Type 1 angiotensin II (ANG II) receptors (AT<jats:sub>1<\/jats:sub>R), which mediate proximal tubule (PT) salt and water reabsorption, undergo endocytosis and recycling. Prior studies in a PT-like model (LLC-PK<jats:sub>Cl4<\/jats:sub>cells expressing rabbit AT<jats:sub>1<\/jats:sub>R) (LLC-PK-AT<jats:sub>1<\/jats:sub>R cells) determined that quinacrine, a nonspecific phospholipase A<jats:sub>2<\/jats:sub>(PLA<jats:sub>2<\/jats:sub>) inhibitor, and the haloenol lactone suicide substrate (HELSS), a Ca<jats:sup>2+<\/jats:sup>-independent PLA<jats:sub>2<\/jats:sub>inhibitor, attenuated apical (AP) AT<jats:sub>1<\/jats:sub>R recycling. Further studies were undertaken to examine the association between AT<jats:sub>1<\/jats:sub>R endocytotic movement and PLA<jats:sub>2<\/jats:sub>activity in this model. AP ANG II (100 nM) increased[Formula: see text]arachidonic acid ([Formula: see text]AA) release 4.4 \u00b1 0.38-fold in LLC-PK-AT<jats:sub>1<\/jats:sub>R cells cultured on permeable supports. Basolateral (BL) ANG II had no significant effect. Reversed-phase high-performance liquid chromatography confirmed that AP ANG II stimulated free [Formula: see text]AA release. Quinacrine, HELSS, and palmitoyl trifluoromethyl ketone, another Ca<jats:sup>2+<\/jats:sup>-independent PLA<jats:sub>2<\/jats:sub>inhibitor, inhibited AP ANG II-stimulated [Formula: see text]AA release, as did inhibiting AP AT<jats:sub>1<\/jats:sub>R internalization with phenylarsine oxide. The role of HELSS-inhibitable AA release in ANG II-mediated<jats:sup>22<\/jats:sup>Na flux was examined, given the effects of AT<jats:sub>1<\/jats:sub>R-mediated PLA<jats:sub>2<\/jats:sub>activity on salt and water reabsorption. AP ANG II (100 nM) stimulated<jats:sup>22<\/jats:sup>Na flux (AP \u2192 BL), a response inhibited by HELSS. Thus, in this model, AP AT<jats:sub>1<\/jats:sub>R activated PLA<jats:sub>2<\/jats:sub>with concomitant<jats:sup>22<\/jats:sup>Na flux (AP \u2192 BL), suggesting a link between AP AT<jats:sub>1<\/jats:sub>R endocytotic movement, AT<jats:sub>1<\/jats:sub>R-stimulated PLA<jats:sub>2<\/jats:sub>activity, and<jats:sup>22<\/jats:sup>Na flux in this model. The effects of HELSS suggest that Ca<jats:sup>2+<\/jats:sup>-independent PLA<jats:sub>2<\/jats:sub>activity may be involved in this AP ANG II response.<\/jats:p>","DOI":"10.1152\/ajprenal.1997.273.4.f554","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T14:56:01Z","timestamp":1514040961000},"page":"F554-F562","source":"Crossref","is-referenced-by-count":16,"title":["Apical ANG II-stimulated PLA<sub>2<\/sub>activity and Na<sup>+<\/sup>flux: a potential role for Ca<sup>2+<\/sup>-independent PLA<sub>2<\/sub>"],"prefix":"10.1152","volume":"273","author":[{"given":"B. N.","family":"Becker","sequence":"first","affiliation":[{"name":"Department of Medicine, Vanderbilt University School of Medicine and the Department of Veterans Affairs Medical Center, Nashville, Tennessee 37232-2372"}]},{"given":"H.-F.","family":"Cheng","sequence":"additional","affiliation":[{"name":"Department of Medicine, Vanderbilt University School of Medicine and the Department of Veterans Affairs Medical Center, Nashville, Tennessee 37232-2372"}]},{"given":"R. C.","family":"Harris","sequence":"additional","affiliation":[{"name":"Department of Medicine, Vanderbilt University School of Medicine and the Department of Veterans Affairs Medical Center, Nashville, Tennessee 37232-2372"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.1.445"},{"key":"B2","doi-asserted-by":"crossref","first-page":"9227","DOI":"10.1016\/S0021-9258(17)37098-9","volume":"269","author":"Ackermann E. J.","year":"1994","journal-title":"J. Biol. Chem."},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1995.269.4.C1048"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1111\/j.1432-1033.1995.0199o.x"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1210\/endo-111-6-1830"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1210\/endo-112-6-2007"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1995.268.4.C925"},{"issue":"30","key":"B8","first-page":"F607","volume":"261","author":"Burns K. D.","year":"1991","journal-title":"Am. J. Physiol."},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/0076-6879(90)87045-5"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.18.10855"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1210\/endo-118-6-2312"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1159\/000139303"},{"key":"B13","first-page":"S43","volume":"38","author":"Douglas J. G.","year":"1990","journal-title":"Kidney Int."},{"key":"B14","doi-asserted-by":"crossref","first-page":"9470","DOI":"10.1016\/S0021-9258(18)60555-1","volume":"264","author":"Gassama-Diagne A.","year":"1989","journal-title":"J. Biol. Chem."},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1994.1031"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.85.18.6797"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.79.4.765"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1007\/BF00581370"},{"key":"B19","doi-asserted-by":"crossref","first-page":"7227","DOI":"10.1016\/S0021-9258(20)89634-3","volume":"266","author":"Hazen S. L.","year":"1991","journal-title":"J. Biol. Chem."},{"key":"B20","doi-asserted-by":"crossref","first-page":"2783","DOI":"10.1016\/S0021-9258(18)49915-2","volume":"266","author":"Hunyady L.","year":"1991","journal-title":"J. Biol. Chem."},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.28.4.663"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1994.2603"},{"key":"B23","doi-asserted-by":"crossref","first-page":"20713","DOI":"10.1016\/S0021-9258(19)36837-1","volume":"268","author":"Lehman J. J.","year":"1993","journal-title":"J. Biol. Chem."},{"issue":"35","key":"B24","first-page":"F202","volume":"266","author":"Li L.","year":"1994","journal-title":"Am. J. Physiol."},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.21.12563"},{"key":"B26","doi-asserted-by":"crossref","first-page":"4832","DOI":"10.1016\/S0021-9258(17)37619-6","volume":"269","author":"Lokuta A. J.","year":"1994","journal-title":"J. Biol. Chem."},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.90.21.10255"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1007\/BF01872738"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/0006-2952(94)90216-X"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1042\/bj3070563"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.26.15451"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117141"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.16.9067"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118745"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1021\/bi00189a052"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.128.6.1029"},{"key":"B37","first-page":"199","volume":"14","author":"Romero M. F.","year":"1991","journal-title":"Renal Physiol. Biochem."},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1172\/JCI116139"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1994.266.3.C669"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118630"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1016\/0003-2697(85)90442-7"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.cb.09.110193.001021"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1995.269.2.C435"},{"key":"B44","doi-asserted-by":"crossref","first-page":"7295","DOI":"10.1016\/S0021-9258(17)39606-0","volume":"260","author":"Wolf R. A.","year":"1985","journal-title":"J. Biol. Chem."}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1997.273.4.F554","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:47:49Z","timestamp":1660189669000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1997.273.4.F554"}},"issued":{"date-parts":[[1997,10,1]]},"references-count":44,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1997,10,1]]}},"alternative-id":["10.1152\/ajprenal.1997.273.4.F554"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1997.273.4.f554","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1997,10,1]]}},{"indexed":{"date-parts":[[2026,2,21]],"date-time":"2026-02-21T04:17:39Z","timestamp":1771647459809,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1984,7,1]]},"abstract":"<jats:p> Ammonia and bicarbonate transport by the thick ascending limb of rat kidney was studied to determine whether this segment contributes to the regulation of renal ammonia and net acid excretion. Cortical and medullary thick ascending limbs were perfused in vitro at 1.0-1.5 nl X min-1 X mm-1 with HCO3-buffered solutions. There was no significant net fluid transport. With 4 mM ammonia in bath and perfusate, transepithelial voltage averaged 6-9 mV, lumen positive, and did not differ between the two segments. The mean ammonia concentration in collected tubule fluid was 2.8 mM with cortical segments and 2.3 mM with medullary segments, indicating net absorption of ammonia. Furosemide (10(-4) M) in the perfusate eliminated ammonia absorption in medullary thick ascending limbs and converted net absorption to net secretion in cortical thick ascending limbs. Furosemide reduced transepithelial voltage to near zero in every tubule. Cortical and medullary thick ascending limbs also absorbed bicarbonate, indicating that their tubule fluid was acidified relative to the bath. Therefore, absorption of ammonia could not have occurred by nonionic diffusion. The absorption most likely was due to direct transport of NH4+. The possible mechanisms involved are discussed, and it is proposed that absorption of ammonia by thick ascending limbs provides a source for its accumulation in the renal medulla and secretion into the collecting ducts. <\/jats:p>","DOI":"10.1152\/ajprenal.1984.247.1.f35","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T16:03:09Z","timestamp":1513958589000},"page":"F35-F44","source":"Crossref","is-referenced-by-count":65,"title":["Ammonia and bicarbonate transport by thick ascending limb of rat kidney"],"prefix":"10.1152","volume":"247","author":[{"given":"D. W.","family":"Good","sequence":"first","affiliation":[]},{"given":"M. A.","family":"Knepper","sequence":"additional","affiliation":[]},{"given":"M. B.","family":"Burg","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1984.247.1.F35","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:30:35Z","timestamp":1567967435000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1984.247.1.F35"}},"issued":{"date-parts":[[1984,7,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1984,7,1]]}},"alternative-id":["10.1152\/ajprenal.1984.247.1.F35"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1984.247.1.f35","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1984,7,1]]}},{"indexed":{"date-parts":[[2026,2,21]],"date-time":"2026-02-21T08:45:40Z","timestamp":1771663540540,"version":"3.50.1"},"reference-count":34,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,3,15]]},"abstract":"<jats:p> Autoregulation is critical for protecting the kidney against arterial pressure elevation and is compromised in some forms of hypertension. Evidence indicates that activated lymphocytes contribute importantly to cardiovascular injury in hypertension. We hypothesized that activated lymphocytes contribute to renal vascular dysfunction by impairing autoregulation and P2X<jats:sub>1<\/jats:sub> receptor signaling in ANG II-infused hypertensive rats. Male Sprague-Dawley rats receiving ANG II infusion were treated with a lymphocyte proliferation inhibitor, mycophenolate mofetil (MMF) for 2 wk. Autoregulation was assessed in vitro and in vivo using the blood-perfused juxtamedullary nephron preparation and anesthetized rats, respectively. ANG II-treated rats exhibited impaired autoregulation. At the single vessel level, pressure-mediated afferent arteriolar vasoconstriction was significantly blunted ( P &lt; 0.05 vs. control rats). At the whole kidney level, renal blood flow passively decreased as renal perfusion pressure was reduced. MMF treatment did not alter the ANG II-induced hypertensive state; however, MMF did preserve autoregulation. The autoregulatory profiles in both in vitro or in vivo settings were similar to the responses from control rats despite persistent hypertension. Autoregulatory responses are linked to P2X<jats:sub>1<\/jats:sub> receptor activation. Accordingly, afferent arteriolar responses to ATP and the P2X<jats:sub>1<\/jats:sub> receptor agonist \u03b2,\u03b3-methylene ATP were assessed. ATP- or \u03b2,\u03b3-methylene ATP-induced vasoconstriction was significantly attenuated in ANG II-infused hypertensive rats but was normalized by MMF treatment. Moreover, MMF prevented elevation of plasma transforming growth factor-\u03b21 concentration and lymphocyte and macrophage infiltration in ANG II-infused kidneys. These results suggest that anti-inflammatory treatment with MMF prevents lymphocyte infiltration and preserves autoregulation in ANG II-infused hypertensive rats, likely by normalizing P2X<jats:sub>1<\/jats:sub> receptor activation. <\/jats:p>","DOI":"10.1152\/ajprenal.00286.2012","type":"journal-article","created":{"date-parts":[[2012,12,26]],"date-time":"2012-12-26T20:36:42Z","timestamp":1356554202000},"page":"F801-F807","source":"Crossref","is-referenced-by-count":26,"title":["Immunosuppression preserves renal autoregulatory function and microvascular P2X<sub>1<\/sub> receptor reactivity in ANG II-hypertensive rats"],"prefix":"10.1152","volume":"304","author":[{"given":"Zhengrong","family":"Guan","sequence":"first","affiliation":[{"name":"Department of Physiology, Georgia Health Sciences University, Augusta, Georgia;"}]},{"given":"Matthew I.","family":"Giddens","sequence":"additional","affiliation":[{"name":"Department of Physiology, Georgia Health Sciences University, Augusta, Georgia;"}]},{"given":"David A.","family":"Osmond","sequence":"additional","affiliation":[{"name":"Department of Physiology, Georgia Health Sciences University, Augusta, Georgia;"}]},{"given":"Anthony K.","family":"Cook","sequence":"additional","affiliation":[{"name":"Department of Physiology, Georgia Health Sciences University, Augusta, Georgia;"}]},{"given":"Janet L.","family":"Hobbs","sequence":"additional","affiliation":[{"name":"Department of Experimental Medicine, Georgia Health Sciences University, Augusta, Georgia; and"}]},{"given":"Shali","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Physiology, Georgia Health Sciences University, Augusta, Georgia;"}]},{"given":"Tatsuo","family":"Yamamoto","sequence":"additional","affiliation":[{"name":"Second Department of Medicine, Numazu City Hospital, Shizuoka, Japan"}]},{"given":"Jennifer S.","family":"Pollock","sequence":"additional","affiliation":[{"name":"Department of Experimental Medicine, Georgia Health Sciences University, Augusta, Georgia; and"}]},{"given":"David M.","family":"Pollock","sequence":"additional","affiliation":[{"name":"Department of Experimental Medicine, Georgia Health Sciences University, Augusta, Georgia; and"}]},{"given":"Edward W.","family":"Inscho","sequence":"additional","affiliation":[{"name":"Department of Physiology, Georgia Health Sciences University, Augusta, Georgia;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1007\/s11302-009-9149-z"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.109.133777"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.2010.05428.x"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.4.F799"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00527.2007"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00298.2009"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00221.2006"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-006-0070-9"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00281.2007"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00743.2009"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20070657"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.2010.00714.x"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.110.163576"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1007\/s11302-009-9147-1"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.110.168955"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-200404000-00025"},{"key":"B17","first-page":"S178","volume":"10","author":"Inscho EW","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0b013e32831daf54"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00090.2005"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000251162.14782.d4"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1159\/000051064"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1590\/S1807-59322007000600015"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)64445-8"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1021\/jm00164a057"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1291\/hypres.27.791"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00016.2010"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9629(15)33943-4"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.281.1.F38"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1291\/hypres.31.707"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0b013e3283360a2e"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00345.2004"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2009.66"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1046\/j.0001-6772.2003.01205.x"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000179584.39937.41"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00286.2012","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:40:39Z","timestamp":1567971639000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00286.2012"}},"issued":{"date-parts":[[2013,3,15]]},"references-count":34,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2013,3,15]]}},"alternative-id":["10.1152\/ajprenal.00286.2012"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00286.2012","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2013,3,15]]}},{"indexed":{"date-parts":[[2026,2,25]],"date-time":"2026-02-25T18:01:33Z","timestamp":1772042493132,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1990,10,1]]},"abstract":"<jats:p> To define whether angiotensin I-converting enzyme (ACE) inhibition affects the distribution of renin gene-expressing cells within the kidney, a control group of adult male Wistar-Kyoto rats (C, n = 7) was compared with a group of rats treated with enalapril (E, n = 6) for 5 days. Renin mRNA distribution was assessed using in situ hybridization to a 35S-labeled 28 mer oligonucleotide complementary to rat renin mRNA. Whereas in control rats renin mRNA was confined to a juxtaglomerular location, in enalapril-treated rats, renin mRNA extended proximally along the length of the afferent arteriole. The percent of visible afferent arteriolar length containing renin mRNA was higher in enalapril-treated (71.7 +\/- 2.8%) than in control (49.6 +\/- 2.1%) rats (P less than 0.0001). These findings were accompanied by an increase in the percent of juxtaglomerular apparatuses (JGAs) containing renin mRNA (71 +\/- 2.2 vs. 49 +\/- 2.9%; E vs. C, P less than 0.0001). Also, the intensity of the JGA hybridization signals was higher in enalapril-treated (757 +\/- 59 grains\/JGA) than in control (167 +\/- 11 grains\/JGA) rats (P less than 0.00001). We conclude that the increased kidney renin gene expression elicited by ACE inhibition is the result of an increase in renin mRNA content per JGA, an increase in the number of JGAs expressing the renin gene, and a recruitment of renin gene-expressing cells along the afferent arteriole. <\/jats:p>","DOI":"10.1152\/ajprenal.1990.259.4.f660","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T22:24:25Z","timestamp":1513981465000},"page":"F660-F665","source":"Crossref","is-referenced-by-count":44,"title":["Recruitment of renin gene-expressing cells in adult rat kidneys"],"prefix":"10.1152","volume":"259","author":[{"given":"R. A.","family":"Gomez","sequence":"first","affiliation":[{"name":"Department of Pediatrics, University of Virginia School of Medicine, Charlottesville 22908."}]},{"given":"R. L.","family":"Chevalier","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, University of Virginia School of Medicine, Charlottesville 22908."}]},{"given":"A. D.","family":"Everett","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, University of Virginia School of Medicine, Charlottesville 22908."}]},{"given":"J. P.","family":"Elwood","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, University of Virginia School of Medicine, Charlottesville 22908."}]},{"given":"M. J.","family":"Peach","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, University of Virginia School of Medicine, Charlottesville 22908."}]},{"given":"K. R.","family":"Lynch","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, University of Virginia School of Medicine, Charlottesville 22908."}]},{"given":"R. M.","family":"Carey","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, University of Virginia School of Medicine, Charlottesville 22908."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1990.259.4.F660","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:17:17Z","timestamp":1567970237000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1990.259.4.F660"}},"issued":{"date-parts":[[1990,10,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1990,10,1]]}},"alternative-id":["10.1152\/ajprenal.1990.259.4.F660"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1990.259.4.f660","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1990,10,1]]}},{"indexed":{"date-parts":[[2026,2,17]],"date-time":"2026-02-17T04:48:54Z","timestamp":1771303734921,"version":"3.50.1"},"reference-count":92,"publisher":"American Physiological Society","issue":"11","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,12,1]]},"abstract":"<jats:p>The DCT (distal convoluted tubule) is the site of microregulation of water reabsorption and ion handling in the kidneys, which is mainly under the control of aldosterone. Aldosterone binds to and activates mineralocorticoid receptors, which ultimately lead to increased sodium reabsorption in the distal part of the nephron. Impairment of mineralocorticoid signal transduction results in resistance to aldosterone and mineralocorticoids, and, therefore, causes disturbances in electrolyte balance. Pseudohypoaldosteronism type II (PHAII) or familial hyperkalemic hypertension (FHHt) is a rare, autosomal dominant syndrome characterized by hypertension, hyperkalemia, metabolic acidosis, elevated or low aldosterone levels, and decreased plasma renin activity. PHAII is caused by mutations in the WNK isoforms (with no lysine kinase), which regulate the Na-Cl and Na-K-Cl cotransporters (NCC and NKCC2, respectively) and the renal outer medullary potassium (ROMK) channel in the DCT. This review focuses on new candidate genes such as KLHL3 and Cullin3, which are instrumental to unraveling novel signal transductions pathways involving NCC, to better understand the cause of PHAII along with the molecular mechanisms governing the pathophysiology of PHAII and its clinical manifestations.<\/jats:p>","DOI":"10.1152\/ajprenal.00440.2013","type":"journal-article","created":{"date-parts":[[2013,10,10]],"date-time":"2013-10-10T16:01:17Z","timestamp":1381420877000},"page":"F1513-F1520","source":"Crossref","is-referenced-by-count":48,"title":["A molecular update on pseudohypoaldosteronism type II"],"prefix":"10.1152","volume":"305","author":[{"given":"Ganesh","family":"Pathare","sequence":"first","affiliation":[{"name":"Department of Physiology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands"}]},{"given":"Joost G. J.","family":"Hoenderop","sequence":"additional","affiliation":[{"name":"Department of Physiology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands"}]},{"given":"Ren\u00e9 J. M.","family":"Bindels","sequence":"additional","affiliation":[{"name":"Department of Physiology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands"}]},{"given":"Pedro","family":"San-Cristobal","sequence":"additional","affiliation":[{"name":"Department of Physiology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2011020132"},{"key":"B2","doi-asserted-by":"crossref","first-page":"836","DOI":"10.1681\/ASN.V134836","volume":"13","author":"Biner HL","year":"2002","journal-title":"J Am Soc Nephrol"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1172\/JCI6821"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00968.x"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-002-0945-8"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1038\/nature10814"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000333"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1200947109"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2009.03.013"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.084111"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.242728499"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M206293200"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.23.24.9208-9221.2003"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1086\/303020"},{"key":"B15","first-page":"55","volume":"31","author":"Disse-Nicodeme S","year":"2001","journal-title":"Adv Nephrol Necker Hosp"},{"key":"B16","first-page":"122","volume":"111","author":"DuBose TD","year":"2000","journal-title":"Trans Am Clin Climatol Assoc"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.4.F616"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1038\/emboj.2011.78"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00391.2005"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00011.2004"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00311.2004"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00159.2009"},{"key":"B23","doi-asserted-by":"crossref","first-page":"17713","DOI":"10.1016\/S0021-9258(17)32499-7","volume":"269","author":"Gamba G","year":"1994","journal-title":"J Biol Chem"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2265.2005.02229.x"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1038\/emboj.2013.173"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00468.2005"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000174326.96918.d6"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.8.2.93"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1111\/j.1445-5994.1986.tb01145.x"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1042\/bj20021375"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1126\/science.2063193"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M110.103432"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1038\/nm.2497"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1038\/ncpneph0638"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00187.2006"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0308434100"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200409000-00012"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1038\/ng1271"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.24.14552"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1677\/joe.0.1690437"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5001851"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1038\/ng1877"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1007\/s00018-006-6011-0"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(01)00241-0"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.0085.2001"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1038\/ng.2218"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfm641"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1210\/jc.2004-0037"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1210\/jcem.87.7.8449"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M510042200"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1038\/nm.2337"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1007\/s10157-011-0491-4"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1007\/s00418-004-0742-5"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005111197"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000089830.97681.3B"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1038\/sj.jhh.1000705"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1172\/JCI200421560"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.6.F900"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1042\/BJ20121903"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2006.08.101"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2010.130"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1002\/emmm.200900058"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.025312"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1159\/000224334"},{"key":"B65","first-page":"657","volume":"123","author":"Ronzaud C","year":"2013","journal-title":"J Clin Invest"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1159\/000139639"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0813238106"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.1016\/j.mce.2003.10.017"},{"key":"B69","doi-asserted-by":"publisher","DOI":"10.1210\/jc.2002-021932"},{"key":"B70","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1304592110"},{"key":"B71","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.10.7.2361"},{"key":"B72","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00280.2005"},{"key":"B73","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2013.06.104"},{"key":"B74","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-010-0848-7"},{"key":"B75","doi-asserted-by":"publisher","DOI":"10.1007\/s00381-006-0254-9"},{"key":"B76","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1304230110"},{"key":"B77","doi-asserted-by":"publisher","DOI":"10.1042\/BJ20051180"},{"key":"B78","doi-asserted-by":"publisher","DOI":"10.1042\/BJ20060220"},{"key":"B79","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0603109103"},{"key":"B80","doi-asserted-by":"publisher","DOI":"10.1016\/j.celrep.2013.02.024"},{"key":"B81","doi-asserted-by":"publisher","DOI":"10.1126\/science.1062844"},{"key":"B82","volume-title":"GeneReviews","author":"Wilson FH","year":"1993"},{"key":"B83","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.242735399"},{"key":"B84","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-006-0106-6"},{"key":"B85","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.275.22.16795"},{"key":"B86","doi-asserted-by":"publisher","DOI":"10.1172\/JCI32033"},{"key":"B87","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009121295"},{"key":"B88","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2007.03.009"},{"key":"B89","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.2336103100"},{"key":"B90","doi-asserted-by":"publisher","DOI":"10.1016\/j.mce.2011.04.023"},{"key":"B91","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00032.2011"},{"key":"B92","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008121275"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00440.2013","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,3,8]],"date-time":"2022-03-08T18:17:22Z","timestamp":1646763442000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00440.2013"}},"issued":{"date-parts":[[2013,12,1]]},"references-count":92,"journal-issue":{"issue":"11","published-print":{"date-parts":[[2013,12,1]]}},"alternative-id":["10.1152\/ajprenal.00440.2013"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00440.2013","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2013,12,1]]}},{"indexed":{"date-parts":[[2026,2,17]],"date-time":"2026-02-17T12:58:31Z","timestamp":1771333111453,"version":"3.50.1"},"reference-count":54,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2010,4]]},"abstract":"<jats:p>Macrophages are heterogeneous immune cell populations that include classically activated and alternatively activated (M2) macrophages. We examined the anti-inflammatory effect of ANG II type 1 receptor (AT<jats:sub>1<\/jats:sub>R) blocker (ARB) on glomerular inflammation in a rat model of anti-glomerular basement membrane (GBM) glomerulonephritis (GN). The study focused on infiltrating CD8<jats:sup>+<\/jats:sup>and CD4<jats:sup>+<\/jats:sup>cells and macrophages, as well as the heterogeneity of intraglomerular macrophages. Wistar-Kyoto rats were treated with high-dose olmesartan (3 mg\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7day<jats:sup>\u22121<\/jats:sup>), low-dose olmesartan (0.3 mg\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7day<jats:sup>\u22121<\/jats:sup>), or vehicle (control) 7 days before induction of anti-GBM GN. Control rats showed mainly CD8<jats:sup>+<\/jats:sup>cells and ED1<jats:sup>+<\/jats:sup>macrophages, with a few CD4<jats:sup>+<\/jats:sup>cells infiltrating the glomeruli. Necrotizing and crescentic glomerular lesions developed by day 7 with the increase of proteinuria. AT<jats:sub>1<\/jats:sub>R was expressed on CD8<jats:sup>+<\/jats:sup>and CD4<jats:sup>+<\/jats:sup>cells and on ED1<jats:sup>+<\/jats:sup>macrophages. Low-dose ARB had no anti-inflammatory effects in anti-GBM GN. However, high-dose ARB reduced glomerular infiltration of CD8<jats:sup>+<\/jats:sup>cells and ED1<jats:sup>+<\/jats:sup>macrophages and suppressed necrotizing and crescentic lesions by days 5 to 7 ( P &lt; 0.05). In addition, high-dose ARB reduced the numbers of ED3<jats:sup>+<\/jats:sup>-activated macrophages, suppressed glomerular TNF-\u03b1 and IFN-\u03b3 production, and downregulated M1-related chemokine and cytokines (monocyte chemoattractant protein type 1, IL-6, and IL-12). High-dose ARB also enhanced ED2<jats:sup>+<\/jats:sup>M2 macrophages by day 7 with upregulation of glomerular IL-4 and IL-13 and augmented CCL17, IL-1 receptor antagonist, and IL-10. We concluded that high-dose ARB inhibits glomerular inflammation by increasing the numbers of M2 macrophages and upregulation of anti-inflammatory cytokines and by suppressing M1 macrophage development with downregulation of M1-related proinflammatory cytokines.<\/jats:p>","DOI":"10.1152\/ajprenal.00374.2009","type":"journal-article","created":{"date-parts":[[2010,1,14]],"date-time":"2010-01-14T02:28:08Z","timestamp":1263436088000},"page":"F870-F882","source":"Crossref","is-referenced-by-count":54,"title":["ANG II receptor blockade enhances anti-inflammatory macrophages in anti-glomerular basement membrane glomerulonephritis"],"prefix":"10.1152","volume":"298","author":[{"given":"Kaoru","family":"Aki","sequence":"first","affiliation":[{"name":"Departments of 1Analytic Human Pathology and"},{"name":"Pediatrics, Nippon Medical School, Tokyo; and"}]},{"given":"Akira","family":"Shimizu","sequence":"additional","affiliation":[{"name":"Departments of 1Analytic Human Pathology and"}]},{"given":"Yukinari","family":"Masuda","sequence":"additional","affiliation":[{"name":"Departments of 1Analytic Human Pathology and"}]},{"given":"Naomi","family":"Kuwahara","sequence":"additional","affiliation":[{"name":"Departments of 1Analytic Human Pathology and"}]},{"given":"Takashi","family":"Arai","sequence":"additional","affiliation":[{"name":"Departments of 1Analytic Human Pathology and"}]},{"given":"Arimi","family":"Ishikawa","sequence":"additional","affiliation":[{"name":"Departments of 1Analytic Human Pathology and"}]},{"given":"Emiko","family":"Fujita","sequence":"additional","affiliation":[{"name":"Departments of 1Analytic Human Pathology and"}]},{"given":"Akiko","family":"Mii","sequence":"additional","affiliation":[{"name":"Departments of 1Analytic Human Pathology and"}]},{"given":"Yasuhiro","family":"Natori","sequence":"additional","affiliation":[{"name":"Department of Health Chemistry, School of Pharmacy, Iwate Medical University, Iwate, Japan"}]},{"given":"Yoshitaka","family":"Fukunaga","sequence":"additional","affiliation":[{"name":"Pediatrics, Nippon Medical School, Tokyo; and"}]},{"given":"Yuh","family":"Fukuda","sequence":"additional","affiliation":[{"name":"Departments of 1Analytic Human Pathology and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2007.06.010"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/j.amjmed.2003.09.034"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(99)10365-9"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/sj.jhh.1002101"},{"key":"B5","first-page":"589","volume":"54","author":"Dijkstra CD","year":"1985","journal-title":"Immunology"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00362.x"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/j.vph.2006.05.002"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200105000-00007"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.108.772491"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2007.02.001"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1038\/nri978"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.02231205"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2009.090290"},{"key":"B14","doi-asserted-by":"crossref","first-page":"845","DOI":"10.1182\/blood.V94.3.845.415k09_845_852","volume":"94","author":"Hashimoto S","year":"1999","journal-title":"Blood"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1797.2007.00878.x"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfi105"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1093\/intimm\/11.1.81"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/j.cardiores.2006.07.014"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfh558"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1006\/cimm.1996.0186"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1992.221"},{"key":"B22","first-page":"993","volume":"15","author":"Kitching AR","year":"2000","journal-title":"Histol Histopathol"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00773.x"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2249.1997.tb08322.x"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004060492"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/S1471-4906(01)01941-X"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/j.it.2004.09.015"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1186\/1742-4682-3-1"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.2741\/2692"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)61731-2"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1038\/labinvest.2008.128"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2007.03.084"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1189\/jlb.0602325"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1038\/nri2448"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000018408.51388.57"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-199917040-00012"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.09911.x"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1172\/JCI36150"},{"key":"B39","first-page":"S5","volume":"10","author":"Ruilope LM","year":"2008","journal-title":"Medscape J Med Suppl"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200105000-00005"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006040356"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007020149"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1016\/j.amjhyper.2004.11.032"},{"key":"B44","first-page":"268","volume":"11","author":"Schreiner GF","year":"1991","journal-title":"Semin Nephrol"},{"key":"B45","first-page":"1231","volume":"151","author":"Shimizu A","year":"1997","journal-title":"Am J Pathol"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000141038.28733.F2"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1084\/jem.176.1.287"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1097\/HJH.0b013e3282f9b58a"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1016\/S1357-2725(02)00271-6"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2249.2008.03758.x"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.107.099028"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002275"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5001846"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.2174\/156652407781387073"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00374.2009","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2020,5,26]],"date-time":"2020-05-26T18:41:56Z","timestamp":1590518516000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00374.2009"}},"issued":{"date-parts":[[2010,4]]},"references-count":54,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2010,4]]}},"alternative-id":["10.1152\/ajprenal.00374.2009"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00374.2009","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2010,4]]}},{"indexed":{"date-parts":[[2026,2,18]],"date-time":"2026-02-18T00:21:47Z","timestamp":1771374107942,"version":"3.50.1"},"reference-count":71,"publisher":"American Physiological Society","issue":"4","funder":[{"name":"NIH","award":["RO1HL048459"],"award-info":[{"award-number":["RO1HL048459"]}]},{"name":"NIH","award":["R21CA121212"],"award-info":[{"award-number":["R21CA121212"]}]},{"name":"NIH","award":["DK87389"],"award-info":[{"award-number":["DK87389"]}]},{"name":"NIH","award":["DK94768"],"award-info":[{"award-number":["DK94768"]}]},{"name":"NIH","award":["R01DK097598"],"award-info":[{"award-number":["R01DK097598"]}]},{"name":"NIH","award":["R21DK081835"],"award-info":[{"award-number":["R21DK081835"]}]},{"name":"NIH","award":["DK84077"],"award-info":[{"award-number":["DK84077"]}]},{"name":"NIH","award":["DK94768"],"award-info":[{"award-number":["DK94768"]}]},{"name":"NIH","award":["R01DK097598"],"award-info":[{"award-number":["R01DK097598"]}]},{"name":"NIH","award":["R21DK081835"],"award-info":[{"award-number":["R21DK081835"]}]},{"name":"NIH","award":["R01DK056799"],"award-info":[{"award-number":["R01DK056799"]}]},{"name":"NIH","award":["R21DK081835"],"award-info":[{"award-number":["R21DK081835"]}]},{"name":"NCI","award":["P30 CA016056"],"award-info":[{"award-number":["P30 CA016056"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2015,8,15]]},"abstract":"<jats:p>Modified vascular smooth muscle cells of the kidney afferent arterioles have recently been shown to serve as progenitors for glomerular epithelial cells in response to glomerular injury. To determine whether such cells of renin lineage (CoRL) serve as progenitors for other cells in kidney disease characterized by both glomerular and tubulointerstitial injury, permanent genetic cell fate mapping of adult CoRL using Ren1cCreER \u00d7 Rs-tdTomato-R reporter mice was performed. TdTomato-labeled CoRL were almost completely restricted to the juxtaglomerular compartment in healthy kidneys. Following 2 wk of antibody-mediated focal segmental glomerulosclerosis (FSGS) or 16 wk of \u215a nephrectomy-induced chronic kidney diseases, tdTomato-mapped CoRL were identified in both interstitial and glomerular compartments. In the interstitium, PDGF\u03b2 receptor (R)-expressing cells significantly increased, and a portion of these expressed tdTomato. This was accompanied by a decrease in native pericyte number, but an increase in the number of tdTomato cells that coexpressed the pericyte markers PDGF\u03b2-R and NG2. These cells surrounded vessels and coexpressed the pericyte markers CD73 and CD146, but not the endothelial marker ERG. Within glomeruli of reporter mice with the \u215a nephrectomy model, a subset of labeled CoRL migrated to the glomerular tuft and coexpressed podocin and synaptopodin. By contrast, labeled CoRL were not detected in glomerular or interstitial compartments following uninephrectomy. These observations indicate that in addition to supplying new adult podocytes to glomeruli, CoRL have the capacity to become new adult pericytes in the setting of interstitial disease. We conclude that CoRL have the potential to function as progenitors for multiple adult cell types in kidney disease.<\/jats:p>","DOI":"10.1152\/ajprenal.00438.2014","type":"journal-article","created":{"date-parts":[[2015,6,11]],"date-time":"2015-06-11T11:22:07Z","timestamp":1434021727000},"page":"F341-F358","source":"Crossref","is-referenced-by-count":57,"title":["Cells of renin lineage are adult pluripotent progenitors in experimental glomerular disease"],"prefix":"10.1152","volume":"309","author":[{"given":"Jeffrey W.","family":"Pippin","sequence":"first","affiliation":[{"name":"Division of Nephrology, University of Washington, Seattle, Washington;"}]},{"given":"Natalya V.","family":"Kaverina","sequence":"additional","affiliation":[{"name":"Division of Nephrology, University of Washington, Seattle, Washington;"}]},{"given":"Diana G.","family":"Eng","sequence":"additional","affiliation":[{"name":"Division of Nephrology, University of Washington, Seattle, Washington;"}]},{"given":"Ronald D.","family":"Krofft","sequence":"additional","affiliation":[{"name":"Division of Nephrology, University of Washington, Seattle, Washington;"}]},{"given":"Sean T.","family":"Glenn","sequence":"additional","affiliation":[{"name":"Department of Molecular and Cellular Biology, Roswell Park Cancer Institute, Buffalo, New York; and"}]},{"given":"Jeremy S.","family":"Duffield","sequence":"additional","affiliation":[{"name":"Division of Nephrology, University of Washington, Seattle, Washington;"},{"name":"Biogen IDEC, Cambridge, Massachusetts"}]},{"given":"Kenneth W.","family":"Gross","sequence":"additional","affiliation":[{"name":"Department of Molecular and Cellular Biology, Roswell Park Cancer Institute, Buffalo, New York; and"}]},{"given":"Stuart J.","family":"Shankland","sequence":"additional","affiliation":[{"name":"Division of Nephrology, University of Washington, Seattle, Washington;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"crossref","first-page":"201","DOI":"10.1681\/ASN.V52201","volume":"5","author":"Alpers CE","year":"1994","journal-title":"J Am Soc Nephrol"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1002\/jcb.10594"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.5527\/wjn.v2.i1.11"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2009.548"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0024640"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2011.208"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5320(83)90133-8"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1186\/1471-2369-14-74"},{"key":"B9","first-page":"909","volume":"24","author":"Diaz-Flores L","year":"2009","journal-title":"Histol Histopathol"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1172\/JCI72267"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1038\/kisup.2014.2"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/j.tcb.2007.06.006"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.93.20.10887"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-013-2688-0"},{"key":"B15","doi-asserted-by":"crossref","first-page":"8361","DOI":"10.1016\/S0021-9258(19)38892-1","volume":"265","author":"Gougos A","year":"1990","journal-title":"J Biol Chem"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/j.ajpath.2013.04.009"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1038\/nm.3405"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002454"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/S1357-2725(01)00022-X"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119592"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2010.090517"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1164\/rccm.201212-2297OC"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00725.2010"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2012.08.037"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1016\/j.stem.2012.05.015"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0092115"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/j.stemcr.2014.08.008"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(93)90515-R"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2012080791"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1242\/dev.01604"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2008.080433"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1101\/cshperspect.a008300"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00058.x"},{"key":"B34","author":"Maezawa Y","journal-title":"J Am Soc Nephrol"},{"key":"B35","author":"Miyazaki Y","journal-title":"Nephrol Dial Transplant"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfs556"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.139.1.193"},{"key":"B38","author":"Nakagawa N","journal-title":"J Am Soc Nephrol"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2014.406"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00428.2009"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00003.x"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00020.2002"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2003-09-3070"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00699.2013"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1016\/j.ajpath.2013.04.024"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1126\/science.284.5411.143"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1126\/science.276.5309.71"},{"key":"B48","doi-asserted-by":"crossref","first-page":"5771","DOI":"10.1242\/dev.126.24.5771","volume":"126","author":"Quaggin SE","year":"1999","journal-title":"Development"},{"key":"B49","first-page":"253","volume":"14","author":"Ranieri E","year":"2001","journal-title":"J Nephrol"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1126\/science.3299708"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2012.290"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00228.2013"},{"key":"B53","doi-asserted-by":"crossref","first-page":"544","DOI":"10.1681\/ASN.V132544","volume":"13","author":"Satchell SC","year":"2002","journal-title":"J Am Soc Nephrol"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013040376"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1016\/S1534-5807(04)00134-0"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00428.2014"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1827.1998.tb03920.x"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.268.2.F240"},{"key":"B59","first-page":"1503","volume":"27","author":"Smith SW","year":"2012","journal-title":"Histol Histopathol"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfp454"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014030265"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1634\/stemcells.21-5-527"},{"key":"B63","doi-asserted-by":"crossref","first-page":"2673","DOI":"10.1681\/ASN.V12122673","volume":"12","author":"Takahashi T","year":"2001","journal-title":"J Am Soc Nephrol"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00614.2011"},{"key":"B65","doi-asserted-by":"crossref","first-page":"231","DOI":"10.1681\/ASN.V92231","volume":"9","author":"Thomas SE","year":"1998","journal-title":"J Am Soc Nephrol"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1016\/j.yexcr.2003.12.030"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005080835"},{"key":"B68","doi-asserted-by":"crossref","first-page":"2125","DOI":"10.1681\/ASN.V10102125","volume":"10","author":"Tufro A","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B69","doi-asserted-by":"publisher","DOI":"10.1016\/j.micron.2012.04.013"},{"key":"B70","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00020.2013"},{"key":"B71","doi-asserted-by":"publisher","DOI":"10.1159\/000342808"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00438.2014","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,5,12]],"date-time":"2022-05-12T15:54:34Z","timestamp":1652370874000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00438.2014"}},"issued":{"date-parts":[[2015,8,15]]},"references-count":71,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2015,8,15]]}},"alternative-id":["10.1152\/ajprenal.00438.2014"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00438.2014","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2015,8,15]]}},{"indexed":{"date-parts":[[2026,2,17]],"date-time":"2026-02-17T20:15:35Z","timestamp":1771359335477,"version":"3.50.1"},"reference-count":57,"publisher":"American Physiological Society","issue":"6","funder":[{"DOI":"10.13039\/100000738","name":"U.S. Department of Veterans Affairs","doi-asserted-by":"publisher","award":["I01 BX004024"],"award-info":[{"award-number":["I01 BX004024"]}],"id":[{"id":"10.13039\/100000738","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000850","name":"National Heart and Lung Institute","doi-asserted-by":"publisher","award":["R35 HL135749"],"award-info":[{"award-number":["R35 HL135749"]}],"id":[{"id":"10.13039\/501100000850","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000850","name":"National Heart and Lung Institute","doi-asserted-by":"publisher","award":["P01 HL116264"],"award-info":[{"award-number":["P01 HL116264"]}],"id":[{"id":"10.13039\/501100000850","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK 020595"],"award-info":[{"award-number":["DK 020595"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK105160"],"award-info":[{"award-number":["DK105160"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100001440","name":"ADA Foundation","doi-asserted-by":"publisher","award":["1-15-BS-172"],"award-info":[{"award-number":["1-15-BS-172"]}],"id":[{"id":"10.13039\/100001440","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100005384","name":"American Physiological Society","doi-asserted-by":"publisher","award":["Research Career Enhancement Award"],"award-info":[{"award-number":["Research Career Enhancement Award"]}],"id":[{"id":"10.13039\/100005384","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"HHS | NIH | National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["T32 HL134643"],"award-info":[{"award-number":["T32 HL134643"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2019,12,1]]},"abstract":"<jats:p>Diabetic kidney disease (DKD) is one of the leading pathological causes of decreased renal function and progression to end-stage kidney failure. To explore and characterize age-related changes in DKD and associated glomerular damage, we used a rat model of type 2 diabetic nephropathy (T2DN) at 12 wk and older than 48 wk. We compared their disease progression with control nondiabetic Wistar and diabetic Goto-Kakizaki (GK) rats. During the early stages of DKD, T2DN and GK animals revealed significant increases in blood glucose and kidney-to-body weight ratio. Both diabetic groups had significantly altered renin-angiotensin-aldosterone system function. Thereafter, during the later stages of disease progression, T2DN rats demonstrated a remarkable increase in renal damage compared with GK and Wistar rats, as indicated by renal hypertrophy, polyuria accompanied by a decrease in urine osmolarity, high cholesterol, a significant prevalence of medullary protein casts, and severe forms of glomerular injury. Urinary nephrin shedding indicated loss of the glomerular slit diaphragm, which also correlates with the dramatic elevation in albuminuria and loss of podocin staining in aged T2DN rats. Furthermore, we used scanning ion microscopy topographical analyses to detect and quantify the pathological remodeling in podocyte foot projections of isolated glomeruli from T2DN animals. In summary, T2DN rats developed renal and physiological abnormalities similar to clinical observations in human patients with DKD, including progressive glomerular damage and a significant decrease in renin-angiotensin-aldosterone system plasma levels, indicating these rats are an excellent model for studying the progression of renal damage in type 2 DKD.<\/jats:p>","DOI":"10.1152\/ajprenal.00246.2019","type":"journal-article","created":{"date-parts":[[2019,9,30]],"date-time":"2019-09-30T14:24:06Z","timestamp":1569853446000},"page":"F1450-F1461","source":"Crossref","is-referenced-by-count":51,"title":["Progression of diabetic kidney disease in T2DN rats"],"prefix":"10.1152","volume":"317","author":[{"given":"Oleg","family":"Palygin","sequence":"first","affiliation":[{"name":"Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin"},{"name":"Cardiovascular Center, Medical College of Wisconsin, Milwaukee, Wisconsin"}]},{"given":"Denisha","family":"Spires","sequence":"additional","affiliation":[{"name":"Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin"}]},{"given":"Vladislav","family":"Levchenko","sequence":"additional","affiliation":[{"name":"Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin"}]},{"given":"Ruslan","family":"Bohovyk","sequence":"additional","affiliation":[{"name":"Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin"}]},{"given":"Mykhailo","family":"Fedoriuk","sequence":"additional","affiliation":[{"name":"Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0812-824X","authenticated-orcid":false,"given":"Christine A.","family":"Klemens","sequence":"additional","affiliation":[{"name":"Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin"},{"name":"Cardiovascular Center, Medical College of Wisconsin, Milwaukee, Wisconsin"}]},{"given":"Olga","family":"Sykes","sequence":"additional","affiliation":[{"name":"Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4411-3643","authenticated-orcid":false,"given":"John D.","family":"Bukowy","sequence":"additional","affiliation":[{"name":"Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin"}]},{"suffix":"Jr.","given":"Allen W.","family":"Cowley","sequence":"additional","affiliation":[{"name":"Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin"}]},{"given":"Jozef","family":"Lazar","sequence":"additional","affiliation":[{"name":"Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin"}]},{"given":"Daria V.","family":"Ilatovskaya","sequence":"additional","affiliation":[{"name":"Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5190-8356","authenticated-orcid":false,"given":"Alexander","family":"Staruschenko","sequence":"additional","affiliation":[{"name":"Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin"},{"name":"Cardiovascular Center, Medical College of Wisconsin, Milwaukee, Wisconsin"},{"name":"Clement J. Zablocki Veterans Affairs Medical Center, Milwaukee, Wisconsin"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.11491116"},{"key":"B2","first-page":"8","volume":"11","author":"Anguiano L","year":"2019","journal-title":"ASN Kidney News"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1177\/1470320317705232"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/S2213-8587(13)70208-0"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00636.x"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00353.x"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-019-40639-x"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009070721"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2017111210"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.11111016"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.3390\/jcm4050998"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2012.07.011"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.07505.x"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1038\/srep26428"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1620\/tjem.119.85"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/j.ebiom.2019.01.006"},{"key":"B17","first-page":"598","volume":"106","author":"Kasiske BL","year":"1985","journal-title":"J Lab Clin Med"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.2337\/diab.41.11.1422"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.2147\/IJNRD.S103784"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.4172\/2155-6156.S9-005"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.113.203869"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00320.x"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2018.02.003"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00143.2018"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1038\/ncpendmet1066"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa1611925"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.53.3.735"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1038\/nmeth.1306"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(14)62459-4"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1172\/jci.insight.92331"},{"key":"B31","volume-title":"Kidney Disease in Diabetes","author":"Pavkov ME","year":"2018"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa1811744"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1155\/2012\/428950"},{"key":"B34","doi-asserted-by":"crossref","first-page":"2382","DOI":"10.1681\/ASN.V10112382","volume":"10","author":"Price DA","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1984.147"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1007\/s00125-018-4654-7"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.52"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa042167"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1111\/dom.13639"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004110970"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00234.2006"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1007\/s13300-016-0167-x"},{"key":"B43","first-page":"624","volume":"4","author":"Sengupta P","year":"2013","journal-title":"Int J Prev Med"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M111.327866"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00155.2018"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00182.2018"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010010010"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.2174\/157339905774574374"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2016060666"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.2337\/dc14-1296"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1002\/cphy.c100049"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00941.x"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1007\/s00125-015-3525-8"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.117.028268"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1185\/03007995.2014.919907"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00262.2010"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006070798"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00246.2019","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,9,30]],"date-time":"2022-09-30T11:41:04Z","timestamp":1664538064000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00246.2019"}},"issued":{"date-parts":[[2019,12,1]]},"references-count":57,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2019,12,1]]}},"alternative-id":["10.1152\/ajprenal.00246.2019"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00246.2019","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2019,12,1]]}},{"indexed":{"date-parts":[[2026,2,13]],"date-time":"2026-02-13T15:22:46Z","timestamp":1770996166265,"version":"3.50.1"},"reference-count":42,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2000,3,1]]},"abstract":"<jats:p>The purpose of these experiments was to investigate the mechanisms whereby transforming growth factor-\u03b2 (TGF-\u03b2) antagonizes the action of adrenocorticoid hormones on Na<jats:sup>+<\/jats:sup>transport by the rat inner medullary collecting duct in primary culture. Steroid hormones 1) increased Na<jats:sup>+<\/jats:sup>transport by three- to fourfold, 2) increased the maximum capacity of the Na<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>pump by 30\u201350%, 3) increased the steady-state levels of the \u03b1<jats:sub>1<\/jats:sub>-subunit of the Na<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-ATPase by \u223c30%, and 4) increased the steady-state levels of the \u03b1-subunit of the rat epithelial Na<jats:sup>+<\/jats:sup>channel (\u03b1-rENaC) by nearly fourfold. TGF-\u03b2 blocked the effects of steroids on the increase in Na<jats:sup>+<\/jats:sup>transport and the stimulation of the Na<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-ATPase and pump capacity. However, there was no effect of TGF-\u03b2 on the steroid-induced increase in mRNA levels of \u03b1-rENaC. The effects of TGF-\u03b2 were not secondary to the decrease in Na<jats:sup>+<\/jats:sup>transport per se, inasmuch as benzamil inhibited the increase in Na<jats:sup>+<\/jats:sup>transport but did not block the increase in pump capacity or Na<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-ATPase mRNA. The results indicate that TGF-\u03b2 does not inactivate the steroid receptor or its translocation to the nucleus. Rather, they indicate complex pathways involving interruption of the enhancement of pump activity and activation\/inactivation of pathways distal to the steroid-induced increase in the transcription of \u03b1-rENaC.<\/jats:p>","DOI":"10.1152\/ajprenal.2000.278.3.f425","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T12:57:46Z","timestamp":1514033866000},"page":"F425-F433","source":"Crossref","is-referenced-by-count":20,"title":["Mechanisms of inactivation of the action of aldosterone on collecting duct by TGF-\u03b2"],"prefix":"10.1152","volume":"278","author":[{"given":"Russell F.","family":"Husted","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, University of Iowa, and Department of Veterans Affairs Medical Center, Iowa City, Iowa 52242"}]},{"given":"Rita D.","family":"Sigmund","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Iowa, and Department of Veterans Affairs Medical Center, Iowa City, Iowa 52242"}]},{"given":"John B.","family":"Stokes","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Iowa, and Department of Veterans Affairs Medical Center, Iowa City, Iowa 52242"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"crossref","first-page":"7799","DOI":"10.1016\/S0021-9258(19)38999-9","volume":"265","author":"Barlet-Bas C.","year":"1990","journal-title":"J. Biol. Chem."},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1994.266.5.C1278"},{"key":"B3","doi-asserted-by":"crossref","first-page":"10859","DOI":"10.1016\/S0021-9258(18)99098-8","volume":"266","author":"Bhutada A.","year":"1991","journal-title":"J. Biol. Chem."},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/0003-2697(87)90021-2"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.81.7.1991"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.266.6.F926"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1997.272.5.C1482"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1992.263.4.C810"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1210\/endo-127-1-32"},{"key":"B10","doi-asserted-by":"crossref","first-page":"10338","DOI":"10.1016\/S0021-9258(18)34025-0","volume":"257","author":"Geering K.","year":"1982","journal-title":"J. Biol. Chem."},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1988.255.6.F1160"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1172\/JCI114736"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.267.5.F767"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.2.F433"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1007\/s002329900182"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1007\/BF00370240"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1007\/BF00234994"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1172\/JCI116003"},{"key":"B19","doi-asserted-by":"crossref","first-page":"13736","DOI":"10.1016\/S0021-9258(17)36706-6","volume":"269","author":"Lingueglia E.","year":"1994","journal-title":"J. Biol. Chem."},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1990.318"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.273.3.F372"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.102.1.25"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.102.1.43"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.407"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1988.255.3.F421"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.18.12431"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1993.264.4.C875"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1982.62.4.1131"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1021\/bi00373a001"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.256.5.F862"},{"key":"B31","first-page":"202","volume":"13","author":"Stokes J. B.","year":"1993","journal-title":"Semin. Nephrol."},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1998.274.6.C1699"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.1.F7"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1007\/BF00232796"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1210\/mend-3-9-1369"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.104.5.1231"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118344"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.2.F304"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.1998.275.6.G1227"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1007\/BF00232020"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1172\/JCI116781"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.4.F635"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.2000.278.3.F425","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:41:20Z","timestamp":1660189280000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.2000.278.3.F425"}},"issued":{"date-parts":[[2000,3,1]]},"references-count":42,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2000,3,1]]}},"alternative-id":["10.1152\/ajprenal.2000.278.3.F425"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.2000.278.3.f425","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2000,3,1]]}},{"indexed":{"date-parts":[[2026,2,19]],"date-time":"2026-02-19T23:41:14Z","timestamp":1771544474669,"version":"3.50.1"},"reference-count":46,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2004,10]]},"abstract":"<jats:p>Chronic acidosis is a stimulus for proteolysis in muscle in vivo, but the mechanism of this response is unknown. We tested the hypothesis that acidosis or TNF-\u03b1, a cytokine whose production increases in acidosis, regulates proteolysis by inhibiting insulin signaling through phosphoinositide 3-kinase (PI3K). In cultured L6 myotubes, acidified (pH 7.1) media did not accelerate the basal protein degradation rate, but it inhibited insulin\u2019s ability to suppress proteolysis. Insulin receptor substrate-1 (IRS-1)-associated PI3K activity was not altered in cells acidified for 10 min but was strongly inhibited in cells incubated at pH 7.1 for 24 h. Phosphorylation of Akt was also suppressed by acidification for 24 h. Acidification did not induce changes in IRS-1 abundance, insulin-stimulated IRS-1 tyrosine phosphorylation, or the amount of PI3K p85 regulatory subunit. In contrast to acidification, TNF-\u03b1 suppressed proteolysis in the presence or absence of insulin but had no effect on IRS-1-associated PI3K activity. To establish that the PI3K pathway can regulate protein degradation in muscle, we measured proteolysis in cells after inhibition of PI3K activity with LY-294002 or infection with an adenovirus encoding a dominant negative PI3K p85\u03b1-subunit. Both approaches inhibited insulin-induced suppression of proteolysis to a degree similar to that seen with acidification. We conclude that acidosis accelerates protein degradation by impairing insulin signaling through PI3K in muscle cells.<\/jats:p>","DOI":"10.1152\/ajprenal.00440.2003","type":"journal-article","created":{"date-parts":[[2004,6,1]],"date-time":"2004-06-01T00:13:27Z","timestamp":1086048807000},"page":"F700-F706","source":"Crossref","is-referenced-by-count":62,"title":["Acidosis impairs insulin receptor substrate-1-associated phosphoinositide 3-kinase signaling in muscle cells: consequences on proteolysis"],"prefix":"10.1152","volume":"287","author":[{"given":"Harold A.","family":"Franch","sequence":"first","affiliation":[]},{"given":"Sina","family":"Raissi","sequence":"additional","affiliation":[]},{"given":"Xiaonan","family":"Wang","sequence":"additional","affiliation":[]},{"given":"Bin","family":"Zheng","sequence":"additional","affiliation":[]},{"given":"James L.","family":"Bailey","sequence":"additional","affiliation":[]},{"given":"S. Russ","family":"Price","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118566"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.9.5086"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.1.F198"},{"key":"R4","doi-asserted-by":"crossref","unstructured":"Combaret L, Tilignac T, Claustre A, Voisin L, Taillandier D, Obled C, Tanaka K, and Attaix D.Torbafylline (HWA 448) inhibits enhanced skeletal muscle ubiquitin-proteasome-dependent proteolysis in cancer and septic rats.Biochem J361: 185\u2013192, 2002.","DOI":"10.1042\/bj3610185"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.1999.276.5.E849"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118499"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1172\/JCI18330"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1991.260.2.C277"},{"key":"R9","doi-asserted-by":"crossref","unstructured":"Feinstein R, Kanety H, Papa MZ, Lunenfeld B, and Karasik A.Tumor necrosis factor-\u03b1 suppresses insulin-induced tyrosine phosphorylation of insulin receptor and its substrates.J Biol Chem268: 26055\u201326058, 1993.","DOI":"10.1016\/S0021-9258(19)74276-8"},{"key":"R10","doi-asserted-by":"crossref","unstructured":"Franch HA.Modification of the epidermal growth factor response by ammonia in renal cell hypertrophy.J Am Soc Nephrol11: 1631\u20131638, 2000.","DOI":"10.1681\/ASN.V1191631"},{"key":"R11","unstructured":"Franch HA, Curtis PV, and Mitch WE.Mechanisms of renal tubular cell hypertrophy: mitogen-induced suppression of proteolysis.Am J Physiol Cell Physiol273: C843\u2013C851, 1997."},{"key":"R12","unstructured":"Franch HAand Mitch WE.Catabolism in uremia: the impact of metabolic acidosis.J Am Soc Nephrol9: S78\u2013S81, 1998."},{"key":"R13","doi-asserted-by":"crossref","unstructured":"Franch H, Wang X, Sooparb S, Brown NS, and Du J.Phoshatidylinositol 3-kinase activity is required for epidermal growth factor to suppress proteolysis.J Am Soc Nephrol13: 903\u2013908, 2002.","DOI":"10.1681\/ASN.V134903"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118217"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.48.10.1930"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.11.7455"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.1991.260.5.E727"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1051\/rnd:19990104"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1042\/bj2600377"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1126\/science.289.5488.2363"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.40.23780"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1002\/dmr.5610040805"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1172\/JCI7917"},{"key":"R24","doi-asserted-by":"crossref","unstructured":"Kuru S, Inukai A, Kato T, Liang Y, Kimura S, and Sobue G.Expression of tumor necrosis factor-\u03b1 in regenerating muscle fibers in inflammatory and non-inflammatory myopathies.Acta Neuropathol (Berl)105: 217\u2013224, 2003.","DOI":"10.1007\/s00401-002-0635-4"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1210\/endo.131.5.1385098"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1096\/fj.03-0251com"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1096\/fj.02-0759com"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1172\/JCI116124"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00023.x"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M200501200"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.96"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1985.155"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1172\/JCI112924"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1999.276.5.C1132"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1053\/ajkd.2001.29249"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1053\/jren.2003.50019"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118968"},{"key":"R38","doi-asserted-by":"crossref","unstructured":"Rodrigeuz-Viciana P, Warne PH, Khwaja A, Marte BM, Pappin D, Das P, Waterfield MD, Ridley A, and Downward J.Role of phosphoinostitide 3-OH kinase in cell transformation and control of the actin cytoskeleton by Ras.Cell89: 401\u2013410, 1997.","DOI":"10.1016\/S0092-8674(00)80226-3"},{"key":"R39","doi-asserted-by":"crossref","unstructured":"Sacheck JM, Ohtsuka A, McLary SC, and Goldberg AL.IGF-1 stimulates muscle growth by suppressing protein breakdown and expression of atrophy-related ubiquitin-ligases, atrogin-1 and MuRF1.Am J Physiol Endocrinol Metab. First published April 20, 2004;10.1152\/ajpendo.00073.2004.","DOI":"10.1152\/ajpendo.00073.2004"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(04)00400-3"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.43.26690"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1999.277.2.C320"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.22.3.965-977.2002"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1006\/excr.1999.4701"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1172\/JCI6609"},{"key":"R46","doi-asserted-by":"publisher","DOI":"10.1152\/jappl.1996.81.4.1501"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00440.2003","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,6,22]],"date-time":"2021-06-22T18:39:39Z","timestamp":1624387179000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00440.2003"}},"issued":{"date-parts":[[2004,10]]},"references-count":46,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2004,10]]}},"alternative-id":["10.1152\/ajprenal.00440.2003"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00440.2003","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2004,10]]}},{"indexed":{"date-parts":[[2026,2,19]],"date-time":"2026-02-19T03:00:56Z","timestamp":1771470056973,"version":"3.50.1"},"reference-count":39,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2005,11]]},"abstract":"<jats:p>Peroxisome proliferator-activated receptor-\u03b3 (PPAR\u03b3) are ligand-activated transcription factors that regulate cell growth, inflammation, lipid metabolism, and insulin sensitivity. We recently demonstrated that PPAR\u03b3 agonists limit high glucose-induced inflammation in a model of proximal tubular cells (PTC; Panchapakesan U, Pollock CA, and Chen XM. Am J Physiol Renal Physiol 287: F528\u2013F534, 2004). However, the role of PPAR\u03b3 in the excess extracellular matrix production is largely unknown. We evaluated the effect of 24- to 48-h 8 \u03bcM l-805645 or 10 \u03bcM pioglitazone on 25 mM d-glucose-induced markers of fibrosis in HK-2 cells. High d-glucose induced nuclear binding of activator protein-1 (AP-1) to 140.8 \u00b1 10.9% ( P &lt; 0.05), which was attenuated with L-805645 and pioglitazone to 82.3 \u00b1 14.4 ( P &lt; 0.01 vs. high d-glucose) and 99.3 \u00b1 12.2% ( P &lt; 0.05 vs. high d-glucose), respectively. High d-glucose increased total production of transforming growth factor (TGF)-\u03b2<jats:sub>1<\/jats:sub>139.6 \u00b1 6.5% ( P &lt; 0.05), which was reversed with L-805645 and pioglitazone to 68.73 \u00b1 5.7 ( P &lt; 0.01 vs. high d-glucose) and 112 \u00b1 13.6% ( P &lt; 0.05 vs. high d-glucose). L-805645 and pioglitazone reduced high d-glucose-induced fibronectin from 156.0 \u00b1 24.9 ( P &lt; 0.05) to 81.9 \u00b1 16.0 and 57.4 \u00b1 12.7%, respectively (both P &lt; 0.01 vs. high d-glucose). Collagen IV was not induced by high d-glucose. L-805645 and pioglitazone suppressed collagen IV to 68.0 \u00b1 14.5 ( P &lt; 0.05) and 46.5 \u00b1 11.6% ( P &lt; 0.01) vs. high d-glucose, respectively. High d-glucose increased the nuclear binding of NF-\u03baB to 167 \u00b1 22.4% ( P &lt; 0.05), which was not modified with PPAR\u03b3 agonists. In conclusion, PPAR\u03b3 agonists exert antifibrotic effects in human PTC in high glucose by attenuating the increase in AP-1, TGF-\u03b2<jats:sub>1<\/jats:sub>, and the downstream production of the extracellular matrix protein fibronectin.<\/jats:p>","DOI":"10.1152\/ajprenal.00097.2005","type":"journal-article","created":{"date-parts":[[2005,5,11]],"date-time":"2005-05-11T02:13:45Z","timestamp":1115777625000},"page":"F1153-F1158","source":"Crossref","is-referenced-by-count":66,"title":["PPAR\u03b3 agonists exert antifibrotic effects in renal tubular cells exposed to high glucose"],"prefix":"10.1152","volume":"289","author":[{"given":"U.","family":"Panchapakesan","sequence":"first","affiliation":[]},{"given":"S.","family":"Sumual","sequence":"additional","affiliation":[]},{"given":"C. A.","family":"Pollock","sequence":"additional","affiliation":[]},{"given":"X.","family":"Chen","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.2337\/diacare.26.8.2421"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1016\/S0167-4889(00)00054-9"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1136\/jcp.2003.012989"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1038\/sj.jhh.1001444"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1089\/15209150260007381"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa011161"},{"key":"R7","doi-asserted-by":"crossref","unstructured":"Buckingham RE, Al-Barazanji KA, Toseland CD, Slaughter M, Connor SC, West A, Bond B, Turner NC, and Clapham JC.Peroxisome proliferator-activated receptor-gamma agonist, rosiglitazone, protects against nephropathy and pancreatic islet abnormalities in Zucker fatty rats.Diabetes47: 1326\u20131334, 1998.","DOI":"10.2337\/diabetes.47.8.1326"},{"key":"R8","unstructured":"Chen J, Sun Z, Ma J, Gu Y, Yang H, and Lin S.Abstract: non-metabolic protective effects of pioglitazone on diabetic nephropathy induced by streptozotocin in uninephrectomized rat (Abstract).J Am Soc Nephrol14: 392A, 2003."},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(03)13636-7"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.236"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(95)90193-0"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00054.x"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1358\/dnp.2002.15.3.840011"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.53.1.200"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.2337\/diacare.21.12.2135"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00643.x"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(95)90194-9"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1210\/jcem.86.1.7157"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1016\/j.leukres.2004.09.010"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa011303"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.0590051899.x"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00418.x"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1016\/0378-1119(94)90707-2"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)81574-3"},{"key":"R25","unstructured":"National Institute of Diabetes and Digestive and Kidney Diseases.US Renal Data System. Annual Data Report: Atlas of End-Stage Renal Disease in the United States.Bethesda, MD: National Institute of Diabetes and Digestive and Kidney Diseases, 2003."},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.37.2.722"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00445.2003"},{"key":"R28","doi-asserted-by":"crossref","unstructured":"Ping D, Boekhoudt GH, Rogers EM, and Boss JM.Nuclear factor-\u03baB p65 mediates the assembly and activation of the TNF-responsive element of the murine monocyte chemoattractant-1 gene.J Immunol162: 727\u2013734, 1999.","DOI":"10.4049\/jimmunol.162.2.727"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00277.x"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa042167"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)81575-5"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1136\/bmj.317.7160.703"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00311.x"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-291X(03)00599-0"},{"key":"R35","doi-asserted-by":"crossref","unstructured":"Weigert C, Sauer U, Brodbeck K, Pfeiffer A, Haring HU, and Schleicher ED.AP-1 proteins mediate hyperglycemia-induced activation of the human TGF-\u03b21promoter in mesangial cells.J Am Soc Nephrol11: 2007\u20132016, 2000.","DOI":"10.1681\/ASN.V11112007"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1016\/S0959-437X(99)80021-5"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00574.x"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004040278"},{"key":"R39","unstructured":"Zhang Y, Park CW, Zheng F, Fan X, Striker GE, Breyer MD, and Guan Y.Endogenous PPAR\u03b3 activity ameliorates diabetic nephropathy (Abstract).J Am Soc Nephrol14: 392A, 2003."}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00097.2005","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,5,3]],"date-time":"2023-05-03T06:00:53Z","timestamp":1683093653000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00097.2005"}},"issued":{"date-parts":[[2005,11]]},"references-count":39,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2005,11]]}},"alternative-id":["10.1152\/ajprenal.00097.2005"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00097.2005","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2005,11]]}},{"indexed":{"date-parts":[[2026,2,19]],"date-time":"2026-02-19T08:20:20Z","timestamp":1771489220520,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1981,6,1]]},"abstract":"<jats:p> Radiochemical microprocedures were developed for the determination of hexokinase and phosphoenolpyruvate carboxykinase (PEPCK) activity in single microdissected segments of the mature rabbit nephron dissected from fresh tissue after collagenase treatment. All results were related to tubular length and tubular protein content. Hexokinase activity was found to be lowest in the proximal convoluted tubule and to increase along the following nephron segments, with highest activity in the connecting tubule. The gluconeogenic enzyme PEPCK, on the other hand, was exclusively found in the proximal tubule. Early and late portions of the convoluted segment exhibited the same specific activity, but only 50% was found in the pars recta. All other renal structures exhibited only insignificant activity of PEPCK. The results show that renal glucose metabolism and gluconeogenesis are clearly separated. As previously shown for the cytosolic rat enzyme, rabbit mitochondrial PEPCK is also exclusively a proximal tubular enzyme, thus confirming the dominant role of this segment in mammalian renal gluconeogenesis. The high activity of hexokinase in the segments of the distal tubule points to the role of glucose as metabolic fuel, glycogen precursor, and other glucose-6-phosphate-using pathways in these structures. <\/jats:p>","DOI":"10.1152\/ajprenal.1981.240.6.f492","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T14:21:36Z","timestamp":1513952496000},"page":"F492-F500","source":"Crossref","is-referenced-by-count":13,"title":["Distribution of hexokinase and phosphoenolpyruvate carboxykinase along the rabbit nephron"],"prefix":"10.1152","volume":"240","author":[{"given":"A.","family":"Vandewalle","sequence":"first","affiliation":[]},{"given":"G.","family":"Wirthensohn","sequence":"additional","affiliation":[]},{"given":"H. G.","family":"Heidrich","sequence":"additional","affiliation":[]},{"given":"W. G.","family":"Guder","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1981.240.6.F492","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:21:34Z","timestamp":1567966894000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1981.240.6.F492"}},"issued":{"date-parts":[[1981,6,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1981,6,1]]}},"alternative-id":["10.1152\/ajprenal.1981.240.6.F492"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1981.240.6.f492","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1981,6,1]]}},{"indexed":{"date-parts":[[2026,2,28]],"date-time":"2026-02-28T19:44:00Z","timestamp":1772307840183,"version":"3.50.1"},"reference-count":54,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2007,8]]},"abstract":"<jats:p>Oxidized low-density lipoproteins (oxLDL) and their scavenger receptor (SR) binding partners play a central role in atherosclerosis and by analogy may play a role in chronic kidney disease pathogenesis. The present study was designed to investigate in C57BL\/6 mice the effects of hypercholesterolemia on renal injury severity and oxLDL generation after unilateral ureteral obstruction (UUO). The expression profiles of CD36, SR class AI\/II (SR-A), lectin-like receptor for oxidized low-density lipoprotein-1 (Lox-1), and SR that binds phosphatidylserine and oxLDL (SR-PSOX\/CXCL16) were examined. Four experimental groups were studied: sham and UUO male mice on either a high-fat Western diet or a control diet. Significantly more oxLDL accumulated in the tubulointerstitium of hypercholesterolemic mice compared with normocholesterolemic mice after 14 days of UUO ( P &lt; 0.01). Total kidney collagen was significantly higher in the obstructed kidneys of hypercholesterolemic mice compared with normocholesterolemic mice on day 14 ( P &lt; 0.01). After 14 days of obstruction, the number of interstitial F4\/80+ macrophages and NF-\u03baB activation increased in hypercholesterolemic mice compared with normocholesterolemic mice ( P &lt; 0.01). In normal kidneys, CD36, SR-A, Lox-1, and CXCL16 were primarily localized to renal tubular epithelia. After ureteral obstruction, CD36 increased at day 7; SR-A and Lox-1 progressively decreased in a time-dependent manner; and CXCL16 increased significantly with the onset of obstruction ( P &lt; 0.01). Strong tubular expression suggests that in addition to inflammatory interstitial cells, renal tubular scavenger receptors may help to orchestrate the inflammatory and fibrogenic pathways that are activated by oxLDL.<\/jats:p>","DOI":"10.1152\/ajprenal.00063.2007","type":"journal-article","created":{"date-parts":[[2007,5,31]],"date-time":"2007-05-31T01:04:40Z","timestamp":1180573480000},"page":"F575-F585","source":"Crossref","is-referenced-by-count":65,"title":["Atherogenic scavenger receptor modulation in the tubulointerstitium in response to chronic renal injury"],"prefix":"10.1152","volume":"293","author":[{"given":"Daryl M.","family":"Okamura","sequence":"first","affiliation":[]},{"given":"Jes\u00fas M.","family":"L\u00f3pez-Guisa","sequence":"additional","affiliation":[]},{"given":"Katie","family":"Koelsch","sequence":"additional","affiliation":[]},{"given":"Sarah","family":"Collins","sequence":"additional","affiliation":[]},{"given":"Allison A.","family":"Eddy","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.172.10.6362"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1186\/1471-2199-7-8"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20040731"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.105.540583"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1152\/ajplung.00474.2004"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M406202200"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00752.x"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000130428.85603.6B"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000184250.37607.da"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.37.25959"},{"key":"R11","doi-asserted-by":"crossref","unstructured":"Coller SP, Paulnock DM.Signaling pathways initiated in macrophages after engagement of type A scavenger receptors.J Leukoc Biol70: 142\u2013148, 2001.","DOI":"10.1189\/jlb.70.1.142"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1159\/000093673"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.275.17.12633"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.173.10.6427"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1172\/JCI21514"},{"key":"R16","doi-asserted-by":"crossref","unstructured":"Drukker A, Eddy AA.Failure of antioxidant therapy to attenuate interstitial disease in rats with reversible nephrotic syndrome.J Am Soc Nephrol9: 243\u2013251, 1998.","DOI":"10.1681\/ASN.V92243"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1172\/JCI14006"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1172\/JCI9259"},{"key":"R19","unstructured":"Gao J, Liu DP, Huang Y, Dong WJ, Wu M, Feng DX, Liang CC.Excessive expression of the scavenger receptor class A type I can significantly affect the serum lipids.Sheng Wu Hua Xue Yu Sheng Wu Wu Li Xue Bao (Shanghai)35: 117\u2013121, 2003."},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.172.6.3678"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.176.1.43"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1161\/01.ATV.0000012402.85056.45"},{"key":"R23","unstructured":"Huh HY, Pearce SF, Yesner LM, Schindler JL, Silverstein RL.Regulated expression of CD36 during monocyte-to-macrophage differentiation: potential role of CD36 in foam cell formation.Blood87: 2020\u20132028, 1996."},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1161\/01.ATV.20.8.1953"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M507599200"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1189\/jlb.0504270"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1172\/JCI11902"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M209649200"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(98)70145-3"},{"key":"R30","unstructured":"Lipsky RH, Eckert DM, Tang Y, Ockenhouse CF.The carboxyl-terminal cytoplasmic domain of CD36 is required for oxidized low-density lipoprotein modulation of NF-kappaB activity by tumor necrosis factor-alpha.Recept Signal Transduct7: 1\u201311, 1997."},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00327.x"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.275.23.17661"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1161\/hq1001.096652"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-200501000-00017"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M208788200"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1189\/jlb.0104014"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.2000.tb06307.x"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1016\/j.str.2005.03.016"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1016\/0021-9150(87)90249-8"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9378(97)70070-X"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00587.x"},{"key":"R42","doi-asserted-by":"crossref","unstructured":"Ryeom SW, Sparrow JR, Silverstein RL.CD36 participates in the phagocytosis of rod outer segments by retinal pigment epithelium.J Cell Sci109: 387\u2013395, 1996.","DOI":"10.1242\/jcs.109.2.387"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1007\/PL00013428"},{"key":"R44","unstructured":"Sakaguchi H, Takeya M, Suzuki H, Hakamata H, Kodama T, Horiuchi S, Gordon S, van der Laan LJ, Kraal G, Ishibashi S, Kitamura N, Takahashi K.Role of macrophage scavenger receptors in diet-induced atherosclerosis in mice.Lab Invest78: 423\u2013434, 1998."},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.C400163200"},{"key":"R46","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.171.4.1647"},{"key":"R47","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00449.2003"},{"key":"R48","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pmed.0020045"},{"key":"R49","doi-asserted-by":"publisher","DOI":"10.1038\/386292a0"},{"key":"R50","doi-asserted-by":"publisher","DOI":"10.1291\/hypres.26.117"},{"key":"R51","doi-asserted-by":"publisher","DOI":"10.2337\/db06-0359"},{"key":"R52","doi-asserted-by":"crossref","unstructured":"Whitman SC, Rateri DL, Szilvassy SJ, Cornicelli JA, Daugherty A.Macrophage-specific expression of class A scavenger receptors in LDL receptor(\u2212\/\u2212) mice decreases atherosclerosis and changes spleen morphology.J Lipid Res43: 1201\u20131208, 2002.","DOI":"10.1194\/jlr.M200116-JLR200"},{"key":"R53","doi-asserted-by":"publisher","DOI":"10.1161\/01.ATV.16.8.1019"},{"key":"R54","doi-asserted-by":"publisher","DOI":"10.1007\/s00408-004-2525-0"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00063.2007","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,5,12]],"date-time":"2023-05-12T02:45:14Z","timestamp":1683859514000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00063.2007"}},"issued":{"date-parts":[[2007,8]]},"references-count":54,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2007,8]]}},"alternative-id":["10.1152\/ajprenal.00063.2007"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00063.2007","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2007,8]]}},{"indexed":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T03:50:36Z","timestamp":1772164236290,"version":"3.50.1"},"reference-count":29,"publisher":"American Physiological Society","issue":"11","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2014,6,1]]},"abstract":"<jats:p>\n                    Nephron number ( N\n                    <jats:sub>glom<\/jats:sub>\n                    ) and size (V\n                    <jats:sub>glom<\/jats:sub>\n                    ) are correlated with risk for chronic cardiovascular and kidney disease and may be predictive of renal allograft viability. Unfortunately, there are no techniques to assess N\n                    <jats:sub>glom<\/jats:sub>\n                    and V\n                    <jats:sub>glom<\/jats:sub>\n                    in intact kidneys. This work demonstrates the use of cationized ferritin (CF) as a magnetic resonance imaging (MRI) contrast agent to measure N\n                    <jats:sub>glom<\/jats:sub>\n                    and V\n                    <jats:sub>glom<\/jats:sub>\n                    in viable human kidneys donated to science. The kidneys were obtained from patients with varying levels of cardiovascular and renal disease. CF was intravenously injected into three viable human kidneys. A fourth control kidney was perfused with saline. After fixation, immunofluorescence and electron microscopy confirmed binding of CF to the glomerulus. The intact kidneys were imaged with three-dimensional MRI and CF-labeled glomeruli appeared as punctate spots. Custom software identified, counted, and measured the apparent volumes of CF-labeled glomeruli, with an \u223c6% false positive rate. These measurements were comparable to stereological estimates. The MRI-based technique yielded a novel whole kidney distribution of glomerular volumes. Histopathology demonstrated that the distribution of CF-labeled glomeruli may be predictive of glomerular and vascular disease. Variations in CF distribution were quantified using image texture analyses, which be a useful marker of glomerular sclerosis. This is the first report of direct measurement of glomerular number and volume in intact human kidneys.\n                  <\/jats:p>","DOI":"10.1152\/ajprenal.00092.2014","type":"journal-article","created":{"date-parts":[[2014,3,20]],"date-time":"2014-03-20T00:20:28Z","timestamp":1395274828000},"page":"F1381-F1390","source":"Crossref","is-referenced-by-count":97,"title":["MRI-based glomerular morphology and pathology in whole human kidneys"],"prefix":"10.1152","volume":"306","author":[{"given":"Scott C.","family":"Beeman","sequence":"first","affiliation":[{"name":"Department of Radiology, Washington University School of Medicine, Saint Louis, Missouri;"}]},{"given":"Luise A.","family":"Cullen-McEwen","sequence":"additional","affiliation":[{"name":"Department of Anatomy and Developmental Biology, Monash University, Melbourne, Victoria, Australia;"}]},{"given":"Victor G.","family":"Puelles","sequence":"additional","affiliation":[{"name":"Department of Anatomy and Developmental Biology, Monash University, Melbourne, Victoria, Australia;"}]},{"given":"Min","family":"Zhang","sequence":"additional","affiliation":[{"name":"School of Computing, Informatics, and Decision Systems Engineering, Arizona State University, Tempe, Arizona;"}]},{"given":"Teresa","family":"Wu","sequence":"additional","affiliation":[{"name":"School of Computing, Informatics, and Decision Systems Engineering, Arizona State University, Tempe, Arizona;"}]},{"given":"Edwin J.","family":"Baldelomar","sequence":"additional","affiliation":[{"name":"Department of Physics, College of Natural Sciences, University of Hawaii at Manoa, Honolulu, Hawaii;"}]},{"given":"John","family":"Dowling","sequence":"additional","affiliation":[{"name":"Department of Anatomical Pathology, Monash Medical Centre, Clayton, Victoria, Australia;"}]},{"given":"Jennifer R.","family":"Charlton","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Division of Nephrology, University of Virginia Medical Center, Charlottesville, Virginia;"}]},{"given":"Michael S.","family":"Forbes","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Division of Nephrology, University of Virginia Medical Center, Charlottesville, Virginia;"}]},{"given":"Amanda","family":"Ng","sequence":"additional","affiliation":[{"name":"Monash Biomedical Imaging, Monash University, Melbourne, Australia; and"}]},{"given":"Qi-zhu","family":"Wu","sequence":"additional","affiliation":[{"name":"Monash Biomedical Imaging, Monash University, Melbourne, Australia; and"}]},{"given":"James A.","family":"Armitage","sequence":"additional","affiliation":[{"name":"Department of Anatomy and Developmental Biology, Monash University, Melbourne, Victoria, Australia;"}]},{"given":"Gary F.","family":"Egan","sequence":"additional","affiliation":[{"name":"Monash Biomedical Imaging, Monash University, Melbourne, Australia; and"}]},{"given":"John F.","family":"Bertram","sequence":"additional","affiliation":[{"name":"Department of Anatomy and Developmental Biology, Monash University, Melbourne, Victoria, Australia;"}]},{"given":"Kevin M.","family":"Bennett","sequence":"additional","affiliation":[{"name":"Department of Biology, College of Natural Sciences, University of Hawaii at Manoa, Honolulu, Hawaii"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1002\/mrm.24301"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1002\/mrm.24619"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00044.2011"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00714.2012"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1002\/mrm.21684"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-013-2600-y"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-011-1843-8"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1007\/BF00381877"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1093\/ajh\/1.4.335"},{"key":"B10","unstructured":"Centers for Disease Control and Prevention.\n                      National\n                      chronic kidney disease fact sheet: general information and national estimates on chronic kidney disease in the United States, 2010."},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1002\/cmmi.1578"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-61779-851-1_10"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-61779-851-1_30"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00767.x"},{"key":"B15","first-page":"26","volume":"65","author":"Damadian R","year":"1965","journal-title":"J Lab Clin Med"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/0022-5320(72)90087-1"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa041031"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfr273"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0b013e3282f9b1a5"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1159\/000327044"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1006\/nimg.2002.1132"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-200411000-00022"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1002\/ar.1092320205"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfr539"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1148\/radiol.13121352"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013040376"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000125670.64996.BB"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.00600206"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1002\/mrm.21761"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00092.2014","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:53:09Z","timestamp":1567972389000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00092.2014"}},"issued":{"date-parts":[[2014,6,1]]},"references-count":29,"journal-issue":{"issue":"11","published-print":{"date-parts":[[2014,6,1]]}},"alternative-id":["10.1152\/ajprenal.00092.2014"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00092.2014","relation":{"has-review":[{"id-type":"doi","id":"10.3410\/f.718319233.793496641","asserted-by":"object"}]},"ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2014,6,1]]}},{"indexed":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T03:50:07Z","timestamp":1772164207167,"version":"3.50.1"},"reference-count":85,"publisher":"American Physiological Society","issue":"1","funder":[{"DOI":"10.13039\/100014989","name":"Chan Zuckerberg Initiative","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100014989","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000738","name":"U.S. Department of Veterans Affairs","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000738","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2025,7,1]]},"abstract":"<jats:p>African American women experience a disproportionate burden of hypertension and chronic kidney disease, yet their molecular underpinnings remain understudied. This study uniquely integrates transcriptomic data from 344 African American women to uncover 95 female-specific genes jointly associated with hypertension and reduced kidney function. These genes implicate immune activation, cytoskeletal remodeling, and metabolic dysregulation as key contributors to renal decline. By identifying sex-specific molecular pathways, this work advances precision medicine approaches to address kidney health disparities.<\/jats:p>","DOI":"10.1152\/ajprenal.00067.2025","type":"journal-article","created":{"date-parts":[[2025,5,30]],"date-time":"2025-05-30T13:40:21Z","timestamp":1748612421000},"page":"F59-F70","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["Intersecting transcriptomic landscapes of hypertension and kidney function in African American women"],"prefix":"10.1152","volume":"329","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5484-5875","authenticated-orcid":false,"given":"Malak","family":"Abbas","sequence":"first","affiliation":[{"name":"National Institutes of Health","place":["United States"]}]},{"given":"Pamela","family":"Martin","sequence":"additional","affiliation":[{"name":"Meharry Medical College","place":["United States"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4090-0391","authenticated-orcid":false,"given":"Merry L.","family":"Lindsey","sequence":"additional","affiliation":[{"name":"Meharry Medical College","place":["United States"]},{"name":"Veterans Affairs Medical Center","place":["United States"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1605-7250","authenticated-orcid":false,"given":"Eric S.","family":"Bennett","sequence":"additional","affiliation":[{"name":"Cardio-Renal Institute, Wright State University","place":["United States"]}]},{"given":"Thomas L.","family":"Brown","sequence":"additional","affiliation":[{"name":"Cardio-Renal Institute, Wright State University","place":["United States"]}]},{"given":"Chike","family":"Nzerue","sequence":"additional","affiliation":[{"name":"Meharry Medical College","place":["United States"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7026-7737","authenticated-orcid":false,"given":"Clintoria R.","family":"Williams","sequence":"additional","affiliation":[{"name":"Cardio-Renal Institute, Wright State University","place":["United States"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1180-2792","authenticated-orcid":false,"given":"Amadou","family":"Gaye","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/00k63dq23","id-type":"ROR","asserted-by":"publisher"}],"name":"Meharry Medical College","place":["United States"]}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.122.321762"},{"key":"B2","unstructured":"WHO. Hypertension. https:\/\/www.who.int\/news-room\/fact-sheets\/detail\/hypertension, 2023."},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.15585\/mmwr.mm7309a1"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1161\/CIR.0000000000000597"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/j.jacc.2021.06.017"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa0907355"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1161\/JAHA.117.007988"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2007.09.023"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2012.369"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2019.04.032"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1038\/s41591-024-02858-2"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCGEN.123.004259"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1016\/j.kisu.2017.07.004"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/physiol.00026.2016"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-021-83589-z"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1038\/s41371-024-00898-2"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1186\/s12967-018-1664-7"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1161\/JAHA.119.012508"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/ddu478"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1038\/s41467-024-53452-6"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1038\/s41467-024-50297-x"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/s41562-024-01909-5"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1038\/s41467-019-11704-w"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.111.180729"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1111\/cts.12511"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/j.isci.2023.106686"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.3389\/fendo.2021.774436"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-023-46555-5"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1161\/JAHA.124.034417"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.3390\/biomedicines11010118"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1007\/s10528-023-10389-7"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.121.18026"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/ddac245"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1146\/annurev-biodatasci-122220-112550"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1038\/s41591-021-01672-4"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1007\/s11606-021-07073-0"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1053\/j.ackd.2015.08.004"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002374"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00197.2024"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1152\/physiolgenomics.00144.2021"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0313252"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1038\/s41591-022-01869-1"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-024-71669-9"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00332.2024"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1007\/s40615-021-01040-5"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2021.08.003"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa2102953"},{"key":"B48","unstructured":"BroadInstitute. Analysis pipelines for the GTEx Consortium and TOPMed. GitHub. https:\/\/github.com\/broadinstitute\/gtex-pipeline 2015."},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1186\/gb-2010-11-3-r25"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1111\/j.2517-6161.1995.tb02031.x"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.3389\/fgene.2016.00225"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1002\/pro.4172"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2020.08.035"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-022-21634-1"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1136\/jmedgenet-2012-101442"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1042\/CS20210625"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1016\/j.metabol.2023.155718"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.3390\/biomedicines10102642"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.120.314458"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.2006.01610.x"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00051.2003"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.3390\/ijms24087465"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.3390\/cimb44040114"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1016\/j.ajhg.2018.01.015"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.3390\/biomedicines9020182"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pmed.0030274"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.3389\/fimmu.2024.1303115"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.4110\/in.2014.14.3.123"},{"key":"B69","doi-asserted-by":"publisher","DOI":"10.1126\/scisignal.aan4931"},{"key":"B70","doi-asserted-by":"publisher","DOI":"10.1186\/s12943-023-01826-7"},{"key":"B71","doi-asserted-by":"publisher","DOI":"10.1016\/j.heliyon.2023.e16961"},{"key":"B72","doi-asserted-by":"publisher","DOI":"10.3389\/fimmu.2022.791158"},{"key":"B73","doi-asserted-by":"publisher","DOI":"10.1093\/ckj\/sfac196"},{"key":"B74","doi-asserted-by":"publisher","DOI":"10.1055\/s-2007-1020057"},{"key":"B75","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00557.2012"},{"key":"B76","doi-asserted-by":"publisher","DOI":"10.3390\/biom13101450"},{"key":"B77","doi-asserted-by":"publisher","DOI":"10.1038\/s41581-024-00913-2"},{"key":"B78","doi-asserted-by":"publisher","DOI":"10.1016\/j.xkme.2024.100826"},{"key":"B79","doi-asserted-by":"publisher","DOI":"10.1016\/j.biopha.2023.115674"},{"key":"B80","doi-asserted-by":"publisher","DOI":"10.3390\/cells9020405"},{"key":"B81","doi-asserted-by":"publisher","DOI":"10.1002\/path.5631"},{"key":"B82","doi-asserted-by":"publisher","DOI":"10.1385\/IR:36:1:197"},{"key":"B83","doi-asserted-by":"publisher","DOI":"10.3389\/fimmu.2014.00491"},{"key":"B84","doi-asserted-by":"publisher","unstructured":"Hoffmann M, Willruth LL, Dietrich A, Lee HK, Knabl L, Trummer N, Baumbach J, Furth PA, Hennighausen L, List M. Blood transcriptomics analysis offers insights into variant-specific immune response to SARS-CoV-2 (Preprint). bioRxiv, 2023. doi:10.1101\/2023.11.03.564190. 38076885","DOI":"10.1101\/2023.11.03.564190"},{"key":"B85","doi-asserted-by":"publisher","DOI":"10.1016\/j.celrep.2020.03.063"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00067.2025","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,12,3]],"date-time":"2025-12-03T14:35:28Z","timestamp":1764772528000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00067.2025"}},"issued":{"date-parts":[[2025,7,1]]},"references-count":85,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2025,7,1]]}},"alternative-id":["10.1152\/ajprenal.00067.2025"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00067.2025","relation":{"has-preprint":[{"id-type":"doi","id":"10.1101\/2025.01.16.633488","asserted-by":"object"}]},"ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2025,7,1]]},"assertion":[{"value":"2025-02-25","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2025-04-05","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2025-05-27","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2025-06-18","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T03:50:07Z","timestamp":1772164207237,"version":"3.50.1"},"reference-count":44,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2009,8]]},"abstract":"<jats:p>\n                    Extracellular nucleotides are local, short-lived signaling molecules that inhibit renal tubular transport via both luminal and basolateral P2 receptors. Apparently, the renal epithelium itself is able to release nucleotides. The mechanism and circumstances under which nucleotide release is stimulated remain elusive. Here, we investigate the phenomenon of nucleotide secretion in intact, perfused mouse medullary thick ascending limb (mTAL) and cortical collecting duct (CCD). The nucleotide secretion was monitored by a biosensor adapted to register nucleotides in the tubular outflow. Intracellular Ca\n                    <jats:sup>2+<\/jats:sup>\n                    concentration ([Ca\n                    <jats:sup>2+<\/jats:sup>\n                    ]\n                    <jats:sub>i<\/jats:sub>\n                    ) was measured simultaneously in the biosensor cells and the renal tubule with fluo 4. We were able to identify spontaneous tubular nucleotide secretion in resting perfused mTAL. In this preparation, 10 nM AVP and 1-desamino-8-d-arginine vasopressin (dDAVP) induced robust [Ca\n                    <jats:sup>2+<\/jats:sup>\n                    ]\n                    <jats:sub>i<\/jats:sub>\n                    oscillations, whereas AVP in the CCD induced large, slow, and transient [Ca\n                    <jats:sup>2+<\/jats:sup>\n                    ]\n                    <jats:sub>i<\/jats:sub>\n                    elevations. Importantly, we identify that AVP\/dDAVP triggers tubular secretion of nucleotides in the mTAL. After addition of AVP\/dDAVP, the biosensor registered bursts of nucleotides in the tubular perfusate, corresponding to a tubular nucleotide concentration of \u223c0.2\u20130.3 \u03bcM. A very similar response was observed after AVP stimulation of CCDs. Thus AVP stimulated tubular secretion of nucleotides in a burst-like pattern with peak tubular nucleotide concentrations in the low-micromolar range. We speculate that local nucleotide signaling is an intrinsic feedback element of hormonal control of renal tubular transport.\n                  <\/jats:p>","DOI":"10.1152\/ajprenal.00190.2009","type":"journal-article","created":{"date-parts":[[2009,6,10]],"date-time":"2009-06-10T21:09:15Z","timestamp":1244668155000},"page":"F341-F349","source":"Crossref","is-referenced-by-count":26,"title":["AVP-stimulated nucleotide secretion in perfused mouse medullary thick ascending limb and cortical collecting duct"],"prefix":"10.1152","volume":"297","author":[{"given":"Elvin","family":"Odgaard","sequence":"first","affiliation":[]},{"given":"Helle A.","family":"Praetorius","sequence":"additional","affiliation":[]},{"given":"Jens","family":"Leipziger","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2000.00361.x"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1997.sp021927"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2004.072306"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1007\/BF00585935"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.270.4.F623"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-007-0366-4"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1007\/BF00582110"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbamcr.2004.06.004"},{"key":"R9","doi-asserted-by":"crossref","unstructured":"Hayashi S\n                      , Hazama A, Dutta AK, Sabirov RZ, Okada Y.\n                      Detecting ATP release by a biosensor method.\n                      Sci STKE\n                      2004: l14, 2004.","DOI":"10.1126\/stke.2582004pl14"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006070700"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M302680200"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-291X(05)81265-3"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.6.F863"},{"key":"R14","unstructured":"Knepper MA\n                      , Nielsen S, Chou CL, DiGiovanni SR.\n                      Mechanism of vasopressin action in the renal collecting duct.\n                      Semin Nephrol\n                      14\n                      : 302\u2013321, 1994."},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1124\/mol.64.4.785"},{"key":"R16","doi-asserted-by":"crossref","unstructured":"Lehrmann H\n                      , Thomas J, Kim SJ, Jacobi C, Leipziger J.\n                      Luminal P2Y\n                      2\n                      receptor-mediated inhibition of Na\n                      +\n                      absorption in isolated perfused mouse CCD.\n                      J Am Soc Nephrol\n                      13\n                      : 10\u201318, 2002.","DOI":"10.1681\/ASN.V13110"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00075.2002"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1124\/mol.105.021436"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1111\/j.1460-9568.2004.03831.x"},{"key":"R20","doi-asserted-by":"crossref","unstructured":"Macfarlane SR\n                      , Seatter MJ, Kanke T, Hunter GD, Plevin R.\n                      Proteinase-activated receptors.\n                      Pharmacol Rev\n                      53\n                      : 245\u2013282, 2001.","DOI":"10.1016\/S0031-6997(24)01493-5"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00196.2007"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1007\/BF00372961"},{"key":"R23","unstructured":"Okada S\n                      , Paradiso AM, Lazarowski ER, Boucher RC.\n                      A calcium-dependent pathway in swelling-induced ATP release from airway epithelial cells.\n                      J Physiol\n                      567\n                      : C53, 2006."},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1038\/359241a0"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.275.16.11735"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.91.8.3275"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M807129200"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2008.155085"},{"key":"R29","unstructured":"Praetorius HA\n                      , Leipziger J.\n                      ATP release from non-excitable cells.\n                      Purinergic Signal.\n                      In press."},{"key":"R30","doi-asserted-by":"crossref","unstructured":"Rieg T\n                      , Bundey RA, Chen Y, Deschenes G, Junger WG, Insel PA, Vallon V.\n                      Mice lacking P2Y\n                      2\n                      receptors have salt-insensitive hypertension and facilitated renal Na\n                      +\n                      and water reabsorption.\n                      FASEB\n                      J 13, 3717\u20133726. 2007.","DOI":"10.1096\/fj.07-8807com"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.90784.2008"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.267.2.F289"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-2952(97)00070-1"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.6.F945"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1007\/s00232-001-0059-4"},{"key":"R36","unstructured":"Unwin RJ\n                      , Bailey MA, Burnstock G.\n                      Purinergic signaling along the renal tubule: the current state of play.\n                      News Physiol Sci\n                      18\n                      : 237\u2013241, 2003."},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00432.2007"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005111171"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.256.5.F957"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2008.153015"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1016\/0076-6879(90)91015-X"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90542.2008"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2001.012606"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90311.2008"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00190.2009","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,2,9]],"date-time":"2025-02-09T21:43:43Z","timestamp":1739137423000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00190.2009"}},"issued":{"date-parts":[[2009,8]]},"references-count":44,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2009,8]]}},"alternative-id":["10.1152\/ajprenal.00190.2009"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00190.2009","relation":{"has-review":[{"id-type":"doi","id":"10.3410\/f.1162122.622587","asserted-by":"object"}]},"ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2009,8]]}},{"indexed":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T03:49:38Z","timestamp":1772164178654,"version":"3.50.1"},"reference-count":53,"publisher":"American Physiological Society","issue":"2","funder":[{"DOI":"10.13039\/100006812","name":"Center for Integrated Healthcare, U.S. Department of Veterans Affairs (VISN 2 Center for Integrated Healthcare)","doi-asserted-by":"publisher","award":["IK2BX002240"],"award-info":[{"award-number":["IK2BX002240"]}],"id":[{"id":"10.13039\/100006812","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100006812","name":"Center for Integrated Healthcare, U.S. Department of Veterans Affairs (VISN 2 Center for Integrated Healthcare)","doi-asserted-by":"publisher","award":["1I01BX002984"],"award-info":[{"award-number":["1I01BX002984"]}],"id":[{"id":"10.13039\/100006812","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)","doi-asserted-by":"publisher","award":["R01DK087707"],"award-info":[{"award-number":["R01DK087707"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000901","name":"Juvenile Diabetes Research Foundation International (JDRF)","doi-asserted-by":"publisher","award":["201302131"],"award-info":[{"award-number":["201302131"]}],"id":[{"id":"10.13039\/100000901","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2017,8,1]]},"abstract":"<jats:p>Enhanced expression of cyclooxygenase 2 (COX2) in podocytes contributes to glomerular injury in diabetic kidney disease, but some basal level of podocyte COX2 expression might be required to promote podocyte attachment and\/or survival. To investigate the role of podocyte COX2 expression in diabetic kidney disease, we deleted COX2 specifically in podocytes in a mouse model of Type 1 diabetes mellitus (Akita mice). Podocyte-specific knockout (KO) of COX2 did not affect renal morphology or albuminuria in nondiabetic mice. Albuminuria was significantly increased in wild-type (WT) and KO Akita mice compared with nondiabetic controls, and the increase in albuminuria was significantly greater in KO Akita mice compared with WT Akita mice at both 16 and 20 wk of age. At the 20-wk time point, mesangial expansion was also increased in WT and KO Akita mice compared with nondiabetic animals, and these histologic abnormalities were not improved by KO of COX2. Tubular injury was seen only in diabetic mice, but there were no significant differences between groups. Thus, KO of COX2 enhanced albuminuria and did not improve the histopathologic features of diabetic kidney disease. These data suggest that 1) KO of COX2 in podocytes does not ameliorate diabetic kidney disease in Akita mice, and 2) some basal level of podocyte COX2 expression in podocytes is necessary to attenuate the adverse effects of diabetes on glomerular filtration barrier function.<\/jats:p>","DOI":"10.1152\/ajprenal.00614.2016","type":"journal-article","created":{"date-parts":[[2017,5,11]],"date-time":"2017-05-11T09:57:05Z","timestamp":1494496625000},"page":"F430-F439","source":"Crossref","is-referenced-by-count":10,"title":["Podocyte-specific knockout of cyclooxygenase 2 exacerbates diabetic kidney disease"],"prefix":"10.1152","volume":"313","author":[{"given":"Liming","family":"Wang","sequence":"first","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Duke University and Durham Veterans Affairs Medical Centers, Durham, North Carolina;"}]},{"given":"Yonggang","family":"Sha","sequence":"additional","affiliation":[{"name":"Division of Hematologic Malignancies and Cellular Therapy, Department of Medicine, Duke University Medical Center, Durham, North Carolina;"}]},{"given":"Jingyi","family":"Bai","sequence":"additional","affiliation":[{"name":"Duke University, Durham, North Carolina;"}]},{"given":"William","family":"Eisner","sequence":"additional","affiliation":[{"name":"Division of Hematological Malignancies, Department of Medicine, Duke University Medical Center, Durham, North Carolina; and"}]},{"given":"Matthew A.","family":"Sparks","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Duke University and Durham Veterans Affairs Medical Centers, Durham, North Carolina;"}]},{"given":"Anne F.","family":"Buckley","sequence":"additional","affiliation":[{"name":"Department of Pathology, Duke University Medical Center, Durham, North Carolina"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3858-0317","authenticated-orcid":false,"given":"Robert F.","family":"Spurney","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Duke University and Durham Veterans Affairs Medical Centers, Durham, North Carolina;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa011161"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0033942"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009010039"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010111149"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00520.x"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2011060577"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.52.4.1031"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/11.7.1256"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00240.2001"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/j.tcb.2007.06.006"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1172\/JCI44774"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00204.2005"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90515.2008"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002192"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1042\/BST0360543"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1982.82"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.128"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2818.1979.tb00149.x"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1159\/000113538"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00019.x"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1172\/JCI10228"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0096987"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2010.090578"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00044.x"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2012111078"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa011303"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/j.ecl.2010.05.011"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000019782.37851.BF"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1007\/s001250051447"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1002\/gene.10164"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.2337\/diacare.27.2007.S79"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1002\/dvg.20335"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1042\/CS20120543"},{"key":"B34","unstructured":"National Research Council (U.S.). Committee for the Update of the Guide for the Care and Use of Laboratory Animals., Institute for Laboratory Animal Research (U.S.), and National Academies Press (U.S.).\n                      Guide for the Care and Use of Laboratory Animals\n                      . Washington, D.C.: National Academies Press, 2011, p. xxv."},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00413.x"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.01259.2010"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00527.x"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)64357-X"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008090955"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1002\/ar.20625"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013080859"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfn644"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0805806106"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1210\/me.2011-0029"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2011.472"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008010113"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1172\/JCI76767"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.51.10.3083"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.01089.2003"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002222"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.54.6.1626"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1002\/9780470942390.mo100149"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00416.x"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00614.2016","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:08:06Z","timestamp":1567969686000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00614.2016"}},"issued":{"date-parts":[[2017,8,1]]},"references-count":53,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2017,8,1]]}},"alternative-id":["10.1152\/ajprenal.00614.2016"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00614.2016","relation":{"has-review":[{"id-type":"doi","id":"10.3410\/f.727605373.793533309","asserted-by":"object"}]},"ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2017,8,1]]}},{"indexed":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T05:55:34Z","timestamp":1772171734634,"version":"3.50.1"},"reference-count":50,"publisher":"American Physiological Society","issue":"7","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2014,10,1]]},"abstract":"<jats:p>Carbonic anhydrase 2 regulates acid-base homeostasis, and recent findings have indicated a correlation between cellular control of acid-base status and the innate defense of the kidney. Mice deficient in carbonic anhydrase 2 ( Car2<jats:sup>\u2212\/\u2212<\/jats:sup>mice) have metabolic acidosis, impaired urine acidification, and are deficient in normal intercalated cells. The objective of the present study was to evaluate the biological consequences of carbonic anhydrase 2 deficiency in a murine model of pyelonephritis. Infection susceptibility and transcription of bacterial response components in Car2<jats:sup>\u2212\/\u2212<\/jats:sup>mice were compared with wild-type littermate controls. Car2<jats:sup>\u2212\/\u2212<\/jats:sup>mice had increased kidney bacterial burdens along with decreased renal bacterial clearance after inoculation compared with wild-type mice. Standardization of the urine pH and serum HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup>levels did not substantially alter kidney infection susceptibility between wild-type and Car2<jats:sup>\u2212\/\u2212<\/jats:sup>mice; thus, factors other than acid-base status are responsible. Car2<jats:sup>\u2212\/\u2212<\/jats:sup>mice had significantly increased neutrophil-gelatinase-associated lipocalin mRNA and protein and expression at baseline and a marked decreased ability to upregulate key bacterial response genes during pyelonephritis. Our findings provide in vivo evidence that supports a role for carbonic anhydrase 2 and intercalated cells in promoting renal bacterial clearance. Decreased carbonic anhydrase expression results in increased antimicrobial peptide production by cells other than renal intercalated cells, which is not sufficient to prevent infection after a bacterial challenge.<\/jats:p>","DOI":"10.1152\/ajprenal.00344.2014","type":"journal-article","created":{"date-parts":[[2014,8,21]],"date-time":"2014-08-21T06:52:48Z","timestamp":1408603968000},"page":"F869-F880","source":"Crossref","is-referenced-by-count":38,"title":["Carbonic anhydrase 2 deficiency leads to increased pyelonephritis susceptibility"],"prefix":"10.1152","volume":"307","author":[{"given":"David S.","family":"Hains","sequence":"first","affiliation":[{"name":"Division of Nephrology, Le Bonheur Children's Hospital, Memphis, Tennessee;"}]},{"given":"Xi","family":"Chen","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Le Bonheur Children's Hospital, Memphis, Tennessee;"},{"name":"Center for Clinical and Translational Medicine, The Research Institute at Nationwide Children's Hospital, Columbus, Ohio;"}]},{"given":"Vijay","family":"Saxena","sequence":"additional","affiliation":[{"name":"Center for Clinical and Translational Medicine, The Research Institute at Nationwide Children's Hospital, Columbus, Ohio;"}]},{"given":"Evan","family":"Barr-Beare","sequence":"additional","affiliation":[{"name":"Center for Clinical and Translational Medicine, The Research Institute at Nationwide Children's Hospital, Columbus, Ohio;"}]},{"given":"Weisi","family":"Flemming","sequence":"additional","affiliation":[{"name":"Center for Clinical and Translational Medicine, The Research Institute at Nationwide Children's Hospital, Columbus, Ohio;"}]},{"given":"Robert","family":"Easterling","sequence":"additional","affiliation":[{"name":"Center for Clinical and Translational Medicine, The Research Institute at Nationwide Children's Hospital, Columbus, Ohio;"}]},{"given":"Brian","family":"Becknell","sequence":"additional","affiliation":[{"name":"Center for Clinical and Translational Medicine, The Research Institute at Nationwide Children's Hospital, Columbus, Ohio;"},{"name":"Division of Nephrology, Nationwide Children's Hospital, Columbus, Ohio;"},{"name":"Department of Pediatrics, The Ohio State University, Columbus, Ohio;"}]},{"given":"George J.","family":"Schwartz","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, The University of Rochester, Rochester, New York"}]},{"given":"Andrew L.","family":"Schwaderer","sequence":"additional","affiliation":[{"name":"Center for Clinical and Translational Medicine, The Research Institute at Nationwide Children's Hospital, Columbus, Ohio;"},{"name":"Division of Nephrology, Nationwide Children's Hospital, Columbus, Ohio;"},{"name":"Department of Pediatrics, The Ohio State University, Columbus, Ohio;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1038\/nrmicro2546"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1007\/s004080000012"},{"key":"B3","first-page":"159","volume":"2","author":"Breton S","year":"2001","journal-title":"J Pancreas"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.6.F761"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1983.245.1.F110"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1002\/jlb.55.3.343"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfp160"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1016\/0041-008X(88)90051-8"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1221496110"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.177.7.4773"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pgen.1002336"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00552.2009"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.178.3.1829"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1002\/art.20600"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002473"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1099\/00222615-48-6-535"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1172\/JCI107604"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1186\/1471-2369-13-25"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1007\/BF00257206"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M111880200"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1002\/immu.200390018"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1172\/JCI105921"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1038\/10061"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0508007102"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1007\/s00335-007-9049-x"},{"key":"B26","author":"Lowry R","journal-title":"VassarStats: Website for Statistical Computation"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1007\/s00223-007-9098-x"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1038\/nm.2290"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M111.310953"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002020"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1089\/mdr.1998.4.37"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1158\/0008-5472.CAN-07-5575"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000023430.92674.E5"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1007\/BF00856522"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1007\/BF00849255"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1189\/jlb.1107725"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.071516798"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.260.4.F506"},{"key":"B39","doi-asserted-by":"crossref","first-page":"6492","DOI":"10.1016\/S0021-9258(19)84589-1","volume":"261","author":"Simchowitz L","year":"1986","journal-title":"J Biol Chem"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.bi.64.070195.002111"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0031712"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2011.109"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2012.410"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00060.x"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010101072"},{"key":"B46","doi-asserted-by":"crossref","first-page":"4849","DOI":"10.4049\/jimmunol.162.8.4849","volume":"162","author":"Trevani AS","year":"1999","journal-title":"J Immunol"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.05780612"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1128\/AAC.01378-12"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1172\/JCI67911"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1038\/nature10510"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00344.2014","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,7,16]],"date-time":"2023-07-16T04:50:07Z","timestamp":1689483007000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00344.2014"}},"issued":{"date-parts":[[2014,10,1]]},"references-count":50,"journal-issue":{"issue":"7","published-print":{"date-parts":[[2014,10,1]]}},"alternative-id":["10.1152\/ajprenal.00344.2014"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00344.2014","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2014,10,1]]}},{"indexed":{"date-parts":[[2026,3,5]],"date-time":"2026-03-05T05:22:33Z","timestamp":1772688153552,"version":"3.50.1"},"reference-count":65,"publisher":"American Physiological Society","issue":"4","funder":[{"DOI":"10.13039\/100000968","name":"American Heart Association","doi-asserted-by":"publisher","award":["15POST25130003"],"award-info":[{"award-number":["15POST25130003"]}],"id":[{"id":"10.13039\/100000968","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK116987"],"award-info":[{"award-number":["DK116987"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK120533"],"award-info":[{"award-number":["DK120533"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK120846"],"award-info":[{"award-number":["DK120846"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2021,10,1]]},"abstract":"<jats:p> It has been established that renal proximal tubule (PT) injury is a primary cause of the development of chronic kidney disease, but the underlying molecular mechanism remains to be defined. Here, we show that cyclophilin D, a mitochondrial matrix protein, in the PT causes kidney fibrogenesis in obstructive nephropathy. Our data suggest that targeting PT cyclophilin D could be beneficial to prevent fibrosis progression. <\/jats:p>","DOI":"10.1152\/ajprenal.00171.2021","type":"journal-article","created":{"date-parts":[[2021,8,16]],"date-time":"2021-08-16T11:39:01Z","timestamp":1629113941000},"page":"F431-F442","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":10,"title":["Proximal tubule cyclophilin D mediates kidney fibrogenesis in obstructive nephropathy"],"prefix":"10.1152","volume":"321","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9620-351X","authenticated-orcid":true,"given":"Hee-Seong","family":"Jang","sequence":"first","affiliation":[{"name":"Department of Urology, Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, New York"},{"name":"Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5402-5260","authenticated-orcid":true,"given":"Mi Ra","family":"Noh","sequence":"additional","affiliation":[{"name":"Department of Urology, Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, New York"},{"name":"Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska"}]},{"given":"Ligyeom","family":"Ha","sequence":"additional","affiliation":[{"name":"Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska"}]},{"given":"Jinu","family":"Kim","sequence":"additional","affiliation":[{"name":"Department of Anatomy, Jeju National University School of Medicine, Jeju, South Korea"},{"name":"Interdisciplinary Graduate Program in Advanced Convergence Technology & Science, Jeju National University, Jeju, South Korea"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0985-3213","authenticated-orcid":true,"given":"Babu J.","family":"Padanilam","sequence":"additional","affiliation":[{"name":"Department of Urology, Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, New York"},{"name":"Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMc1504848"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI93563"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2015.3"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2015030309"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2015010006"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2012.208"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2011.379"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2015060647"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2012.20"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1172\/JCI45361"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00170.2015"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/j.matbio.2018.02.006"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00164.2016"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00571.2013"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2016070761"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.3389\/fmed.2020.00065"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1253\/circj.cj-13-0321"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1007\/s00018-016-2202-5"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1007\/s00018-017-2502-4"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.119.316306"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1038\/nature03434"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/nature03317"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0505294102"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00239.2009"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00033.2011"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2019.08.019"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1305538110"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1158\/0008-5472.CAN-05-3241"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbadis.2014.06.022"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbadis.2018.02.001"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00059.2011"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00017.2014"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1016\/j.redox.2020.101548"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1155\/2014\/602149"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbadis.2013.02.016"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1038\/s41581-021-00394-7"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00110.2012"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2010.090345"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-015-3169-4"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1038\/srep44892"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013121270"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00072.2019"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2021.03.024"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1038\/nm.2144"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0000000000000605"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1126\/scitranslmed.aav4754"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1172\/JCI122313"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0906430106"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1016\/j.devcel.2005.11.006"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0904875106"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1016\/j.jhep.2014.07.008"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1002\/2211-5463.13091"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1139\/bcb-2014-0120"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.115.07085"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2018.12.064"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1111\/1440-1681.12881"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.3390\/ijms22010271"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1093\/cvr\/cvaa053"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1038\/s41419-020-02864-5"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M111.243469"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00414.2014"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M112.433045"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1172\/JCI43171"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-017-10076-9"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1038\/srep15981"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00171.2021","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,9,14]],"date-time":"2021-09-14T17:16:32Z","timestamp":1631639792000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00171.2021"}},"issued":{"date-parts":[[2021,10,1]]},"references-count":65,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2021,10,1]]}},"alternative-id":["10.1152\/ajprenal.00171.2021"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00171.2021","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2021,10,1]]},"assertion":[{"value":"2021-05-03","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2021-07-22","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2021-08-02","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2021-09-14","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2025,7,16]],"date-time":"2025-07-16T13:53:57Z","timestamp":1752674037920},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1986,11,1]]},"abstract":"<jats:p> Intracellular pH (pHi) was estimated in paired hemibladders isolated from Dominican toads (Bufo marinus) by the tissue distribution of [14C]5,5'-dimethyl-2,4-oxazolidinedione and [3H]inulin. Tissues were incubated with isotopes for 30 min to correlate changes in pHi with the approximate time of peak vasopressin (VP)-induced water flow. At serosal pH 7.1 in the presence of an osmotic gradient, the intracellular hydrogen ion concentration [( H+]i) after 30 min of VP (20 mU\/ml) stimulation was 8.29 +\/- 0.23 X 10(-8) M (pHi 7.08) compared with 5.19 +\/- 0.46 X 10(-8) M (pHi 7.28) in unstimulated paired controls (n = 5, P less than 0.001). The cyclic AMP (cAMP) analogue 8-(p-chlorophenylthio)-cAMP (10(-5) M) mimicked the VP effects. A similar change was observed at serosal bath pH 8.2, where [H+]i was 1.67 +\/- 0.06 X 10(-8) M (pHi 7.78) with VP vs. 1.11 +\/- 0.04 X 10(-8) M (pHi 7.95) in matched controls (n = 8, P less than 0.001). In all cases, the hydroosmotic response was associated with a significant decrease in inulin space. When the osmotic gradient was eliminated with Ringer solution or isotonic sorbitol in the mucosal bath, VP produced a smaller decrease in pHi (approximately 0.08 pH units) at both serosal pH. 31P-nuclear magnetic resonance spectra showed a similar downward trend in pHi with cell swelling. When vasopressin was removed from the bath, pHi and inulin space in stimulated hemibladders returned to pretreatment values within 30 min, and the tissues were again capable of a maximum hydroosmotic response if rechallenged with the hormone.(ABSTRACT TRUNCATED AT 250 WORDS) <\/jats:p>","DOI":"10.1152\/ajprenal.1986.251.5.f897","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T00:52:48Z","timestamp":1513990368000},"page":"F897-F903","source":"Crossref","is-referenced-by-count":1,"title":["Fluctuations in intracellular pH associated with vasopressin stimulation"],"prefix":"10.1152","volume":"251","author":[{"given":"A. S.","family":"Brem","sequence":"first","affiliation":[]},{"given":"M.","family":"Pacholski","sequence":"additional","affiliation":[]},{"given":"R. G.","family":"Lawler","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1986.251.5.F897","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:34:30Z","timestamp":1567971270000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1986.251.5.F897"}},"issued":{"date-parts":[[1986,11,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1986,11,1]]}},"alternative-id":["10.1152\/ajprenal.1986.251.5.F897"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1986.251.5.f897","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1986,11,1]]}},{"indexed":{"date-parts":[[2025,5,20]],"date-time":"2025-05-20T18:10:04Z","timestamp":1747764604044,"version":"3.41.0"},"reference-count":36,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2002,12,1]]},"abstract":"<jats:p>The present clinical taxonomy of distal renal tubular acidoses includes \u201cgradient,\u201d \u201csecretory,\u201d and \u201cvoltage\u201d defects. These categories refer to presumed collecting duct defects in which the epithelium may be abnormally permeable and unable to sustain an ion gradient, in which luminal proton ATPases are defective, or in which electrogenic Na<jats:sup>+<\/jats:sup>reabsorption is impaired and luminal electronegativity is reduced. Classification of affected individuals is based on urinary pH and ion concentrations during spontaneous acidosis and during SO[Formula: see text] infusion, as well as urinary Pco<jats:sub>2<\/jats:sub>during HCO[Formula: see text] loading. A model of rat CD has been developed that has been used to examine determinants of urinary acidification (Weinstein AM. Am J Physiol Renal Physiol 283: F1252\u2013F1266, 2002) and the interplay of HCO[Formula: see text] and PO[Formula: see text] loads to generate a disequlibrium pH and equilibrium Pco<jats:sub>2<\/jats:sub>. In this paper, pure forms of gradient, voltage, and secretory defects are simulated, with attention to variability in the locus of the defect in the cortical (CCD), outer medullary (OMCD), or inner medullary collecting duct (IMCD). The objective of these calculations is to discover whether the intuitive description of these defects is sustained quantitatively. The most important positive finding is that the locus of the transport defect along the CD plays a critical role in the apparent severity of the lesion, with more proximal defects being less severe and more easily correctable. In particular, model calculations suggest that for gradient or secretory defects to be clinically detectable they need to involve the OMCD and\/or IMCD. Additionally, the calculations reveal a possible mechanism for CD K<jats:sup>+<\/jats:sup>wasting, which does not involve failure of H<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-ATPase but derives from a paracellular anion leak and thereby a more electronegative lumen. The most important negative finding is the lack of support for the category of renal tubular acidosis associated with a voltage defect. Although CD lesions that present with both K<jats:sup>+<\/jats:sup>and H<jats:sup>+<\/jats:sup>secretory defects suggest mediation by transepithelial electrical potential difference (PD), both PD changes and proton pump PD sensitivity appear too small to account for the observed abnormalities.<\/jats:p>","DOI":"10.1152\/ajprenal.00164.2002","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:36:32Z","timestamp":1425414992000},"page":"F1267-F1280","source":"Crossref","is-referenced-by-count":12,"title":["A mathematical model of rat collecting duct III. Paradigms for distal acidification defects"],"prefix":"10.1152","volume":"283","author":[{"given":"Alan M.","family":"Weinstein","sequence":"first","affiliation":[{"name":"Department of Physiology and Biophysics, Weill Medical College of Cornell University, New York, New York 10021"}]}],"member":"24","reference":[{"doi-asserted-by":"publisher","key":"B1","DOI":"10.1085\/jgp.86.2.215"},{"doi-asserted-by":"publisher","key":"B2","DOI":"10.1038\/ki.1980.23"},{"doi-asserted-by":"publisher","key":"B3","DOI":"10.1152\/ajprenal.1980.239.6.F515"},{"doi-asserted-by":"publisher","key":"B4","DOI":"10.1038\/ki.1977.48"},{"key":"B5","first-page":"81","volume":"4","author":"Arruda JAL","year":"1980","journal-title":"Miner Electrolyte Metab"},{"doi-asserted-by":"publisher","key":"B6","DOI":"10.1152\/ajprenal.1982.242.1.F23"},{"doi-asserted-by":"publisher","key":"B7","DOI":"10.1038\/ki.1986.220"},{"doi-asserted-by":"publisher","key":"B8","DOI":"10.1146\/annurev.med.52.1.471"},{"doi-asserted-by":"publisher","key":"B9","DOI":"10.1085\/jgp.56.1.100"},{"doi-asserted-by":"publisher","key":"B10","DOI":"10.1016\/S0378-5173(97)00417-1"},{"key":"B11","doi-asserted-by":"crossref","first-page":"701","DOI":"10.1016\/S0022-3565(25)11094-X","volume":"261","author":"Dafnis E","year":"1992","journal-title":"J Pharmacol Exp Ther"},{"doi-asserted-by":"publisher","key":"B12","DOI":"10.1152\/ajprenal.1992.262.3.F449"},{"doi-asserted-by":"publisher","key":"B13","DOI":"10.1016\/S0272-6386(99)70164-2"},{"doi-asserted-by":"publisher","key":"B15","DOI":"10.1172\/JCI111805"},{"doi-asserted-by":"publisher","key":"B16","DOI":"10.1152\/ajprenal.1993.265.6.F875"},{"doi-asserted-by":"publisher","key":"B17","DOI":"10.1038\/262698a0"},{"doi-asserted-by":"publisher","key":"B18","DOI":"10.1038\/ki.1977.39"},{"doi-asserted-by":"publisher","key":"B19","DOI":"10.1007\/BF00582344"},{"doi-asserted-by":"publisher","key":"B20","DOI":"10.1042\/cs0560555"},{"doi-asserted-by":"publisher","key":"B21","DOI":"10.1056\/NEJM196801182780302"},{"key":"B22","first-page":"983","volume":"93","author":"Mehta PK","year":"1979","journal-title":"J Lab Clin Med"},{"key":"B23","first-page":"455","volume":"89","author":"Nascimento L","year":"1977","journal-title":"J Lab Clin Med"},{"key":"B24","first-page":"463","volume":"89","author":"Roscoe JM","year":"1977","journal-title":"J Lab Clin Med"},{"doi-asserted-by":"publisher","key":"B25","DOI":"10.1038\/ki.1976.40"},{"doi-asserted-by":"publisher","key":"B26","DOI":"10.1038\/ki.1990.11"},{"key":"B27","first-page":"202","volume":"11","author":"Sabatini S","year":"1991","journal-title":"Semin Nephrol"},{"doi-asserted-by":"publisher","key":"B28","DOI":"10.1016\/0006-291X(89)92232-8"},{"key":"B29","doi-asserted-by":"crossref","first-page":"953","DOI":"10.1681\/ASN.V34953","volume":"3","author":"Schlueter W","year":"1992","journal-title":"J Am Soc Nephrol"},{"doi-asserted-by":"publisher","key":"B30","DOI":"10.1172\/JCI106270"},{"key":"B31","doi-asserted-by":"crossref","first-page":"1233","DOI":"10.1152\/ajplegacy.1976.231.4.1233","volume":"231","author":"Thirakomen K","year":"1976","journal-title":"Am J Physiol"},{"doi-asserted-by":"publisher","key":"B32","DOI":"10.1152\/ajprenal.1998.274.5.F841"},{"doi-asserted-by":"publisher","key":"B33","DOI":"10.1152\/ajprenal.1998.274.5.F856"},{"doi-asserted-by":"publisher","key":"B34","DOI":"10.1152\/ajprenal.2000.279.1.F24"},{"doi-asserted-by":"publisher","key":"B35","DOI":"10.1152\/ajprenal.2001.280.6.F1072"},{"doi-asserted-by":"publisher","key":"B36","DOI":"10.1152\/ajprenal.00162.2002"},{"doi-asserted-by":"publisher","key":"B37","DOI":"10.1152\/ajprenal.00163.2002"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00164.2002","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,5,20]],"date-time":"2025-05-20T17:51:33Z","timestamp":1747763493000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00164.2002"}},"issued":{"date-parts":[[2002,12,1]]},"references-count":36,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2002,12,1]]}},"alternative-id":["10.1152\/ajprenal.00164.2002"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00164.2002","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2002,12,1]]}},{"indexed":{"date-parts":[[2025,5,20]],"date-time":"2025-05-20T18:10:04Z","timestamp":1747764604949,"version":"3.41.0"},"reference-count":42,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2003,2,1]]},"abstract":"<jats:p>We examined the hemodynamic and tubular transport mechanisms by which platelet-activating factor (PAF) regulates salt and water excretion. In anesthetized, renally denervated male Wistar rats, with raised systemic blood pressure and renal arterial blood pressure maintained at normal levels, intrarenal PAF infusion at 2.5 ng \u00b7 min<jats:sup>\u22121<\/jats:sup>\u00b7 kg<jats:sup>\u22121<\/jats:sup>resulted in a small fall in systemic blood pressure (no change in renal arterial blood pressure) and an increase in renal blood flow and urinary water, sodium, and potassium excretion rates. The PAF-induced changes in cardiovascular and renal hemodynamic function were abolished and renal excretory function greatly attenuated by treating rats with a nitric oxide synthase inhibitor. To determine whether a tubular site of action was involved in the natriuretic effect of PAF, cortical proximal tubules were enzymatically dissociated from male Wistar rat kidneys, and oxygen consumption rates (Qo<jats:sub>2<\/jats:sub>) were used as an integrated index of transcellular sodium transport. PAF at 1 nM maximally inhibited Qo<jats:sub>2<\/jats:sub>in both untreated and nystatin-stimulated (sodium entry into renal cell is not rate limiting) proximal tubules by \u223c20%. Blockade of PAF receptors or Na<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-ATPase pump activity with BN-52021 or ouabain, respectively, abolished the effect of PAF on nystatin-stimulated proximal tubule Qo<jats:sub>2<\/jats:sub>. Inhibition of nitric oxide synthase or guanylate cyclase systems did not alter PAF-mediated inhibition of nystatin-stimulated proximal tubule Qo<jats:sub>2<\/jats:sub>, whereas phospholipase A<jats:sub>2<\/jats:sub>or cytochrome- P-450 monooxygenase inhibition resulted in a 40\u201360% reduction. These findings suggest that stimulation of PAF receptors on the proximal tubule decreases transcellular sodium transport by activating phospholipase A<jats:sub>2<\/jats:sub>and the cytochrome- P-450 monooxygenase pathways that lead to the inhibition of an ouabain-sensitive component of the basolateral Na<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-ATPase pump. Thus PAF can activate both an arachidonate pathway-mediated suppression of proximal tubule sodium transport and a nitric oxide pathway-mediated dilatory action on renal hemodynamics that likely contributes to the natriuresis and diuresis observed in vivo.<\/jats:p>","DOI":"10.1152\/ajprenal.00117.2002","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:37:06Z","timestamp":1425415026000},"page":"F274-F281","source":"Crossref","is-referenced-by-count":3,"title":["Platelet-activating factor and solute transport processes in the kidney"],"prefix":"10.1152","volume":"284","author":[{"given":"Rajash K.","family":"Handa","sequence":"first","affiliation":[{"name":"Department of Physiology and Pharmacology, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157"}]},{"given":"Jack W.","family":"Strandhoy","sequence":"additional","affiliation":[{"name":"Department of Physiology and Pharmacology, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157"}]},{"given":"Carlos E.","family":"Giammattei","sequence":"additional","affiliation":[{"name":"Department of Physiology and Pharmacology, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157"}]},{"given":"Shelly E.","family":"Handa","sequence":"additional","affiliation":[{"name":"Department of Physiology and Pharmacology, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1996.1179"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1992.38"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/S0008-6363(01)00328-5"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/0168-0102(94)90149-X"},{"key":"B5","first-page":"579","volume":"37","author":"Dillingham MA","year":"1990","journal-title":"Kidney Int"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1006\/mvre.2000.2250"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0704311"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1984.46"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-198900076-00084"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.258.6.F1504"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.261.1.F108"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.270.1.F141"},{"key":"B13","doi-asserted-by":"crossref","first-page":"1486","DOI":"10.1016\/S0022-3565(25)13099-1","volume":"277","author":"Handa RK","year":"1996","journal-title":"J Pharmacol Exp Ther"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.2.F290"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1016\/S0163-7827(99)00016-8"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/S0090-6980(98)00031-8"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1172\/JCI116339"},{"key":"B18","first-page":"987","volume":"89","author":"Knight TF","year":"1977","journal-title":"J Lab Clin Med"},{"key":"B19","first-page":"9","volume":"18","author":"Kraut JA","year":"1992","journal-title":"Miner Electrolyte Metab"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1995.268.3.R796"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.2000.278.5.R1117"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00450.x"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1986.2"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.258.5.F1295"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.1997.tb02096.x"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1097\/00005344-199117003-00002"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/0167-4889(93)90031-J"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.2000.80.4.1669"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117431"},{"key":"B30","doi-asserted-by":"crossref","first-page":"19414","DOI":"10.1016\/S0021-9258(17)45387-7","volume":"265","author":"Noris M","year":"1990","journal-title":"J Biol Chem"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1007\/BF02536555"},{"key":"B32","doi-asserted-by":"crossref","first-page":"1391","DOI":"10.1681\/ASN.V891391","volume":"8","author":"Perico N","year":"1997","journal-title":"J Am Soc Nephrol"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1097\/00005344-199905000-00006"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00021.2001"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.8.9.737"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1986.251.1.F1"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.1997.tb02097.x"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1016\/0014-2999(92)90693-X"},{"key":"B39","first-page":"42","volume":"68","author":"Vavilova GL","year":"1996","journal-title":"Ukr Biokhim Zh"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.6.4.489"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1997.273.3.R1126"},{"key":"B42","doi-asserted-by":"crossref","first-page":"743","DOI":"10.1016\/S0022-3565(25)13041-3","volume":"253","author":"Yoo J","year":"1990","journal-title":"J Pharmacol Exp Ther"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00117.2002","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,5,20]],"date-time":"2025-05-20T17:51:34Z","timestamp":1747763494000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00117.2002"}},"issued":{"date-parts":[[2003,2,1]]},"references-count":42,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2003,2,1]]}},"alternative-id":["10.1152\/ajprenal.00117.2002"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00117.2002","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2003,2,1]]}},{"indexed":{"date-parts":[[2025,9,25]],"date-time":"2025-09-25T16:19:49Z","timestamp":1758817189855,"version":"3.37.3"},"reference-count":53,"publisher":"American Physiological Society","issue":"10","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2016,5,15]]},"abstract":"<jats:p>The development of ANG II-dependent hypertension involves increased infiltration of macrophages (M\u03a6) and T cells into the kidney and the consequent elevation of intrarenal cytokines including IL-6, which facilitates the progression of hypertension and associated kidney injury. Intrarenal renin-angiotensin system (RAS) activation, including proximal tubular angiotensinogen (AGT) stimulation, has also been regarded as a cardinal mechanism contributing to these diseases. However, the interaction between immune cells and intrarenal RAS activation has not been fully delineated. Therefore, the present study investigated whether ANG II-treated M\u03a6 induce AGT upregulation in renal proximal tubular cells (PTCs). M\u03a6 were treated with 0\u201310<jats:sup>\u22126<\/jats:sup>M ANG II for up to 48 h. PTCs were incubated with the collected medium from M\u03a6. In ANG II-treated M\u03a6, IL-6 mRNA and protein levels were increased (1.86 \u00b1 0.14, protein level, ratio to control); moreover, IL-6 levels were higher than TNF-\u03b1 and IL-1\u03b2 in culture medium isolated from ANG II-treated M\u03a6. Elevated AGT expression (1.69 \u00b1 0.04, ratio to control) accompanied by phosphorylated STAT3 were observed in PTCs that received culture medium from ANG II-treated M\u03a6. The addition of a neutralizing IL-6 antibody to the collected medium attenuated phosphorylation of STAT3 and AGT augmentation in PTCs. Furthermore, a JAK2 inhibitor also suppressed STAT3 phosphorylation and AGT augmentation in PTCs. These results demonstrate that ANG II-induced IL-6 elevation in M\u03a6 enhances activation of the JAK-STAT pathway and consequent AGT upregulation in PTCs, suggesting involvement of an immune response in driving intrarenal RAS activity.<\/jats:p>","DOI":"10.1152\/ajprenal.00482.2015","type":"journal-article","created":{"date-parts":[[2016,3,24]],"date-time":"2016-03-24T02:20:30Z","timestamp":1458786030000},"page":"F1000-F1007","source":"Crossref","is-referenced-by-count":24,"title":["Macrophage-derived IL-6 contributes to ANG II-mediated angiotensinogen stimulation in renal proximal tubular cells"],"prefix":"10.1152","volume":"310","author":[{"given":"Ryan","family":"O'Leary","sequence":"first","affiliation":[{"name":"Department of Physiology and Hypertension and Renal Center of Excellence, Tulane University School of Medicine, New Orleans, Louisiana"}]},{"given":"Harrison","family":"Penrose","sequence":"additional","affiliation":[{"name":"Department of Physiology and Hypertension and Renal Center of Excellence, Tulane University School of Medicine, New Orleans, Louisiana"}]},{"given":"Kayoko","family":"Miyata","sequence":"additional","affiliation":[{"name":"Department of Physiology and Hypertension and Renal Center of Excellence, Tulane University School of Medicine, New Orleans, Louisiana"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6505-9722","authenticated-orcid":false,"given":"Ryousuke","family":"Satou","sequence":"additional","affiliation":[{"name":"Department of Physiology and Hypertension and Renal Center of Excellence, Tulane University School of Medicine, New Orleans, Louisiana"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00163.2003"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.110.158071"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1023\/A:1007133710837"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00507.2006"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00527.2007"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.3389\/fphys.2014.00396"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00019.2008"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1089\/jir.2010.0073"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.112.203679"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.2.F218"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1172\/JCI114454"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.00324.2011"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00433.2006"},{"key":"B14","first-page":"99","volume":"14","author":"Jamaluddin M","year":"2000","journal-title":"Mol Endocrinol"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1093\/cvr\/cvn120"},{"key":"B16","doi-asserted-by":"crossref","first-page":"431","DOI":"10.1681\/ASN.V123431","volume":"12","author":"Kobori H","year":"2001","journal-title":"JASN"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004080676"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000122875.91100.28"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1034\/j.1600-0463.2002.1101201.x"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00708.2005"},{"key":"B21","first-page":"252","volume":"10","author":"Li J","year":"1996","journal-title":"Mol Endocrinol"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/j.jss.2012.07.002"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.00277.2006"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1159\/000104094"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.116.303697"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.2008.04938.x"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1161\/hy0202.103821"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1016\/j.coph.2011.01.009"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1159\/000098004"},{"key":"B30","first-page":"1331","volume":"130","author":"Ohtani R","year":"1992","journal-title":"Endocrinology"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009060625"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00059.2006"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1053\/j.gastro.2005.07.055"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1016\/j.atherosclerosis.2006.10.013"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.62.s82.4.x"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000210"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00047.2008"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1016\/j.mce.2009.06.013"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1096\/fj.11-195198"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00078.2010"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1993.177"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00283.2015"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.98.1.73"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00049.2012"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.115.306010"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.2169\/internalmedicine.42.383"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfm509"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1038\/ajh.2012.16"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1016\/j.coph.2014.12.003"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.114.03863"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008060628"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.111.173328"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00446.2014"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00482.2015","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,6,16]],"date-time":"2022-06-16T02:47:59Z","timestamp":1655347679000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00482.2015"}},"issued":{"date-parts":[[2016,5,15]]},"references-count":53,"journal-issue":{"issue":"10","published-print":{"date-parts":[[2016,5,15]]}},"alternative-id":["10.1152\/ajprenal.00482.2015"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00482.2015","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2016,5,15]]}},{"indexed":{"date-parts":[[2025,5,6]],"date-time":"2025-05-06T20:10:02Z","timestamp":1746562202484,"version":"3.40.5"},"reference-count":47,"publisher":"American Physiological Society","issue":"6","funder":[{"DOI":"10.13039\/100017618","name":"HHS | NIH | NIDDK | Division of Diabetes, Endocrinology, and Metabolic Diseases","doi-asserted-by":"publisher","award":["DK133220"],"award-info":[{"award-number":["DK133220"]}],"id":[{"id":"10.13039\/100017618","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100017618","name":"HHS | NIH | NIDDK | Division of Diabetes, Endocrinology, and Metabolic Diseases","doi-asserted-by":"publisher","award":["DK136491"],"award-info":[{"award-number":["DK136491"]}],"id":[{"id":"10.13039\/100017618","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2025,6,1]]},"abstract":"<jats:p> We investigated the role of Kir4.1\/Kir5.1 in mediating the effect of short-term Ang-II on Na-Cl cotransporter (NCC) expression\/activity. We demonstrated that Kir4.1\/Kir5.1 in the distal convoluted tubule is required for short-term Ang-II-induced stimulation of with-no-lysine-kinase 4 (WNK4), ste20-proline-alanine-rich kinase (SPAK), and NCC. However, sustained Ang-II stimulation is expected to activate WNK4, SPAK, and NCC by Kir4.1\/Kir5.1-independent mechanism. <\/jats:p>","DOI":"10.1152\/ajprenal.00004.2025","type":"journal-article","created":{"date-parts":[[2025,4,17]],"date-time":"2025-04-17T07:39:56Z","timestamp":1744875596000},"page":"F775-F786","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Kir4.1\/Kir5.1 of distal convoluted tubule is required for short-term angiotensin-II-induced stimulation of Na-Cl cotransporter"],"prefix":"10.1152","volume":"328","author":[{"given":"Xin-Peng","family":"Duan","sequence":"first","affiliation":[{"name":"Xuzhou Medical University","place":["People\u2019s Republic of China"]},{"id":[{"id":"https:\/\/ror.org\/03dkvy735","id-type":"ROR","asserted-by":"publisher"}],"name":"New York Medical College","place":["United States"]}]},{"given":"Xin-Xin","family":"Meng","sequence":"additional","affiliation":[{"name":"Zhuhai Campus of Zunyi Medical University","place":["People\u2019s Republic of China"]},{"name":"Harbin Medical University","place":["People\u2019s Republic of China"]}]},{"given":"Yu","family":"Xiao","sequence":"additional","affiliation":[{"name":"Qiqihar Medical College","place":["People\u2019s Republic of China"]},{"id":[{"id":"https:\/\/ror.org\/03dkvy735","id-type":"ROR","asserted-by":"publisher"}],"name":"New York Medical College","place":["United States"]}]},{"given":"Cheng-Biao","family":"Zhang","sequence":"additional","affiliation":[{"name":"Xuzhou Medical University","place":["People\u2019s Republic of China"]},{"id":[{"id":"https:\/\/ror.org\/03dkvy735","id-type":"ROR","asserted-by":"publisher"}],"name":"New York Medical College","place":["United States"]}]},{"given":"Ruimin","family":"Gu","sequence":"additional","affiliation":[{"name":"Harbin Medical University","place":["People\u2019s Republic of China"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1760-2684","authenticated-orcid":false,"given":"Dao-Hong","family":"Lin","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/03dkvy735","id-type":"ROR","asserted-by":"publisher"}],"name":"New York Medical College","place":["United States"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7503-9554","authenticated-orcid":false,"given":"Wen-Hui","family":"Wang","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/03dkvy735","id-type":"ROR","asserted-by":"publisher"}],"name":"New York Medical College","place":["United States"]}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.253.3.F546"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.24.14552"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.90.7.2749"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.6.F900"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1038\/ng0196-24"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00044.2018"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.242735399"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00030.2009"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2017.10.023"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.202112902"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2018080799"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0813238106"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1418342111"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00465.2014"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2016090948"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1146\/annurev-physiol-021115-105431"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2011.07.009"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00232.2019"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.123.21389"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00096.2022"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2014.12.006"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1411705111"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2001.012961"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1101400108"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1172\/jci.insight.92331"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2016090935"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00555.2020"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00072.202.1"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.0000000000000429"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2011.03.001"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00306.2021"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.200208737"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1200947109"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1038\/ng1271"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2015.289"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00064.2007"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2010.290"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1172\/JCI113847"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00335.2019"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1620315114"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00412.2018"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00022.2018"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa0810276"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00284.2020"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1161\/JAHA.119.014996"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1304592110"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2016.10.127"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00004.2025","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,5,6]],"date-time":"2025-05-06T19:29:11Z","timestamp":1746559751000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00004.2025"}},"issued":{"date-parts":[[2025,6,1]]},"references-count":47,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2025,6,1]]}},"alternative-id":["10.1152\/ajprenal.00004.2025"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00004.2025","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2025,6,1]]},"assertion":[{"value":"2025-01-06","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2025-02-01","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2025-04-07","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2025-05-06","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2025,5,29]],"date-time":"2025-05-29T19:05:46Z","timestamp":1748545546149,"version":"3.37.3"},"reference-count":22,"publisher":"American Physiological Society","issue":"6","funder":[{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)","doi-asserted-by":"publisher","award":["R01DK107694-01"],"award-info":[{"award-number":["R01DK107694-01"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000057","name":"HHS | NIH | National Institute of General Medical Sciences (NIGMS)","doi-asserted-by":"publisher","award":["COBRE","P30GM103337"],"award-info":[{"award-number":["COBRE","P30GM103337"]}],"id":[{"id":"10.13039\/100000057","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2016,12,1]]},"abstract":"<jats:p>The pleiotropic actions of the renin-angiotensin system (RAS) depend on the availability of angiotensinogen (AGT) which generates angiotensin I (ANG I) when cleaved by renin. Thus, quantification of the intact AGT (iAGT) concentrations is important to evaluate the actual renin substrate available. The iAGT conformation exists as oxidized AGT (oxi-AGT) and reduced AGT (red-AGT) in a disulfide bond, and oxi-AGT has a higher affinity for renin, which may exacerbate RAS-associated diseases. Accordingly, we determined iAGT, oxi-AGT, and red-AGT levels in plasma from rats and mice. Blood samples were obtained by cardiac puncture and then immediately mixed with an inhibitor solution containing a renin inhibitor. Total AGT (tAGT) levels were measured by tAGT ELISA which detects both cleaved and iAGT. iAGT levels were determined by iAGT ELISA which was found to only detect red-AGT. Thus, it was necessary to treat samples with dithiothreitol, a reducing agent, to quantify total iAGT concentration. tAGT levels in rat and mouse plasma were 1,839 \u00b1 139 and 1,082 \u00b1 77 ng\/ml, respectively. iAGT levels were 53% of tAGT in rat plasma but only 22% in mouse plasma, probably reflecting the greater plasma renin activity in mice. The ratios of oxi-AGT and red-AGT were \u223c4:1 (rat) and 16:1 (mouse). Plasma iAGT consists of oxi-AGT and red-AGT, suggesting that oxidative stress can influence ANG I generation by the AGT conformation switch. Furthermore, the lower availability of plasma iAGT in mice suggests that it may serve as a limiting factor in ANG I formation in this species.<\/jats:p>","DOI":"10.1152\/ajprenal.00320.2016","type":"journal-article","created":{"date-parts":[[2016,8,11]],"date-time":"2016-08-11T01:20:19Z","timestamp":1470878419000},"page":"F1211-F1216","source":"Crossref","is-referenced-by-count":7,"title":["Quantification of intact plasma AGT consisting of oxidized and reduced conformations using a modified ELISA"],"prefix":"10.1152","volume":"311","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6505-9722","authenticated-orcid":false,"given":"Ryousuke","family":"Satou","sequence":"first","affiliation":[{"name":"Department of Physiology and Hypertension, Renal Center of Excellence, Tulane University School of Medicine, New Orleans, Louisiana; and"}]},{"given":"Hiroyuki","family":"Kobori","sequence":"additional","affiliation":[{"name":"Graduate School of Health Sciences, International University of Health and Welfare, Tokyo, Japan"}]},{"given":"Akemi","family":"Katsurada","sequence":"additional","affiliation":[{"name":"Department of Physiology and Hypertension, Renal Center of Excellence, Tulane University School of Medicine, New Orleans, Louisiana; and"}]},{"given":"Kayoko","family":"Miyata","sequence":"additional","affiliation":[{"name":"Department of Physiology and Hypertension, Renal Center of Excellence, Tulane University School of Medicine, New Orleans, Louisiana; and"}]},{"given":"L. Gabriel","family":"Navar","sequence":"additional","affiliation":[{"name":"Department of Physiology and Hypertension, Renal Center of Excellence, Tulane University School of Medicine, New Orleans, Louisiana; and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"crossref","first-page":"7364","DOI":"10.1016\/S0021-9258(18)32187-2","volume":"258","author":"Catanzaro DF","year":"1983","journal-title":"J Biol Chem"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000227932.13687.60"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000254350.62876.b1"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.30.6.1325"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1086\/515452"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00588.2007"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1124\/pr.59.3.3"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.2005.04217.x"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000032100.23772.98"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1161\/ATVBAHA.115.306740"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.2008.04938.x"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1086\/420793"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1161\/hy0202.103821"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0135905"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000210"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1096\/fj.11-195198"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004060490"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1097\/HJH.0b013e328332031a"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.115.05166"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1097\/FJC.0b013e3181953e44"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1038\/ajh.2012.16"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/nature09505"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00320.2016","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,7,5]],"date-time":"2022-07-05T19:19:34Z","timestamp":1657048774000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00320.2016"}},"issued":{"date-parts":[[2016,12,1]]},"references-count":22,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2016,12,1]]}},"alternative-id":["10.1152\/ajprenal.00320.2016"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00320.2016","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2016,12,1]]}},{"indexed":{"date-parts":[[2025,9,25]],"date-time":"2025-09-25T15:06:40Z","timestamp":1758812800154},"reference-count":33,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2001,5,1]]},"abstract":"<jats:p> Carbonic anhydrase (CA) IV facilitates renal acidification by catalyzing the dehydration of luminal H<jats:sub>2<\/jats:sub>CO<jats:sub>3<\/jats:sub>. CA IV is expressed in proximal tubules, medullary collecting ducts, and A-intercalated cells of the mature rabbit kidney (Schwartz GJ, Kittelberger AM, Barnhart DA, and Vijayakumar S. Am J Physiol 278: F894\u2013F904, 2000). In view of the maturation of HCO[Formula: see text] transport in the proximal tubule and collecting duct, the ontogeny of CA IV expression was examined. During the first 2 wk, CA IV mRNA was expressed in maturing cortex and medulla at \u223c20% of adult levels. The maturational increase was gradual in cortex over 3\u20135 wk of age but surged in the medulla, so that mRNA levels appeared higher than those in the adult medulla. In situ hybridization showed very little CA IV mRNA at 5 days, with increases in deep cortex and medullary collecting ducts by 21 days. Expression of CA IV protein in the cortex and medulla was minimal at 3 days of age but then apparent in the juxtamedullary region, A-intercalated cells and medullary collecting ducts by 18 days; there was little labeling of the proximal straight tubules of the medullary rays. Thus CA IV expression may be regulated to accommodate the maturational increase in HCO[Formula: see text] absorption in the proximal tubule. In the medullary collecting duct, there is a more robust maturation of CA IV mRNA and protein, commensurate with the high rate of HCO[Formula: see text] absorption in the neonatal segment. <\/jats:p>","DOI":"10.1152\/ajprenal.2001.280.5.f895","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T14:16:58Z","timestamp":1514038618000},"page":"F895-F903","source":"Crossref","is-referenced-by-count":23,"title":["Maturation of carbonic anhydrase IV expression in rabbit kidney"],"prefix":"10.1152","volume":"280","author":[{"given":"Cornelia A.","family":"Winkler","sequence":"first","affiliation":[{"name":"Department of Pediatrics, University of Rochester School of Medicine, Rochester, New York 14642"}]},{"given":"Ann M.","family":"Kittelberger","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, University of Rochester School of Medicine, Rochester, New York 14642"}]},{"given":"Richard H.","family":"Watkins","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, University of Rochester School of Medicine, Rochester, New York 14642"}]},{"given":"William M.","family":"Maniscalco","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, University of Rochester School of Medicine, Rochester, New York 14642"}]},{"given":"George J.","family":"Schwartz","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, University of Rochester School of Medicine, Rochester, New York 14642"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1165\/ajrcmb\/3.5.491"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI114465"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1203\/00006450-199204000-00021"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115237"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1991.261.5.R1204"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.266.2.F185"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1983.245.1.F110"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.87.19.7457"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1172\/JCI105623"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1983.245.3.F391"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1966.sp008071"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1007\/s004670050450"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1991.tb09072.x"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1983.245.4.F443"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1203\/00006450-199601000-00001"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.259.5.F801"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/11.6.1759"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/0003-9861(95)90015-2"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1038\/353076a0"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1988.230"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.266.1.F57"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.262.2.F199"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.253.4.F622"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.6.F894"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.4.F510"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1983.245.3.F382"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1203\/00006450-200008000-00014"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.5.F883"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.2.F259"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.1.F139"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1177\/13.1.44"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.260.5.F738"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.272.4.F551"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.2001.280.5.F895","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:58:16Z","timestamp":1567976296000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.2001.280.5.F895"}},"issued":{"date-parts":[[2001,5,1]]},"references-count":33,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2001,5,1]]}},"alternative-id":["10.1152\/ajprenal.2001.280.5.F895"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.2001.280.5.f895","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2001,5,1]]}},{"indexed":{"date-parts":[[2025,7,30]],"date-time":"2025-07-30T15:27:33Z","timestamp":1753889253014},"reference-count":19,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2007,12]]},"DOI":"10.1152\/ajprenal.00482.2007","type":"journal-article","created":{"date-parts":[[2007,10,18]],"date-time":"2007-10-18T01:04:53Z","timestamp":1192669493000},"page":"F1766-F1767","source":"Crossref","is-referenced-by-count":3,"title":["VASP: a TRPC4-associated phosphoprotein that mediates PKG-induced inhibition of store-operated calcium influx"],"prefix":"10.1152","volume":"293","author":[{"given":"Roger G.","family":"O'Neil","sequence":"first","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1016\/j.ceca.2006.08.011"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006091067"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1007\/s00418-001-0353-3"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1016\/j.ceca.2007.03.009"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004070591"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.105.089052"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.cellbio.19.050103.103356"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.275.10.6758"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1016\/S0962-8924(03)00130-2"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1016\/j.cub.2005.05.055"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1152\/physiol.00050.2004"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.03462"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200502019"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00268.2005"},{"key":"R15","doi-asserted-by":"crossref","unstructured":"Wang X, Pluznick JL, Settles DC, Sansom SC. Association of VASP with TRPC4 in PKG-mediated inhibition of the store-operated calcium response in mesangial cells. Am J Physiol Renal Physiol. doi:10.1152\/ajprenal.00365.2007.","DOI":"10.1152\/ajprenal.00365.2007"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00068.2004"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1016\/j.ceca.2007.03.004"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1016\/j.ceca.2007.03.003"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1038\/ncb1590"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00482.2007","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T22:39:53Z","timestamp":1567982393000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00482.2007"}},"issued":{"date-parts":[[2007,12]]},"references-count":19,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2007,12]]}},"alternative-id":["10.1152\/ajprenal.00482.2007"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00482.2007","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2007,12]]}},{"indexed":{"date-parts":[[2025,8,2]],"date-time":"2025-08-02T04:36:53Z","timestamp":1754109413806,"version":"3.37.3"},"reference-count":51,"publisher":"American Physiological Society","issue":"2","funder":[{"DOI":"10.13039\/100000050","name":"HHS | NIH | National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["HL128053"],"award-info":[{"award-number":["HL128053"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK128304"],"award-info":[{"award-number":["DK128304"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2024,2,1]]},"abstract":"<jats:p> A diet containing amounts of fructose consumed by 17 million Americans causes salt-sensitive hypertension. Oxidative stress is an initiating cause of this model of fructose-induced salt-sensitive hypertension increasing blood pressure. This salt-sensitive hypertension is prevented by losartan and thus is angiotensin II (ANG II) dependent. Fructose-induced salt-sensitive hypertension depends on ANG II stimulating oxidative stress in the proximal tubule. A fructose\/high-salt diet augments the ability of ANG II to stimulate proximal tubule O<jats:sub>2<\/jats:sub><jats:sup>\u2212<\/jats:sup> via protein kinase C. <\/jats:p>","DOI":"10.1152\/ajprenal.00289.2023","type":"journal-article","created":{"date-parts":[[2023,12,7]],"date-time":"2023-12-07T09:00:53Z","timestamp":1701939653000},"page":"F249-F256","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":4,"title":["Angiotensin II-stimulated proximal nephron superoxide production and fructose-induced salt-sensitive hypertension"],"prefix":"10.1152","volume":"326","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7517-4636","authenticated-orcid":false,"given":"Beau R.","family":"Forester","sequence":"first","affiliation":[{"name":"Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, Ohio, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6646-3364","authenticated-orcid":false,"given":"Autumn","family":"Brostek","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, Ohio, United States"}]},{"given":"Brett","family":"Schuhler","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, Ohio, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3682-0815","authenticated-orcid":false,"given":"Agustin","family":"Gonzalez-Vicente","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, Ohio, United States"},{"name":"Department of Nephrology and Hypertension, Cleveland Clinic Glickman Urological and Kidney Institute, Cleveland, Ohio, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8647-3815","authenticated-orcid":false,"given":"Jeffrey L.","family":"Garvin","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, Ohio, United States"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/j.nut.2013.08.014"},{"key":"B2","volume":"10","author":"Vos MB","year":"2008","journal-title":"Medscape J Med"},{"key":"B3","first-page":"1","volume":"2011","author":"Ogden CL","year":"2011","journal-title":"NCHS Data Brief"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1080\/10408391003626223"},{"key":"B5","first-page":"1","author":"Ostchega Y","year":"2020","journal-title":"NCHS Data Brief"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.110.165456"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/j.jpeds.2009.01.015"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1161\/01.hyp.10.5.512"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-199917090-00001"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1161\/01.hyp.0000024267.71656.0d"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.14814\/phy2.15489"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.3390\/nu10091244"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1161\/JAHA.114.001559"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00626.2004"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1038\/srep46051"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1161\/01.hyp.37.1.77"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00462.2019"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2011.03.001"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.3390\/nu9080885"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.113.02564"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00247.2018"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/0305-0491(91)90243-7"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00102.2002"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.14814\/phy2.12697"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00457.2011"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M110.109157"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00472.2009"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.4.2015"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1161\/01.cir.99.15.2027"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.14814\/phy2.13162"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.2147\/IBPC.S147674"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.14814\/phy2.15687"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1016\/0024-3205(94)00750-0"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1291\/hypres.31.135"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1016\/0895-7061(96)00035-0"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1161\/01.hyp.26.6.1074"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1990.259.6.H1629"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1999.277.5.H1701"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00183.2017"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1016\/s0895-7061(02)02280-x"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejphar.2015.04.019"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00543.2019"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117268"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1986.251.1.F57"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1016\/0002-9149(61)90159-x"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1038\/ajh.2012.16"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00402.2003"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1097\/HJH.0b013e328353e807"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.112.192302"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1369\/jhc.2009.953190"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00600.2010"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00289.2023","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,2,7]],"date-time":"2024-02-07T14:13:42Z","timestamp":1707315222000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00289.2023"}},"issued":{"date-parts":[[2024,2,1]]},"references-count":51,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2024,2,1]]}},"alternative-id":["10.1152\/ajprenal.00289.2023"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00289.2023","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2024,2,1]]},"assertion":[{"value":"2023-09-12","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2023-11-30","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2023-11-30","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2024-01-16","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2025,9,4]],"date-time":"2025-09-04T13:51:45Z","timestamp":1756993905460},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1991,10,1]]},"abstract":"<jats:p> In Okamoto spontaneously hypertensive rats (SHR), elevated arterial blood pressure is not transmitted to the renal interstitium, and therefore pressure natriuretic and diuretic responses are attenuated. The objective of this study was to determine the effect of increasing renal interstitial hydrostatic pressure (RIHP) by direct renal interstitial volume expansion (DRIVE) on natriuresis and diuresis of SHR and Wistar-Kyoto rats (WKY). Unilateral nephrectomy and implantation of two polyethylene (PE) matrices were performed 3-4 wk before the acute experiment. Four groups of rats, two experimental and two time control, were used. A control clearance period was taken in all groups. In experimental groups and at the beginning and middle of the second period DRIVE was accomplished by bolus injection of a solution of 2.5% human albumin in saline directly into interstitium through one of the PE matrices. In time-control groups saline was infused in renal interstitium at the beginning of the second period. The second PE matrix was used to continuously measure RIHP in all groups. In experimental groups, DRIVE produced a significant increase in RIHP from 3.8 +\/- 0.4 to 5.7 +\/- 0.8 mmHg (P less than 0.05) in SHR and 4.3 +\/- 0.4 to 7.1 +\/- 0.5 mmHg (P less than 0.05) in WKY. In both groups the significant increase in RIHP was associated with significant increases in urinary sodium excretion (UNaV), fractional excretion of sodium (FENa), and urine flow rate (V).(ABSTRACT TRUNCATED AT 250 WORDS) <\/jats:p>","DOI":"10.1152\/ajprenal.1991.261.4.f567","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T18:30:54Z","timestamp":1513967454000},"page":"F567-F570","source":"Crossref","is-referenced-by-count":7,"title":["Direct renal interstitial volume expansion causes exaggerated natriuresis in SHR"],"prefix":"10.1152","volume":"261","author":[{"given":"A. A.","family":"Khraibi","sequence":"first","affiliation":[{"name":"Department of Physiology and Biophysics, Mayo Clinic and Foundation,Rochester, Minnesota 55905."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1991.261.4.F567","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:22:54Z","timestamp":1567956174000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1991.261.4.F567"}},"issued":{"date-parts":[[1991,10,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1991,10,1]]}},"alternative-id":["10.1152\/ajprenal.1991.261.4.F567"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1991.261.4.f567","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1991,10,1]]}},{"indexed":{"date-parts":[[2025,5,3]],"date-time":"2025-05-03T16:28:49Z","timestamp":1746289729372},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1987,2,1]]},"abstract":"<jats:p> The purpose of this study was to clarify how changes in acid-base balance influence the rate of urea synthesis in vivo. Since ureagenesis was increased by an ammonium infusion into rats, regulation seemed to be a function of the blood ammonium concentration. The rate of urea synthesis was constant at a fixed rate of ammonium infusion and independent of the conjugate base infused, chloride or bicarbonate. The steady-state blood ammonium concentration was higher in the rats that developed metabolic acidosis. Thus it appeared that regulation was not directly mediated by this ammonium concentration per se. The rate of urea synthesis was also independent of the blood pH. Accordingly, the rate of urea synthesis was examined as a function of the plasma NH3 concentration. The rate of ureagenesis was found to be directly proportional to the plasma NH3 concentration. Assuming that plasma NH3 levels reflect those in mitochondria, the NH3 concentration yielding half-maximal rates of urea synthesis (close to 2 microM) was in the same range as Km for the rate-limiting step in ureagenesis, carbamoyl phosphate synthetase (EC 6.3.4.16). These results suggest that, at a constant ammonium concentration, the decreased rate of ureagenesis caused by a pH fall in vitro could reflect an acidosis-induced decline in the concentration of true substrate (NH3) for this pathway. <\/jats:p>","DOI":"10.1152\/ajprenal.1987.252.2.f221","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T02:51:37Z","timestamp":1513997497000},"page":"F221-F225","source":"Crossref","is-referenced-by-count":3,"title":["Regulation of urea synthesis by acid-base balance in vivo: role of NH3 concentration"],"prefix":"10.1152","volume":"252","author":[{"given":"S.","family":"Cheema-Dhadli","sequence":"first","affiliation":[]},{"given":"R. L.","family":"Jungas","sequence":"additional","affiliation":[]},{"given":"M. L.","family":"Halperin","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1987.252.2.F221","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:45:41Z","timestamp":1567971941000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1987.252.2.F221"}},"issued":{"date-parts":[[1987,2,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1987,2,1]]}},"alternative-id":["10.1152\/ajprenal.1987.252.2.F221"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1987.252.2.f221","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1987,2,1]]}},{"indexed":{"date-parts":[[2025,5,17]],"date-time":"2025-05-17T19:21:33Z","timestamp":1747509693498},"reference-count":35,"publisher":"American Physiological Society","issue":"11","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2014,12,1]]},"abstract":"<jats:p>The human organic anion transporter 1 (OAT1) is crucial for the excretion of organic anions in renal proximal tubular cells and has been classified as a clinically relevant transporter in the kidneys. Our previous study indicated that renal male-predominant expression of rat Oat1 and Oat3 appears to be regulated by transcription factor B-cell CLL\/lymphoma 6 (BCL6). The aim of this study was to characterize the effect of BCL6 on human OAT1 promoter and on the transcription of OAT1 mediated by hepatocyte nuclear factor-1\u03b1 (HNF-1\u03b1). Luciferase assays were carried out in opossum kidney (OK) cells transiently transfected with promoter constructs of OAT1, expression vectors for BCL6 and HNF-1\u03b1, and the empty control vectors. BCL6 and HNF-1\u03b1 binding on OAT1 promoter was analyzed using electrophoretic mobility shift assay (EMSA). Protein expression of HNF-1\u03b1 was investigated by Western blot analysis. Site-directed mutagenesis was used to introduce mutations into BCL6 and HNF-1\u03b1 binding sites within the OAT1 promoter. BCL6 enhanced the promoter activity of OAT1 independently of predicted BCL6 binding sites but was dependent on HNF-1\u03b1 response element and HNF-1\u03b1 protein. Coexpression of BCL6 and HNF-1\u03b1 induced an additive effect on OAT1 promoter activation compared with BCL6 or HNF-1\u03b1 alone. BCL6 does not bind directly or indirectly to OAT1 promoter but increases the protein expression of HNF-1\u03b1 and thereby indirectly enhances OAT1 gene transcription. BCL6 constitutes a promising candidate gene for the regulation of human OAT1 transcription and other renal and\/or hepatic drug transporters that have been already shown to be activated by HNF-1\u03b1.<\/jats:p>","DOI":"10.1152\/ajprenal.00426.2014","type":"journal-article","created":{"date-parts":[[2014,9,19]],"date-time":"2014-09-19T04:46:29Z","timestamp":1411101989000},"page":"F1283-F1291","source":"Crossref","is-referenced-by-count":10,"title":["Transcriptional regulation of human organic anion transporter 1 by B-cell CLL\/lymphoma 6"],"prefix":"10.1152","volume":"307","author":[{"given":"Waja","family":"Wegner","sequence":"first","affiliation":[{"name":"Department of Systemic Physiology and Pathophysiology, University Medical Center G\u00f6ttingen, G\u00f6ttingen, Germany"}]},{"given":"Gerhard","family":"Burckhardt","sequence":"additional","affiliation":[{"name":"Department of Systemic Physiology and Pathophysiology, University Medical Center G\u00f6ttingen, G\u00f6ttingen, Germany"}]},{"given":"Maja","family":"Henjakovic","sequence":"additional","affiliation":[{"name":"Department of Systemic Physiology and Pathophysiology, University Medical Center G\u00f6ttingen, G\u00f6ttingen, Germany"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0046126"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1097\/MOL.0b013e3283295ee9"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-065X.2012.01112.x"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1055\/s-0037-1615757"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.301.1.145"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/j.pharmthera.2012.07.010"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/S1040-8428(01)00164-0"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M508050200"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1369\/jhc.5A6646.2005"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1038\/nrd3028"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-013-1351-8"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.111.187161"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M703467200"},{"key":"B14","doi-asserted-by":"crossref","first-page":"57","DOI":"10.1242\/dev.128.1.57","volume":"128","author":"Kojima S","year":"2001","journal-title":"Development"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.1103246"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1206755"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009070698"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00029.2004"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/j.bcp.2006.03.016"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/j.pharmthera.2010.02.007"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1210\/me.2009-0242"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1074\/mcp.M500112-MCP200"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00017.2007"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.107.126748"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1182\/blood.V99.7.2408"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1002\/path.2279"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.107.128249"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000024437.62046.AF"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2222.2011.03836.x"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M111.249292"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00528.2007"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1208\/s12248-012-9413-y"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0035556"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/gkr341"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.06312-11"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00426.2014","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,4,17]],"date-time":"2022-04-17T11:08:24Z","timestamp":1650193704000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00426.2014"}},"issued":{"date-parts":[[2014,12,1]]},"references-count":35,"journal-issue":{"issue":"11","published-print":{"date-parts":[[2014,12,1]]}},"alternative-id":["10.1152\/ajprenal.00426.2014"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00426.2014","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2014,12,1]]}},{"indexed":{"date-parts":[[2025,8,3]],"date-time":"2025-08-03T04:10:35Z","timestamp":1754194235114,"version":"3.37.3"},"reference-count":50,"publisher":"American Physiological Society","issue":"2","funder":[{"DOI":"10.13039\/100000050","name":"NHLBI","doi-asserted-by":"crossref","award":["R01HL102042"],"award-info":[{"award-number":["R01HL102042"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2020,8,1]]},"abstract":"<jats:p> Angiotensin II (ANG II) is the key contributor to renal fibrosis and injury. The present study investigated the role of endothelium prolyl hydroxylase 2 (PHD2) in ANG II-mediated renal fibrosis and injury. In vitro, endothelial cells (ECs) were isolated from PHD2<jats:sup>f\/f<\/jats:sup> control [wild-type (WT)] mice or PHD2 EC knockout (PHD2<jats:sup>EC<\/jats:sup>KO) mice. In vivo, WT and PHD2<jats:sup>EC<\/jats:sup>KO mice were infused with ANG II (1,000 ng\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7min<jats:sup>\u22121<\/jats:sup>) for 28 days. Renal fibrosis, reactive oxygen species (ROS), and iron contents were measured. Knockout of PHD2 resulted in a significant increase in the expression of hypoxia-inducible factor (HIF)-1\u03b1 and HIF-2\u03b1 in ECs. Intriguingly, knockout of PHD2 significantly reduced expression of the ANG II type 1 receptor (AT<jats:sub>1<\/jats:sub>R) in ECs. WT mice infused with ANG II caused increases in renal fibrosis, ROS formation, and iron contents. ANG II treatment led to a downregulation of PHD1 expression and upregulation of HIF-1\u03b1 and HIF-2\u03b1 in the renal cortex and medulla. Knockout of PHD2 in EC blunted ANG II-induced downregulation of PHD1 expression. Furthermore, knockout of PHD2 in ECs attenuated ANG II-induced expression of HIF-1\u03b1, HIF-2\u03b1, transforming growth factor-\u03b21, p47 <jats:sup>phox<\/jats:sup>, gp91 <jats:sup>phox<\/jats:sup>, heme oxygenase-1, and ferroportin. This was accompanied by a significant suppression of renal fibrosis, ROS formation, and iron accumulation. In summary, knockout of endothelial PHD2 suppressed the expression of AT<jats:sub>1<\/jats:sub>R in ECs and blunted ANG II-induced downregulation of PHD1 and upregulation of HIF-\u03b1 in the kidney. Our study, for the first time, demonstrates a necessary role of endothelial PHD2 in ANG II-mediated renal fibrosis and injury. <\/jats:p>","DOI":"10.1152\/ajprenal.00032.2020","type":"journal-article","created":{"date-parts":[[2020,7,27]],"date-time":"2020-07-27T10:14:27Z","timestamp":1595844867000},"page":"F345-F357","source":"Crossref","is-referenced-by-count":10,"title":["Endothelial prolyl hydroxylase 2 is necessary for angiotensin II-mediated renal fibrosis and injury"],"prefix":"10.1152","volume":"319","author":[{"given":"Yongzhen","family":"Zhao","sequence":"first","affiliation":[{"name":"Department of Pharmacology and Toxicology, School of Medicine, University of Mississippi Medical Center, Jackson, Mississippi"}]},{"given":"Heng","family":"Zeng","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, School of Medicine, University of Mississippi Medical Center, Jackson, Mississippi"}]},{"given":"Bo","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, School of Medicine, University of Mississippi Medical Center, Jackson, Mississippi"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8266-5895","authenticated-orcid":false,"given":"Xiaochen","family":"He","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, School of Medicine, University of Mississippi Medical Center, Jackson, Mississippi"}]},{"given":"Jian-Xiong","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, School of Medicine, University of Mississippi Medical Center, Jackson, Mississippi"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.116.021494"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.118.039276"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.18632\/oncotarget.11104"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2010.434"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbamcr.2013.02.029"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00155.2013"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(13)60687-X"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.01055-15"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/j.phrs.2017.05.008"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-017-11829-2"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1089\/ars.2011.4271"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1089\/ars.2016.6659"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1038\/labinvest.2017.24"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1155\/2014\/627380"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.3390\/ijms18050950"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1111\/jcmm.13060"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.115.05578"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.110.167106"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1161\/hy09t1.094234"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2015.230"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1291\/hypres.31.175"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1089\/ars.2012.4641"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1097\/MOH.0000000000000494"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1016\/j.lfs.2015.01.005"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00215.2013"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007020149"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0031034"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1038\/s41581-019-0182-z"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1007\/s00395-019-0725-2"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra1011165"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.3390\/ijms20092138"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2017.02.035"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1155\/2013\/612971"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1038\/hr.2010.63"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.118.11176"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2018.02.006"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1002\/jbt.21679"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-018-23839-9"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.3791\/52965"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1111\/jcmm.13117"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.18632\/oncotarget.11585"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00072.2018"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2010.326"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00673.2013"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1089\/ars.2005.7.1337"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1016\/j.phymed.2018.08.002"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfr754"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.117.10156"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-019-47891-1"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1159\/000491968"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00032.2020","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2020,8,7]],"date-time":"2020-08-07T14:34:55Z","timestamp":1596810895000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00032.2020"}},"issued":{"date-parts":[[2020,8,1]]},"references-count":50,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2020,8,1]]}},"alternative-id":["10.1152\/ajprenal.00032.2020"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00032.2020","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2020,8,1]]}},{"indexed":{"date-parts":[[2025,10,31]],"date-time":"2025-10-31T14:06:13Z","timestamp":1761919573832},"reference-count":39,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2012,8,15]]},"abstract":"<jats:p> Tuberous sclerosis complex (TSC) is a multiorgan hamartomatous disease caused by loss of function mutations of either the TSC1 or TSC2 genes. Neurological symptoms of TSC predominate in younger patients, but renal pathologies are a serious aspect of the disease in older children and adults. To study TSC pathogenesis in the kidney, we inactivated the mouse Tsc1 gene in the distal convoluted tubules (DCT). At young ages, Tsc1 conditional knockout (CKO) mice have enlarged kidneys and mild cystogenesis with increased mammalian target of rapamycin complex (mTORC)1 but decreased mTORC2 signaling. Treatment with the mTORC1 inhibitor rapamycin reduces kidney size and cystogenesis. Rapamycin withdrawal led to massive cystogenesis involving both distal as well as proximal tubules. To assess the contribution of decreased mTORC2 signaling in kidney pathogenesis, we also generated Rictor CKO mice. These animals did not have any detectable kidney pathology. Finally, we examined primary cilia in the DCT. Cilia were longer in Tsc1 CKO mice, and rapamycin treatment returned cilia length to normal. Rictor CKO mice had normal cilia in the DCT. Overall, our findings suggest that loss of the Tsc1 gene in the DCT is sufficient for renal cystogenesis. This cytogenesis appears to be mTORC1 but not mTORC2 dependent. Intriguingly, the mechanism may be cell autonomous as well as non-cell autonomous and possibly involves the length and function of primary cilia. <\/jats:p>","DOI":"10.1152\/ajprenal.00141.2012","type":"journal-article","created":{"date-parts":[[2012,6,7]],"date-time":"2012-06-07T02:43:43Z","timestamp":1339037023000},"page":"F584-F592","source":"Crossref","is-referenced-by-count":28,"title":["Cystogenesis and elongated primary cilia in <i>Tsc1<\/i>-deficient distal convoluted tubules"],"prefix":"10.1152","volume":"303","author":[{"given":"Eric A.","family":"Armour","sequence":"first","affiliation":[{"name":"Department of Neurology and Vanderbilt Kennedy Center for Research on Human Development, Vanderbilt University, Nashville, Tennessee"}]},{"given":"Robert P.","family":"Carson","sequence":"additional","affiliation":[{"name":"Department of Neurology and Vanderbilt Kennedy Center for Research on Human Development, Vanderbilt University, Nashville, Tennessee"}]},{"given":"Kevin C.","family":"Ess","sequence":"additional","affiliation":[{"name":"Department of Neurology and Vanderbilt Kennedy Center for Research on Human Development, Vanderbilt University, Nashville, Tennessee"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.genom.7.080505.115610"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/0925-4773(96)00544-8"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/j.nbd.2011.08.024"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(93)90618-Z"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1212\/WNL.0b013e3181e04325"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra055323"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0009239"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/ddn384"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1042\/BJ20081668"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/ddn325"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1158\/0008-5472.CAN-09-0975"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1016\/j.molmed.2011.06.003"},{"key":"B14","author":"Inoki K","year":"2004","journal-title":"Nature Genetics"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1111\/j.1460-9568.2004.03763.x"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2006.08.033"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1242\/dmm.005587"},{"key":"B18","first-page":"1206","volume":"59","author":"Kobayashi T","year":"1999","journal-title":"Cancer Res"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/11.5.525"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1038\/ng1076"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1111\/j.1464-410X.2004.05046.x"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.151.3.709"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-1809.1994.tb01881.x"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1086\/514888"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1016\/j.cub.2004.06.054"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1136\/jmg.33.11.962"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0509694103"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1016\/j.devcel.2006.08.013"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/j.semcdb.2004.11.005"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1038\/nm.1865"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1002\/ana.10283"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008101105"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1002\/ana.21058"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1016\/0090-4295(91)80261-5"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2006.01.016"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.91.24.11413"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1016\/S1357-4310(98)01245-3"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1112834109"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/ddp398"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/ddq180"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00141.2012","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T00:29:40Z","timestamp":1567988980000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00141.2012"}},"issued":{"date-parts":[[2012,8,15]]},"references-count":39,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2012,8,15]]}},"alternative-id":["10.1152\/ajprenal.00141.2012"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00141.2012","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2012,8,15]]}},{"indexed":{"date-parts":[[2025,12,10]],"date-time":"2025-12-10T12:41:43Z","timestamp":1765370503082,"version":"3.37.3"},"reference-count":113,"publisher":"American Physiological Society","issue":"6","funder":[{"DOI":"10.13039\/100016674","name":"NoVo Foundation","doi-asserted-by":"publisher","award":["NNF22OC0080736"],"award-info":[{"award-number":["NNF22OC0080736"]}],"id":[{"id":"10.13039\/100016674","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100008392","name":"Sundhed og Sygdom, Det Frie Forskningsr\u00e5d","doi-asserted-by":"publisher","award":["2034-00195B"],"award-info":[{"award-number":["2034-00195B"]}],"id":[{"id":"10.13039\/100008392","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2024,12,1]]},"abstract":"<jats:p> Experimental studies have shown that V-type ATPase-driven H<jats:sup>+<\/jats:sup> secretion is dependent on transepithelial voltage. On this basis, the \u201cvoltage hypothesis\u201d of urinary acidification by the collecting duct was derived. Accordingly, it has been supposed that the lumen-negative potential created by the reabsorption of Na<jats:sup>+<\/jats:sup> via the epithelial Na<jats:sup>+<\/jats:sup> channel (ENaC) enhances electrogenic H<jats:sup>+<\/jats:sup> secretion via V-type H<jats:sup>+<\/jats:sup>-ATPase. This concept continues to be widely used to explain acid\/base disorders. Importantly, however, a solid proof of principle for the voltage hypothesis in physiologically relevant situations has not been reached. Rather, it has been challenged by recent in vivo functional studies. In this review, we outline the arguments and experimental observations explaining why voltage-coupled H<jats:sup>+<\/jats:sup> secretion in the collecting duct often appears poorly applicable for rationalizing changes in H<jats:sup>+<\/jats:sup> secretion as a function of more or less ENaC function in the collecting duct. <\/jats:p>","DOI":"10.1152\/ajprenal.00023.2024","type":"journal-article","created":{"date-parts":[[2024,9,26]],"date-time":"2024-09-26T08:00:26Z","timestamp":1727337626000},"page":"F931-F945","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["Revisiting voltage-coupled H<sup>+<\/sup> secretion in the collecting duct"],"prefix":"10.1152","volume":"327","author":[{"given":"Niklas","family":"Ayasse","sequence":"first","affiliation":[{"name":"Vth Department of Medicine, University Hospital Mannheim, Medical Faculty Mannheim of the University of Heidelberg, Mannheim, Germany"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5216-2891","authenticated-orcid":false,"given":"Peder","family":"Berg","sequence":"additional","affiliation":[{"name":"Department of Biomedicine, Physiology, Aarhus University, Aarhus, Denmark"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6398-1035","authenticated-orcid":false,"given":"Mads V.","family":"S\u00f8rensen","sequence":"additional","affiliation":[{"name":"Department of Biomedicine, Physiology, Aarhus University, Aarhus, Denmark"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7446-054X","authenticated-orcid":false,"given":"Samuel L.","family":"Svendsen","sequence":"additional","affiliation":[{"name":"Department of Biomedicine, Physiology, Aarhus University, Aarhus, Denmark"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3192-1297","authenticated-orcid":false,"given":"Alan M.","family":"Weinstein","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, Weill Medical College of Cornell University, New York, New York, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6719-7034","authenticated-orcid":false,"given":"Jens","family":"Leipziger","sequence":"additional","affiliation":[{"name":"Department of Biomedicine, Physiology, Aarhus University, Aarhus, Denmark"}]}],"member":"24","reference":[{"key":"B1","first-page":"831","volume":"27","author":"Malnic G","year":"1994","journal-title":"Braz J Med Biol Res"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.07400715"},{"key":"B3","first-page":"23","volume-title":"Acid-Base and Electrolyte Disorders","author":"Alpern RJ","year":"2002"},{"key":"B4","first-page":"1935","volume-title":"The Kidney: Physiology and Pathophysiology","author":"Hamm LL","year":"2000"},{"key":"B5","first-page":"407","volume":"95","author":"Arruda JA","year":"1980","journal-title":"J Lab Clin Med"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1989.97"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1172\/JCI111805"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002220"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002506"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1159\/000332580"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.12391213"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0b013e32820ac850"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00296.2015"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00154.2015"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1111\/apha.13013"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00444.2020"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2017.04.017"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2017.05.009"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.10391012"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2019060613"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.10311013"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00011.2019"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1111\/apha.13591"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1113\/JP281285"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1161\/01.cir.21.5.879"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1007\/BF00584094"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2021010042"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.09750913"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90356.2008"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1986.220"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1985.154"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1986.148"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000023430.92674.E5"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1977.233.6.F502"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1977.233.1.F46"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1985.sp015588"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1976.110"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.86.2.215"},{"key":"B39","first-page":"264","volume":"210","author":"Husted RF","year":"1979","journal-title":"J Pharmacol Exp Ther"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1982.242.5.F521"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1172\/JCI111170"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1982.204"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1978.234.2.F141"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.266.2.F218"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.2000.80.1.277"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1152\/ajplegacy.1971.220.3.624"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.ph.38.030176.000320"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.08880914"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1986.250.1.F1"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014111067"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00175.2022"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.V72260"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00399.2006"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1986.250.1.F70"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.V134836"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00217.2002"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2020010071"},{"key":"B58","first-page":"S51","volume":"33","author":"Jacobson HR","year":"1991","journal-title":"Kidney Int Suppl"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1172\/JCI112264"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.202112902"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.V1011"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5001851"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00044.2005"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1159\/000173130"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1982.243.4.F330"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.V13110"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1007\/BF00584761"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-022-02732-5"},{"key":"B69","doi-asserted-by":"publisher","DOI":"10.1172\/JCI113833"},{"key":"B70","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-009-0656-0"},{"key":"B71","doi-asserted-by":"publisher","DOI":"10.1002\/cphy.c100073"},{"key":"B72","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.0000000000000259"},{"key":"B73","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115322"},{"key":"B74","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(89)80199-4"},{"key":"B75","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-008-0484-7"},{"key":"B76","doi-asserted-by":"publisher","DOI":"10.1016\/S0223-5234(03)00100-4"},{"key":"B77","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00013.2022"},{"key":"B78","doi-asserted-by":"publisher","DOI":"10.1186\/s13613-016-0168-y"},{"key":"B79","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1993.143"},{"key":"B80","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00013.2022"},{"key":"B81","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00415.2012"},{"key":"B82","doi-asserted-by":"publisher","DOI":"10.1172\/JCI63492"},{"key":"B83","doi-asserted-by":"publisher","DOI":"10.1007\/s00240-011-0397-3"},{"key":"B84","doi-asserted-by":"publisher","DOI":"10.1007\/s001980050235"},{"key":"B85","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.01320217"},{"key":"B86","doi-asserted-by":"publisher","DOI":"10.1007\/BF00587289"},{"key":"B87","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90723.2008"},{"key":"B88","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00605.2013"},{"key":"B89","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1097-010X(19971201)279:5<443::AID-JEZ6>3.0.CO;2-O"},{"key":"B90","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.0124.2001"},{"key":"B91","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.66.032102.112025"},{"key":"B92","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbagen.2010.05.002"},{"key":"B93","doi-asserted-by":"publisher","DOI":"10.1111\/apha.12707"},{"key":"B94","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.265.6.F875"},{"key":"B95","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.143"},{"key":"B96","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-119-4-199308150-00008"},{"key":"B97","doi-asserted-by":"publisher","DOI":"10.1016\/0922-4106(91)90008-6"},{"key":"B98","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00273.2023"},{"key":"B99","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2736(88)90238-6"},{"key":"B100","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2736(94)90059-0"},{"key":"B101","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2020101406"},{"key":"B102","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.281.6.F1117"},{"key":"B103","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00270.2006"},{"key":"B104","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1980.23"},{"key":"B105","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1985.201"},{"key":"B106","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.V34953"},{"key":"B107","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00164.2002"},{"key":"B108","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1983.245.5.F593"},{"key":"B109","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.260.5.F680"},{"key":"B110","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2017111163"},{"key":"B111","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008020166"},{"key":"B112","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM197709152971104"},{"key":"B113","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00162.2002"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00023.2024","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,11,11]],"date-time":"2024-11-11T20:49:09Z","timestamp":1731358149000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00023.2024"}},"issued":{"date-parts":[[2024,12,1]]},"references-count":113,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2024,12,1]]}},"alternative-id":["10.1152\/ajprenal.00023.2024"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00023.2024","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2024,12,1]]},"assertion":[{"value":"2024-01-18","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2024-09-17","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2024-09-17","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2024-11-11","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2025,12,5]],"date-time":"2025-12-05T03:35:30Z","timestamp":1764905730434},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1997,4,1]]},"abstract":"<jats:p> Most of the classic functions of the renin-angiotensin system are mediated by type 1 (AT1) angiotensin receptors, of which two subtypes, AT1A and AT1B, have been identified. However, distinct functions for these two AT1 receptors have been difficult to separate. We examined the pressor effects of angiotensin II in Agtr1A -\/- mice, which lack AT1A receptors. In enalapril-pretreated Agtr1A -\/- mice, angiotensin II caused significant and dose-proportional increases in mean arterial pressure. This pressor response was not blocked by pretreatment with sympatholytic agents but was completely inhibited by the AT1-receptor antagonists, losartan and candesartan, suggesting that it is directly mediated by AT1B receptors. Chronic treatment of Agtr1A -\/- mice with losartan reduced systolic blood pressure from 80 +\/- 5 to 72 +\/- 4 mmHg (P &lt; 0.04), suggesting a role for AT1B receptors in chronic blood pressure regulation. These studies provide the first demonstration of in vivo pressor effects mediated by AT1B receptors and demonstrate that, when AT1A receptors are absent, the AT1B receptor contributes to the regulation of resting blood pressure. <\/jats:p>","DOI":"10.1152\/ajprenal.1997.272.4.f515","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T03:11:57Z","timestamp":1513998717000},"page":"F515-F520","source":"Crossref","is-referenced-by-count":51,"title":["Angiotensin II responses in AT1A receptor-deficient mice: a role for AT1B receptors in blood pressure regulation"],"prefix":"10.1152","volume":"272","author":[{"given":"M. I.","family":"Oliverio","sequence":"first","affiliation":[{"name":"Department of Medicine, Duke University and Durham Veterans Affairs Medical Centers, North Carolina 27705, USA."}]},{"given":"C. F.","family":"Best","sequence":"additional","affiliation":[{"name":"Department of Medicine, Duke University and Durham Veterans Affairs Medical Centers, North Carolina 27705, USA."}]},{"given":"H. S.","family":"Kim","sequence":"additional","affiliation":[{"name":"Department of Medicine, Duke University and Durham Veterans Affairs Medical Centers, North Carolina 27705, USA."}]},{"given":"W. J.","family":"Arendshorst","sequence":"additional","affiliation":[{"name":"Department of Medicine, Duke University and Durham Veterans Affairs Medical Centers, North Carolina 27705, USA."}]},{"given":"O.","family":"Smithies","sequence":"additional","affiliation":[{"name":"Department of Medicine, Duke University and Durham Veterans Affairs Medical Centers, North Carolina 27705, USA."}]},{"given":"T. M.","family":"Coffman","sequence":"additional","affiliation":[{"name":"Department of Medicine, Duke University and Durham Veterans Affairs Medical Centers, North Carolina 27705, USA."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1997.272.4.F515","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:15:28Z","timestamp":1567959328000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1997.272.4.F515"}},"issued":{"date-parts":[[1997,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1997,4,1]]}},"alternative-id":["10.1152\/ajprenal.1997.272.4.F515"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1997.272.4.f515","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1997,4,1]]}},{"indexed":{"date-parts":[[2025,12,11]],"date-time":"2025-12-11T22:47:55Z","timestamp":1765493275549},"reference-count":51,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2015,1,15]]},"abstract":"<jats:p>High NaCl in the renal medullary interstitial fluid powers the concentration of urine but can damage cells. The transcription factor nuclear factor of activated T cells 5 (NFAT5) activates the expression of osmoprotective genes. We studied whether PKC-\u03b1 contributes to the activation of NFAT5. PKC-\u03b1 protein abundance was greater in the renal medulla than in the cortex. Knockout of PKC-\u03b1 reduced NFAT5 protein abundance and expression of its target genes in the inner medulla. In human embryonic kidney (HEK)-293 cells, high NaCl increased PKC-\u03b1 activity, and small interfering RNA-mediated knockdown of PKC-\u03b1 attenuated high NaCl-induced NFAT5 transcriptional activity. Expression of ERK1\/2 protein and phosphorylation of ERK1\/2 were higher in the renal inner medulla than in the cortex. Knockout of PKC-\u03b1 decreased ERK1\/2 phosphorylation in the inner medulla, as did knockdown of PKC-\u03b1 in HEK-293 cells. Also, knockdown of ERK2 reduced high NaCl-dependent NFAT5 transcriptional activity in HEK-293 cells. Combined knockdown of PKC-\u03b1 and ERK2 had no greater effect than knockdown of either alone. Knockdown of either PKC-\u03b1 or ERK2 reduced the high NaCl-induced increase of NFAT5 transactivating activity. We have previously found that the high NaCl-induced increase of phosphorylation of Ser<jats:sup>591<\/jats:sup>on Src homology 2 domain-containing phosphatase 1 (SHP-1-S591-P) contributes to the activation of NFAT5 in cell culture, and here we found high levels of SHP-1-S591-P in the inner medulla. PKC-\u03b1 has been previously shown to increase SHP-1-S591-P, which raised the possibility that PKC-\u03b1 might be acting through SHP-1. However, we did not find that knockout of PKC-\u03b1 in the renal medulla or knockdown in HEK-293 cells affected SHP-1-S591-P. We conclude that PKC-\u03b1 contributes to high NaCl-dependent activation of NFAT5 through ERK1\/2 but not through SHP-1-S591.<\/jats:p>","DOI":"10.1152\/ajprenal.00471.2014","type":"journal-article","created":{"date-parts":[[2014,11,13]],"date-time":"2014-11-13T05:06:37Z","timestamp":1415855197000},"page":"F140-F148","source":"Crossref","is-referenced-by-count":20,"title":["PKC-\u03b1 contributes to high NaCl-induced activation of NFAT5 (TonEBP\/OREBP) through MAPK ERK1\/2"],"prefix":"10.1152","volume":"308","author":[{"given":"Hong","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland;"}]},{"given":"Joan D.","family":"Ferraris","sequence":"additional","affiliation":[{"name":"Systems Biology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland; and"}]},{"given":"Janet D.","family":"Klein","sequence":"additional","affiliation":[{"name":"Renal Division, School of Medicine, Emory University, Atlanta, Georgia"}]},{"given":"Jeff M.","family":"Sands","sequence":"additional","affiliation":[{"name":"Renal Division, School of Medicine, Emory University, Atlanta, Georgia"}]},{"given":"Maurice B.","family":"Burg","sequence":"additional","affiliation":[{"name":"Systems Biology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland; and"}]},{"given":"Xiaoming","family":"Zhou","sequence":"additional","affiliation":[{"name":"Department of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1215934110"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00056.2006"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20111569"},{"key":"B4","doi-asserted-by":"crossref","first-page":"2221","DOI":"10.1681\/ASN.V12112221","volume":"12","author":"Cha JH","year":"2001","journal-title":"J Am Soc Nephrol"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbagen.2011.01.004"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuropharm.2014.01.039"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/S0076-6879(07)28016-4"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.241637298"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1159\/000095855"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1038\/onc.2011.618"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.3389\/fphys.2012.00313"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1161\/ATVBAHA.111.232165"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.3.F405"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0602911103"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.14814\/phy2.12000"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.2006.01551.x"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M402970200"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00664.2011"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1038\/nature11868"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.0901298"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M109.093690"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.3858\/emm.2008.40.6.596"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.13.7214"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1038\/nm.1960"},{"key":"B25","first-page":"237","volume":"20","author":"Mak KM","year":"2012","journal-title":"Neurosignals"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0019186"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1186\/1471-2199-9-13"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M004678200"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.2174\/138920210793360961"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/j.cellsig.2005.05.016"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0610906104"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1371\/journal.ppat.1002620"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1016\/j.ceb.2009.01.019"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1038\/sj.embor.embor939"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.601"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2002-08-2384"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2006.03.138"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1359\/jbmr.070322"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1007\/s00125-002-0996-1"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M209980200"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00484.2012"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1038\/nature11984"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M910237199"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00274.2003"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1007\/s10571-012-9889-0"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00303.2001"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00463.2004"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1002795107"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00218.2013"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00006.2014"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.2000.278.1.C102"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00471.2014","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,4,22]],"date-time":"2022-04-22T03:56:39Z","timestamp":1650599799000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00471.2014"}},"issued":{"date-parts":[[2015,1,15]]},"references-count":51,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2015,1,15]]}},"alternative-id":["10.1152\/ajprenal.00471.2014"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00471.2014","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2015,1,15]]}},{"indexed":{"date-parts":[[2025,12,12]],"date-time":"2025-12-12T13:20:48Z","timestamp":1765545648391},"reference-count":47,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2010,12]]},"abstract":"<jats:p>The 5\/6<jats:sup>th<\/jats:sup>nephrectomy or ablation\/infarction (A\/I) preparation has been used as a classic model of chronic kidney disease (CKD). We observed increased kidney oxygen consumption (Q<jats:sub>O<jats:sub>2<\/jats:sub><\/jats:sub>) and altered renal hemodynamics in the A\/I kidney that were normalized after combined angiotensin II (ANG II) blockade. Studies suggest hypoxia inducible factor as a protective influence in A\/I. We induced hypoxia-inducible factor (HIF) and HIF target proteins by two different methods, cobalt chloride (CoCl<jats:sub>2<\/jats:sub>) and dimethyloxalyglycine (DMOG), for the first week after creation of A\/I and compared the metabolic and renal hemodynamic outcomes to combined ANG II blockade. We also examined the HIF target proteins expressed by using Western blots and real-time PCR. Treatment with DMOG, CoCl<jats:sub>2<\/jats:sub>, and ANG II blockade normalized kidney oxygen consumption factored by Na reabsorption and increased both renal blood flow and glomerular filtration rate. At 1 wk, CoCl<jats:sub>2<\/jats:sub>and DMOG increased kidney expression of HIF by Western blot. In the untreated A\/I kidney, VEGF, heme oxygenase-1, and GLUT1 were all modestly increased. Both ANG II blockade and CoCl<jats:sub>2<\/jats:sub>therapy increased VEGF and GLUT1 but the cobalt markedly so. ANG II blockade decreased heme oxygenase-1 expression while CoCl<jats:sub>2<\/jats:sub>increased it. By real-time PCR, erythropoietin and GLUT1 were only increased by CoCl<jats:sub>2<\/jats:sub>therapy. Cell proliferation was modestly increased by ANG II blockade but markedly after cobalt therapy. Metabolic and hemodynamic abnormalities were corrected equally by ANG II blockade and HIF therapies. However, the molecular patterns differed significantly between ANG II blockade and cobalt therapy. HIF induction may prove to be protective in this model of CKD.<\/jats:p>","DOI":"10.1152\/ajprenal.00153.2010","type":"journal-article","created":{"date-parts":[[2010,9,30]],"date-time":"2010-09-30T02:47:30Z","timestamp":1285814850000},"page":"F1365-F1373","source":"Crossref","is-referenced-by-count":60,"title":["Renal protection in chronic kidney disease: hypoxia-inducible factor activation vs. angiotensin II blockade"],"prefix":"10.1152","volume":"299","author":[{"given":"Aihua","family":"Deng","sequence":"first","affiliation":[{"name":"Division of Nephrology-Hypertension, School of Medicine, and O'Brien Center for Acute Kidney Injury Research, University of California, and Veterans Affairs San Diego Healthcare System, San Diego, California"}]},{"given":"Mary Ann K.","family":"Arndt","sequence":"additional","affiliation":[{"name":"Division of Nephrology-Hypertension, School of Medicine, and O'Brien Center for Acute Kidney Injury Research, University of California, and Veterans Affairs San Diego Healthcare System, San Diego, California"}]},{"given":"Joseph","family":"Satriano","sequence":"additional","affiliation":[{"name":"Division of Nephrology-Hypertension, School of Medicine, and O'Brien Center for Acute Kidney Injury Research, University of California, and Veterans Affairs San Diego Healthcare System, San Diego, California"}]},{"given":"Prabhleen","family":"Singh","sequence":"additional","affiliation":[{"name":"Division of Nephrology-Hypertension, School of Medicine, and O'Brien Center for Acute Kidney Injury Research, University of California, and Veterans Affairs San Diego Healthcare System, San Diego, California"}]},{"given":"Timo","family":"Rieg","sequence":"additional","affiliation":[{"name":"Division of Nephrology-Hypertension, School of Medicine, and O'Brien Center for Acute Kidney Injury Research, University of California, and Veterans Affairs San Diego Healthcare System, San Diego, California"}]},{"given":"Scott","family":"Thomson","sequence":"additional","affiliation":[{"name":"Division of Nephrology-Hypertension, School of Medicine, and O'Brien Center for Acute Kidney Injury Research, University of California, and Veterans Affairs San Diego Healthcare System, San Diego, California"}]},{"given":"Tong","family":"Tang","sequence":"additional","affiliation":[{"name":"Division of Nephrology-Hypertension, School of Medicine, and O'Brien Center for Acute Kidney Injury Research, University of California, and Veterans Affairs San Diego Healthcare System, San Diego, California"}]},{"given":"Roland C.","family":"Blantz","sequence":"additional","affiliation":[{"name":"Division of Nephrology-Hypertension, School of Medicine, and O'Brien Center for Acute Kidney Injury Research, University of California, and Veterans Affairs San Diego Healthcare System, San Diego, California"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.35.3.800"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.01324.2007"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/S0169-328X(98)00301-5"},{"key":"B4","doi-asserted-by":"crossref","first-page":"704","DOI":"10.1182\/blood.V82.3.704.704","volume":"82","author":"Beck I","year":"1993","journal-title":"Blood"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0903978106"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/S0891-5849(02)01112-7"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/S0024-3205(00)00693-7"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00343.2005"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00450.x"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.481"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M511408200"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(01)00507-4"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1126\/science.2849206"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00773.x"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.398"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008070804"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1988.254.2.F267"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00150.x"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.107.4.1359"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1096\/fj.02-0963fje"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1042\/bst0310510"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1159\/000146075"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1096\/fj.02-1134fje"},{"key":"B24","doi-asserted-by":"crossref","first-page":"1448","DOI":"10.1681\/ASN.V1271448","volume":"12","author":"Kang DH","year":"2001","journal-title":"J Am Soc Nephrol"},{"key":"B25","doi-asserted-by":"crossref","first-page":"1434","DOI":"10.1681\/ASN.V1271434","volume":"12","author":"Kang DH","year":"2001","journal-title":"J Am Soc Nephrol"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00474.x"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1096\/fj.02-0168fje"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1001\/jama.293.1.90"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/S0960-894X(03)00539-0"},{"key":"B30","author":"Nagel S","year":"2010","journal-title":"J Cereb Blood Flow Metab"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005070757"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.258.5.F1354"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1097\/00005344-198900133-00007"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.2002.tb04680.x"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1039\/a902197c"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000095676.90936.80"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1159\/000186368"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00621.x"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1159\/000045735"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1042\/BJ20070389"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.88.13.5680"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.12.12.5447"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfp454"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00935.x"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1038\/labinvest.3700328"},{"key":"B46","doi-asserted-by":"crossref","first-page":"3610","DOI":"10.1182\/blood.V82.12.3610.3610","volume":"82","author":"Wang GL","year":"1993","journal-title":"Blood"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.055003808.x"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00153.2010","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,11,10]],"date-time":"2021-11-10T21:44:48Z","timestamp":1636580688000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00153.2010"}},"issued":{"date-parts":[[2010,12]]},"references-count":47,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2010,12]]}},"alternative-id":["10.1152\/ajprenal.00153.2010"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00153.2010","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2010,12]]}},{"indexed":{"date-parts":[[2026,1,24]],"date-time":"2026-01-24T23:39:50Z","timestamp":1769297990866,"version":"3.49.0"},"reference-count":46,"publisher":"American Physiological Society","issue":"1","funder":[{"DOI":"10.13039\/501100004488","name":"Hrvatska Zaklada za Znanost (Croatian Science Foundation)","doi-asserted-by":"publisher","award":["1481"],"award-info":[{"award-number":["1481"]}],"id":[{"id":"10.13039\/501100004488","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001659","name":"Deutsche Forschungsgemeinschaft (DFG)","doi-asserted-by":"publisher","award":["DFG998\/5-3"],"award-info":[{"award-number":["DFG998\/5-3"]}],"id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Croatian Ministry of Science, Education & Sports","award":["022-0222148-2146"],"award-info":[{"award-number":["022-0222148-2146"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2016,7,1]]},"abstract":"<jats:p>The initial step in renal secretion of organic anions (OAs) is mediated by transporters in the basolateral membrane (BLM). Contributors to this process are primary active Na<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-ATPase (EC 3.6.3.9), secondary active Na<jats:sup>+<\/jats:sup>-dicarboxylate cotransporter 3 (NaDC3\/SLC13A3), and tertiary active OA transporters (OATs) OAT1\/SLC22A6, OAT2\/SLC22A7, and OAT3\/SLC22A8. In human kidneys, we analyzed the localization of these transporters by immunochemical methods in tissue cryosections and isolated membranes. The specificity of antibodies was validated with human embryonic kidney-293 cells stably transfected with functional OATs. Na<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-ATPase was immunolocalized to the BLM along the entire human nephron. NaDC3-related immunostaining was detected in the BLM of proximal tubules and in the BLM and\/or luminal membrane of principal cells in connecting segments and collecting ducts. The thin and thick ascending limbs, macula densa, and distal tubules exhibited no reactivity with the anti-NaDC3 antibody. OAT1\u2013OAT3-related immunostaining in human kidneys was detected only in the BLM of cortical proximal tubules; all three OATs were stained more intensely in S1\/S2 segments compared with S3 segment in medullary rays, whereas the S3 segment in the outer stripe remained unstained. Expression of NaDC3, OAT1, OAT2, and OAT3 proteins exhibited considerable interindividual variability in both male and female kidneys, and sex differences in their expression could not be detected. Our experiments provide a side-by-side comparison of basolateral transporters cooperating in renal OA secretion in the human kidney.<\/jats:p>","DOI":"10.1152\/ajprenal.00113.2016","type":"journal-article","created":{"date-parts":[[2016,4,7]],"date-time":"2016-04-07T05:24:15Z","timestamp":1460006655000},"page":"F227-F238","source":"Crossref","is-referenced-by-count":36,"title":["Distribution of organic anion transporters NaDC3 and OAT1-3 along the human nephron"],"prefix":"10.1152","volume":"311","author":[{"given":"Davorka","family":"Breljak","sequence":"first","affiliation":[{"name":"Molecular Toxicology Unit, Institute for Medical Research and Occupational Health, Zagreb, Croatia;"}]},{"given":"Marija","family":"Ljubojevi\u0107","sequence":"additional","affiliation":[{"name":"Molecular Toxicology Unit, Institute for Medical Research and Occupational Health, Zagreb, Croatia;"}]},{"given":"Yohannes","family":"Hagos","sequence":"additional","affiliation":[{"name":"Center of Physiology and Pathophysiology, Institute of Systemic Physiology and Pathophysiology, University of G\u00f6ttingen, G\u00f6ttingen, Germany;"}]},{"given":"Vedran","family":"Micek","sequence":"additional","affiliation":[{"name":"Molecular Toxicology Unit, Institute for Medical Research and Occupational Health, Zagreb, Croatia;"}]},{"given":"Daniela","family":"Balen Eror","sequence":"additional","affiliation":[{"name":"Molecular Toxicology Unit, Institute for Medical Research and Occupational Health, Zagreb, Croatia;"}]},{"given":"Ivana","family":"Vrhovac Maduni\u0107","sequence":"additional","affiliation":[{"name":"Molecular Toxicology Unit, Institute for Medical Research and Occupational Health, Zagreb, Croatia;"}]},{"given":"Hrvoje","family":"Brzica","sequence":"additional","affiliation":[{"name":"Molecular Toxicology Unit, Institute for Medical Research and Occupational Health, Zagreb, Croatia;"}]},{"given":"Dean","family":"Karaica","sequence":"additional","affiliation":[{"name":"Molecular Toxicology Unit, Institute for Medical Research and Occupational Health, Zagreb, Croatia;"}]},{"given":"Nikola","family":"Radovi\u0107","sequence":"additional","affiliation":[{"name":"Department of Urology, Clinical Hospital Dubrava, Zagreb, Croatia;"}]},{"given":"Ognjen","family":"Kraus","sequence":"additional","affiliation":[{"name":"University Hospital Sisters of Mercy, Zagreb, Croatia;"}]},{"given":"Naohiko","family":"Anzai","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, Dokkyo Medical University School of Medicine, Tochigi, Japan; and"}]},{"given":"Hermann","family":"Koepsell","sequence":"additional","affiliation":[{"name":"Department of Molecular Plant Physiology and Biophysics, Julius-von-Sachs-Institute and Institute of Anatomy and Cell Biology, University of W\u00fcrzburg, W\u00fcrzburg, Germany"}]},{"given":"Gerhard","family":"Burckhardt","sequence":"additional","affiliation":[{"name":"Center of Physiology and Pathophysiology, Institute of Systemic Physiology and Pathophysiology, University of G\u00f6ttingen, G\u00f6ttingen, Germany;"}]},{"given":"Birgitta C.","family":"Burckhardt","sequence":"additional","affiliation":[{"name":"Center of Physiology and Pathophysiology, Institute of Systemic Physiology and Pathophysiology, University of G\u00f6ttingen, G\u00f6ttingen, Germany;"}]},{"given":"Ivan","family":"Saboli\u0107","sequence":"additional","affiliation":[{"name":"Molecular Toxicology Unit, Institute for Medical Research and Occupational Health, Zagreb, Croatia;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00619.2004"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.20553"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00180.2008"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1177\/23.11.127810"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/j.mam.2012.12.001"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/0003-2697(76)90527-3"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00201.2012"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.5772\/20319"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.301.1.145"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1124\/dmd.32.6.620"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1016\/j.pharmthera.2012.07.010"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1124\/mol.59.5.1277"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1172\/JCI5392"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1124\/dmd.111.042036"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.301.3.797"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M508050200"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-012-1140-9"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.300.3.746"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00140.2015"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-003-1081-4"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1095\/biolreprod64.6.1699"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.1.F122"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1979.237.2.F114"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00169.2011"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.6.3422"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1124\/mol.62.1.7"},{"key":"B27","doi-asserted-by":"crossref","first-page":"848","DOI":"10.1681\/ASN.V134848","volume":"13","author":"Kojima R","year":"2002","journal-title":"J Am Soc Nephrol"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1016\/j.taap.2004.10.004"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014111067"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00029.2004"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00207.2006"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1124\/pr.55.2.1"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1146\/annurev-pharmtox-011112-140317"},{"key":"B34","doi-asserted-by":"crossref","first-page":"866","DOI":"10.1681\/ASN.V134866","volume":"13","author":"Motohashi H","year":"2002","journal-title":"J Am Soc Nephrol"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00525.2011"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.106.113076"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-013-1369-y"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-007-0308-1"},{"key":"B39","first-page":"7","volume":"113","author":"Sabolic I","year":"2011","journal-title":"Period Biol"},{"key":"B40","doi-asserted-by":"crossref","first-page":"913","DOI":"10.1681\/ASN.V105913","volume":"10","author":"Sabolic I","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1992.263.6.C1225"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1023\/B:PHAM.0000012153.71993.cb"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1159\/000356419"},{"key":"B44","doi-asserted-by":"crossref","first-page":"464","DOI":"10.1681\/ASN.V103464","volume":"10","author":"Tojo A","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-014-1619-7"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1093\/gerona\/58.10.B879"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00113.2016","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,6,17]],"date-time":"2022-06-17T06:46:49Z","timestamp":1655448409000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00113.2016"}},"issued":{"date-parts":[[2016,7,1]]},"references-count":46,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2016,7,1]]}},"alternative-id":["10.1152\/ajprenal.00113.2016"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00113.2016","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2016,7,1]]}},{"indexed":{"date-parts":[[2026,1,15]],"date-time":"2026-01-15T09:34:03Z","timestamp":1768469643872,"version":"3.49.0"},"reference-count":90,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2001,9,1]]},"abstract":"<jats:p>The epithelial Na<jats:sup>+<\/jats:sup>channel (ENaC) plays a key role in the regulation of Na<jats:sup>+<\/jats:sup>and water absorption in several epithelia, including those of the distal nephron, distal colon, and lung. Accordingly, mutations in ENaC leading to reduced or increased channel activity cause human diseases such as pseudohypoaldosteronism type I or Liddle's syndrome, respectively. The gain of ENaC function in Liddle's syndrome is associated with increased activity and stability of the channel at the plasma membrane. Thus understanding the regulation of channel processing and trafficking to and stability at the cell surface is of fundamental importance. This review describes some of the recent advances in our understanding of ENaC trafficking, including the role of glycosylation, ENaC solubility in nonionic detergent, targeting signal(s) and hormones. It also describes the regulation of ENaC stability at the cell surface and the roles of the ubiquitin ligase Nedd4 (and ubiquitination) and clathrin-mediated endocytosis in that regulation.<\/jats:p>","DOI":"10.1152\/ajprenal.2001.281.3.f391","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T14:12:44Z","timestamp":1514038364000},"page":"F391-F399","source":"Crossref","is-referenced-by-count":99,"title":["Trafficking and cell surface stability of ENaC"],"prefix":"10.1152","volume":"281","author":[{"given":"Daniela","family":"Rotin","sequence":"first","affiliation":[{"name":"Program in Cell Biology and Biochemistry, The Hospital for Sick Children, and Biochemistry Department, University of Toronto, Toronto, Ontario, Canada, M5G 1X8; and"}]},{"given":"Voula","family":"Kanelis","sequence":"additional","affiliation":[{"name":"Program in Cell Biology and Biochemistry, The Hospital for Sick Children, and Biochemistry Department, University of Toronto, Toronto, Ontario, Canada, M5G 1X8; and"}]},{"given":"Laurent","family":"Schild","sequence":"additional","affiliation":[{"name":"Institut de Pharmacologie, Lausanne, Switzerland CH-1005"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI5713"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.43.27295"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.53.37834"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1172\/JCI3971"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.30.17704"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1002\/j.1460-2075.1996.tb00965.x"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199401203300305"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1007\/BF01869456"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1038\/361467a0"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1994.267.6.C1682"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1038\/367463a0"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.46.32889"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1038\/ng0396-248"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.5.2514"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.35.22693"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.14.8317"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.52.32919"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.127.6.1907"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.1.F46"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1007\/s004240050898"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1997.272.1.C131"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1042\/bj3450503"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/17.2.344"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.93.26.15370"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.1.F112"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1997.77.2.359"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.10.2.455"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.45.30012"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/16.5.899"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1038\/ng0995-76"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.25.11495"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.C000906200"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.18.12525"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.biochem.67.1.425"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1096\/fasebj.11.14.9409540"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1038\/77923"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.94.21.11710"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1530\/eje.0.1380691"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.111.6.825"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.53.37845"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1096\/fj.00-0191com"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1038\/87562"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.266.3.F506"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.22.13469"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1016\/0006-291X(92)91747-E"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.142.6.1413"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(93)81336-X"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.2.F252"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.4.F675"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1172\/JCI7840"},{"key":"B51","doi-asserted-by":"crossref","first-page":"1813","DOI":"10.1681\/ASN.V8121813","volume":"8","author":"May A","year":"1997","journal-title":"J Am Soc Nephrol"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1995.268.5.C1157"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1152\/ajplung.1994.266.6.L728"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.4.1727"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.24.16973"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1126\/science.282.5392.1327"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.102.1.25"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.149.7.1473"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.51.32329"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1042\/bj3360705"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1999.276.6.C1346"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.43.30345"},{"key":"B63","doi-asserted-by":"crossref","first-page":"12981","DOI":"10.1016\/S0021-9258(18)99972-2","volume":"269","author":"Renard S","year":"1994","journal-title":"J Biol Chem"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.051603198"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1002\/j.1460-2075.1994.tb06766.x"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1007\/s00232001079"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1021\/bi00184a033"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.30.20812"},{"key":"B69","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.12.5699"},{"key":"B70","doi-asserted-by":"publisher","DOI":"10.1002\/j.1460-2075.1996.tb00594.x"},{"key":"B71","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.41.25537"},{"key":"B72","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(94)90250-X"},{"key":"B73","doi-asserted-by":"publisher","DOI":"10.1038\/42408"},{"key":"B74","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.2.681"},{"key":"B75","doi-asserted-by":"crossref","first-page":"24379","DOI":"10.1016\/S0021-9258(19)51094-8","volume":"269","author":"Snyder PM","year":"1994","journal-title":"J Biol Chem"},{"key":"B76","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(95)90212-0"},{"key":"B77","doi-asserted-by":"publisher","DOI":"10.1002\/j.1460-2075.1996.tb00593.x"},{"key":"B78","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/16.21.6325"},{"key":"B79","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1997.272.6.C1871"},{"key":"B80","doi-asserted-by":"publisher","DOI":"10.1038\/ng0696-248"},{"key":"B81","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118606"},{"key":"B82","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.46.30344"},{"key":"B83","doi-asserted-by":"publisher","DOI":"10.1038\/77929"},{"key":"B84","doi-asserted-by":"publisher","DOI":"10.1006\/geno.1995.1188"},{"key":"B85","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.13.4.2031"},{"key":"B86","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M003822200"},{"key":"B87","doi-asserted-by":"publisher","DOI":"10.1053\/ajkd.2001.22072"},{"key":"B88","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1999.79.1.73"},{"key":"B89","doi-asserted-by":"publisher","DOI":"10.1038\/77891"},{"key":"B90","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.33.23286"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.2001.281.3.F391","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:44:33Z","timestamp":1660189473000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.2001.281.3.F391"}},"issued":{"date-parts":[[2001,9,1]]},"references-count":90,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2001,9,1]]}},"alternative-id":["10.1152\/ajprenal.2001.281.3.F391"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.2001.281.3.f391","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2001,9,1]]}},{"indexed":{"date-parts":[[2026,1,15]],"date-time":"2026-01-15T21:37:06Z","timestamp":1768513026917,"version":"3.49.0"},"reference-count":51,"publisher":"American Physiological Society","issue":"11","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2014,12,1]]},"abstract":"<jats:p> Stress-activated kinases p38 MAPK and JNK promote renal fibrosis; however, how the pathways by which these kinases are activated in kidney disease remain poorly defined. Apoptosis signal-regulating kinase 1 (ASK1\/MAPKKK5) is a member of the MAPKKK family that can induce activation of p38 and JNK. The present study examined whether ASK1 induces p38\/JNK activation and renal fibrosis in unilateral ureteric obstruction (UUO) using wild-type (WT) and Ask1-deficient ( Ask1<jats:sup>\u2212\/\u2212<\/jats:sup>) mice. Basal p38 and JNK activation in WT kidneys was increased three- to fivefold in day 7 UUO mice in association with renal fibrosis. In contrast, there was no increase in p38 activation in Ask1<jats:sup>\u2212\/\u2212<\/jats:sup> UUO mice, whereas JNK activation was only partially increased. The progressive increase in kidney collagen (hydroxyproline) content seen on days 7 and 12 of UUO in WT mice was significantly reduced in Ask1<jats:sup>\u2212\/\u2212<\/jats:sup> UUO mice in association with reduced \u03b1-smooth muscle actin-positive myofibroblast accumulation. However, cultured WT and Ask1<jats:sup>\u2212\/\u2212<\/jats:sup> renal fibroblasts showed equivalent proliferation and matrix production, indicating that ASK1 acts indirectly on fibroblasts. Tubular epithelial cells are the main site of p38 activation in the obstructed kidney. Angiotensin II and H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>, but not IL-1 or lipopolysaccharide, induced p38 activation and upregulation of transforming growth factor-\u03b2<jats:sub>1<\/jats:sub>, platelet-derived growth factor-B, and monocyte chemoattractant protein-1 production was suppressed in Ask1<jats:sup>\u2212\/\u2212<\/jats:sup> tubular epithelial cells. In addition, macrophage accumulation was significantly inhibited in Ask1<jats:sup>\u2212\/\u2212<\/jats:sup> UUO mice. In conclusion, ASK1 is an important upstream activator of p38 and JNK signaling in the obstructed kidney, and ASK1 is a potential therapeutic target in renal fibrosis. <\/jats:p>","DOI":"10.1152\/ajprenal.00211.2014","type":"journal-article","created":{"date-parts":[[2014,10,9]],"date-time":"2014-10-09T00:24:21Z","timestamp":1412814261000},"page":"F1263-F1273","source":"Crossref","is-referenced-by-count":91,"title":["ASK1\/p38 signaling in renal tubular epithelial cells promotes renal fibrosis in the mouse obstructed kidney"],"prefix":"10.1152","volume":"307","author":[{"given":"Frank Y.","family":"Ma","sequence":"first","affiliation":[{"name":"Department of Nephrology and Monash University Department of Medicine, Monash Medical Centre, Clayton, Victoria, Australia"}]},{"given":"Greg H.","family":"Tesch","sequence":"additional","affiliation":[{"name":"Department of Nephrology and Monash University Department of Medicine, Monash Medical Centre, Clayton, Victoria, Australia"}]},{"given":"David J.","family":"Nikolic-Paterson","sequence":"additional","affiliation":[{"name":"Department of Nephrology and Monash University Department of Medicine, Monash Medical Centre, Clayton, Victoria, Australia"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1797.2012.01567.x"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/nri3495"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1159\/000313493"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1002\/dvdy.21750"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1002\/iub.1078"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1002\/path.2228"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.109.154179"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00252.2007"},{"key":"B9","doi-asserted-by":"crossref","first-page":"1405","DOI":"10.1111\/j.1440-1681.2008.05023.x","volume":"35","author":"Evans RG","year":"2008","journal-title":"Clin Exp Pharmacol Physiol"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002404"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1007\/s11248-006-9052-0"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1136\/ard.2009.119479"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.00914-13"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2008.070726"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1159\/000339500"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.183"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfp214"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfq147"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)63292-0"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1158\/1078-0432.CCR-05-0981"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1177\/43.1.7822770"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/labinvest.2011.42"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1007\/s004410050009"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006060604"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.2741\/s17"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00010.2007"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00018.2011"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1038\/ni1200"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00414.x"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.109.135392"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1038\/hr.2011.175"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1016\/j.ajpath.2013.11.030"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007020149"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006010050"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1016\/j.jbior.2012.09.006"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1159\/000045538"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000048715.12315.FD"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000109669.23650.56"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000108520.63445.E0"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1155\/2014\/670106"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1159\/000096859"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1016\/j.lfs.2008.10.004"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000089828.73014.C8"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2007.10.122"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1997.7580"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1093\/embo-reports\/kve046"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1002\/jcb.24227"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1053\/ajkd.2001.29206"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1111\/nep.12271"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-008-0593-3"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00698.2013"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00211.2014","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T23:56:59Z","timestamp":1567987019000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00211.2014"}},"issued":{"date-parts":[[2014,12,1]]},"references-count":51,"journal-issue":{"issue":"11","published-print":{"date-parts":[[2014,12,1]]}},"alternative-id":["10.1152\/ajprenal.00211.2014"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00211.2014","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2014,12,1]]}},{"indexed":{"date-parts":[[2026,1,18]],"date-time":"2026-01-18T11:47:15Z","timestamp":1768736835842,"version":"3.49.0"},"reference-count":46,"publisher":"American Physiological Society","issue":"5","funder":[{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["103740"],"award-info":[{"award-number":["103740"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["UC2DK126024"],"award-info":[{"award-number":["UC2DK126024"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["T32DK007126"],"award-info":[{"award-number":["T32DK007126"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["1L60DK130173-01"],"award-info":[{"award-number":["1L60DK130173-01"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2024,5,1]]},"abstract":"<jats:p> The molecular drivers of successful and failed repair in the proximal tubule after acute kidney injury (AKI) are incompletely understood. We identified Traf2 and Nck interacting kinase ( Tnik) to be exclusively expressed in failed-repair proximal tubule cells after AKI. We tested the effect of si TNIK depletion in two proximal tubule cell lines followed by bulk RNA-sequencing analysis. Our results indicate that TNIK acts to suppress inflammatory signaling and apoptosis in injured renal proximal tubule epithelial cells to promote cell survival. <\/jats:p>","DOI":"10.1152\/ajprenal.00262.2023","type":"journal-article","created":{"date-parts":[[2024,3,14]],"date-time":"2024-03-14T08:01:38Z","timestamp":1710403298000},"page":"F827-F838","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":8,"title":["<i>TNIK<\/i> depletion induces inflammation and apoptosis in injured renal proximal tubule epithelial cells"],"prefix":"10.1152","volume":"326","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4049-7384","authenticated-orcid":false,"given":"Shayna T. J.","family":"Bradford","sequence":"first","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Washington University in St. Louis School of Medicine, St. Louis, Missouri, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7866-2544","authenticated-orcid":false,"given":"Haojia","family":"Wu","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Washington University in St. Louis School of Medicine, St. Louis, Missouri, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5240-5531","authenticated-orcid":false,"given":"Yuhei","family":"Kirita","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Kyoto Prefectural University of Medicine, Kyoto, Japan"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7020-8400","authenticated-orcid":false,"given":"Changfeng","family":"Chen","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Washington University in St. Louis School of Medicine, St. Louis, Missouri, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0968-5283","authenticated-orcid":false,"given":"Nicole P.","family":"Malvin","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Washington University in St. Louis School of Medicine, St. Louis, Missouri, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3320-9869","authenticated-orcid":false,"given":"Yasuhiro","family":"Yoshimura","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Washington University in St. Louis School of Medicine, St. Louis, Missouri, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0358-9442","authenticated-orcid":false,"given":"Yoshiharu","family":"Muto","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Washington University in St. Louis School of Medicine, St. Louis, Missouri, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6420-8703","authenticated-orcid":false,"given":"Benjamin D.","family":"Humphreys","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Washington University in St. Louis School of Medicine, St. Louis, Missouri, United States"},{"name":"Department of Developmental Biology, Washington University in St. Louis School of Medicine, St. Louis, Missouri, United States"}]}],"member":"24","reference":[{"key":"B1","first-page":"85","volume":"37","author":"Makris K","year":"2016","journal-title":"Clin Biochem Rev"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1093\/toxsci\/kfy159"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra1214243"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/j.stem.2008.01.014"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1310653110"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.2005477117"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/s41586-023-05769-3"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/physiol.00139.2005"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M406370200"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.43.30729"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1038\/ncb2537"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1038\/emboj.2009.285"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1038\/ncomms12586"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1038\/s41467-021-24878-z"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.0905-17.2017"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pbio.1001376"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1002\/hep4.1835"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0110180"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2022.09.026"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.0000000000000057"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/s41467-021-22368-w"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1172\/jci.insight.97497"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0033258"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/jappl.2000.88.4.1474"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2006.02.002"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.0902023"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1007\/BF02915110"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1172\/JCI135773"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1038\/s41581-023-00694-0"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.3390\/cancers12051258"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1084\/jem.182.5.1545"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1007\/s10495-018-1502-7"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1023\/a:1016119328968"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1038\/371346a0"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.2174\/1389201023378265"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1186\/1478-811X-8-31"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.2004683117"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.3389\/fimmu.2018.01999"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1101\/gad.12.18.2821"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1038\/nri1184"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1016\/s0962-8924(01)01980-8"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.35.22681"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1042\/BST20110641"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1016\/s0092-8674(00)00116-1"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2011090887"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2018030309"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00262.2023","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,5,2]],"date-time":"2024-05-02T18:56:12Z","timestamp":1714676172000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00262.2023"}},"issued":{"date-parts":[[2024,5,1]]},"references-count":46,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2024,5,1]]}},"alternative-id":["10.1152\/ajprenal.00262.2023"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00262.2023","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2024,5,1]]},"assertion":[{"value":"2023-08-28","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2024-03-05","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2024-03-05","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2024-05-02","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,1,17]],"date-time":"2026-01-17T06:57:03Z","timestamp":1768633023608,"version":"3.49.0"},"reference-count":53,"publisher":"American Physiological Society","issue":"3","funder":[{"DOI":"10.13039\/100001463","name":"American Society of Nephrology","doi-asserted-by":"publisher","award":["Ben J. Lipps Fellowship"],"award-info":[{"award-number":["Ben J. Lipps Fellowship"]}],"id":[{"id":"10.13039\/100001463","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001674","name":"Fondation Leducq","doi-asserted-by":"publisher","award":["Potassium in Hypertension"],"award-info":[{"award-number":["Potassium in Hypertension"]}],"id":[{"id":"10.13039\/501100001674","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK054231"],"award-info":[{"award-number":["DK054231"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK093501"],"award-info":[{"award-number":["DK093501"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK110375"],"award-info":[{"award-number":["DK110375"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK110375"],"award-info":[{"award-number":["DK110375"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2023,3,1]]},"abstract":"<jats:p> Regulation of the Cl<jats:sup>\u2212<\/jats:sup>\/[Formula: see text] exchanger pendrin has been suggested to explain the aldosterone paradox. A high-K<jats:sup>+<\/jats:sup> diet has been proposed to downregulate a pendrin-mediated K<jats:sup>+<\/jats:sup>-sparing NaCl reabsorption pathway to maximize urinary K<jats:sup>+<\/jats:sup> excretion. Here, we challenged the hypothesis, revealing that the accompanying anion, not K<jats:sup>+<\/jats:sup>, drives pendrin expression. Pendrin is downregulated with a high-KCl diet, preventing acidosis, and upregulated with an alkaline-rich high-K<jats:sup>+<\/jats:sup> diet, preventing metabolic alkalosis. Pendrin regulation is prioritized for acid-base balance. <\/jats:p>","DOI":"10.1152\/ajprenal.00128.2022","type":"journal-article","created":{"date-parts":[[2023,1,19]],"date-time":"2023-01-19T18:54:22Z","timestamp":1674154462000},"page":"F256-F266","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":11,"title":["Pendrin regulation is prioritized by anion in high-potassium diets"],"prefix":"10.1152","volume":"324","author":[{"given":"Ebrahim","family":"Tahaei","sequence":"first","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States"}]},{"given":"Truyen D.","family":"Pham","sequence":"additional","affiliation":[{"name":"Department of Medicine, Emory University School of Medicine, Atlanta, Georgia, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2956-2811","authenticated-orcid":false,"given":"Lama","family":"Al-Qusairi","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9368-0601","authenticated-orcid":false,"given":"Rick","family":"Grimm","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2786-8849","authenticated-orcid":false,"given":"Susan M.","family":"Wall","sequence":"additional","affiliation":[{"name":"Department of Medicine, Emory University School of Medicine, Atlanta, Georgia, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0719-8705","authenticated-orcid":false,"given":"Paul A.","family":"Welling","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States"},{"name":"Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00472.2020"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1172\/jci.insight.130553"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-018-2151-y"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1042\/cs0830567"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0b013e32833c34ec"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00011.2019"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.2.F356"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/s41371-020-00439-7"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.116.08519"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00378.2021"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2013.10.005"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2125.1981.tb01231.x"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1161\/01.cir.52.1.146"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.00035.2015"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2019080804"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00671.x"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1159\/000335100"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-020-02423-z"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005101054"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00211.2004"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00655.2020"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1210\/en.2004-1102"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.141241098"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2018.05.001"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2017080826"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-61779-474-2_12"},{"key":"B27","first-page":"412","volume":"110","author":"Farkas RA","year":"1987","journal-title":"J Lab Clin Med"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1982.242.1.F46"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2017030243"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000088321.67254.B7"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013111156"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/physiol.00049.2010"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5001634"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00454.2003"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009080817"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00114.2011"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00361.2006"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00486.2007"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1016\/0002-8703(65)90047-5"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1210\/jcem-25-7-884"},{"key":"B41","first-page":"15","volume":"48","author":"Siltanen P","year":"1959","journal-title":"Ann Med Intern Fenn"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1016\/0002-9343(65)90172-5"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000145863.96091.89"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013030279"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00474.2005"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-017-2049-0"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2011.03.022"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1016\/j.devcel.2019.10.005"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2018090912"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.381"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2019050551"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2019.12.022"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2021.06.020"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00128.2022","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,2,17]],"date-time":"2023-02-17T15:07:27Z","timestamp":1676646447000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00128.2022"}},"issued":{"date-parts":[[2023,3,1]]},"references-count":53,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2023,3,1]]}},"alternative-id":["10.1152\/ajprenal.00128.2022"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00128.2022","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2023,3,1]]},"assertion":[{"value":"2022-05-03","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2022-12-21","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2023-01-16","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2023-02-17","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,1,17]],"date-time":"2026-01-17T08:48:57Z","timestamp":1768639737524,"version":"3.49.0"},"reference-count":65,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2014,9,1]]},"abstract":"<jats:p> Visceral leishmaniasis patients have been reported to have a urine concentration defect. Concentration of urine by the renal inner medulla is essentially dependent on a transcription factor, NFAT5\/TonEBP, because it activates expression of osmoprotective genes betaine\/glycine transporter 1 (BGT1) and sodium\/myo-inositol transporter (SMIT), and water channel aquaporin-2, all of which are imperative for concentrating urine. Leishmania parasites evade macrophage immune defenses by activating protein tyrosine phosphatases, among which SHP-1 is critical. We previously demonstrated that SHP-1 inhibits tonicity-dependent activation of NFAT5\/TonEBP in HEK293 cells through screening a genome-wide small interfering (si) RNA library against phosphatases (Zhou X, Gallazzini M, Burg MB, Ferraris JD. Proc Natl Acad Sci USA 107: 7072\u20137077, 2010). We sought to examine whether Leishmania can activate SHP-1 and inhibit NFAT5\/TonEBP activity in the renal inner medulla in a murine model of visceral leishmaniasis by injection of female BALB\/c mice with a single intravenous dose of 5 \u00d7 10<jats:sup>5<\/jats:sup> L. chagasi metacyclic promastigotes. We found that SHP-1 is expressed in the kidney inner medulla. L. chagasi activates SHP-1 with an increase in stimulatory phosphorylation of SHP-1-Y536 in the region. L. chagasi reduces expression of NFAT5\/TonEBP mRNA and protein as well as expression of its targeted genes: BGT1, SMIT, and aquaporin-2. The culture supernatant from L. chagasi metacyclic promastigotes increases SHP-1 protein abundance and potently inhibits NFAT5 transcriptional activity in mIMCD3 cells. However, L. chagasi in our animal model has no significant effect on urinary concentration. We conclude that L. chagasi, most likely through its secreted virulence factors, activates SHP-1 and reduces NFAT5\/TonEBP gene expression, which leads to reduced NFAT5\/TonEBP transcriptional activity in the kidney inner medulla. <\/jats:p>","DOI":"10.1152\/ajprenal.00006.2014","type":"journal-article","created":{"date-parts":[[2014,7,3]],"date-time":"2014-07-03T07:25:53Z","timestamp":1404372353000},"page":"F516-F524","source":"Crossref","is-referenced-by-count":16,"title":["<i>Leishmania infantum-chagasi<\/i> activates SHP-1 and reduces NFAT5\/TonEBP activity in the mouse kidney inner medulla"],"prefix":"10.1152","volume":"307","author":[{"given":"Xiaoming","family":"Zhou","sequence":"first","affiliation":[{"name":"Department of Medicine, Uniformed Services University of Health Sciences, Bethesda, Maryland"}]},{"given":"Hong","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Medicine, Uniformed Services University of Health Sciences, Bethesda, Maryland"}]},{"given":"Nancy L.","family":"Koles","sequence":"additional","affiliation":[{"name":"Department of Medicine, Uniformed Services University of Health Sciences, Bethesda, Maryland"}]},{"given":"Aihong","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Medicine, Uniformed Services University of Health Sciences, Bethesda, Maryland"}]},{"given":"Naomi E.","family":"Aronson","sequence":"additional","affiliation":[{"name":"Department of Medicine, Uniformed Services University of Health Sciences, Bethesda, Maryland"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1101\/cshperspect.a006114"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0035671"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1590\/S0036-46652013000200007"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.1004237"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.2307\/3279142"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1215934110"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.1001232"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1128\/AAC.39.9.2167"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00056.2006"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20111569"},{"key":"B11","first-page":"1251","volume":"22","author":"Chong ZZ","year":"2007","journal-title":"Histol Histopathol"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1354\/vp.40-6-677"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1159\/000324914"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-6143.2010.03125.x"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1038\/nm1397"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1155\/2012\/930257"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.241637298"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M414126200"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.00853-05"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0403139101"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1126\/scisignal.2000213"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejcb.2008.01.006"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.3389\/fphys.2012.00313"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0018724"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1016\/j.advenzreg.2011.09.003"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.3389\/fimmu.2012.00251"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1097\/CCM.0b013e31824e1186"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1189\/jlb.0611326"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M109.093690"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00588.2005"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1590\/0037-8682-0033-2012"},{"key":"B32","first-page":"430","volume":"20","author":"Lima Verde FA","year":"2007","journal-title":"J Nephrol"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0308703100"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.2174\/187152011794941154"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-065X.2008.00760.x"},{"key":"B36","first-page":"237","volume":"20","author":"Mak KM","year":"2012","journal-title":"Neurosignals"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0019186"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2011-09-377069"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M004678200"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.1100076"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2010.100367"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2011.251"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1186\/1471-2369-13-44"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.167.6.3391"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1126\/science.282.5396.2085"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1016\/j.cellsig.2005.05.016"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.265.3.F416"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.E10-02-0133"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1002\/0471142735.im1902s28"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1155\/2012\/819512"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1186\/gb-2008-9-2-r35"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1006\/smim.1998.0125"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1016\/S1995-7645(12)60084-4"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-3024.1985.tb00098.x"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1016\/j.arr.2006.10.001"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1359\/jbmr.070322"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1016\/j.bcp.2005.12.017"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1016\/S0074-7696(02)15009-1"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1016\/j.exppara.2007.06.012"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1016\/j.micinf.2007.05.012"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00076.2012"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00463.2004"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1002795107"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00218.2013"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00591.2012"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00006.2014","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T01:01:46Z","timestamp":1567990906000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00006.2014"}},"issued":{"date-parts":[[2014,9,1]]},"references-count":65,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2014,9,1]]}},"alternative-id":["10.1152\/ajprenal.00006.2014"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00006.2014","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2014,9,1]]}},{"indexed":{"date-parts":[[2026,1,17]],"date-time":"2026-01-17T09:04:22Z","timestamp":1768640662033,"version":"3.49.0"},"reference-count":51,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2008,8]]},"abstract":"<jats:p> We previously showed that the 12\/15-lipoxygenase (12\/15-LO) pathway of arachidonate acid metabolism is involved in multiple events related to diabetic nephropathy (DN), including glomerular hypertrophy and extracellular matrix deposition (Kang SW, Adler SG, Nast CC, LaPage J, Gu JL, Nadler JL, Natarajan R. Kidney Int 59: 1354\u20131362, 2001; Kang SW, Natarajan R, Shahed A, Nast CC, LaPage J, Mundel P, Kashtan C, Adler SG. J Am Soc Nephrol 14: 3178\u20133187, 2003; Kim YS, Lanting L, Adler SG, Natarajan R. Kindney Int 64: 1702\u20131714, 2003; Reddy MA, Adler SG, Kim YS, Lanting L, Rossi JJ, Kang SW, Nadler JL, Shahed A, Natarajan R. Am J Physiol Renal Physiol 283: F985\u2013F994, 2002). In this study, we investigated whether in vivo delivery of small interfering RNAs (siRNAs) targeting 12\/15-LO can ameliorate renal injury and DN in a streptozotocin-injected mouse model of type 1 diabetes. To achieve greater in vivo access and siRNA expression in the kidney, we used double-stranded 12\/15-LO siRNA oligonucleotides conjugated with cholesterol. Diabetic DBA\/2J mice were injected subcutaneously with either cholesterol-tagged 12\/15-LO siRNA, mismatched control siRNA, or vehicle alone, twice weekly for 7 wk. Relative to controls, mice that received 12\/15-LO siRNA showed significant reduction in albuminuria, kidney-to-body weight ratios, glomerular mesangial matrix expansion, renal structural damage, and monocyte\/macrophage infiltration. These effects were associated with lower renal cortical or glomerular levels of profibrotic markers transforming growth factor-\u03b2, connective tissue growth factor, type I and type IV collagens, plasminogen activator inhibitor 1, and fibronectin. The diabetes-induced increase in glomerular cyclin-dependent kinase inhibitors that are associated with hypertrophy was also prevented by siRNA administration. Our results show for the first time that systemic delivery of cholesterol-tagged siRNAs targeting 12\/15-LO has renoprotective effects under diabetic conditions and therefore could be a novel therapeutic approach for DN. <\/jats:p>","DOI":"10.1152\/ajprenal.90268.2008","type":"journal-article","created":{"date-parts":[[2008,6,18]],"date-time":"2008-06-18T21:37:27Z","timestamp":1213825047000},"page":"F605-F617","source":"Crossref","is-referenced-by-count":66,"title":["Effects of cholesterol-tagged small interfering RNAs targeting 12\/15-lipoxygenase on parameters of diabetic nephropathy in a mouse model of type 1 diabetes"],"prefix":"10.1152","volume":"295","author":[{"given":"Hang","family":"Yuan","sequence":"first","affiliation":[]},{"given":"Linda","family":"Lanting","sequence":"additional","affiliation":[]},{"given":"Zhong-Gao","family":"Xu","sequence":"additional","affiliation":[]},{"given":"Shu-Lian","family":"Li","sequence":"additional","affiliation":[]},{"given":"Piotr","family":"Swiderski","sequence":"additional","affiliation":[]},{"given":"Sumanth","family":"Putta","sequence":"additional","affiliation":[]},{"given":"Mahesh","family":"Jonnalagadda","sequence":"additional","affiliation":[]},{"given":"Mitsuo","family":"Kato","sequence":"additional","affiliation":[]},{"given":"Rama","family":"Natarajan","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00988.x"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-4684-5700-1_3"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00214.x"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004110967"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.105.100347"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1007\/s00125-005-1673-y"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/gkg393"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1038\/nrd2310"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1261\/rna.459807"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1038\/35078107"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1016\/S0005-2760(96)00107-5"},{"key":"R12","doi-asserted-by":"crossref","unstructured":"Giunti S, Tesch GH, Pinach S, Burt DJ, Cooper ME, Cavallo-Perin P, Camussi G, Gruden G. Monocyte chemoattractant protein-1 has prosclerotic effects both in a mouse model of experimental diabetes and in vitro in human mesangial cells. Diabetologia 51: 198\u2013207, 2008.","DOI":"10.1007\/s00125-007-0837-3"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1096\/fj.06-6713com"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1210\/endo.134.1.8275971"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1038\/nature02870"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2007.06.148"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.0590041354.x"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000099702.16315.DE"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.280"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006070754"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0611192104"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1038\/nrg2006"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00286.x"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004070568"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1993.18"},{"key":"R26","unstructured":"Kuan CJ, Al-Douahji M, Shankland SJ. The cyclin kinase inhibitor p21WAF1, CIP1 is increased in experimental diabetic nephropathy: potential role in glomerular hypertrophy. J Am Soc Nephrol 9: 986\u2013993, 1998."},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000133025.23732.46"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1194\/jlr.M400328-JLR200"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004080720"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1016\/j.plefa.2004.06.004"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1038\/nbt1122"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.23.13375"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000031828.58276.02"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1161\/01.ATV.0000133606.69732.4c"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1097-4652(199611)169:2<391::AID-JCP19>3.0.CO;2-C"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.23.1_Suppl.I142"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.90.11.4947"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00181.2002"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M111305200"},{"key":"R40","doi-asserted-by":"crossref","unstructured":"Rincon-Choles H, Kasinath BS, Gorin Y, Abboud HE. Angiotensin II and growth factors in the pathogenesis of diabetic nephropathy. Kidney Int Suppl 82: 8\u201311, 2002.","DOI":"10.1046\/j.1523-1755.62.s82.3.x"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.2337\/diab.44.10.1139"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1038\/nature03121"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.2337\/db07-1119"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00009.x"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00750.x"},{"key":"R46","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00260.2007"},{"key":"R47","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)64056-4"},{"key":"R48","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1992.330"},{"key":"R49","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000137"},{"key":"R50","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2760(92)90297-9"},{"key":"R51","unstructured":"Ziyadeh FN, Sharma K. Role of transforming growth factor-beta in diabetic glomerulosclerosis and renal hypertrophy. Kidney Int Suppl 51: S34\u2013S36, 1995."}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.90268.2008","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:50:28Z","timestamp":1567968628000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.90268.2008"}},"issued":{"date-parts":[[2008,8]]},"references-count":51,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2008,8]]}},"alternative-id":["10.1152\/ajprenal.90268.2008"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.90268.2008","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2008,8]]}},{"indexed":{"date-parts":[[2026,1,30]],"date-time":"2026-01-30T09:51:31Z","timestamp":1769766691206,"version":"3.49.0"},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1983,2,1]]},"abstract":"<jats:p> In paired micropuncture studies in the Munich-Wistar rat we examined the mechanism of diuresis after acute induction of modest hyperglycemia (430-460 mg\/dl) in the absence of an increase in total body water. The major reasons for the diuresis were an increase in nephron filtration rate (SNGFR) (from 30.3 +\/- 1.8 to 35.3 +\/- 1.6 nl\/min) and a reduction in absolute proximal reabsorption (APR) (from 14.0 +\/- 0.6 to 9.8 +\/- 1.2 nl\/min). All determinants of SNGFR were measured and a reduction in systemic oncotic pressure was the sole reason for the increase in SNGFR; vascular resistances did not change. Late proximal tubular fluid-to-plasma glucose concentration ratio was 0.96 +\/- 0.04; therefore, the osmotic effects of unreabsorbed glucose could not account for the reduction in APR. Directly measured net renal interstitial pressure increased by 5 mmHg and the peritubular capillary effective reabsorptive pressure decreased (from 15.5 to 10.9 mmHg) in direct proportion to the reduction in APR, changes that could contribute to the reduction in APR. Equal elevations in glucose concentration in tubule and plasma may have also eliminated effective osmotic pressure gradients for water movement and influenced APR. As a result of increases in late proximal tubular flow rate, loop of Henle tubular reabsorption and absolute tubular reabsorption beyond the distal tubule both increased with hyperglycemia. The major reduction in APR was secondary to altered \"physical factors\" and osmotic effects of glucose that are not dependent on creation of unfavorable chemical gradients for Na+ reabsorption. <\/jats:p>","DOI":"10.1152\/ajprenal.1983.244.2.f185","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T15:21:01Z","timestamp":1513956061000},"page":"F185-F194","source":"Crossref","is-referenced-by-count":6,"title":["Mechanism of diuresis following acute modest hyperglycemia in the rat"],"prefix":"10.1152","volume":"244","author":[{"given":"R. C.","family":"Blantz","sequence":"first","affiliation":[]},{"given":"B. J.","family":"Tucker","sequence":"additional","affiliation":[]},{"given":"L.","family":"Gushwa","sequence":"additional","affiliation":[]},{"given":"O. W.","family":"Peterson","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1983.244.2.F185","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:28:00Z","timestamp":1567967280000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1983.244.2.F185"}},"issued":{"date-parts":[[1983,2,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1983,2,1]]}},"alternative-id":["10.1152\/ajprenal.1983.244.2.F185"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1983.244.2.f185","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1983,2,1]]}},{"indexed":{"date-parts":[[2025,9,12]],"date-time":"2025-09-12T18:39:31Z","timestamp":1757702371741},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1990,10,1]]},"abstract":"<jats:p> Experiments were performed in anesthetized rats to examine whether angiotensin II corrects the attenuation of tubuloglomerular feedback (TGF) responses produced by acute extracellular volume expansion. Volume expansion was achieved by an infusion of isotonic saline at a rate of 9 ml\/h. When urine flow had stabilized, an increase in loop of Henle flow from 0 to 45 nl\/min caused a fall in stop-flow pressure (PSF) by 3.7 +\/- 0.3 mmHg and in single-nephron glomerular filtration rate (SNGFR) by 5.1 +\/- 1.7 nl\/min. During continued saline administration angiotensin II was infused at 16, 48, or 96 ng.kg-1.min-1 while renal arterial pressure was held constant by suprarenal aortic clamping. The mean responses of PSF increased to 5.9 +\/- 0.6, 9.8 +\/- 0.7, and 14.9 +\/- 1.7 mmHg. Angiotensin II infused at 54 ng.kg-1.min-1 increased the SNGFR response to 15.1 +\/- 2.1 nl\/min, whereas kidney GFR and distal SNGFR fell. Subcapsular pressure was not significantly altered by angiotensin II infusion (16 ng.kg-1.min-1). Plasma angiotensin (y, pg\/ml) as a function of angiotensin II infusion rate (x, ng.kg-1.min-1 for approximately 20 min) was found to fit the function y = 2.89 + 3.53x. An infusion of approximately 15 ng.kg-1.min-1 restored plasma angiotensin levels in the volume-expanded rats to hydropenic values. These data confirm that angiotensin II may play a role as a physiological regulator of TGF sensitivity. <\/jats:p>","DOI":"10.1152\/ajprenal.1990.259.4.f565","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T17:24:25Z","timestamp":1513963465000},"page":"F565-F572","source":"Crossref","is-referenced-by-count":18,"title":["Restoration of tubuloglomerular feedback in volume-expanded rats by angiotensin II"],"prefix":"10.1152","volume":"259","author":[{"given":"J.","family":"Schnermann","sequence":"first","affiliation":[{"name":"Department of Physiology, University of Michigan, Ann Arbor 48109."}]},{"given":"J. P.","family":"Briggs","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Michigan, Ann Arbor 48109."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1990.259.4.F565","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:17:10Z","timestamp":1567955830000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1990.259.4.F565"}},"issued":{"date-parts":[[1990,10,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1990,10,1]]}},"alternative-id":["10.1152\/ajprenal.1990.259.4.F565"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1990.259.4.f565","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1990,10,1]]}},{"indexed":{"date-parts":[[2025,9,12]],"date-time":"2025-09-12T18:37:54Z","timestamp":1757702274459},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1984,4,1]]},"abstract":"<jats:p> Experiments were performed on chronically salt-loaded rats to determine whether resetting of tubuloglomerular feedback is caused by changes in the sensitivity of the juxtaglomerular apparatus itself or by changes of tubular fluid composition. The feedback response was quantified in both salt-loaded and salt-deplete rats by measuring early proximal flow rate (EPF) during loop perfusion at 40, 10, and 0 nl\/min using tubular fluid harvested from both groups and with Ringer solution. In salt-loaded rats endogenous tubular fluid produced only a small feedback response (EPF40-0 = 1.9 +\/- 1.5 nl\/min), whereas exogenous tubular fluid from salt-deplete rats or Ringer solution produced normal feedback responses (EPF40-0 = 15.4 +\/- 2.0 and 10.6 +\/- 1.7 nl\/min, respectively). In salt-deplete rats, endogenous tubular fluid and Ringer solution produced feedback responses of similar magnitude (EPF40-0 = 14.2 +\/- 1.8 and 13.0 +\/- 2.0 nl\/min, respectively) but exogenous tubular fluid from salt-loaded rats elicited only a small feedback response (EPF40-0 = 1.5 +\/- 1.6 nl\/min), indistinguishable from that seen in salt-loaded rats with endogenous tubular fluid. It is concluded that an inhibitory factor in the tubular fluid of chronically salt-loaded rats causes a reduction in tubuloglomerular feedback response. <\/jats:p>","DOI":"10.1152\/ajprenal.1984.246.4.f495","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T16:28:42Z","timestamp":1513960122000},"page":"F495-F500","source":"Crossref","is-referenced-by-count":3,"title":["Resetting of tubuloglomerular feedback: evidence for a humoral factor in tubular fluid"],"prefix":"10.1152","volume":"246","author":[{"given":"D. A.","family":"Haberle","sequence":"first","affiliation":[]},{"given":"J. M.","family":"Davis","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1984.246.4.F495","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:32:56Z","timestamp":1567967576000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1984.246.4.F495"}},"issued":{"date-parts":[[1984,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1984,4,1]]}},"alternative-id":["10.1152\/ajprenal.1984.246.4.F495"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1984.246.4.f495","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1984,4,1]]}},{"indexed":{"date-parts":[[2025,9,12]],"date-time":"2025-09-12T18:19:36Z","timestamp":1757701176701},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1990,9,1]]},"abstract":"<jats:p> The steady-state behavior of the tubuloglomerular feedback system has been studied in detail, but little is known about its dynamics. However, kinetic data can provide insight regarding the contribution of feedback to autoregulatory responses. Accordingly, experiments were conducted in anesthetized, euvolemic, spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats to characterize the time course of changes in proximal tubular stop-flow pressure after step changes in the rate of orthograde perfusion of Henle's loop. We studied the responses both to increase in perfusion rate, which produced preglomerular vasoconstriction, and decreases in perfusion rate, which produced preglomerular vasodilation. In both strains, the pattern of induced stop-flow pressure transients consisted of a pure delay followed by a monoexponential decay to a new steady state. In SHR rats, delay times were shorter than in WKY rats, but response time constants were not significantly different in the two strains. However, response time constants for dilation were longer than for constriction in both strains. The delay times and relatively large response time constants observed indicate that tubuloglomerular feedback cannot mediate rapid autoregulatory responses to fluctuations in renal perfusion pressure. The response time of tubuloglomerular feedback is probably limited by both the time lag associated with fluid transit through the loop of Henle and a relatively slow rate-limiting step in the signal transduction process at the macula densa. <\/jats:p>","DOI":"10.1152\/ajprenal.1990.259.3.f529","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T22:21:18Z","timestamp":1513981278000},"page":"F529-F534","source":"Crossref","is-referenced-by-count":23,"title":["Tubuloglomerular feedback kinetics in spontaneously hypertensive and Wistar-Kyoto rats"],"prefix":"10.1152","volume":"259","author":[{"given":"F. H.","family":"Daniels","sequence":"first","affiliation":[{"name":"Department of Biomedical Engineering, Duke University, Durham27706."}]},{"given":"W. J.","family":"Arendshorst","sequence":"additional","affiliation":[{"name":"Department of Biomedical Engineering, Duke University, Durham27706."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1990.259.3.F529","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:17:01Z","timestamp":1567970221000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1990.259.3.F529"}},"issued":{"date-parts":[[1990,9,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1990,9,1]]}},"alternative-id":["10.1152\/ajprenal.1990.259.3.F529"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1990.259.3.f529","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1990,9,1]]}},{"indexed":{"date-parts":[[2025,9,12]],"date-time":"2025-09-12T19:46:14Z","timestamp":1757706374303},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1983,11,1]]},"abstract":"<jats:p> The use of pathogen-free rats allows the dissection and in vitro perfusion of several rat nephron segments not previously studied. In the present experiments, net urea fluxes were measured in isolated perfused cortical and medullary thick ascending limbs and cortical collecting ducts from pathogen-free Sprague-Dawley rats. No evidence for active transport of urea was found in either cortical or medullary thick ascending limbs. Permeabilities were calculated from urea fluxes measured with 5 mM urea either in the bath or perfusate and with no urea on the opposite side of the epithelium. Permeability coefficients (cm\/s X 10(-5) +\/- SE) in different portions of the thick ascending limb were: inner stripe, short-looped nephrons, 0.9 +\/- 0.2; inner stripe, long-looped nephrons, 0.6 +\/- 0.2 (not significantly different vs. short loops); outer stripe, 1.4 +\/- 0.3 (P less than 0.05 vs. inner stripe); and cortical, 1.5 +\/- 0.3 (P less than 0.05 vs. inner stripe). The relatively high urea permeability of thick ascending limbs in the outer stripe of the outer medulla and medullary rays is likely to permit substantial passive absorption of urea from these segments in vivo. This will contribute to dilution of the tubule fluid in thick ascending limbs and thus indirectly enhance urinary concentrating ability. In cortical collecting ducts, the urea permeability was relatively low both in the presence of 100 microU\/ml arginine vasopressin in the bath (0.5 +\/- 0.1 X 10(-5) cm\/s) and in its absence (0.4 +\/- 0.1). These permeability values are similar to values previously measured in rabbit cortical collecting ducts. <\/jats:p>","DOI":"10.1152\/ajprenal.1983.245.5.f634","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T09:40:50Z","timestamp":1513935650000},"page":"F634-F639","source":"Crossref","is-referenced-by-count":14,"title":["Urea transport in isolated thick ascending limbs and collecting ducts from rats"],"prefix":"10.1152","volume":"245","author":[{"given":"M. A.","family":"Knepper","sequence":"first","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1983.245.5.F634","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T14:24:48Z","timestamp":1567952688000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1983.245.5.F634"}},"issued":{"date-parts":[[1983,11,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1983,11,1]]}},"alternative-id":["10.1152\/ajprenal.1983.245.5.F634"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1983.245.5.f634","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1983,11,1]]}},{"indexed":{"date-parts":[[2025,7,1]],"date-time":"2025-07-01T14:25:34Z","timestamp":1751379934745,"version":"3.37.3"},"reference-count":30,"publisher":"American Physiological Society","issue":"2","funder":[{"DOI":"10.13039\/100000061","name":"HHS | NIH | Fogarty International Center","doi-asserted-by":"publisher","award":["D43TW009345"],"award-info":[{"award-number":["D43TW009345"]}],"id":[{"id":"10.13039\/100000061","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health","doi-asserted-by":"publisher","award":["D43TW010132"],"award-info":[{"award-number":["D43TW010132"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health","doi-asserted-by":"publisher","award":["1R25TW011213"],"award-info":[{"award-number":["1R25TW011213"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000061","name":"HHS | NIH | Fogarty International Center","doi-asserted-by":"publisher","award":["D43TW010928"],"award-info":[{"award-number":["D43TW010928"]}],"id":[{"id":"10.13039\/100000061","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2024,8,1]]},"abstract":"<jats:p> In this study, we report an increased risk of developing acute kidney injury (AKI) during hospitalization, worsening AKI, and death among females with sickle cell anemia (SCA) hospitalized with an acute pain crisis compared with males. The sex differences in AKI were not explained by socioeconomic differences, severity of pain, or disease severity among females compared with males. Together, these data suggest that female children with SCA may be at increased risk of AKI. <\/jats:p>","DOI":"10.1152\/ajprenal.00385.2023","type":"journal-article","created":{"date-parts":[[2024,6,27]],"date-time":"2024-06-27T08:01:50Z","timestamp":1719475310000},"page":"F304-F313","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":2,"title":["Sex-disaggregated analysis of acute kidney injury in hospitalized children with sickle cell anemia in Uganda"],"prefix":"10.1152","volume":"327","author":[{"given":"Andrea","family":"Weckman","sequence":"first","affiliation":[{"name":"Michael G. DeGroote School of Medicine, McMaster University, Hamilton, Ontario, Canada"}]},{"given":"Chloe R.","family":"McDonald","sequence":"additional","affiliation":[{"name":"Sandra A. Rotman Laboratories, Sandra Rotman Centre for Global Health, University Health Network-Toronto General Hospital, Toronto, Ontario, Canada"}]},{"given":"Shubaya K.","family":"Naggayi","sequence":"additional","affiliation":[{"name":"Global Health Uganda Research Collaboration, Kampala, Uganda"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7019-809X","authenticated-orcid":false,"given":"Danielle E.","family":"Soranno","sequence":"additional","affiliation":[{"name":"Department of Pediatric Nephrology, Indiana University School of Medicine, Indianapolis, Indiana, United States"},{"name":"Department of Bioengineering, Purdue University, West Lafayette, Indiana, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5328-6511","authenticated-orcid":false,"given":"Andrea L.","family":"Conroy","sequence":"additional","affiliation":[{"name":"Global Health Uganda Research Collaboration, Kampala, Uganda"},{"name":"Ryan White Center for Pediatric Infectious Disease and Global Health, Department of Pediatrics, Indiana University School of Medicine, Indianapolis, Indiana, United States"}]},{"given":"Anthony","family":"Batte","sequence":"additional","affiliation":[{"name":"Global Health Uganda Research Collaboration, Kampala, Uganda"},{"name":"Child Health and Development Centre, College of Health Sciences, Makerere University, Kampala, Uganda"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1136\/archdisschild-2013-303773"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2016-09-702324"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.3389\/fped.2022.886674"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.3390\/children10020261"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1111\/bjh.16384"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-017-3623-6"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2015.8"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.3389\/fmolb.2019.00140"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1186\/s12882-022-02731-9"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2022.04.006"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2022.04.010"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2017.181"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1038\/s41581-020-00338-7"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1182\/bloodadvances.2019001237"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0258638"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.4037\/ajcc2010624"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/j.cpem.2017.09.005"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2017-06-788935"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1542\/peds.2017-1904"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1097\/MCC.0000000000001091"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199406093302303"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-017-3650-3"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1016\/j.whi.2008.01.006"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfq083"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-016-3370-0"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1007\/s00134-023-07194-6"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(03)13917-7"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1136\/archdischild-2013-303889"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.7189\/jogh.07.010418"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-023-06154-y"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00385.2023","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,8,9]],"date-time":"2024-08-09T14:31:09Z","timestamp":1723213869000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00385.2023"}},"issued":{"date-parts":[[2024,8,1]]},"references-count":30,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2024,8,1]]}},"alternative-id":["10.1152\/ajprenal.00385.2023"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00385.2023","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2024,8,1]]},"assertion":[{"value":"2023-12-04","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2024-06-13","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2024-06-18","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2024-08-09","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2025,6,25]],"date-time":"2025-06-25T17:12:43Z","timestamp":1750871563442},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1996,9,1]]},"abstract":"<jats:p> Renal glomerular capillary tufts have been believed to arise from angiogenic ingrowth of extrinsic vessels. We found, however, that when embryonic day 12 (E12) mouse kidneys were maintained in culture for 6 days and then grafted into anterior eye chambers of adult transgenic ROSA26 host mice (which carry the beta-galactosidase transgene), glomerular endothelial cells within the grafts were predominantly of intrinsic, kidney origin. To identify potential endothelial precursors, we immunolabled kidneys with antibodies against the vascular endothelial growth factor receptor, flk-1. Numerous discrete cells expressing flk-1 were scattered throughout the nephrogenic mesenchyme of both E12 and newborn kidneys, and with development these cells became concentrated in microvessels, glomerular vascular clefts, and glomerular tufts. In adults, flk-1 was weakly expressed in glomeruli but absent elsewhere. To examine abilities of flk-1-positive cells to establish glomeruli, E12 kidneys were grafted into kidney cortices of adult and newborn ROSA26 hosts. Grafts into adults resulted in few glomeruli containing host-derived endothelium, whereas a majority of glomeruli grafted into newborns contained host cells. Cells of graft origin were found in vessels forming in renal cortices of newborn hosts, but not in adults. Our findings indicate that embryonic kidney cells expressing flk-1 are angioblasts that create microvessels and glomeruli by vasculogenesis. <\/jats:p>","DOI":"10.1152\/ajprenal.1996.271.3.f744","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T01:31:13Z","timestamp":1513992673000},"page":"F744-F753","source":"Crossref","is-referenced-by-count":21,"title":["Evidence that embryonic kidney cells expressing flk-1 are intrinsic, vasculogenic angioblasts"],"prefix":"10.1152","volume":"271","author":[{"given":"B.","family":"Robert","sequence":"first","affiliation":[{"name":"Department of Comparative Medicine, University of Alabama atBirmingham 35294-0019, USA."}]},{"given":"P. L.","family":"St John","sequence":"additional","affiliation":[{"name":"Department of Comparative Medicine, University of Alabama atBirmingham 35294-0019, USA."}]},{"given":"D. P.","family":"Hyink","sequence":"additional","affiliation":[{"name":"Department of Comparative Medicine, University of Alabama atBirmingham 35294-0019, USA."}]},{"given":"D. R.","family":"Abrahamson","sequence":"additional","affiliation":[{"name":"Department of Comparative Medicine, University of Alabama atBirmingham 35294-0019, USA."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1996.271.3.F744","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:06:07Z","timestamp":1567958767000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1996.271.3.F744"}},"issued":{"date-parts":[[1996,9,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1996,9,1]]}},"alternative-id":["10.1152\/ajprenal.1996.271.3.F744"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1996.271.3.f744","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1996,9,1]]}},{"indexed":{"date-parts":[[2025,6,29]],"date-time":"2025-06-29T05:10:01Z","timestamp":1751173801600,"version":"3.41.0"},"reference-count":45,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1998,8,1]]},"abstract":"<jats:p>Experiments were performed to investigate vasopressin type 2 receptor (V<jats:sub>2<\/jats:sub>)-mediated renal water reabsorption and the renal expression of the vasopressin-regulated water channel aquaporin-2 (AQP-2) in cirrhotic rats with sodium retention but without ascites. In addition, the expression of the furosemide-sensitive type 1 Na-K-2Cl cotransporter (BSC-1) and the natriuretic response to an intravenous test dose furosemide (7.5 mg\/kg) during acute V<jats:sub>2<\/jats:sub>-receptor blockade was measured. Acute V<jats:sub>2<\/jats:sub>-receptor blockade with the selective nonpeptide antagonist OPC-31260 (800 \u03bcg \u22c5 kg<jats:sup>\u22121<\/jats:sup>\u22c5 h<jats:sup>\u22121<\/jats:sup>) was performed during conditions in which volume depletion was prevented by computer-driven, servo-controlled intravenous volume replacement with 150 mM glucose. OPC-31260 produced a significantly smaller increase in urine flow rate (\u221226%) and free water clearance (\u221218%) in cirrhotic rats than in control rats. The natriuretic response to an intravenous test dose furosemide (7.5 mg\/kg) was significantly increased in cirrhotic rats (+52%), but pretreatment with OPC-31260 did not affect the natriuretic response to furosemide in neither cirrhotic nor in control rats. Semiquantitative immunoblotting showed a significant downregulation of AQP-2 in the renal cortex (\u221272%) and in the outer medulla (\u221244%). The relative expression of BSC-1 in the outer medulla was unchanged in cirrhotic rats. The corticopapillary gradient of Na was significantly increased in cirrhotic rats. Since daily urine flow rate was similar in cirrhotic and sham-operated rats, we suggest that non-vasopressin-mediated water reabsorption is increased in cirrhotic rats probably as a result of an increased corticomedullary gradient due to exaggerated NaCl reabsorption in the thick ascending limb of Henle\u2019s loop.<\/jats:p>","DOI":"10.1152\/ajprenal.1998.275.2.f216","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T17:17:09Z","timestamp":1514049429000},"page":"F216-F225","source":"Crossref","is-referenced-by-count":19,"title":["Decreased vasopressin-mediated renal water reabsorption in rats with compensated liver cirrhosis"],"prefix":"10.1152","volume":"275","author":[{"given":"Thomas E. N.","family":"Jonassen","sequence":"first","affiliation":[{"name":"Department of Pharmacology, the Panum Institute, University of Copenhagen, DK-2200 Copenhagen N; and"}]},{"given":"S\u00f8ren","family":"Nielsen","sequence":"additional","affiliation":[{"name":"Department of Cell Biology, Institute of Anatomy, University of Aarhus, DK-8000 Aarhus, Denmark"}]},{"given":"Sten","family":"Christensen","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, the Panum Institute, University of Copenhagen, DK-2200 Copenhagen N; and"}]},{"given":"J\u00f8rgen S\u00f8berg","family":"Petersen","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, the Panum Institute, University of Copenhagen, DK-2200 Copenhagen N; and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"crossref","first-page":"15","DOI":"10.1681\/ASN.V8115","volume":"8","author":"Apostol E.","year":"1997","journal-title":"J. Am. Soc. Nephrol."},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1042\/cs0850129"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1677\/joe.0.1270213"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1172\/JCI111901"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.91.19.8984"},{"issue":"40","key":"B6","first-page":"F619","volume":"271","author":"Ecelbarger C. A.","year":"1996","journal-title":"Am. J. Physiol."},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119352"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1136\/jcp.13.2.156"},{"issue":"32","key":"B9","first-page":"R129","volume":"263","author":"Frandsen R.","year":"1992","journal-title":"Am. J. Physiol."},{"issue":"39","key":"B10","first-page":"F657","volume":"270","author":"Fr\u00f8kjaer J.","year":"1996","journal-title":"Am. J. Physiol."},{"issue":"38","key":"B11","first-page":"F926","volume":"269","author":"Furita N.","year":"1995","journal-title":"Am. J. Physiol."},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1985.65.3.760"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1002\/hep.1840050215"},{"issue":"42","key":"B14","first-page":"R568","volume":"273","author":"Jonassen T. E. N.","year":"1997","journal-title":"Am. J. Physiol."},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1210\/endo.135.2.8033816"},{"key":"B16","first-page":"305","volume":"65","author":"Kountouras J.","year":"1984","journal-title":"Br. J. Exp. Pathol."},{"key":"B17","doi-asserted-by":"crossref","first-page":"451","DOI":"10.1152\/ajplegacy.1959.196.2.451","volume":"196","author":"Levinsky N. G.","year":"1959","journal-title":"Am. J. Physiol."},{"issue":"2","key":"B18","first-page":"F586","volume":"233","author":"Levy M.","year":"1977","journal-title":"Am. J. Physiol."},{"issue":"22","key":"B19","first-page":"F664","volume":"253","author":"Levy M.","year":"1987","journal-title":"Am. J. Physiol."},{"issue":"36","key":"B20","first-page":"F86","volume":"267","author":"Leyssac P. P.","year":"1994","journal-title":"Am. J. Physiol."},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1994.266.1.C189"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117863"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118628"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1995.269.3.C655"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.4.1013"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.90.24.11663"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.254"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.94.10.5450"},{"key":"B29","first-page":"102","volume":"10","author":"Petersen J. S.","year":"1987","journal-title":"Renal Physiol."},{"key":"B30","doi-asserted-by":"crossref","first-page":"1103","DOI":"10.1016\/S0022-3565(25)10905-1","volume":"262","author":"Petersen J. S.","year":"1992","journal-title":"J. Pharmacol. Exp. Ther."},{"key":"B31","doi-asserted-by":"crossref","first-page":"1","DOI":"10.1016\/S0022-3565(25)20338-X","volume":"258","author":"Petersen J. S.","year":"1991","journal-title":"J. Pharmacol. Exp. Ther."},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1007\/BF00233445"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117079"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1007\/BF00587521"},{"issue":"32","key":"B35","first-page":"F1128","volume":"263","author":"Shirley D.","year":"1992","journal-title":"Am. J. Physiol."},{"issue":"40","key":"B36","first-page":"F414","volume":"271","author":"Terris J.","year":"1996","journal-title":"Am. J. Physiol."},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1159\/000183252"},{"key":"B38","doi-asserted-by":"crossref","first-page":"23451","DOI":"10.1016\/S0021-9258(17)31537-5","volume":"269","author":"Ushida S.","year":"1994","journal-title":"J. Biol. Chem."},{"issue":"40","key":"B39","first-page":"F223","volume":"271","author":"Walter S. J.","year":"1996","journal-title":"Am. J. Physiol."},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1007\/BF02584009"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1016\/0016-5085(93)91026-E"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1002\/hep.1840080422"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119312"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1995.268.6.C1546"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.1992.tb09058.x"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1998.275.2.F216","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,6,29]],"date-time":"2025-06-29T04:40:13Z","timestamp":1751172013000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1998.275.2.F216"}},"issued":{"date-parts":[[1998,8,1]]},"references-count":45,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1998,8,1]]}},"alternative-id":["10.1152\/ajprenal.1998.275.2.F216"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1998.275.2.f216","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[1998,8,1]]}},{"indexed":{"date-parts":[[2025,6,29]],"date-time":"2025-06-29T05:10:01Z","timestamp":1751173801820,"version":"3.41.0"},"reference-count":51,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1999,3,1]]},"abstract":"<jats:p>High potassium intake is known to attenuate hypertension, glomerular lesion, ischemic damage, and stroke-associated death. Our recent studies showed that expression of recombinant kallikrein by somatic gene delivery reduced high blood pressure, cardiac hypertrophy, and renal injury in hypertensive animal models. The aim of this study is to explore the potential role of the tissue kallikrein-kinin system in blood pressure reduction and renal protection in spontaneously hypertensive rats (SHR) on a high-potassium diet. Young SHR were given drinking water with or without 1% potassium chloride for 6 wk. Systolic blood pressure was significantly reduced beginning at 1 wk, and the effect lasted for 6 wk in the potassium-supplemented group compared with that in the control group. Potassium supplement induced 70 and 40% increases in urinary kallikrein levels and renal bradykinin B<jats:sub>2<\/jats:sub>receptor density, respectively ( P &lt; 0.05), but did not change serum kininogen levels. Similarly, Northern blot analysis showed that renal kallikrein mRNA levels increased 2.7-fold, whereas hepatic kininogen mRNA levels remained unchanged in rats with high potassium intake. No difference was observed in \u03b2-actin mRNA levels in the kidney or liver of either group. Competitive RT-PCR showed a 1.7-fold increase in renal bradykinin B<jats:sub>2<\/jats:sub>receptor mRNA levels in rats with high potassium intake. Potassium supplement significantly increased water intake, urine excretion, urinary kinin, cAMP, and cGMP levels. This study suggests that upregulation of the tissue kallikrein-kinin system may be attributed, in part, to blood pressure-lowering and diuretic effects of high potassium intake.<\/jats:p>","DOI":"10.1152\/ajprenal.1999.276.3.f476","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T18:10:12Z","timestamp":1514052612000},"page":"F476-F484","source":"Crossref","is-referenced-by-count":17,"title":["Potassium supplement upregulates the expression of renal kallikrein and bradykinin B<sub>2<\/sub>receptor in SHR"],"prefix":"10.1152","volume":"276","author":[{"given":"Lan","family":"Jin","sequence":"first","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, South Carolina 29425"}]},{"given":"Lee","family":"Chao","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, South Carolina 29425"}]},{"given":"Julie","family":"Chao","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, South Carolina 29425"}]}],"member":"24","reference":[{"issue":"21","key":"B1","first-page":"F964","volume":"252","author":"Ader J.","year":"1987","journal-title":"Am. J. Physiol."},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1042\/cs0750527"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.13.1.3"},{"key":"B5","doi-asserted-by":"crossref","first-page":"1","DOI":"10.1016\/S0031-6997(25)00058-4","volume":"44","author":"Bhoola K. D.","year":"1992","journal-title":"Pharmacol. Rev."},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1089\/hum.1998.9.1-21"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1089\/hum.1996.7.8-901"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1016\/0304-4165(88)90033-5"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/0076-6879(88)59009-2"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117264"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1210\/endo-103-1-60"},{"key":"B12","doi-asserted-by":"crossref","first-page":"1529","DOI":"10.1681\/ASN.V2101529","volume":"2","author":"Ellis D.","year":"1992","journal-title":"J. Am. Soc. Nephrol."},{"key":"B13","first-page":"69","volume":"49","author":"Favaro S.","year":"1975","journal-title":"Clin. Sci. Mol. Med."},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1984.sp015363"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1164\/ajrccm.153.3.8630573"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-198608000-00006"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.22.2.161"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.26.3.425"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1089\/hum.1997.8.15-1753"},{"key":"B20","doi-asserted-by":"crossref","first-page":"25","DOI":"10.1016\/S0031-6997(25)06820-6","volume":"47","author":"Linz W.","year":"1995","journal-title":"Pharmacol. Rev."},{"key":"B21","doi-asserted-by":"crossref","first-page":"265","DOI":"10.1016\/S0021-9258(19)52451-6","volume":"193","author":"Lowry O. H.","year":"1951","journal-title":"J. Biol. Chem."},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.30.3.358"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.35.6.820"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1159\/000138700"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.3181\/00379727-180-42152"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/0090-6980(80)90004-0"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/0003-2697(80)90515-1"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-4615-9546-5_22"},{"issue":"17","key":"B30","first-page":"F382","volume":"248","author":"Nasjletti A.","year":"1985","journal-title":"Am. J. Physiol."},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-198906000-00009"},{"key":"B32","first-page":"189","volume":"95","author":"Obika L. F.","year":"1987","journal-title":"Arch. Int. Physiol. Biochim. Biophys."},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.17.2.242"},{"key":"B36","doi-asserted-by":"crossref","first-page":"581","DOI":"10.1016\/S0022-3565(25)19955-2","volume":"252","author":"Schini V. B.","year":"1990","journal-title":"J. Pharmacol. Exp. Ther."},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1986.14"},{"key":"B38","first-page":"721","volume":"91","author":"Shimamoto K.","year":"1978","journal-title":"J. Lab. Clin. Med."},{"key":"B39","first-page":"172","volume":"94","author":"Shimamoto K.","year":"1979","journal-title":"J. Lab. Clin. Med."},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.3109\/10641969609081030"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.9.5.444"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1139\/y86-145"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-198812040-00003"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.24.6.770"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1987.146"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117847"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1016\/0167-4781(94)90264-X"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.23.2.236"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(94)90658-0"},{"key":"B50","doi-asserted-by":"crossref","first-page":"729","DOI":"10.1016\/S0022-3565(25)10817-3","volume":"262","author":"Wiemer G.","year":"1992","journal-title":"J. Pharmacol. Exp. Ther."},{"issue":"18","key":"B51","first-page":"H907","volume":"249","author":"Workman M. L.","year":"1985","journal-title":"Am. J. Physiol."},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-198911000-00003"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.25.4.715"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1007\/BF01851781"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1093\/oxfordjournals.aje.a112282"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1999.276.3.F476","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,6,29]],"date-time":"2025-06-29T04:40:56Z","timestamp":1751172056000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1999.276.3.F476"}},"issued":{"date-parts":[[1999,3,1]]},"references-count":51,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1999,3,1]]}},"alternative-id":["10.1152\/ajprenal.1999.276.3.F476"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1999.276.3.f476","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[1999,3,1]]}},{"indexed":{"date-parts":[[2025,4,2]],"date-time":"2025-04-02T14:22:58Z","timestamp":1743603778335},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1983,12,1]]},"abstract":"<jats:p> This Editorial Review describes the mechanisms that have been identified for mediating active H + secretion across the luminal membrane of the proximal tubular cell. These include Na+-H+ exchange, Na+-phosphate cotransport, organic anion-OH- exchange, ATP-driven H+ transport, and redox-driven H+ transport. Of these, Na+-H+ exchange appears to bethe most important. Indeed, there is no conclusive evidence against the concept that luminal membrane Na+-H- exchange is the principal if not the sole mechanism for mediating active H+ secretion in the proximal tubule. The transport properties of the Na+-H+ exchanger, particularly its striking sensitivity to intracellular pH, can explain many aspects of howthe rate of active H+ secretion in the proximal tubule is regulated in response to various physiologic stimuli. Certainly, important physiologic roles for other H+ secretory mechanisms, especially those involving primary active H+ secretion,have not been excluded. Nevertheless, there is not yet definitive proof that ATP-driven or redox-driven H+ pumps are located on the luminal membrane itself or that they significantly contribute to transtubular H+ secretion. <\/jats:p>","DOI":"10.1152\/ajprenal.1983.245.6.f647","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T10:02:26Z","timestamp":1513936946000},"page":"F647-F659","source":"Crossref","is-referenced-by-count":19,"title":["Mechanisms of active H+ secretion in the proximal tubule"],"prefix":"10.1152","volume":"245","author":[{"given":"P. S.","family":"Aronson","sequence":"first","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1983.245.6.F647","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T14:25:26Z","timestamp":1567952726000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1983.245.6.F647"}},"issued":{"date-parts":[[1983,12,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1983,12,1]]}},"alternative-id":["10.1152\/ajprenal.1983.245.6.F647"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1983.245.6.f647","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1983,12,1]]}},{"indexed":{"date-parts":[[2025,4,2]],"date-time":"2025-04-02T14:23:01Z","timestamp":1743603781365},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1997,4,1]]},"abstract":"<jats:p> PKD1, the gene that is mutated in approximately 85% of autosomal dominant polycystic kidney disease (ADPKD) cases in humans, has recently been identified (Eur. PKD Consortium. Cell 77: 881-894, 1994; also, erratum in Cell 78: 1994). The longest open-reading frame of PKD1 encodes polycystin, a novel approximately 460-kDa protein that contains a series of NH2-terminal adhesive domains (J. Hughes, C. J. Ward, B. Peral, R. Aspinwall, K. Clark, J. San Millan, V. Gamble, and P. C. Harris. Nat. Genet. 10: 151-160, 1995; and Int. PKD Consortium. Cell 81: 289\u2013298, 1995) and several putative transmembrane segments. To extend studies of polycystin to an experimentally accessible animal, we have isolated a cDNA clone encoding the 3' end of Pkd1, the mouse homologue of PKD1, and raised a specific antibody to recombinant murine polycystin. This antibody was used to determine the subcellular localization and tissue distribution of the protein by Western analysis and immunocytochemistry. In the mouse, polycystin is an approximately 400-kDa molecule that is predominantly found in membrane fractions of tissue and cell extracts. It is expressed in many tissues including kidney, liver, pancreas, heart, intestine, lung, and brain. Renal expression, which is confined to tubular epithelia, is highest in late fetal and early neonatal life and drops 20-fold by the third postnatal week, maintaining this level into adulthood. Thus the temporal profile of polycystin expression coincides with kidney tubule differentiation and maturation. <\/jats:p>","DOI":"10.1152\/ajprenal.1997.272.4.f451","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T03:11:57Z","timestamp":1513998717000},"page":"F451-F459","source":"Crossref","is-referenced-by-count":16,"title":["Distribution and developmentally regulated expression of murine polycystin"],"prefix":"10.1152","volume":"272","author":[{"given":"L.","family":"Geng","sequence":"first","affiliation":[{"name":"Renal Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA."}]},{"given":"Y.","family":"Segal","sequence":"additional","affiliation":[{"name":"Renal Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA."}]},{"given":"A.","family":"Pavlova","sequence":"additional","affiliation":[{"name":"Renal Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA."}]},{"given":"E. J.","family":"Barros","sequence":"additional","affiliation":[{"name":"Renal Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA."}]},{"given":"C.","family":"Lohning","sequence":"additional","affiliation":[{"name":"Renal Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA."}]},{"given":"W.","family":"Lu","sequence":"additional","affiliation":[{"name":"Renal Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA."}]},{"given":"S. K.","family":"Nigam","sequence":"additional","affiliation":[{"name":"Renal Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA."}]},{"given":"A. M.","family":"Frischauf","sequence":"additional","affiliation":[{"name":"Renal Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA."}]},{"given":"S. T.","family":"Reeders","sequence":"additional","affiliation":[{"name":"Renal Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA."}]},{"given":"J.","family":"Zhou","sequence":"additional","affiliation":[{"name":"Renal Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1997.272.4.F451","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:15:24Z","timestamp":1567959324000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1997.272.4.F451"}},"issued":{"date-parts":[[1997,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1997,4,1]]}},"alternative-id":["10.1152\/ajprenal.1997.272.4.F451"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1997.272.4.f451","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1997,4,1]]}},{"indexed":{"date-parts":[[2025,4,2]],"date-time":"2025-04-02T14:40:02Z","timestamp":1743604802602,"version":"3.40.3"},"reference-count":49,"publisher":"American Physiological Society","issue":"3","funder":[{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["K01DK119375"],"award-info":[{"award-number":["K01DK119375"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["R01DK129255-01A1"],"award-info":[{"award-number":["R01DK129255-01A1"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100031146","name":"OU Health | Harold Hamm Diabetes Center, OU Health","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100031146","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100001296","name":"PKD Foundation","doi-asserted-by":"publisher","award":["1065555"],"award-info":[{"award-number":["1065555"]}],"id":[{"id":"10.13039\/100001296","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2025,3,1]]},"abstract":"<jats:p> Due to the growing obesity pandemic, almost one third of all children are born to mothers with obesity; however, the impact of maternal obesity on polycystic kidney disease (PKD) is unknown. In this manuscript, we found that maternal obesity did not worsen PKD severity in Pkd1<jats:sup>RC\/RC<\/jats:sup> mice at 3 mo or 1 yr of age when weaned onto normal chow diet. However, rechallenging pups born to obese mothers worsened PKD severity in female but not male mice. <\/jats:p>","DOI":"10.1152\/ajprenal.00227.2024","type":"journal-article","created":{"date-parts":[[2025,2,5]],"date-time":"2025-02-05T16:19:41Z","timestamp":1738772381000},"page":"F316-F327","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["The impact of maternal obesity on polycystic kidney disease progression in a mouse model"],"prefix":"10.1152","volume":"328","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4888-5306","authenticated-orcid":false,"given":"Sarah J.","family":"Miller","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/0457zbj98","id-type":"ROR","asserted-by":"publisher"}],"name":"University of Oklahoma Health Sciences Center","place":["United States"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7805-5197","authenticated-orcid":false,"given":"Kaitlyn","family":"Hill","sequence":"additional","affiliation":[{"name":"University of Oklahoma Health Sciences Center","place":["United States"]}]},{"given":"Isabella","family":"Darby","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/0457zbj98","id-type":"ROR","asserted-by":"publisher"}],"name":"University of Oklahoma Health Sciences Center","place":["United States"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8624-721X","authenticated-orcid":false,"given":"Fariha","family":"Nusrat","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/0457zbj98","id-type":"ROR","asserted-by":"publisher"}],"name":"University of Oklahoma Health Sciences Center","place":["United States"]}]},{"given":"Jacob E.","family":"Friedman","sequence":"additional","affiliation":[{"name":"University of Oklahoma Health Sciences Center","place":["United States"]},{"name":"University of Oklahoma Health Sciences Center","place":["United States"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6147-212X","authenticated-orcid":false,"given":"Michael C.","family":"Rudolph","sequence":"additional","affiliation":[{"name":"University of Oklahoma Health Sciences Center","place":["United States"]},{"name":"University of Oklahoma Health Sciences Center","place":["United States"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1798-8046","authenticated-orcid":false,"given":"Kurt A.","family":"Zimmerman","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/0457zbj98","id-type":"ROR","asserted-by":"publisher"}],"name":"University of Oklahoma Health Sciences Center","place":["United States"]}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1126\/science.272.5266.1339"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(94)90137-6"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.med.60.101707.125712"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1007\/978-3-319-51436-9_12"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.02320220"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1055\/s-0035-1557868"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1038\/oby.2007.621"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1002\/hep.23205"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1007\/s00198-009-1118-4"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00351.2004"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00310.2010"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbadis.2013.07.006"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1194\/jlr.M800033-JLR200"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1017\/S000711450820749X"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1038\/s41467-018-06929-0"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.33696\/immunology.2.061"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.34067\/KID.0000882021"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2011010084"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.14814\/phy2.13951"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2018.06.025"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00065.x"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1993.79"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2012.446"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.15252\/embj.201798615"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2018080810"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2018050518"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.34067\/KID.0001052019"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2021030278"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/j.amjmed.2012.12.018"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/j.xkme.2021.03.004"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1016\/j.isci.2021.103697"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2017070819"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.16871020"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.3390\/nu15122749"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1038\/nmeth.2089"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-0716-3437-0_12"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-022-19657-9"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1097\/ALN.0b013e3181799d45"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.3389\/fendo.2021.585887"},{"volume-title":"Endotext","year":"2000","author":"Purnell JQ","key":"B40"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-023-38703-8"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.2174\/1876894600901010059"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2021.01.028"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1172\/JCI64313"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1002\/hep4.1139"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1016\/j.celrep.2023.112393"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2018090931"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.2337\/db19-1218"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(92)90362-g"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00227.2024","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,4,2]],"date-time":"2025-04-02T14:11:12Z","timestamp":1743603072000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00227.2024"}},"issued":{"date-parts":[[2025,3,1]]},"references-count":49,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2025,3,1]]}},"alternative-id":["10.1152\/ajprenal.00227.2024"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00227.2024","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2025,3,1]]},"assertion":[{"value":"2024-08-05","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2024-09-08","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2025-01-27","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2025-02-18","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2025,8,23]],"date-time":"2025-08-23T05:15:45Z","timestamp":1755926145895},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1990,8,1]]},"abstract":"<jats:p> It is well known that prostaglandin E2 (PGE2) both inhibits arginine vasopressin (AVP)-stimulated water permeability (hydraulic conductivity, Lp) in the cortical collecting duct (CCD) or, if administered alone, modestly increases Lp in the CCD. These bifunctional effects on Lp correspond to PGE2's capacity to inhibit AVP-stimulated adenylate cyclase (AC) activity, or to singularly stimulate AC activity in the collecting duct. The present studies suggest that the inhibitory effect of PGE2 on Lp may also be mediated by phosphatidylinositol (PI) hydrolysis. Using in vitro microperfused rabbit CCDs, we show that PGE2 releases Ca from intracellular stores. We also demonstrate that the inhibitory effect of PGE2 on AVP-stimulated Lp in the CCD is significantly reversed by the protein kinase C (PKC) inhibitor, staurosporine (SSP). Although PGE2 does not reduce an established water flow response to 8-(4-chlorophenylthio)-adenosine 3',5'-cyclic monophosphate (8-CPTcAMP), when the sequence of addition is reversed and PGE2 is added first, marked inhibition of 8-CPTcAMP-induced Lp is observed. This provides independent evidence that PGE2 can act through a mechanism separate from modulating AC activity. PGE2 inhibition of 8-CPTcAMP-induced Lp is reversed by SSP pretreatment. Finally, SSP pretreatment also markedly potentiates the capacity of PGE2 itself to increase Lp. We conclude that PGE2 releases Ca from intracellular stores and, by activating PKC, inhibits AVP-induced osmotic water flow. This suggests an important role for PI hydrolysis in mediating PGE2's effects on the CCD. <\/jats:p>","DOI":"10.1152\/ajprenal.1990.259.2.f318","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T22:26:51Z","timestamp":1513981611000},"page":"F318-F325","source":"Crossref","is-referenced-by-count":46,"title":["PGE2 inhibits AVP-induced water flow in cortical collecting ducts by protein kinase C activation"],"prefix":"10.1152","volume":"259","author":[{"given":"R. L.","family":"Hebert","sequence":"first","affiliation":[{"name":"Department of Medicine, Vanderbilt University, Nashville,Tennessee."}]},{"given":"H. R.","family":"Jacobson","sequence":"additional","affiliation":[{"name":"Department of Medicine, Vanderbilt University, Nashville,Tennessee."}]},{"given":"M. D.","family":"Breyer","sequence":"additional","affiliation":[{"name":"Department of Medicine, Vanderbilt University, Nashville,Tennessee."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1990.259.2.F318","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:19:02Z","timestamp":1567970342000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1990.259.2.F318"}},"issued":{"date-parts":[[1990,8,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1990,8,1]]}},"alternative-id":["10.1152\/ajprenal.1990.259.2.F318"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1990.259.2.f318","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1990,8,1]]}},{"indexed":{"date-parts":[[2025,8,23]],"date-time":"2025-08-23T05:00:27Z","timestamp":1755925227828},"reference-count":42,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2004,9]]},"abstract":"<jats:p>In previous studies examining the role of glucocorticoids and thyroid hormone on the maturation of the Na<jats:sup>+<\/jats:sup>\/H<jats:sup>+<\/jats:sup>antiporter (NHE3), we found attenuation in the maturational increase in proximal tubule apical Na<jats:sup>+<\/jats:sup>\/H<jats:sup>+<\/jats:sup>antiporter activity but no change in NHE3 mRNA abundance in either glucocorticoid-deficient or hypothyroid rats. In addition, prevention of the maturational increase in either hormone failed to totally prevent the maturational increase in Na<jats:sup>+<\/jats:sup>\/H<jats:sup>+<\/jats:sup>antiporter activity. We hypothesized that one hormone played a compensatory role when the other was deficient. The present study examined whether combined deficiency of thyroid and glucocorticoid hormones would completely prevent the maturation of the Na<jats:sup>+<\/jats:sup>\/H<jats:sup>+<\/jats:sup>antiporter. Adrenalectomy was performed in 9-day-old hypothyroid Sprague-Dawley rats, a time before the normal postnatal maturational increase in these hormones occurs. Nine- and 30-day-old adrenalectomized (ADX), hypothyroid rats had comparable NHE3 mRNA abundance, which was 5- to 10-fold less than 30-day-old ADX, hypothyroid rats that received corticosterone-thyroxine replacement and 30-day-old sham control rats ( P &lt; 0.05). Brush-border membrane NHE3 protein abundance was comparable in 9- and 30-day-old ADX, hypothyroid groups and \u223c20-fold lower than both the 30-day replacement and 30-day sham groups ( P &lt; 0.05). Similarly, the replacement and sham groups had higher sodium-dependent proton secretion than 9- and 30-day-old ADX, hypothyroid groups ( P &lt; 0.05). We conclude that combined deficiency of both hormones totally prevents the maturational increase in NHE3 mRNA and protein abundance and Na<jats:sup>+<\/jats:sup>\/H<jats:sup>+<\/jats:sup>antiporter activity.<\/jats:p>","DOI":"10.1152\/ajprenal.00005.2004","type":"journal-article","created":{"date-parts":[[2004,5,4]],"date-time":"2004-05-04T00:19:03Z","timestamp":1083629943000},"page":"F521-F527","source":"Crossref","is-referenced-by-count":24,"title":["Maturation of the Na<sup>+<\/sup>\/H<sup>+<\/sup>antiporter (NHE3) in the proximal tubule of the hypothyroid adrenalectomized rat"],"prefix":"10.1152","volume":"287","author":[{"given":"Neena","family":"Gupta","sequence":"first","affiliation":[]},{"given":"Vangipuram","family":"Dwarakanath","sequence":"additional","affiliation":[]},{"given":"Michel","family":"Baum","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI112602"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.404"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1996.270.2.C585"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1172\/JCI114465"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1203\/00006450-199204000-00021"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.270.1.F164"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.268.5.F815"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00879.x"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.267.3.F437"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.467"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.261.5.F746"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1985.248.5.R524"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.3.F629"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1999.276.1.C102"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1172\/JCI9260"},{"key":"R16","doi-asserted-by":"crossref","unstructured":"Chomczynmski Pand Sacchi N.Single-step method of RNA isolation by acid guanidine thiocyanate-phenol-chloroform extraction.Anal Biochem162: 156\u2013159, 1987.","DOI":"10.1016\/0003-2697(87)90021-2"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1016\/0016-6480(74)90127-0"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.1982.242.1.E33"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.3758\/BF03332971"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1016\/0014-4886(85)90039-1"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1172\/JCI105623"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.79.16.4932"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00784.x"},{"key":"R24","doi-asserted-by":"crossref","unstructured":"Henning SJ.Plasma concentrations of total and free corticosterone during development in the rat.Am J Physiol Endocrinol Metab Gastrointest Physiol235: E451\u2013E456, 1978.","DOI":"10.1152\/ajpendo.1978.235.5.E451"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.18.10551"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.81.2.630"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1985.248.2.F233"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.82.11.3606"},{"key":"R29","doi-asserted-by":"crossref","unstructured":"Loffing J, Lotscher M, Kaissling B, Biber J, Murer H, Seikaly M, Alpern RJ, Levi M, Baum M, and Moe OW.Renal Na\/H exchanger NHE-3 and Na-PO4 cotransporter NaPi-2 protein expression in glucocorticoid excess and deficient states.J Am Soc Nephrol9: 1560\u20131567, 1998.","DOI":"10.1681\/ASN.V991560"},{"key":"R30","doi-asserted-by":"crossref","unstructured":"Lowry OH, Rosebrough NJ, Farr AL, and Randall RJ.Protein measurements with the Folin phenol reagent.J Biol Chem193: 265\u2013275, 1951.","DOI":"10.1016\/S0021-9258(19)52451-6"},{"key":"R31","unstructured":"Meserve LAand Juarez de Ku LM.Effect of thiouracil-induced hypothyroidism on time course of adrenal response in 15 day old rats.Growth Dev Aging57: 25\u201330, 1993."},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1055\/s-2007-1019004"},{"key":"R33","doi-asserted-by":"crossref","unstructured":"Orlowski J, Kandasamy RA, and Shull GE.Molecular cloning of putative members of the Na\/H exchanger gene family. cDNA cloning, deduced amino acid sequence, and mRNA tissue expression of the rat Na\/H exchanger NHE-1 and two structurally related proteins.J Biol Chem267: 9331\u20139339, 1992.","DOI":"10.1016\/S0021-9258(19)50428-8"},{"key":"R34","doi-asserted-by":"crossref","unstructured":"Roos Aand Boron WF.Intracellular pH.Physiol Rev61: 297\u2013434, 1981.","DOI":"10.1152\/physrev.1981.61.2.296"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1983.245.3.F382"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1203\/00006450-200008000-00014"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1998.274.3.H883"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1007\/BF00788662"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1203\/00006450-198003000-00014"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.2.F298"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.51.32749"},{"key":"R42","doi-asserted-by":"crossref","unstructured":"Yagil R, Lerner Z, Etzion Z, and Berlyne GM.Acid-base changes in milk and blood of rats in acidosis and alkalosis.Am J Physiol231: 132\u2013135, 1976.","DOI":"10.1152\/ajplegacy.1976.231.1.132"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00005.2004","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,6,17]],"date-time":"2021-06-17T07:53:07Z","timestamp":1623916387000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00005.2004"}},"issued":{"date-parts":[[2004,9]]},"references-count":42,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2004,9]]}},"alternative-id":["10.1152\/ajprenal.00005.2004"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00005.2004","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2004,9]]}},{"indexed":{"date-parts":[[2025,8,12]],"date-time":"2025-08-12T21:37:45Z","timestamp":1755034665783},"reference-count":10,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2017,11,1]]},"DOI":"10.1152\/ajprenal.00283.2017","type":"journal-article","created":{"date-parts":[[2017,6,14]],"date-time":"2017-06-14T20:25:30Z","timestamp":1497471930000},"page":"F1084-F1086","source":"Crossref","is-referenced-by-count":9,"title":["An essential MIF-CD74 signaling axis in kidney tubular regeneration, with prospects for precision medicine and pharmacological augmentation"],"prefix":"10.1152","volume":"313","author":[{"given":"Idit","family":"Shachar","sequence":"first","affiliation":[{"name":"Department of Immunology, Weizmann Institute of Science, Rehovot, Israel"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.93.15.7849"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.2174\/1389557515666150203144111"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(13)60647-9"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1159\/000145463"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1102941108"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00683.2016"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1172\/JCI73061"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/onc.2010.191"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1172\/JCI81937"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M203503200"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00283.2017","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T21:34:03Z","timestamp":1567978443000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00283.2017"}},"issued":{"date-parts":[[2017,11,1]]},"references-count":10,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2017,11,1]]}},"alternative-id":["10.1152\/ajprenal.00283.2017"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00283.2017","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2017,11,1]]}},{"indexed":{"date-parts":[[2025,4,13]],"date-time":"2025-04-13T13:05:59Z","timestamp":1744549559996},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1987,8,1]]},"abstract":"<jats:p> Rat renal papillary collecting duct (PCD) cells were isolated using collagenase and hyaluronidase digestion and a three-step low-speed centrifugation. As assessed by binding of the lectin Dolichos biflorus and determination of vasopressin-sensitive adenylate cyclase and Na+-K+-ATPase, the enrichment of PCD cells over a crude papillary cell preparation was 1.8, 2.4, and 1.4, respectively. Microscopic evaluation indicated that the preparation was greater than 90% pure PCD cells. The isolated cells were viable as evident from the high K\/Na ratio of intracellular electrolytes measured by electron probe analysis (5.3), from the high ATP\/ADP ratio (2.15), and the metabolic response to alterations in Na transport. Exposure to 2 mM ouabain or removal of Na reduced O2 consumption by 25-35%; the uncoupler carboxylcyanide-m-chlorophenylhydrazone more than doubled O2 consumption. In the presence of 14 mM glucose and at a PO2 of 100 Torr the cells produced substantial quantities of lactate. This aerobic glycolysis may account for greater than 20% of the ATP production. In the presence of rotenone, glycolysis increased by 56% and was able to maintain the cellular ATP level at 65% of control. In the absence of any exogenous substrate PCD cells respired normally and had a close to normal ATP content, but lactate production was markedly decreased. These results demonstrate that viable PCD cells can be isolated from rat kidney. At normal PO2 and in the presence of D-glucose the cells show a substantial amount of aerobic glycolysis, although their mitochondrial respiration is not rate limiting. In the absence of glucose the cells derive the majority of their energy from an as yet unidentified endogenous substrate. <\/jats:p>","DOI":"10.1152\/ajprenal.1987.253.2.f251","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T01:59:02Z","timestamp":1513994342000},"page":"F251-F262","source":"Crossref","is-referenced-by-count":34,"title":["Purification of rat papillary collecting duct cells: functional and metabolic assessment"],"prefix":"10.1152","volume":"253","author":[{"given":"J. B.","family":"Stokes","sequence":"first","affiliation":[]},{"given":"C.","family":"Grupp","sequence":"additional","affiliation":[]},{"given":"R. K.","family":"Kinne","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1987.253.2.F251","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:40:20Z","timestamp":1567971620000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1987.253.2.F251"}},"issued":{"date-parts":[[1987,8,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1987,8,1]]}},"alternative-id":["10.1152\/ajprenal.1987.253.2.F251"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1987.253.2.f251","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1987,8,1]]}},{"indexed":{"date-parts":[[2025,4,13]],"date-time":"2025-04-13T00:52:23Z","timestamp":1744505543695},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1982,2,1]]},"DOI":"10.1152\/ajprenal.1982.242.2.f140","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T13:47:23Z","timestamp":1513950443000},"page":"F140-F148","source":"Crossref","is-referenced-by-count":5,"title":["Renal function in conscious rats with chronic unilateral renal denervation"],"prefix":"10.1152","volume":"242","author":[{"given":"P. R.","family":"Rogenes","sequence":"first","affiliation":[]},{"given":"C. W.","family":"Gottschalk","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1982.242.2.F140","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:17:46Z","timestamp":1567966666000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1982.242.2.F140"}},"issued":{"date-parts":[[1982,2,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1982,2,1]]}},"alternative-id":["10.1152\/ajprenal.1982.242.2.F140"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1982.242.2.f140","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1982,2,1]]}},{"indexed":{"date-parts":[[2025,4,22]],"date-time":"2025-04-22T12:26:16Z","timestamp":1745324776490},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1979,1,1]]},"DOI":"10.1152\/ajprenal.1979.236.1.f40","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T15:37:30Z","timestamp":1513957050000},"page":"F40-F47","source":"Crossref","is-referenced-by-count":3,"title":["Feedback control of glomerular filtration rate: site of the effector mechanism"],"prefix":"10.1152","volume":"236","author":[{"given":"J. P.","family":"Briggs","sequence":"first","affiliation":[]},{"given":"F. S.","family":"Wright","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1979.236.1.F40","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:02:19Z","timestamp":1567954939000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1979.236.1.F40"}},"issued":{"date-parts":[[1979,1,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1979,1,1]]}},"alternative-id":["10.1152\/ajprenal.1979.236.1.F40"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1979.236.1.f40","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1979,1,1]]}},{"indexed":{"date-parts":[[2025,4,8]],"date-time":"2025-04-08T23:35:47Z","timestamp":1744155347957},"reference-count":32,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1998,10,1]]},"abstract":"<jats:p>Laminin is a major component of the extracellular matrix whose expression is regulated by growth factors. The laminin \u03b31-chain promoter contains a newly identified transcriptional element denoted bcn-1 that is both active and inducible in mesangial cells. In this study, we explored activation of the bcn-1 element in other renal and nonrenal cells. Treatment of rat glomerular epithelial cells (GEC) with phorbol 12-myristate 13-acetate (PMA) increased activity of the bcn-1 transcriptional element, within the context of the native laminin \u03b31-chain promoter or when cloned upstream of a heterologous promoter. Treatment of GEC with PMA induced nuclear DNA-binding activity, BCN-1, which was recognized by the bcn-1 motif in a gel shift assay. These results provide evidence that the bcn-1 motif and its cognate BCN-1 factor(s) may regulate transcription of the laminin \u03b31-chain in GEC. The bcn-1 element and its cognate BCN-1 DNA-binding activity were also inducible in monkey kidney COS-7 and in human T cell Jurkat lines. SDS-PAGE of in situ ultraviolet cross-linked nucleoproteins from GEC, COS, and Jurkat cells revealed one major 110\u2013115 kDa adduct in all three cell lines. These results demonstrate that the bcn-1 element is active in renal and nonrenal cells from different mammalian species where the same protein contributes to the inducible BCN-1 DNA-binding activity.<\/jats:p>","DOI":"10.1152\/ajprenal.1998.275.4.f518","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T16:39:30Z","timestamp":1514047170000},"page":"F518-F526","source":"Crossref","is-referenced-by-count":2,"title":["Inducible transcriptional activity of bcn-1 element from laminin \u03b31-chain gene promoter in renal and nonrenal cells"],"prefix":"10.1152","volume":"275","author":[{"given":"Hideaki","family":"Suzuki","sequence":"first","affiliation":[{"name":"Department of Medicine, University of Washington, Seattle, Washington 98195"}]},{"given":"Oleg N.","family":"Denisenko","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Washington, Seattle, Washington 98195"}]},{"given":"Yu","family":"Suzuki","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Washington, Seattle, Washington 98195"}]},{"given":"Daniel S.","family":"Schullery","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Washington, Seattle, Washington 98195"}]},{"given":"Karol","family":"Bomsztyk","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Washington, Seattle, Washington 98195"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.14.12.7704"},{"key":"B2","doi-asserted-by":"crossref","first-page":"9413","DOI":"10.1016\/S0021-9258(19)38864-7","volume":"265","author":"Bomsztyk K.","year":"1990","journal-title":"J. Biol. Chem."},{"key":"B3","first-page":"1116","volume":"7","author":"Brasier A. R.","year":"1989","journal-title":"Biotechniques"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1126\/science.3529394"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/0945-053X(94)90184-8"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/24.7.1360"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/0003-2697(87)90021-2"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/11.5.1475"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.87.9.3264"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(12)80329-5"},{"key":"B12","first-page":"485","volume":"66","author":"Floege J.","year":"1992","journal-title":"Lab. Invest."},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1991.235"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1084\/jem.152.6.1709"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(81)90282-8"},{"key":"B16","doi-asserted-by":"crossref","first-page":"1388","DOI":"10.1681\/ASN.V291388","volume":"2","author":"Johnson R. J.","year":"1992","journal-title":"J. Am. Soc. Nephrol."},{"key":"B17","doi-asserted-by":"crossref","first-page":"221","DOI":"10.1016\/S0021-9258(18)52424-8","volume":"266","author":"Kallunki T.","year":"1991","journal-title":"J. Biol. Chem."},{"key":"B18","doi-asserted-by":"crossref","first-page":"2793","DOI":"10.1016\/S0021-9258(18)53843-6","volume":"268","author":"Lin C. S.","year":"1993","journal-title":"J. Biol. Chem."},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.cb.03.110187.000421"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.87.24.10028"},{"key":"B21","doi-asserted-by":"crossref","first-page":"8384","DOI":"10.1016\/S0021-9258(18)68489-3","volume":"263","author":"Ogawa K.","year":"1988","journal-title":"J. Biol. Chem."},{"issue":"42","key":"B22","first-page":"F411","volume":"273","author":"O\u2019Neill B. O.","year":"1997","journal-title":"Am. J. Physiol."},{"key":"B23","doi-asserted-by":"crossref","first-page":"13340","DOI":"10.1016\/S0021-9258(18)37710-X","volume":"263","author":"Paik Y. K.","year":"1988","journal-title":"J. Biol. Chem."},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1988.143"},{"key":"B25","doi-asserted-by":"crossref","first-page":"2021","DOI":"10.4049\/jimmunol.146.6.2021","volume":"146","author":"Rayhel E. J.","year":"1991","journal-title":"J. Immunol."},{"issue":"37","key":"B26","first-page":"F273","volume":"268","author":"Richardson C. A.","year":"1995","journal-title":"Am. J. Physiol."},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.74.12.5463"},{"key":"B28","doi-asserted-by":"crossref","first-page":"17111","DOI":"10.1016\/S0021-9258(18)45498-1","volume":"262","author":"Sasaki M.","year":"1987","journal-title":"J. Biol. Chem."},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.78.12.7575"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.31.18981"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1016\/S0955-0674(96)80102-5"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.47.1.1"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1016\/0006-291X(90)91996-6"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1998.275.4.F518","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,8,30]],"date-time":"2023-08-30T05:41:35Z","timestamp":1693374095000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1998.275.4.F518"}},"issued":{"date-parts":[[1998,10,1]]},"references-count":32,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1998,10,1]]}},"alternative-id":["10.1152\/ajprenal.1998.275.4.F518"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1998.275.4.f518","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1998,10,1]]}},{"indexed":{"date-parts":[[2025,8,6]],"date-time":"2025-08-06T12:56:07Z","timestamp":1754484967009},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1988,5,1]]},"abstract":"<jats:p> Although the mammalian colon is thought to absorb large quantities of total ammonia, principally in the form of NH3, quantitative support for this hypothesis is lacking. In rat distal colon, we observed that NH3 was approximately 400 times more permeant than NH+4. In addition, colonic HCO-3 secretion influenced total ammonia (NH3 plus NH+4) absorption; that is, alteration of HCO-3 secretion caused a parallel change in total ammonia absorption. Perfusion with total ammonia also caused net HCO-3 secretion to switch to net absorption, and, in the setting of preexisting HCO-3 absorption, perfusate containing total ammonia enhanced HCO-3 absorption. These events suggest that colonic HCO-3 secretion titrates luminal NH+4 to NH3, permitting NH3 to diffuse from the lumen, while HCO-3 is titrated to carbon dioxide and also diffuses from the lumen. In support of titration of NH+4 and HCO-3, the magnitude of induced HCO-3 absorption approximated total ammonia absorption. This titration relationship suggests that, in kinetic studies, total ammonia absorption will be limited by a fixed rate of HCO-3 secretion. A model was developed that simulated these events. <\/jats:p>","DOI":"10.1152\/ajprenal.1988.254.5.f657","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T03:22:43Z","timestamp":1513999363000},"page":"F657-F667","source":"Crossref","is-referenced-by-count":7,"title":["Bicarbonate secretion modulates ammonium absorption in rat distal colon in vivo"],"prefix":"10.1152","volume":"254","author":[{"given":"R. M.","family":"Cohen","sequence":"first","affiliation":[{"name":"Department of Medicine, Veterans Administration Medical Center,University of Pennsylvania School of Medicine, Philadelphia 19104."}]},{"given":"R. L.","family":"Stephenson","sequence":"additional","affiliation":[{"name":"Department of Medicine, Veterans Administration Medical Center,University of Pennsylvania School of Medicine, Philadelphia 19104."}]},{"given":"G. M.","family":"Feldman","sequence":"additional","affiliation":[{"name":"Department of Medicine, Veterans Administration Medical Center,University of Pennsylvania School of Medicine, Philadelphia 19104."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1988.254.5.F657","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:51:07Z","timestamp":1567972267000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1988.254.5.F657"}},"issued":{"date-parts":[[1988,5,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1988,5,1]]}},"alternative-id":["10.1152\/ajprenal.1988.254.5.F657"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1988.254.5.f657","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1988,5,1]]}},{"indexed":{"date-parts":[[2025,10,25]],"date-time":"2025-10-25T12:25:51Z","timestamp":1761395151131},"reference-count":34,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1999,2,1]]},"abstract":"<jats:p>Patients with proteinuria tend to develop progressive renal disease with proximal tubular cell atrophy and interstitial scarring. It has been suggested that the nephrotoxicity of albuminuric states may be due to the protein molecule itself or by lipids, such as lysophosphatidic acid (LPA), that albumin carries. LPA was found to cause a transient increase in intracytoplasmic free Ca<jats:sup>2+<\/jats:sup>([Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>) in opossum kidney proximal tubule cells (OK) that was maximal at 100 \u03bcM LPA and was dose dependent with an EC<jats:sub>50<\/jats:sub>of 2.6 \u00d7 10<jats:sup>\u22126<\/jats:sup>M. This Ca<jats:sup>2+<\/jats:sup>mobilization was from both internal stores and across the plasma membrane and was pertussis toxin (PTX) insensitive. Treatment of OK cells with 100 \u03bcM LPA for 5 min was found to cause a twofold increase in [<jats:sup>3<\/jats:sup>H]thymidine incorporation and a three- to fivefold increase over control after 24 h. This was highly PTX sensitive and insensitive to pretreatment with the tyrosine kinase inhibitors genistein and herbimycin A. These findings may be of significance in the progression of renal disease and indicate the potential importance of lipids in modulating proximal tubule cell function and growth.<\/jats:p>","DOI":"10.1152\/ajprenal.1999.276.2.f191","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T18:14:22Z","timestamp":1514052862000},"page":"F191-F198","source":"Crossref","is-referenced-by-count":3,"title":["Lysophosphatidic acid-induced calcium mobilization and proliferation in kidney proximal tubular cells"],"prefix":"10.1152","volume":"276","author":[{"given":"Richard J.","family":"Dixon","sequence":"first","affiliation":[{"name":"Department of Cell Physiology and Pharmacology, Leicester University School of Medicine; and"}]},{"given":"Ken","family":"Young","sequence":"additional","affiliation":[{"name":"Department of Cell Physiology and Pharmacology, Leicester University School of Medicine; and"}]},{"given":"Nigel J.","family":"Brunskill","sequence":"additional","affiliation":[{"name":"Department of Cell Physiology and Pharmacology, Leicester University School of Medicine; and"},{"name":"Department of Nephrology, Leicester General Hospital, Leicester LE1 9HN, United Kingdom"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1990.14"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1159\/000402883"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1159\/000167514"},{"key":"B4","first-page":"345","volume":"2","author":"Burton C. J.","year":"1994","journal-title":"Exp. Nephrol."},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(96)90512-0"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1159\/000168199"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.me.35.020184.001135"},{"key":"B8","first-page":"719","volume":"135","author":"Eddy A. A.","year":"1989","journal-title":"Am. J. Pathol."},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.218"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(95)90295-3"},{"key":"B11","first-page":"26","volume":"1","author":"Frank J.","year":"1992","journal-title":"Exp. Nephrol."},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.11.6151"},{"key":"B13","doi-asserted-by":"crossref","first-page":"3440","DOI":"10.1016\/S0021-9258(19)83641-4","volume":"260","author":"Grynkewicz G.","year":"1989","journal-title":"J. Biol. Chem."},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.88.6.2051"},{"key":"B15","unstructured":"Heptinstall R. H.Pathology of the Kidney3rd ed.III1983617724Little, BrownBoston"},{"key":"B16","first-page":"186","volume":"1198","author":"Jalink K.","year":"1994","journal-title":"Biochim. Biophys. Acta"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.222"},{"key":"B18","first-page":"598","volume":"3","author":"Kees-Folts D.","year":"1992","journal-title":"J. Am. Soc. Nephrol."},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1007\/BF02616032"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1991.63"},{"issue":"42","key":"B21","first-page":"F575","volume":"273","author":"Levine J. S.","year":"1997","journal-title":"Am. J. Physiol."},{"issue":"28","key":"B22","first-page":"F485","volume":"259","author":"Miyauchi A.","year":"1990","journal-title":"Am. J. Physiol."},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.22.12949"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1016\/S0955-0674(97)80059-2"},{"key":"B25","doi-asserted-by":"crossref","first-page":"1247","DOI":"10.1681\/ASN.V881247","volume":"8","author":"Neverov N.","year":"1997","journal-title":"J. Am. Soc. Nephrol."},{"issue":"19","key":"B26","first-page":"F217","volume":"250","author":"Pollack A. S.","year":"1986","journal-title":"Am. J. Physiol."},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/0143-4160(90)90016-N"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1016\/S0046-8177(70)80061-2"},{"issue":"37","key":"B29","first-page":"F1177","volume":"268","author":"Thomas M. E.","year":"1995","journal-title":"Am. J. Physiol."},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1159\/000168653"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(90)90801-K"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(89)90868-4"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1990.103"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1991.52"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1999.276.2.F191","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:55:22Z","timestamp":1660190122000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1999.276.2.F191"}},"issued":{"date-parts":[[1999,2,1]]},"references-count":34,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1999,2,1]]}},"alternative-id":["10.1152\/ajprenal.1999.276.2.F191"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1999.276.2.f191","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1999,2,1]]}},{"indexed":{"date-parts":[[2025,10,23]],"date-time":"2025-10-23T05:27:12Z","timestamp":1761197232500},"reference-count":53,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2014,7,15]]},"abstract":"<jats:p>The present study tested the hypothesis that the multiligand endocytic receptor megalin is partially involved in the uptake of ANG II and downstream signaling responses in mouse proximal tubule cells (mPCT) by interacting with AT<jats:sub>1a<\/jats:sub>receptors. mPCT cells of wild-type (WT) and AT<jats:sub>1a<\/jats:sub>receptor-deficient (AT<jats:sub>1a<\/jats:sub>-KO) mice were treated with vehicle, the AT<jats:sub>1<\/jats:sub>receptor blocker losartan (10 \u03bcM), or a selective megalin small interfering (si) RNA for 48 h. The uptake of fluorescein (FITC)-labeled ANG II (10 nM, 37\u00b0C) and downstream signaling responses were analyzed by fluorescence imaging and Western blotting. AT<jats:sub>1a<\/jats:sub>receptors and megalin were abundantly expressed in mPCT cells, whereas AT<jats:sub>1a<\/jats:sub>receptors were absent in AT<jats:sub>1a<\/jats:sub>-KO mPCT cells ( P &lt; 0.01). In WT mPCT cells, FITC-ANG II uptake was visualized at 30 min in the cytoplasm and in the nuclei 1 h after exposure. Losartan alone completely blocked the uptake of FITC-ANG II, whereas megalin siRNA inhibited only 30% of the response ( P &lt; 0.01). The remaining FITC-ANG II uptake in the presence of megalin siRNA was completely abolished by losartan. ANG II induced threefold increases in phosphorylated MAP kinases ERK1\/2 and a onefold increase in phosphorylated sodium and hydrogen exchanger 3 (NHE3) proteins, which were also blocked by losartan and megalin-siRNA. By contrast, losartan and megalin siRNA had no effects on these signaling proteins in AT<jats:sub>1a<\/jats:sub>-KO mPCT cells. We conclude that the uptake of ANG II and downstream MAP kinases ERK1\/2 and NHE3 signaling responses in mPCT cells are mediated primarily by AT<jats:sub>1a<\/jats:sub>receptors. However, megalin may also play a partial role in these responses to ANG II.<\/jats:p>","DOI":"10.1152\/ajprenal.00693.2013","type":"journal-article","created":{"date-parts":[[2014,4,17]],"date-time":"2014-04-17T05:10:16Z","timestamp":1397711416000},"page":"F222-F233","source":"Crossref","is-referenced-by-count":22,"title":["Mechanisms of AT<sub>1a<\/sub>receptor-mediated uptake of angiotensin II by proximal tubule cells: a novel role of the multiligand endocytic receptor megalin"],"prefix":"10.1152","volume":"307","author":[{"given":"Xiao C.","family":"Li","sequence":"first","affiliation":[{"name":"Laboratory of Receptor and Signal Transduction, Department of Pharmacology and Toxicology, Cardiovascular and Renal Research Center, Division of Nephrology, Department of Medicine, University of Mississippi Medical Center, Jackson, Mississippi"}]},{"given":"Jia L.","family":"Zhuo","sequence":"additional","affiliation":[{"name":"Laboratory of Receptor and Signal Transduction, Department of Pharmacology and Toxicology, Cardiovascular and Renal Research Center, Division of Nephrology, Department of Medicine, University of Mississippi Medical Center, Jackson, Mississippi"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.25.17518"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.42.26497"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.264.5.F891"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1210\/er.2003-0001"},{"key":"B5","doi-asserted-by":"crossref","first-page":"2733","DOI":"10.1002\/cphy.c120002","volume":"2","author":"Chappell MC","year":"2012","journal-title":"Compr Physiol"},{"key":"B6","first-page":"500","volume":"122","author":"Chatelet F","year":"1986","journal-title":"Am J Pathol"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2010.169"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.4.F562"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1038\/nrm778"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1038\/nm.2541"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.15.5.451"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00305.2011"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.4.F900"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00277.2012"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00206.2001"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00164.2005"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00243.2004"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2011.03.001"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1985.248.5.F621"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1210\/mend.11.9.9975"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.79.18.5557"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.211291398"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)65238-8"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00091.2008"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00405.2005"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00329.2010"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90734.2008"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00219.2012"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00489.2006"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00463.2006"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00398.2007"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00432.2007"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2011.161"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.252.4.F573"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00002.2010"},{"key":"B36","first-page":"S81","author":"Navar LG","year":"1987","journal-title":"Kidney Int"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.110.163519"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M110.150284"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1084\/jem.167.1.213"},{"key":"B40","doi-asserted-by":"crossref","first-page":"4443","DOI":"10.1016\/S0021-9258(18)68946-X","volume":"263","author":"Seetharam B","year":"1988","journal-title":"J Biol Chem"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1097\/01.mnh.0000196148.42460.4f"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-200103001-00010"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1007\/s00259-010-1685-9"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.266.1.F120"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0b013e32832f5775"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.93.16.8460"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1290\/0511076.1"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00314.x"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1992.sp019214"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1161\/hy0102.100780"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1016\/j.peptides.2011.05.012"},{"key":"B52","doi-asserted-by":"crossref","first-page":"1079","DOI":"10.1002\/cphy.c110061","volume":"3","author":"Zhuo JL","year":"2013","journal-title":"Compr Physiol"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1016\/S0895-7061(97)00410-X"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00693.2013","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,4,1]],"date-time":"2022-04-01T20:15:13Z","timestamp":1648844113000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00693.2013"}},"issued":{"date-parts":[[2014,7,15]]},"references-count":53,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2014,7,15]]}},"alternative-id":["10.1152\/ajprenal.00693.2013"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00693.2013","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2014,7,15]]}},{"indexed":{"date-parts":[[2025,10,23]],"date-time":"2025-10-23T11:07:45Z","timestamp":1761217665067},"reference-count":36,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2014,2,15]]},"abstract":"<jats:p>Endothelial cell dysfunction (ECD) is a common feature of chronic renal failure (CRF). Defective nitric oxide (NO) generation due to decreased endothelial nitric oxide synthase (eNOS) activity is a crucial parameter characterizing ECD. Decreased activity of cationic amino acid transporter-1 (CAT-1), the selective arginine transporter of eNOS, has been shown to inhibit eNOS in uremia. Recently, we failed to demonstrate a decrease in glomerular arginine transport in uremic female rats (Schwartz IF, Grupper A, Soetendorp H, Hillel O, Laron I, Chernichovski T, Ingbir M, Shtabski A, Weinstein T, Chernin G, Shashar M, Hershkoviz R, Schwartz D. Am J Physiol Renal Physiol 303: F396\u2013F404, 2012). The current experiments were designed to determine whether sexual dimorphism which characterizes glomerular arginine transport system in uremia involves the systemic vasculature as well and to assess the effect of l-arginine in such conditions. Contractile and vasodilatory responses, ultrastructural changes, and measures of the l-arginine-NO system were performed in thoracic aortas of female rats subjected to \u215a nephrectomy. The contractile response to KCl was significantly reduced, and acetylcholine-induced vasodilation was significantly impaired in aortas from CRF dames compared with healthy rats. Both of these findings were prevented by the administration of arginine in the drinking water. The decrease in both cGMP generation, a measure of eNOS activity, and aortic eNOS and phosphorylated eNOS abundance observed in CRF rats was completely abolished by l-arginine, while arginine transport and CAT-1 protein were unchanged in all experimental groups. Arginine decreased both serum levels of advanced glycation end products and the asymmetrical dimethylarginine\/arginine ratio and restored the endothelial ultrastructure in CRF rats. In conclusion. arginine administration has a profound beneficial effect on ECD, independently of cellular arginine uptake, in CRF female rats.<\/jats:p>","DOI":"10.1152\/ajprenal.00457.2013","type":"journal-article","created":{"date-parts":[[2013,12,12]],"date-time":"2013-12-12T06:38:33Z","timestamp":1386830313000},"page":"F449-F456","source":"Crossref","is-referenced-by-count":8,"title":["<scp>l<\/scp>-Arginine improves endothelial function, independently of arginine uptake, in aortas from chronic renal failure female rats"],"prefix":"10.1152","volume":"306","author":[{"given":"Nachum","family":"Nesher","sequence":"first","affiliation":[{"name":"Department of Cardiothoracic Surgery, Tel Aviv Sourasky Medical Center, Tel Aviv University, Sackler School of Medicine, Tel Aviv, Israel; and"}]},{"given":"Inna","family":"Frolkis","sequence":"additional","affiliation":[{"name":"Department of Cardiothoracic Surgery, Tel Aviv Sourasky Medical Center, Tel Aviv University, Sackler School of Medicine, Tel Aviv, Israel; and"}]},{"given":"Doron","family":"Schwartz","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Tel Aviv Sourasky Medical Center, Tel Aviv University, Sackler School of Medicine, Tel Aviv, Israel;"}]},{"given":"Tamara","family":"Chernichovski","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Tel Aviv Sourasky Medical Center, Tel Aviv University, Sackler School of Medicine, Tel Aviv, Israel;"}]},{"given":"Sharon","family":"Levi","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Tel Aviv Sourasky Medical Center, Tel Aviv University, Sackler School of Medicine, Tel Aviv, Israel;"}]},{"given":"Yael","family":"Pri-Paz","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Tel Aviv Sourasky Medical Center, Tel Aviv University, Sackler School of Medicine, Tel Aviv, Israel;"}]},{"given":"Gil","family":"Chernin","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Tel Aviv Sourasky Medical Center, Tel Aviv University, Sackler School of Medicine, Tel Aviv, Israel;"}]},{"given":"Alexander","family":"Shtabsky","sequence":"additional","affiliation":[{"name":"Department of Pathology, Tel Aviv Sourasky Medical Center, Tel Aviv University, Sackler School of Medicine, Tel Aviv, Israel"}]},{"given":"Yanai","family":"Ben-Gal","sequence":"additional","affiliation":[{"name":"Department of Cardiothoracic Surgery, Tel Aviv Sourasky Medical Center, Tel Aviv University, Sackler School of Medicine, Tel Aviv, Israel; and"}]},{"given":"Yossi","family":"Paz","sequence":"additional","affiliation":[{"name":"Department of Cardiothoracic Surgery, Tel Aviv Sourasky Medical Center, Tel Aviv University, Sackler School of Medicine, Tel Aviv, Israel; and"}]},{"given":"Idit F.","family":"Schwartz","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Tel Aviv Sourasky Medical Center, Tel Aviv University, Sackler School of Medicine, Tel Aviv, Israel;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1042\/bj3240565"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/S1089-8603(02)00132-5"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1006\/niox.1996.0106"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115987"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-010-0797-1"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000086476.48686.7D"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1038\/288373a0"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1007\/BF00400651"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00619.2007"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1053\/meta.2003.50035"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1038\/352725a0"},{"key":"B12","doi-asserted-by":"crossref","first-page":"32299","DOI":"10.1016\/S0021-9258(18)31635-1","volume":"269","author":"Lo TW","year":"1994","journal-title":"J Biol Chem"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1093\/jn\/134.10.2798S"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/S0003-2697(03)00157-X"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.50.31213"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.1993.tb13795.x"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1097\/00005344-199701000-00002"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1097\/00005344-199503000-00008"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00587.2004"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(99)70348-3"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.5.F794"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000067"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00020.2009"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00488.2011"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1016\/0306-3623(95)02054-3"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.62"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.2010.05445.x"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.113.203497"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/0140-6736(92)90865-Z"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/S0009-2797(02)00212-0"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00355.2001"},{"key":"B32","doi-asserted-by":"crossref","first-page":"4443","DOI":"10.1016\/S0021-9258(18)34742-2","volume":"257","author":"White MF","year":"1982","journal-title":"J Biol Chem"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.6.F989"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1097\/FJC.0b013e31802f9923"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.83.2.391"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1159\/000063550"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00457.2013","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,3,19]],"date-time":"2022-03-19T15:19:29Z","timestamp":1647703169000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00457.2013"}},"issued":{"date-parts":[[2014,2,15]]},"references-count":36,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2014,2,15]]}},"alternative-id":["10.1152\/ajprenal.00457.2013"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00457.2013","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2014,2,15]]}},{"indexed":{"date-parts":[[2025,10,23]],"date-time":"2025-10-23T11:13:52Z","timestamp":1761218032670},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1992,2,1]]},"abstract":"<jats:p> The effects of hyperinsulinemia and hyperaminoacidemia on glucose and amino acid metabolism were examined in 16 control and 13 chronic renal failure (CRF) patients under two conditions: 1) euglycemic hyperinsulinemia and 2) amino acid infusion. All studies were performed with continuous indirect calorimetry and [1\u201314C]leucine infusion. In CRF patients insulin-mediated whole body glucose metabolism was reduced by 35% (4.41 +\/- 0.50 vs. 6.76 +\/- 0.73 mg.kg-1.min-1, P less than 0.01), primarily due to a decrease in nonoxidative glucose disposal (1.70 +\/- 0.70 vs. 4.32 +\/- 0.60 mg.kg-1.min-1, P less than 0.01); glucose oxidation was similar in both groups. In the postabsorptive state total leucine turnover (1.56 +\/- 0.06 vs. 1.75 +\/- 0.06), leucine oxidation (0.25 +\/- 0.01 vs. 0.30 +\/- 0.01), and nonoxidative leucine disposal (1.29 +\/- 0.06 vs. 1.40 +\/- 0.07 mumol.kg-1.min-1) were reduced in CRF vs. control subjects (all P less than 0.05). In response to hyperinsulinemia, endogenous leucine flux (index of proteolysis), leucine oxidation, nonoxidative leucine disposal (NOLD) (index of protein synthesis), and net leucine flux into protein were similar in CRF and control subjects. In contrast, the ability of hyperaminoacidemia to enhance NOLD (1.54 +\/- 0.11 vs. 2.10 +\/- 0.10 mumol.kg-1.min-1, P less than 0.01) and net leucine balance (0.27 +\/- 0.05 vs. 0.41 +\/- 0.05, P less than 0.05) was reduced in CRF patients.(ABSTRACT TRUNCATED AT 250 WORDS) <\/jats:p>","DOI":"10.1152\/ajprenal.1992.262.2.f168","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T09:15:07Z","timestamp":1514020507000},"page":"F168-F176","source":"Crossref","is-referenced-by-count":9,"title":["Glucose and amino acid metabolism in chronic renal failure: effect of insulin and amino acids"],"prefix":"10.1152","volume":"262","author":[{"given":"P.","family":"Castellino","sequence":"first","affiliation":[{"name":"Division of Nephrology, University of Texas Health Science Center, San Antonio."}]},{"given":"A.","family":"Solini","sequence":"additional","affiliation":[{"name":"Division of Nephrology, University of Texas Health Science Center, San Antonio."}]},{"given":"L.","family":"Luzi","sequence":"additional","affiliation":[{"name":"Division of Nephrology, University of Texas Health Science Center, San Antonio."}]},{"given":"J. G.","family":"Barr","sequence":"additional","affiliation":[{"name":"Division of Nephrology, University of Texas Health Science Center, San Antonio."}]},{"given":"D. J.","family":"Smith","sequence":"additional","affiliation":[{"name":"Division of Nephrology, University of Texas Health Science Center, San Antonio."}]},{"given":"A.","family":"Petrides","sequence":"additional","affiliation":[{"name":"Division of Nephrology, University of Texas Health Science Center, San Antonio."}]},{"given":"M.","family":"Giordano","sequence":"additional","affiliation":[{"name":"Division of Nephrology, University of Texas Health Science Center, San Antonio."}]},{"given":"C.","family":"Carroll","sequence":"additional","affiliation":[{"name":"Division of Nephrology, University of Texas Health Science Center, San Antonio."}]},{"given":"R. A.","family":"DeFronzo","sequence":"additional","affiliation":[{"name":"Division of Nephrology, University of Texas Health Science Center, San Antonio."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1992.262.2.F168","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:18:24Z","timestamp":1567973904000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1992.262.2.F168"}},"issued":{"date-parts":[[1992,2,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1992,2,1]]}},"alternative-id":["10.1152\/ajprenal.1992.262.2.F168"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1992.262.2.f168","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1992,2,1]]}},{"indexed":{"date-parts":[[2025,11,26]],"date-time":"2025-11-26T16:30:31Z","timestamp":1764174631836},"reference-count":23,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2019,5,1]]},"abstract":"<jats:p> Kidney normothermic machine perfusion (NMP) has historically used a 95% O<jats:sub>2<\/jats:sub>-5% CO<jats:sub>2<\/jats:sub> gas mixture. Using a porcine model of organ retrieval, NMP, and reperfusion, we tested the hypothesis that reducing perfusate oxygenation ([Formula: see text]) would be detrimental to renal function and cause injury. In the minimal ischemic injury experiment, kidneys sustained 10 min of warm ischemia and 2 h of static cold storage before 1 h of NMP with either 95%, 25%, or 12% O<jats:sub>2<\/jats:sub> with 5% CO<jats:sub>2<\/jats:sub> and N<jats:sub>2<\/jats:sub> balance. In the clinical injury experiment, kidneys with 10-min warm ischemia and 17-h static cold storage underwent 1-h NMP with the above gas combinations or 18-h static cold storage as a control. They were then reperfused with whole blood and 95% O<jats:sub>2<\/jats:sub> for 3 h. Overall, reducing [Formula: see text] did not significantly influence renal function in either experiment. Furthermore, there were no differences in the injury markers urinary neutrophil gelatinase-associated lipocalin or tissue high-motility group box protein 1. In the minimal ischemic injury experiment, a [Formula: see text] of 25% significantly reduced renal blood flow and increased vascular resistance. Oxygen delivery, consumption, and extraction (oxygen extraction ratio) were significantly greater at 95% [Formula: see text]. In the clinical injury experiment, renal blood flow was significantly increased at 25% [Formula: see text] and Na<jats:sup>+<\/jats:sup> excretion decreased. At 95% [Formula: see text], the oxygen content and oxygen extraction ratio were significantly increased. During reperfusion, renal blood flow was significantly increased in the 25% group. The control group pH was significantly decreased compared with the 25% group. Our data suggest that reducing [Formula: see text] during NMP does not have detrimental effects on renal function or markers of injury. <\/jats:p>","DOI":"10.1152\/ajprenal.00178.2018","type":"journal-article","created":{"date-parts":[[2019,2,20]],"date-time":"2019-02-20T10:55:35Z","timestamp":1550660135000},"page":"F823-F829","source":"Crossref","is-referenced-by-count":21,"title":["Physiological effects of altering oxygenation during kidney normothermic machine perfusion"],"prefix":"10.1152","volume":"316","author":[{"given":"Thomas D.","family":"Adams","sequence":"first","affiliation":[{"name":"Department of Surgery, University of Cambridge, Addenbrooke\u2019s Hospital, Cambridge, United Kingdom"}]},{"given":"Sarah A.","family":"Hosgood","sequence":"additional","affiliation":[{"name":"Department of Surgery, University of Cambridge, Addenbrooke\u2019s Hospital, Cambridge, United Kingdom"},{"name":"Department of Infection, Immunity and Inflammation, Transplant Group, University of Leicester, Leicester General Hospital, Leicester, United Kingdom"}]},{"given":"Michael L.","family":"Nicholson","sequence":"additional","affiliation":[{"name":"Department of Surgery, University of Cambridge, Addenbrooke\u2019s Hospital, Cambridge, United Kingdom"},{"name":"Department of Infection, Immunity and Inflammation, Transplant Group, University of Leicester, Leicester General Hospital, Leicester, United Kingdom"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1097\/TXD.0000000000000655"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1097\/01.TP.0000081044.37318.E3"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/j.transproceed.2004.11.043"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90230.2008"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00552.2010"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1111\/1440-1681.12031"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/j.redox.2015.08.020"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1111\/1440-1681.12034"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1002\/bjs.9894"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1097\/TP.0000000000001504"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1016\/j.jss.2012.08.001"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1097\/MOT.0000000000000405"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1097\/TP.0000000000001343"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/0034-5687(78)90046-4"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1097\/CCM.0b013e31826a44f6"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1042\/BJ20081386"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.00710.2002"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1183\/09031936.98.12030653"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1111\/1440-1681.12036"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1002\/9781119975427.ch5"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1097\/00007890-200010270-00024"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1111\/j.1432-2277.2001.tb00054.x"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1155\/2015\/864946"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00178.2018","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T13:22:11Z","timestamp":1567948931000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00178.2018"}},"issued":{"date-parts":[[2019,5,1]]},"references-count":23,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2019,5,1]]}},"alternative-id":["10.1152\/ajprenal.00178.2018"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00178.2018","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2019,5,1]]}},{"indexed":{"date-parts":[[2025,11,26]],"date-time":"2025-11-26T16:26:36Z","timestamp":1764174396918,"version":"3.37.3"},"reference-count":44,"publisher":"American Physiological Society","issue":"1","funder":[{"DOI":"10.13039\/100000050","name":"NHLBI","doi-asserted-by":"crossref","award":["HL56259","HL56259-S1"],"award-info":[{"award-number":["HL56259","HL56259-S1"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2018,1,1]]},"abstract":"<jats:p> Hyperinsulinemia has been hypothesized to cause hypertension in obesity, type 2 diabetes, and metabolic syndrome through a renal mechanism. However, it has been challenging to isolate renal mechanisms in chronic experimental models due, in part, to technical difficulties. In this study, we tested the hypothesis that a renal mechanism underlies insulin hypertension. We developed a novel technique to permit continuous insulin infusion through the renal artery in conscious rats for 7 days. Mean arterial pressure increased by ~10 mmHg in rats that were infused intravenously (IV) with insulin and glucose. Renal artery doses were 20% of the intravenous doses and did not raise systemic insulin levels or cause differences in blood glucose. The increase in blood pressure was not different from the IV group. Mean arterial pressure did not change in vehicle-infused rats, and there were no differences in renal injury scoring due to the renal artery catheter. Glomerular filtration rate, plasma renin activity, and urinary sodium excretion did not differ between groups at baseline and did not change significantly with insulin infusion. Thus, by developing a novel approach for chronic, continuous renal artery insulin infusion, we provided new evidence that insulin causes hypertension in rats through actions initiated within the kidney. <\/jats:p>","DOI":"10.1152\/ajprenal.00374.2017","type":"journal-article","created":{"date-parts":[[2017,10,2]],"date-time":"2017-10-02T20:40:29Z","timestamp":1506976829000},"page":"F81-F88","source":"Crossref","is-referenced-by-count":12,"title":["Chronic renal artery insulin infusion increases mean arterial pressure in male Sprague-Dawley rats"],"prefix":"10.1152","volume":"314","author":[{"given":"Debra L.","family":"Irsik","sequence":"first","affiliation":[{"name":"Department of Physiology, Medical College of Georgia at Augusta University, Augusta, Georgia"}]},{"given":"Jian-Kang","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Cellular Biology &amp; Anatomy, Medical College of Georgia at Augusta University, Augusta, Georgia"}]},{"given":"Michael W.","family":"Brands","sequence":"additional","affiliation":[{"name":"Department of Physiology, Medical College of Georgia at Augusta University, Augusta, Georgia"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI100504"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1998.274.5.C1373"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1002\/cphy.c100056"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.37.2.733"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.29.4.1014"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.19.1_Suppl.I83"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1991.260.4.R764"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1996.271.1.R276"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00390.2012"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1093\/ajh\/4.2.164"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1007\/BF00252649"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1172\/JCI107996"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1172\/JCI108463"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM198708063170605"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00675.2011"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.116.303604"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.15.5.519"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.260.5.F663"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.25.5.994"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.258.3.F722"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.116.305697"},{"key":"B22","first-page":"S35","volume":"55","author":"Hall JE","year":"1996","journal-title":"Kidney Int Suppl"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.15.6.547"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00081.2014"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00354.2016"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.31.2.637"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/S0895-7061(97)00217-3"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1988.255.6.F1206"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.2337\/diacare.46.10.1572"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-200103001-00001"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00395.2010"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.111.185215"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.23.6.1012"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2015.04.005"},{"key":"B35","first-page":"155","volume":"5","author":"Niskanen LK","year":"1991","journal-title":"J Hum Hypertens"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1007\/BF00400934"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.115.06425"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1172\/JCI21737"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1007\/BF00400257"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-199103000-00004"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00108.2005"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00447.2006"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-199005000-00014"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00436.2015"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00374.2017","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T23:19:48Z","timestamp":1567984788000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00374.2017"}},"issued":{"date-parts":[[2018,1,1]]},"references-count":44,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2018,1,1]]}},"alternative-id":["10.1152\/ajprenal.00374.2017"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00374.2017","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2018,1,1]]}},{"indexed":{"date-parts":[[2025,11,27]],"date-time":"2025-11-27T06:37:12Z","timestamp":1764225432173},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1990,10,1]]},"abstract":"<jats:p> Renal blood flow, renal sympathetic nerve activity, assessed by the renal overflows of norepinephrine (NE), dopamine (DA), and neuropeptide Y-like immunoreactivity (NPY-LI), as well as plasma renin activity and angiotensin II (ANG II) were evaluated during stepwise increases in lower body negative pressure (LBNP) in 10 healthy volunteers. The fractional extraction of epinephrine (Epi) was used to assess renal catecholamine removal (approximately 50%) from arterial plasma. Renal NE, DA, and NPY-LI overflows at rest were 235 +\/- 31, 30 +\/- 5, and 0.6 +\/- 0.2 pmol\/min, respectively. LBNP increased renal vascular resistance (RVR) by 52% and renal NE overflow by 31%. Renin release increased by 330% (from 64 +\/- 12 units\/min) and arterial ANG II levels by 119%, without altering the renal ANG II extraction (which was approximately 50%). Renal DA and NPY-LI overflows were unaffected. A \u201c;vaso-vagal\u201d reaction in one subject was associated with cessation of renal NE overflow and marked elevations of arterial Epi, renal renin release, and arterial ANG II. Selective unloading of cardiopulmonary baroreceptors by low-level LBNP did not affect RVR, whereas higher levels of LBNP caused renal vasoconstriction probably mediated in part by increased renal sympathetic nerve activity and in part by ANG II. <\/jats:p>","DOI":"10.1152\/ajprenal.1990.259.4.f573","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T22:24:25Z","timestamp":1513981465000},"page":"F573-F579","source":"Crossref","is-referenced-by-count":6,"title":["Renal responses to lower body negative pressure in humans"],"prefix":"10.1152","volume":"259","author":[{"given":"B.","family":"Tidgren","sequence":"first","affiliation":[{"name":"Department of Clinical Physiology, Karolinska Hospital, Stockholm, Sweden."}]},{"given":"P.","family":"Hjemdahl","sequence":"additional","affiliation":[{"name":"Department of Clinical Physiology, Karolinska Hospital, Stockholm, Sweden."}]},{"given":"E.","family":"Theodorsson","sequence":"additional","affiliation":[{"name":"Department of Clinical Physiology, Karolinska Hospital, Stockholm, Sweden."}]},{"given":"J.","family":"Nussberger","sequence":"additional","affiliation":[{"name":"Department of Clinical Physiology, Karolinska Hospital, Stockholm, Sweden."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1990.259.4.F573","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:17:10Z","timestamp":1567970230000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1990.259.4.F573"}},"issued":{"date-parts":[[1990,10,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1990,10,1]]}},"alternative-id":["10.1152\/ajprenal.1990.259.4.F573"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1990.259.4.f573","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1990,10,1]]}},{"indexed":{"date-parts":[[2025,12,1]],"date-time":"2025-12-01T06:25:42Z","timestamp":1764570342441},"reference-count":13,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2007,8]]},"DOI":"10.1152\/ajprenal.00237.2007","type":"journal-article","created":{"date-parts":[[2007,5,31]],"date-time":"2007-05-31T01:04:40Z","timestamp":1180573480000},"page":"F468-F469","source":"Crossref","is-referenced-by-count":10,"title":["Functional duality of progenitor cells influxing into arteriovenous fistula during its neoangiogenesis"],"prefix":"10.1152","volume":"293","author":[{"given":"Yashpal S.","family":"Kanwar","sequence":"first","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)64310-6"},{"key":"R2","doi-asserted-by":"crossref","unstructured":"Caplice NM, Wang S, Tracz M, Croatt AJ, Grande JP, Katusic ZS, Nath KA. Neoangiogenesis and the presence of progenitor cells in the venous limb of an arteriovenous fistula in the rat. Am J Physiol Renal Physiol. First published March 6, 2007; doi:10.1152\/ajprenal.00067.2007.","DOI":"10.1152\/ajprenal.00067.2007"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000099245.08637.CE"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000122041.73808.B5"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.105.535294"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005121325"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1172\/JCI0214940"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)64339-8"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00750.x"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1159\/000067863"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005050615"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1161\/01.ATV.0000178991.71605.18"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(05)80013-7"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00237.2007","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T22:30:52Z","timestamp":1567981852000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00237.2007"}},"issued":{"date-parts":[[2007,8]]},"references-count":13,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2007,8]]}},"alternative-id":["10.1152\/ajprenal.00237.2007"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00237.2007","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2007,8]]}},{"indexed":{"date-parts":[[2025,11,27]],"date-time":"2025-11-27T13:28:31Z","timestamp":1764250111381},"reference-count":85,"publisher":"American Physiological Society","issue":"7","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,4,1]]},"abstract":"<jats:p>Glomerulosclerosis is featured by accumulation of the extracellular matrixes in the glomerulus. We showed previously that activation of the small GTPase RhoA in podocytes induces heavy proteinuria and glomerulosclerosis in the mouse. In the current study, we investigated the mechanism by which RhoA stimulates the production of one of the extracellular matrixes, fibronectin, by podocytes, specifically testing the role of nuclear factor of activated T cells (NFAT). Expression of constitutively active RhoA in cultured podocytes activated the fibronectin promoter, upregulated fibronectin protein, and activated NFAT. Expression of constitutively active NFAT in podocytes also activated the fibronectin promoter and upregulated fibronectin protein. RhoA-induced NFAT activation and fibronectin upregulation were both dependent on the calcium\/calmodulin pathway and Rho kinase. NFAT activation was also observed in vivo in the rat and mouse models of podocyte injury and proteinuria, and NFAT inhibition ameliorated fibronectin upregulation in the latter. RhoA activation induced a rise of intracellular calcium ion concentration ([Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>), which was at least in part dependent on the transient receptor potential canonical 6 (TRPC6) cation channel. The results indicate that RhoA activates NFAT by inducing a rise of [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>in podocytes, which in turn contributes to fibronectin upregulation. This pathway may be responsible for the pathogenesis of certain glomerular diseases such as hypertension-mediated glomerulosclerosis.<\/jats:p>","DOI":"10.1152\/ajprenal.00495.2012","type":"journal-article","created":{"date-parts":[[2013,2,7]],"date-time":"2013-02-07T06:58:13Z","timestamp":1360220293000},"page":"F849-F862","source":"Crossref","is-referenced-by-count":14,"title":["Nuclear factor of activated T cells mediates RhoA-induced fibronectin upregulation in glomerular podocytes"],"prefix":"10.1152","volume":"304","author":[{"given":"Lei","family":"Zhu","sequence":"first","affiliation":[{"name":"Department of Medicine, McGill University Health Centre, Montreal, Quebec, Canada; and"}]},{"given":"Xiao-Yan","family":"Qi","sequence":"additional","affiliation":[{"name":"Department of Medicine and Research Center, Montreal Heart Institute and Universit\u00e9 de Montr\u00e9al, Montreal, Quebec, Canada"}]},{"given":"Lamine","family":"Aoudjit","sequence":"additional","affiliation":[{"name":"Department of Medicine, McGill University Health Centre, Montreal, Quebec, Canada; and"}]},{"given":"Flaviana","family":"Mouawad","sequence":"additional","affiliation":[{"name":"Department of Medicine, McGill University Health Centre, Montreal, Quebec, Canada; and"}]},{"given":"Cindy","family":"Baldwin","sequence":"additional","affiliation":[{"name":"Department of Medicine, McGill University Health Centre, Montreal, Quebec, Canada; and"}]},{"given":"Stanley","family":"Nattel","sequence":"additional","affiliation":[{"name":"Department of Medicine and Research Center, Montreal Heart Institute and Universit\u00e9 de Montr\u00e9al, Montreal, Quebec, Canada"}]},{"given":"Tomoko","family":"Takano","sequence":"additional","affiliation":[{"name":"Department of Medicine, McGill University Health Centre, Montreal, Quebec, Canada; and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00267.2005"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/ncb1400"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1159\/000262317"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/ncb1150"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(04)00003-0"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002553"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M312042200"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1016\/j.ceca.2011.08.008"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2007.11.028"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2007.07.186"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(02)00699-2"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.2337\/db07-0551"},{"key":"B13","doi-asserted-by":"crossref","first-page":"413","DOI":"10.1681\/ASN.V123413","volume":"12","author":"Endlich N","year":"2001","journal-title":"J Am Soc Nephrol"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.40.2.119"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.E06-07-0602"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1097\/HJH.0b013e328336ade3"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1038\/nm.1857"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M709390200"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2012.139"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.23.20.7291-7304.2003"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejphar.2007.04.011"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2011040370"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.383"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1096\/fj.08-108670"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.2337\/db10-1110"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2008.070196"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/j.ceca.2006.03.007"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1007\/s00109-008-0399-y"},{"key":"B29","doi-asserted-by":"crossref","first-page":"1","DOI":"10.1016\/S1016-8478(23)13074-3","volume":"18","author":"Im SH","year":"2004","journal-title":"Mol Cells"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.88.3.325"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.48.3.595"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.E10-12-0929"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00300.x"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2010.137"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1124\/mol.108.051912"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.2741\/3230"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-291X(02)02356-2"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002384"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2008.070057"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0811371106"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(91)90124-H"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008121226"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1161\/ATVBAHA.111.241018"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1204386"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1016\/j.biocel.2011.10.014"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M302401200"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2009.204"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1016\/j.ajpath.2011.06.033"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.110.972778"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1038\/nm994"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1038\/369497a0"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00057.2003"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.2337\/db07-1149"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00419.2007"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1159\/000322242"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.68.040204.100431"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.immunol.15.1.707"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1038\/ng1592"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.268.2.F273"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00729.x"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00077.2008"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000410"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005050571"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M608288200"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0707335"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)65080-8"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.0048.2001"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.1126\/scisignal.2001200"},{"key":"B69","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010080878"},{"key":"B70","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0040589"},{"key":"B71","doi-asserted-by":"publisher","DOI":"10.1210\/me.2011-0029"},{"key":"B72","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2012.01.009"},{"key":"B73","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009121253"},{"key":"B74","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002222"},{"key":"B75","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000109415.17511.18"},{"key":"B76","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfg1070"},{"key":"B77","doi-asserted-by":"publisher","DOI":"10.1126\/science.1106215"},{"key":"B78","doi-asserted-by":"publisher","DOI":"10.1152\/ajplung.00015.2009"},{"key":"B79","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119003"},{"key":"B80","doi-asserted-by":"publisher","DOI":"10.1111\/j.1527-3466.2007.00011.x"},{"key":"B81","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00294.2006"},{"key":"B82","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010111146"},{"key":"B83","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00412.2004"},{"key":"B84","doi-asserted-by":"publisher","DOI":"10.1016\/j.cellsig.2008.09.013"},{"key":"B85","doi-asserted-by":"publisher","DOI":"10.2174\/157339908783502370"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00495.2012","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,5,5]],"date-time":"2024-05-05T17:19:03Z","timestamp":1714929543000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00495.2012"}},"issued":{"date-parts":[[2013,4,1]]},"references-count":85,"journal-issue":{"issue":"7","published-print":{"date-parts":[[2013,4,1]]}},"alternative-id":["10.1152\/ajprenal.00495.2012"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00495.2012","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2013,4,1]]}},{"indexed":{"date-parts":[[2025,11,28]],"date-time":"2025-11-28T17:10:08Z","timestamp":1764349808799},"reference-count":31,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2005,11]]},"abstract":"<jats:p>In high glucose, glomerular mesangial cells (MCs) demonstrate impaired Ca<jats:sup>2+<\/jats:sup>signaling in response to seven-transmembrane receptor stimulation. To identify the mechanism, we first postulated decreased release from intracellular stores. Intracellular Ca<jats:sup>2+<\/jats:sup>was measured in fluo-3-loaded primary cultured rat MCs using confocal fluorescence microscopy. In high glucose (HG) 30 mM for 48 h, the 25 nM ionomycin-stimulated intracellular Ca<jats:sup>2+<\/jats:sup>response was reduced to 82% of that observed in normal glucose (NG). In NG 5.6 mM, Ca<jats:sup>2+<\/jats:sup>responses to endothelin (ET)-1 and platelet-derived growth factor (PDGF) were unchanged in cells cultured in 50 nM Ca<jats:sup>2+<\/jats:sup>vs. 1.8 mM Ca<jats:sup>2+<\/jats:sup>. Depletion of intracellular Ca<jats:sup>2+<\/jats:sup>stores with thapsigargin eliminated ET-1-stimulated Ca<jats:sup>2+<\/jats:sup>responses. Incubation in 30 mM glucose (HG) for 48 h or stimulation with phorbol myristate acetate (PMA) for 10 min eliminated the Ca<jats:sup>2+<\/jats:sup>response to ET-1 but had no effect on the PDGF response. Downregulation of protein kinase C (PKC) with 24-h PMA or inhibition with G\u00f66976 in HG normalized the Ca<jats:sup>2+<\/jats:sup>response to ET-1. Because ET-1 and PDGF stimulate Ca<jats:sup>2+<\/jats:sup>signaling through different phospholipase C pathways, we hypothesized that, in HG, PKC selectively phosphorylates and inhibits PLC-\u03b2<jats:sub>3<\/jats:sub>. Using confocal immunofluorescence imaging, in NG, a 1.6- to 1.7-fold increase in PLC-\u03b2<jats:sub>3<\/jats:sub>Ser<jats:sup>1105<\/jats:sup>phosphorylation was observed following PMA or ET-1 stimulation for 10 min. In HG, immunofluorescent imaging and immunoblotting showed increased PLC-\u03b2<jats:sub>3<\/jats:sub>phosphorylation, without change in total PLC-\u03b2<jats:sub>3<\/jats:sub>, which was reversed with 24-h PMA or G\u00f66976. We conclude that reduced Ca<jats:sup>2+<\/jats:sup>signaling in HG cannot be explained by reduced Ca<jats:sup>2+<\/jats:sup>stores but is due to conventional PKC-dependent phosphorylation and inactivation of PLC-\u03b2<jats:sub>3<\/jats:sub>.<\/jats:p>","DOI":"10.1152\/ajprenal.00434.2004","type":"journal-article","created":{"date-parts":[[2005,7,6]],"date-time":"2005-07-06T03:24:16Z","timestamp":1120620256000},"page":"F1078-F1087","source":"Crossref","is-referenced-by-count":13,"title":["Mesangial cell-reduced Ca<sup>2+<\/sup>signaling in high glucose is due to inactivation of phospholipase C-\u03b2<sub>3<\/sub>by protein kinase C"],"prefix":"10.1152","volume":"289","author":[{"given":"Helena","family":"Frecker","sequence":"first","affiliation":[]},{"given":"Snezana","family":"Munk","sequence":"additional","affiliation":[]},{"given":"Hong","family":"Wang","sequence":"additional","affiliation":[]},{"given":"Catharine","family":"Whiteside","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.261.4.F571"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.47.4.668"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1016\/S0065-2571(97)00014-9"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.2337\/diab.43.1.1"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.0055.2001"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.4.F688"},{"key":"R7","doi-asserted-by":"crossref","unstructured":"Dlugosz JA, Munk S, Zhou X, and Whiteside CI.Endothelin-1-induced mesangial cell contraction involves activation of protein kinase C-\u03b1, \u03b4, and \u03b5.Am J Physiol Renal Physiol275: F423\u2013F432, 1998.","DOI":"10.1152\/ajprenal.1998.275.3.F423"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00284.x"},{"key":"R9","unstructured":"Haugland RP.Fluorescent Ca2+indicators excited by visible light. In:Handbook of Fluorescent Probes and Research Chemicals(6th ed.), edited by Johnson ID and Spence MT. Eugene, OR: Molecular Probes, 1996."},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M302823200"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.1999.276.6.E1067"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.19.7.4961"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1016\/S1359-6101(97)00003-8"},{"key":"R14","doi-asserted-by":"crossref","unstructured":"Kapor-Drezgic J, Zhou X, Babazono T, Dlugosz J, Hohman T, and Whiteside C.Effect of high glucose on mesangial cell protein kinase C-\u03b4 and -\u03b5 is polyol pathway dependent.J Am Soc Nephrol10: 1193\u20131203, 1999.","DOI":"10.1681\/ASN.V1061193"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.35.21187"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M011241200"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.6.F954"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1007\/s001250050710"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.45.29738"},{"key":"R20","doi-asserted-by":"crossref","unstructured":"Nutt LKand O'Neil RG.Effect of elevated glucose on endothelin-induced store-operated and nonstore-operated calcium influx in renal mesangial cells.J Am Soc Nephrol11: 1225\u20131235, 2000.","DOI":"10.1681\/ASN.V1171225"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.275.9.6411"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.2000.80.4.1291"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1016\/0006-291X(90)90354-P"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.302.3.924"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.1.F21"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M007775200"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00232.2001"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1007\/s10157-003-0265-8"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M006266200"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M004276200"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117004"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00434.2004","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,7,13]],"date-time":"2021-07-13T02:02:30Z","timestamp":1626141750000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00434.2004"}},"issued":{"date-parts":[[2005,11]]},"references-count":31,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2005,11]]}},"alternative-id":["10.1152\/ajprenal.00434.2004"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00434.2004","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2005,11]]}},{"indexed":{"date-parts":[[2026,1,31]],"date-time":"2026-01-31T15:57:54Z","timestamp":1769875074705,"version":"3.49.0"},"reference-count":43,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2014,1,1]]},"abstract":"<jats:p>Although the kidney is believed to play a minor role in bile acid (BA) excretion, chronic renal failure (CRF) has been reported to be associated with increased serum bile acid levels and alterations in BA homeostasis. The mechanisms for elevated BA levels are poorly understood in both clinical and experimental studies. This study was designed to examine the effects of naturally progressing CRF of longer duration on the hepatic and renal mRNA and protein levels of the BA-synthesizing enzyme Cyp7a1 and the BA transporters Ntcp, Bsep, Mrp3, Ost-\u03b1, and Ost-\u03b2. Sprague-Dawley rats were randomized to the CRF group (\u215a nephrectomy) or to the sham-operated control group and were analyzed 8 wk after surgery. Results obtained in the CRF rats were compared with those obtained in rats that had undergone uninephrectomy (UNX). The CRF group exhibited significantly increased plasma cholesterol and BA concentrations. Hepatic Cyp7a1 mRNA and protein levels were almost identical in the two groups. Hepatic Mrp3, Ost-\u03b1, and Ost-\u03b2 expression was increased, suggesting increased basolateral efflux of bile acids into the blood. However, no such changes in BA transporter expression were observed in the remnant kidney. In UNX rats, similar changes in plasma BA levels and in the expression of BA transporters were found. We hypothesize that the increase in plasma BA is an early event in the progression of CRF and is caused by increased efflux across the basolateral hepatocyte membrane.<\/jats:p>","DOI":"10.1152\/ajprenal.00114.2013","type":"journal-article","created":{"date-parts":[[2013,11,7]],"date-time":"2013-11-07T02:36:04Z","timestamp":1383791764000},"page":"F130-F137","source":"Crossref","is-referenced-by-count":43,"title":["Effect of chronic renal failure on the hepatic, intestinal, and renal expression of bile acid transporters"],"prefix":"10.1152","volume":"306","author":[{"given":"Zhibo","family":"Gai","sequence":"first","affiliation":[{"name":"Department of Clinical Pharmacology and Toxicology, University Hospital Zurich, Zurich, Switzerland;"}]},{"given":"Lei","family":"Chu","sequence":"additional","affiliation":[{"name":"Minimally Invasive Urology Center, Provincial Hospital Affiliated to Shandong University, Shandong, China;"},{"name":"Tengzhou Central People's Hospital, Shandong, China;"}]},{"given":"Christian","family":"Hiller","sequence":"additional","affiliation":[{"name":"Department of Clinical Pharmacology and Toxicology, University Hospital Zurich, Zurich, Switzerland;"}]},{"given":"Denis","family":"Arsenijevic","sequence":"additional","affiliation":[{"name":"Division of Physiology, Department of Medicine, University of Fribourg, Fribourg, Switzerland; and"}]},{"given":"Carlos A.","family":"Penno","sequence":"additional","affiliation":[{"name":"Division of Molecular and Systems Toxicology, Department of Pharmaceutical Sciences, University of Basel, Basel, Switzerland"}]},{"given":"Jean-Pierre","family":"Montani","sequence":"additional","affiliation":[{"name":"Division of Physiology, Department of Medicine, University of Fribourg, Fribourg, Switzerland; and"}]},{"given":"Alex","family":"Odermatt","sequence":"additional","affiliation":[{"name":"Division of Molecular and Systems Toxicology, Department of Pharmaceutical Sciences, University of Basel, Basel, Switzerland"}]},{"given":"Gerd A.","family":"Kullak-Ublick","sequence":"additional","affiliation":[{"name":"Department of Clinical Pharmacology and Toxicology, University Hospital Zurich, Zurich, Switzerland;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-291X(02)00196-1"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1055\/s-2002-30099"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-145-3-200608010-00006"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1155\/2011\/853501"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(12)70318-9"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009121201"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.16.10046"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1016\/S1097-2765(00)00051-4"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1093\/ajcp\/49.3.404"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/j.clpt.2004.12.023"},{"key":"B11","first-page":"850","volume":"16","author":"Igel-Korcagova A","year":"2003","journal-title":"J Nephrol"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1096\/fasebj.8.15.8001744"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00464.x"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1023\/A:1020575001944"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M109326200"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1172\/JCI109182"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.4.F636"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M111.305789"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/12.7.1381"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1055\/s-2002-30098"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1159\/000186953"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.1993.265.2.E314"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1621\/nrs.08005"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1124\/dmd.107.018192"},{"key":"B25","doi-asserted-by":"crossref","first-page":"3416","DOI":"10.1016\/S0021-9258(19)67810-5","volume":"266","author":"Pandak WM","year":"1991","journal-title":"J Biol Chem"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.282"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1039\/c3ay26520j"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2011.11.006"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/j.jhep.2010.12.004"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118314"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1016\/j.clpt.2004.11.012"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1097-4644(19990901)74:3<386::AID-JCB7>3.0.CO;2-1"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1111\/j.1744-9987.2012.01100.x"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00911.x"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1124\/dmd.108.023630"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1016\/S0889-8553(05)70041-8"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1055\/s-0030-1253225"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1038\/nature04330"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2736(75)90010-3"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.195"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1007\/s00592-011-0286-9"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1159\/000327586"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.00490.2005"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00114.2013","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,3,11]],"date-time":"2022-03-11T19:03:13Z","timestamp":1647025393000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00114.2013"}},"issued":{"date-parts":[[2014,1,1]]},"references-count":43,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2014,1,1]]}},"alternative-id":["10.1152\/ajprenal.00114.2013"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00114.2013","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2014,1,1]]}},{"indexed":{"date-parts":[[2026,2,2]],"date-time":"2026-02-02T22:19:44Z","timestamp":1770070784402,"version":"3.49.0"},"reference-count":35,"publisher":"American Physiological Society","issue":"6","funder":[{"name":"Public welfare project of science technology department of Zhejiang Province","award":["2014C37023"],"award-info":[{"award-number":["2014C37023"]}]},{"DOI":"10.13039\/501100004731","name":"Natural Science Foundation of Zhejiang Province (Zhejiang Provincial Natural Science Foundation)","doi-asserted-by":"publisher","award":["LY17H15000"],"award-info":[{"award-number":["LY17H15000"]}],"id":[{"id":"10.13039\/501100004731","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Medical and health research project of Zhejiang province","award":["2013RCB001"],"award-info":[{"award-number":["2013RCB001"]}]},{"name":"Outstanding young talents fund of traditional chinese medicine in Zhejiang province","award":["2012ZQ004"],"award-info":[{"award-number":["2012ZQ004"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2019,6,1]]},"abstract":"<jats:p> Acute kidney injury (AKI) initiated by sepsis remains a thorny problem despite recent advancements in its clinical management. Having been found to be activated during AKI, fibroblast growth factor-inducible molecule 14 (Fn14) may be a potential therapeutic target because of its involvement in the molecular basis of injury. Here, we report that LPS induces apoptosis of mouse cortical tubule cells mediated by Fn14, for which simultaneous Toll-like receptor (TLR)4 activation is required. Mechanistically, TLR4 activation by lipopolysaccharide, through disassociating E3 ligase SCF<jats:sup>Fbxw7\u03b1<\/jats:sup> from Fn14, dismantles Lys<jats:sup>48<\/jats:sup>-linked polyubiquitination of Fn14 and stabilizes it. Pharmacological deactivation of Fn14 with monoclonal antibody ITEM-2 provides effective protection against lethal sepsis and AKI in mice. Our study underscores an adaptive mechanism whereby TLR4 regulates SCF<jats:sup>Fbxw7\u03b1<\/jats:sup>-dependent Fn14 stabilization during inflammatory tubular damage and further supports investigation of targeting Fn14 in clinical trials of patients with septic AKI. <\/jats:p>","DOI":"10.1152\/ajprenal.00627.2018","type":"journal-article","created":{"date-parts":[[2019,4,24]],"date-time":"2019-04-24T07:53:10Z","timestamp":1556092390000},"page":"F1273-F1281","source":"Crossref","is-referenced-by-count":10,"title":["Regulation of Fn14 stability by SCF<sup>Fbxw7\u03b1<\/sup> during septic acute kidney injury"],"prefix":"10.1152","volume":"316","author":[{"given":"Shi-Jing","family":"Mo","sequence":"first","affiliation":[{"name":"Department of Intensive Care Unit, Zhejiang Provincial People's Hospital, People\u2019s Hospital of Hangzhou Medical College, Hangzhou, Zhejiang, China"}]},{"given":"Wei","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Intensive Care Unit, Zhejiang Provincial People's Hospital, People\u2019s Hospital of Hangzhou Medical College, Hangzhou, Zhejiang, China"}]},{"given":"Jing-Quan","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Intensive Care Unit, Zhejiang Provincial People's Hospital, People\u2019s Hospital of Hangzhou Medical College, Hangzhou, Zhejiang, China"}]},{"given":"Min-Hua","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Intensive Care Unit, Zhejiang Provincial People's Hospital, People\u2019s Hospital of Hangzhou Medical College, Hangzhou, Zhejiang, China"}]},{"given":"Liang","family":"Xu","sequence":"additional","affiliation":[{"name":"Department of Intensive Care Unit, Zhejiang Provincial People's Hospital, People\u2019s Hospital of Hangzhou Medical College, Hangzhou, Zhejiang, China"}]},{"given":"Jun","family":"Hong","sequence":"additional","affiliation":[{"name":"Department of Intensive Care Unit, Zhejiang Provincial People's Hospital, People\u2019s Hospital of Hangzhou Medical College, Hangzhou, Zhejiang, China"}]},{"given":"Qian","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Intensive Care Unit, Zhejiang Provincial People's Hospital, People\u2019s Hospital of Hangzhou Medical College, Hangzhou, Zhejiang, China"}]},{"given":"Xiang-Hong","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Intensive Care Unit, Zhejiang Provincial People's Hospital, People\u2019s Hospital of Hangzhou Medical College, Hangzhou, Zhejiang, China"}]},{"given":"Ren-Hua","family":"Sun","sequence":"additional","affiliation":[{"name":"Department of Intensive Care Unit, Zhejiang Provincial People's Hospital, People\u2019s Hospital of Hangzhou Medical College, Hangzhou, Zhejiang, China"}]},{"given":"Bang-Chuan","family":"Hu","sequence":"additional","affiliation":[{"name":"Department of Intensive Care Unit, Zhejiang Provincial People's Hospital, People\u2019s Hospital of Hangzhou Medical College, Hangzhou, Zhejiang, China"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0913367107"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/nrd1854"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(18)30696-2"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/j.yexcr.2016.07.004"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1111\/ajt.14632"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1038\/nature24154"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1053\/j.gastro.2008.11.017"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2015.01.009"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1038\/502S86a"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2016.186"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1007\/s10753-018-0834-3"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.18632\/oncotarget.20235"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1186\/2110-5820-1-32"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2010.379"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1172\/JCI23486"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1126\/science.1240248"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1146\/annurev-biochem-060310-170328"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1126\/science.1162981"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1716578115"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M113.536300"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M110.194936"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/j.neulet.2015.10.051"},{"key":"B23","first-page":"2063","volume":"369","author":"Moreira J","year":"2013","journal-title":"N Engl J Med"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010101073"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1038\/nrm2468"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2016.03.006"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2009.05.040"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2010.01.022"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/j.canlet.2010.01.027"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1158\/0008-5472.CAN-16-2246"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1146\/annurev-immunol-032713-120156"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbadis.2017.04.012"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1038\/ncomms5436"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1172\/JCI78782"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1016\/j.molcel.2015.12.010"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00627.2018","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,20]],"date-time":"2019-09-20T16:41:05Z","timestamp":1568997665000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00627.2018"}},"issued":{"date-parts":[[2019,6,1]]},"references-count":35,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2019,6,1]]}},"alternative-id":["10.1152\/ajprenal.00627.2018"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00627.2018","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2019,6,1]]}},{"indexed":{"date-parts":[[2026,2,4]],"date-time":"2026-02-04T16:15:57Z","timestamp":1770221757309,"version":"3.49.0"},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1985,9,1]]},"abstract":"<jats:p> In early stages of permanent renal injury or extensive ablation, structural and functional adaptations associated with hypertrophy partially compensate for nephron losses. Glomerulotubular balance is maintained in these conditioned nephrons by intrinsic tubule and peritubular capillary adaptations that parallel single nephron glomerular filtration rate (SNGFR). Studies of Na+-H+ exchange in renal cortical brush border membrane vesicles indicate that tubule functional adaptation is not tied to loss of renal mass per se but rather to factors such as dietary protein content that set the level of SNGFR. Likewise, the structural heterogeneity that follows chronic renal injury or extreme ablation of renal mass is less a consequence of nephron injury than of adaptation linked to dietary protein intake. Indeed, since dietary protein restriction blunts the need for compensatory glomerular hyperfiltration, there is neither a stimulus for nephron hypertrophy nor for enhanced tubule ion and fluid transport. In rats with remnant kidneys, experimentally induced diabetes mellitus, or severe hypertension, increases in glomerular pressures and flows precede proteinuria, glomerular sclerosis, and azotemia. Protein restriction prevents these hemodynamic adaptations as well as the late complications. Similar conclusions appear to be applicable to a wide spectrum of clinical circumstances characterized by reduced nephron number. <\/jats:p>","DOI":"10.1152\/ajprenal.1985.249.3.f324","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T19:12:48Z","timestamp":1513969968000},"page":"F324-F337","source":"Crossref","is-referenced-by-count":78,"title":["Nephron adaptation to renal injury or ablation"],"prefix":"10.1152","volume":"249","author":[{"given":"B. M.","family":"Brenner","sequence":"first","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1985.249.3.F324","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:31:04Z","timestamp":1567956664000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1985.249.3.F324"}},"issued":{"date-parts":[[1985,9,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1985,9,1]]}},"alternative-id":["10.1152\/ajprenal.1985.249.3.F324"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1985.249.3.f324","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1985,9,1]]}},{"indexed":{"date-parts":[[2026,1,30]],"date-time":"2026-01-30T07:51:46Z","timestamp":1769759506873,"version":"3.49.0"},"reference-count":41,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2006,8]]},"abstract":"<jats:p>To examine the mechanisms whereby amino acids modulate nitric oxide (NO) production and blood flow in the renal vasculature, chemiluminescence techniques were used to quantify NO in the renal venous effluent of the isolated, perfused rat kidney as different amino acids were added to the perfusate. The addition of 10<jats:sup>\u22124<\/jats:sup>or 10<jats:sup>\u22123<\/jats:sup>M cationic amino acids (l-ornithine, l-lysine, or l-homoarginine) or neutral amino acids (l-glutamine, l-leucine, or l-serine) to the perfusate decreased NO and increased renal vascular resistance. Perfusion with anionic amino acids (l-glutamate or l-aspartate) had no effect on either parameter. The effects of the cationic and neutral amino acids were reversed with 10<jats:sup>\u22123<\/jats:sup>M l-arginine and prevented by deendothelialization or NO synthase inhibition. The effects of the neutral amino acids but not the cationic amino acids were dependent on extracellular sodium. Cationic and neutral amino acids also decreased calcimycin-induced NO, as assessed by DAF-FM-T fluorescence, in cultured EA.hy926 endothelial cells. Inhibition of system y<jats:sup>+<\/jats:sup>or y<jats:sup>+<\/jats:sup>L by siRNA for the cationic amino acid transporter 1 or the CD98\/4F2 heavy chain diminished the NO-depleting effects of these amino acids. Finally, transport studies in cultured cells demonstrated that cationic or neutral amino acids in the extracellular space stimulate efflux of l-arginine out of the cell. Thus the present experiments demonstrate that cationic and neutral amino acids can modulate NO production in endothelial cells by altering cellular l-arginine transport through y<jats:sup>+<\/jats:sup>and y<jats:sup>+<\/jats:sup>L transport mechanisms.<\/jats:p>","DOI":"10.1152\/ajprenal.00417.2005","type":"journal-article","created":{"date-parts":[[2006,3,30]],"date-time":"2006-03-30T01:12:34Z","timestamp":1143681154000},"page":"F297-F304","source":"Crossref","is-referenced-by-count":63,"title":["Amino acids as modulators of endothelium-derived nitric oxide"],"prefix":"10.1152","volume":"291","author":[{"given":"Masao","family":"Kakoki","sequence":"first","affiliation":[]},{"given":"Hyung-Suk","family":"Kim","sequence":"additional","affiliation":[]},{"given":"Cora-Jean S.","family":"Edgell","sequence":"additional","affiliation":[]},{"given":"Nobuyo","family":"Maeda","sequence":"additional","affiliation":[]},{"given":"Oliver","family":"Smithies","sequence":"additional","affiliation":[]},{"given":"David L.","family":"Mattson","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1016\/0006-291X(89)92281-X"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-291X(05)80876-9"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1042\/bj3490787"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115467"},{"key":"R5","doi-asserted-by":"crossref","unstructured":"Closs EI, Albritton LM, Kim JW, and Cunningham JM.Identification of a low affinity, high capacity transporter of cationic amino acids in mouse liver.J Biol Chem268: 7538\u20137544, 1993.","DOI":"10.1016\/S0021-9258(18)53209-9"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1021\/bi962829p"},{"key":"R7","unstructured":"Closs EI, Scheld JS, Sharafi M, and F\u00f6rstermann U.Substrate supply for nitric oxide synthase in macrophages and endothelial cells: role of cationic amino acid transporters.Mol Pharmacol57: 68\u201374, 2000."},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.83.3.1057"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.26.2.256"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1998.78.2.487"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.80.12.3734"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1038\/35078107"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1016\/0003-2697(81)90019-1"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0703921"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1093\/jn\/121.10.1591"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M210254200"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.23.6.752"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1995.268.6.H2375"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.99.9.1242"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00386.2004"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1161\/hy0202.102700"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1172\/JCI200111260"},{"key":"R23","doi-asserted-by":"crossref","unstructured":"Kikuchi K, Nagano T, Hayakawa H, Hirata Y, and Hirobe M.Real time measurement of nitric oxide produced ex vivo by luminol-H2O2chemiluminescence method.J Biol Chem268: 23106\u201323110, 1993.","DOI":"10.1016\/S0021-9258(19)49432-5"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1016\/S0167-5273(02)00413-8"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.bi.65.070196.001513"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.50.31213"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.22.6.863"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1994.266.6.R1730"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1097\/00005344-199503000-00008"},{"key":"R30","doi-asserted-by":"crossref","unstructured":"Plato CF, Stoos BA, Wang D, and Garvin J.Endogenous nitric oxide inhibits chloride transport in the thick ascending limb.Am J Physiol Renal Physiol276: F159\u2013F163, 1999.","DOI":"10.1152\/ajprenal.1999.276.1.F159"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.87.21.8612"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1016\/S0735-1097(97)00279-9"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.261.5.F779"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115132"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.2002.282.1.C134"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.87.21.8607"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000097761.19223.0D"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1016\/0140-6736(92)90865-Z"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119761"},{"key":"R40","doi-asserted-by":"crossref","unstructured":"White MFand Christensen HN.The two-way flux of cationic amino acids across the plasma membrane of mammalian cells is largely explained by a single transport system.J Biol Chem257: 10069\u201310080, 1982.","DOI":"10.1016\/S0021-9258(18)33986-3"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.2000.278.6.R1506"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00417.2005","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,7,25]],"date-time":"2021-07-25T07:17:41Z","timestamp":1627197461000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00417.2005"}},"issued":{"date-parts":[[2006,8]]},"references-count":41,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2006,8]]}},"alternative-id":["10.1152\/ajprenal.00417.2005"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00417.2005","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2006,8]]}},{"indexed":{"date-parts":[[2026,1,13]],"date-time":"2026-01-13T15:03:35Z","timestamp":1768316615955,"version":"3.49.0"},"reference-count":34,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2007,11]]},"abstract":"<jats:p>Epithelial cells are characterized by the ability to form sheets of cells that surround fluid-filled lumens. Cells in these sheets exhibit a characteristic subcellular polarity, with an apical pole that faces the lumen and a basolateral pole that is in contact with other cells and the extracellular matrix (ECM). To investigate the signaling events required for polarization and lumen formation, we have taken advantage of the ability of Madin-Darby canine kidney (MDCK) cells to dynamically remodel their polarity in response to changes in ECM cues. When MDCK cells are grown in suspension culture, they form multicellular \u201cinside-out\u201d cysts with apical proteins found on the peripheral surface and basolateral markers on the interior surface. When these inside-out cysts are embedded in ECM, they rapidly reorient their polarity: apical proteins become localized to the inside surface, and basolateral proteins are found on the surface that contacts ECM. Here we have characterized the signaling requirements for these early molecular reorientation events. Specifically, expression of a dominant-negative form of Rac1 (DN-Rac1) blocks the reorientation of polarity. Phosphoinositide 3\u2032-kinase is required for apical membrane protein remodeling from the initial apical membrane surface. Cells expressing DN-Rac1 fail to detectably activate the PI 3-kinase\/protein kinase B pathway. Last, we found that atypical protein kinase C (aPKC) is also required for reorientation of polarity, since an inhibitor of atypical PKC blocks reorientation. This effect cannot be overcome by constitutively active Rac1, demonstrating that both Rac1 and atypical PKC are required for reorientation of cellular polarity.<\/jats:p>","DOI":"10.1152\/ajprenal.00053.2007","type":"journal-article","created":{"date-parts":[[2007,9,6]],"date-time":"2007-09-06T01:01:32Z","timestamp":1189040492000},"page":"F1633-F1640","source":"Crossref","is-referenced-by-count":37,"title":["Rac1 is required for reorientation of polarity and lumen formation through a PI 3-kinase-dependent pathway"],"prefix":"10.1152","volume":"293","author":[{"given":"Kathleen D.","family":"Liu","sequence":"first","affiliation":[]},{"given":"Anirban","family":"Datta","sequence":"additional","affiliation":[]},{"given":"Wei","family":"Yu","sequence":"additional","affiliation":[]},{"given":"Paul R.","family":"Brakeman","sequence":"additional","affiliation":[]},{"given":"Tzuu-Shuh","family":"Jou","sequence":"additional","affiliation":[]},{"given":"Michael A.","family":"Matthay","sequence":"additional","affiliation":[]},{"given":"Keith E.","family":"Mostov","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1042\/bst0290001"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(04)00003-0"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1038\/ncb1226"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.E05-01-0061"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)81278-7"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00287.2005"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1038\/nrg1879"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1038\/nature01423"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.E04-12-1049"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1038\/ncb1461"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1016\/S0959-437X(03)00077-7"},{"key":"R12","unstructured":"Hogan BL, Kolodziej PA.Organogenesis: molecular mechanisms of tubulogenesis.Nat Rev Genet3: 513\u2013523, 2002."},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1038\/35019573"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.142.1.85"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1038\/35019582"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2006.11.051"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200502129"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.2174\/1568009043333032"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1016\/S0955-0674(00)00120-4"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1038\/ncb1227"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1038\/ncb0901-831"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1038\/nrm859"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1006\/dbio.1998.9091"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00902.x"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00558.2003"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1016\/j.cub.2004.11.009"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(02)01249-7"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1016\/S0960-9822(02)00843-6"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.cb.01.110185.001331"},{"key":"R30","doi-asserted-by":"crossref","unstructured":"Wang AZ, Ojakian GK, Nelson WJ.Steps in the morphogenesis of a polarized epithelium. I. Uncoupling the roles of cell-cell and cell-substratum contact in establishing plasma membrane polarity in multicellular epithelial (MDCK) cysts.J Cell Sci95: 137\u2013151, 1990.","DOI":"10.1242\/jcs.95.1.137"},{"key":"R31","doi-asserted-by":"crossref","unstructured":"Wang AZ, Ojakian GK, Nelson WJ.Steps in the morphogenesis of a polarized epithelium. II. Disassembly and assembly of plasma membrane domains during reversal of epithelial cell polarity in multicellular epithelial (MDCK) cysts.J Cell Sci95: 153\u2013165, 1990.","DOI":"10.1242\/jcs.95.1.153"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.E04-05-0435"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.E02-06-0350"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1016\/S0962-8924(03)00036-9"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00053.2007","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,8,22]],"date-time":"2021-08-22T21:32:33Z","timestamp":1629667953000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00053.2007"}},"issued":{"date-parts":[[2007,11]]},"references-count":34,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2007,11]]}},"alternative-id":["10.1152\/ajprenal.00053.2007"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00053.2007","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2007,11]]}},{"indexed":{"date-parts":[[2026,1,13]],"date-time":"2026-01-13T13:37:14Z","timestamp":1768311434683,"version":"3.49.0"},"reference-count":47,"publisher":"American Physiological Society","issue":"12","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2014,6,15]]},"abstract":"<jats:p> The emerging role of the transient receptor potential cation channel isotype 6 (TRPC6) as a central contributor to various pathological processes affecting podocytes has generated interest in the development of therapeutics to modulate its function. Recent insights into the regulation of TRPC6 have revealed PKG as a potent negative modulator of TRPC6 conductance and associated signaling via its phosphorylation at two highly conserved amino acid residues: Thr<jats:sup>69<\/jats:sup>\/Thr<jats:sup>70<\/jats:sup> (Thr<jats:sup>69<\/jats:sup> in mice and Thr<jats:sup>70<\/jats:sup> in humans) and Ser<jats:sup>321<\/jats:sup>\/Ser<jats:sup>322<\/jats:sup> (Ser<jats:sup>321<\/jats:sup> in mice and Ser<jats:sup>322<\/jats:sup> in humans). Here, we tested the role of PKG in modulating TRPC6-dependent responses in primary and conditionally immortalized mouse podocytes. TRPC6 was phosphorylated at Thr<jats:sup>69<\/jats:sup> in nonstimulated podocytes, but this declined upon ANG II stimulation or overexpression of constitutively active calcineurin phosphatase. ANG II induced podocyte motility in an in vitro wound assay, and this was reduced 30\u201360% in cells overexpressing a phosphomimetic mutant TRPC6 (TRPC6<jats:sub>T70E\/S322E<\/jats:sub>) or activated PKG ( P &lt; 0.05). Pretreatment of podocytes with the PKG agonists S-nitroso- N-acetyl-dl-penicillamine (nitric oxide donor), 8-bromo-cGMP, Bay 41\u20132772 (soluble guanylate cyclase activator), or phosphodiesterase 5 (PDE5) inhibitor 4-{[3\u2032,4\u2032-(methylenedioxy)benzyl]amino}[7]-6-methoxyquinazoline attenuated ANG II-induced Thr<jats:sup>69<\/jats:sup> dephosphorylation and also inhibited TRPC6-dependent podocyte motility by 30\u201360%. These data reveal that PKG activation strategies, including PDE5 inhibition, ameliorate ANG II-induced podocyte dysmotility by targeting TRPC6 in podocytes, highlighting the potential therapeutic utility of these approaches to treat hyperactive TRPC6-dependent glomerular disease. <\/jats:p>","DOI":"10.1152\/ajprenal.00212.2013","type":"journal-article","created":{"date-parts":[[2014,4,17]],"date-time":"2014-04-17T05:10:16Z","timestamp":1397711416000},"page":"F1442-F1450","source":"Crossref","is-referenced-by-count":32,"title":["Phosphodiesterase 5 inhibition ameliorates angiontensin II-induced podocyte dysmotility via the protein kinase G-mediated downregulation of TRPC6 activity"],"prefix":"10.1152","volume":"306","author":[{"given":"Gentzon","family":"Hall","sequence":"first","affiliation":[{"name":"Division of Nephrology, Duke University Medical Center, Durham, North Carolina;"},{"name":"Center for Human Genetics, Duke University Medical Center, Durham, North Carolina;"}]},{"given":"Janelle","family":"Rowell","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Johns Hopkins University School of Medicine, Baltimore, Maryland;"}]},{"given":"Federica","family":"Farinelli","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Johns Hopkins University School of Medicine, Baltimore, Maryland;"}]},{"given":"Rasheed A.","family":"Gbadegesin","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Duke University Medical Center, Durham, North Carolina;"},{"name":"Center for Human Genetics, Duke University Medical Center, Durham, North Carolina;"},{"name":"Department of Pediatrics, Duke University Medical Center, Durham, North Carolina; and"}]},{"given":"Peter","family":"Lavin","sequence":"additional","affiliation":[{"name":"Trinity Health Kidney Centre, Tallaght Hospital, Trinity College, Dublin, Ireland"}]},{"given":"Guanghong","family":"Wu","sequence":"additional","affiliation":[{"name":"Center for Human Genetics, Duke University Medical Center, Durham, North Carolina;"}]},{"given":"Alison","family":"Homstad","sequence":"additional","affiliation":[{"name":"Center for Human Genetics, Duke University Medical Center, Durham, North Carolina;"}]},{"given":"Andrew","family":"Malone","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Duke University Medical Center, Durham, North Carolina;"},{"name":"Center for Human Genetics, Duke University Medical Center, Durham, North Carolina;"}]},{"given":"Thomas","family":"Lindsey","sequence":"additional","affiliation":[{"name":"Center for Human Genetics, Duke University Medical Center, Durham, North Carolina;"}]},{"given":"Ruiji","family":"Jiang","sequence":"additional","affiliation":[{"name":"Center for Human Genetics, Duke University Medical Center, Durham, North Carolina;"}]},{"given":"Robert","family":"Spurney","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Duke University Medical Center, Durham, North Carolina;"}]},{"given":"Gordon F.","family":"Tomaselli","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Johns Hopkins University School of Medicine, Baltimore, Maryland;"}]},{"given":"David A.","family":"Kass","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Johns Hopkins University School of Medicine, Baltimore, Maryland;"}]},{"given":"Michelle P.","family":"Winn","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Duke University Medical Center, Durham, North Carolina;"},{"name":"Center for Human Genetics, Duke University Medical Center, Durham, North Carolina;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI46458"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/ncb1400"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.2741\/2196"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M408518200"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M605024200"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1517\/14728221003733602"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010050522"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfs391"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1038\/nm.1857"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M206088200"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1016\/S0167-4889(01)00086-6"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00014.2011"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00015.2005"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1007\/s00109-008-0399-y"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2007.060481"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1038\/73456"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M500429200"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.109.208314"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/j.yjmcc.2009.11.015"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1172\/JCI27702"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/j.molcel.2007.01.021"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000022029.50356.2C"},{"key":"B23","first-page":"599","volume":"57","author":"Lewko B","year":"2006","journal-title":"J Physiol Pharmacol"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/jappl.2001.91.3.1421"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M708920200"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00629.2008"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009090991"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006091010"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1007\/BF01464478"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/j.ajpath.2011.06.033"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M109.074104"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1038\/sj.emboj.7601417"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M401973200"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00590.2002"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.114.302614"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1308963111"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000017629.70769.CC"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2008.156083"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115908"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfr457"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1016\/j.ceca.2009.07.006"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1016\/j.ceca.2012.01.001"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1126\/science.1106215"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1007\/978-3-540-34891-7_31"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0405908101"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2011121170"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1159\/000337175"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00212.2013","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T23:53:08Z","timestamp":1567986788000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00212.2013"}},"issued":{"date-parts":[[2014,6,15]]},"references-count":47,"journal-issue":{"issue":"12","published-print":{"date-parts":[[2014,6,15]]}},"alternative-id":["10.1152\/ajprenal.00212.2013"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00212.2013","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2014,6,15]]}},{"indexed":{"date-parts":[[2026,1,8]],"date-time":"2026-01-08T20:04:43Z","timestamp":1767902683943,"version":"3.49.0"},"reference-count":37,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2003,11]]},"abstract":"<jats:p>Lipid abnormalities and activation of the local renin-angiotensin system (RAS) may be involved in the pathogenesis of chronic glomerular disease. This study investigated whether low-density lipoprotein (LDL) activates local RAS in cultured human mesangial cells (HMC) and, at the same time, whether ANG II mediates LDL-induced mesangial cell proliferation, hypertrophy, and superoxide ([Formula: see text]) generation. Quiescent HMC were exposed to 50 to 200 \u03bcg\/ml of LDL or 10<jats:sup>-7<\/jats:sup>to 10<jats:sup>-10<\/jats:sup>M ANG II for 0.5 to 24 h in the presence or absence of 10<jats:sup>-6<\/jats:sup>M losartan, an ANG II type I (AT<jats:sub>1<\/jats:sub>) receptor antagonist, or 10<jats:sup>-5<\/jats:sup>M diphehylendieodonium (DPI) or 10<jats:sup>-4<\/jats:sup>M apocynin, inhibitors of nicotinamide adenine dinucleotide phosphate oxidase. LDL induced an up to threefold increase in the ANG II levels in the culture medium of HMC. LDL upregulated AT<jats:sub>1<\/jats:sub>receptor and angiotensinogen mRNA expression in HMC. LDL incubated with HMC increased [Formula: see text] production by up to 3.3 times compared with the level of control cells. The LDL-induced, increased [Formula: see text] generation was suppressed by losartan, DPI, or apocynin. LDL significantly increased mesangial [<jats:sup>3<\/jats:sup>H]thymidine or [<jats:sup>3<\/jats:sup>H]leucine incorporation, whereas these processes were abrogated by losartan. In conclusion, LDL increases ANG II production by mesangial cells, which in turn results in increased [Formula: see text] production, and cell proliferation and hypertrophy, these effects of ANG II being mediated by the AT<jats:sub>1<\/jats:sub>receptor.<\/jats:p>","DOI":"10.1152\/ajprenal.00160.2003","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:39:33Z","timestamp":1425415173000},"page":"F909-F915","source":"Crossref","is-referenced-by-count":18,"title":["Angiotensin II mediates LDL-induced superoxide generation in mesangial cells"],"prefix":"10.1152","volume":"285","author":[{"given":"So Yeon","family":"Park","sequence":"first","affiliation":[{"name":"Department of Pathology, Seoul National University College of Medicine, Seoul 110-799, Korea"}]},{"given":"Chi Young","family":"Song","sequence":"additional","affiliation":[{"name":"Department of Pathology, Seoul National University College of Medicine, Seoul 110-799, Korea"}]},{"given":"Bong Cho","family":"Kim","sequence":"additional","affiliation":[{"name":"Department of Pathology, Seoul National University College of Medicine, Seoul 110-799, Korea"}]},{"given":"Hye Kyoung","family":"Hong","sequence":"additional","affiliation":[{"name":"Department of Pathology, Seoul National University College of Medicine, Seoul 110-799, Korea"}]},{"given":"Hyun Soon","family":"Lee","sequence":"additional","affiliation":[{"name":"Department of Pathology, Seoul National University College of Medicine, Seoul 110-799, Korea"}]}],"member":"24","reference":[{"key":"REF1","unstructured":"Ardaillou R, Chansel D, Chatziantonou C, and Dussaule JC.Mesangial AT1receptors: expression, signaling, and regulation.J Am Soc Nephrol10: S40-S46, 1999."},{"key":"REF2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.3.F328"},{"key":"REF3","doi-asserted-by":"publisher","DOI":"10.1159\/000020505"},{"key":"REF4","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa011161"},{"key":"REF5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.266.3.F384"},{"key":"REF6","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.27.4.867"},{"key":"REF7","doi-asserted-by":"publisher","DOI":"10.1159\/000049428"},{"key":"REF8","doi-asserted-by":"publisher","DOI":"10.1046\/j.0014-2956.2001.02534.x"},{"key":"REF9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.263.3.F411"},{"key":"REF10","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.74.6.1141"},{"key":"REF11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.263.4.F686"},{"key":"REF12","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa013591"},{"key":"REF13","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/13.12.3096"},{"key":"REF14","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00068.x"},{"key":"REF15","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117251"},{"key":"REF16","doi-asserted-by":"crossref","unstructured":"Keane WF, O'Donnell MP, Kasiske BL, and Kim Y.Oxidative modification of low density lipoproteins by mesangial cells.J Am Soc Nephrol4: 187-194, 1993.","DOI":"10.1681\/ASN.V42187"},{"key":"REF17","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1997.6844"},{"key":"REF18","doi-asserted-by":"publisher","DOI":"10.1016\/0021-9150(94)05514-J"},{"key":"REF19","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00462.x"},{"key":"REF20","doi-asserted-by":"publisher","DOI":"10.1080\/10715760100301221"},{"key":"REF21","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-199816010-00014"},{"key":"REF22","unstructured":"Lassague B, Alexander RW, Nickenig G, Clark M, Murphy TJ, and Griendling KK.Angiotensin II downregulates the vascular smooth muscle AT1receptor by transcriptional and posttranscriptional mechanisms: evidence for homologous and heterologous regulation.Mol Pharmacol48: 601-609, 1995."},{"key":"REF23","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.158"},{"key":"REF24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.3.F369"},{"key":"REF25","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.474"},{"key":"REF26","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00059.x"},{"key":"REF27","unstructured":"Lee HSand Koh HI.Visualization of binding and uptake of oxidized low density lipoproteins by cultured mesangial cells.Lab Invest71: 200-208, 1994."},{"key":"REF28","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-291X(05)80967-2"},{"key":"REF29","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000012569.55432.02"},{"key":"REF30","doi-asserted-by":"crossref","unstructured":"Nickenig Gand Murphy TJ.Downregulation by growth factors of vascular smooth muscle angiotensin receptor gene expression.Mol Pharmacol46: 653-659, 1994.","DOI":"10.1016\/S0026-895X(25)09796-2"},{"key":"REF31","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.95.2.473"},{"key":"REF32","doi-asserted-by":"publisher","DOI":"10.1172\/JCI116491"},{"key":"REF33","doi-asserted-by":"publisher","DOI":"10.1007\/BF00196577"},{"key":"REF34","doi-asserted-by":"crossref","unstructured":"Resink TJ, Bochkov VN, Tkachuk VA, Buhler FR, and Hahn AW.Lipoproteins and angiotensin II exert synergisitic effects on signaling processes in vascular smooth muscle cells.J Hypertens11,Suppl5: S110-S111, 1993.","DOI":"10.1097\/00004872-199312050-00034"},{"key":"REF35","doi-asserted-by":"crossref","unstructured":"Song CY, Kim BC, Hong HK, Kim BK, Kim YS, and Lee HS.Biphasic regulation of plasminogen activator\/inhibitor by LDL in mesangial cells.Am J Physiol Renal Physiol283: F423-F430, 2002.","DOI":"10.1152\/ajprenal.00304.2001"},{"key":"REF36","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117710"},{"key":"REF37","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.15"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00160.2003","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,5,20]],"date-time":"2025-05-20T17:52:09Z","timestamp":1747763529000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00160.2003"}},"issued":{"date-parts":[[2003,11]]},"references-count":37,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2003,11]]}},"alternative-id":["10.1152\/ajprenal.00160.2003"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00160.2003","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2003,11]]}},{"indexed":{"date-parts":[[2026,1,10]],"date-time":"2026-01-10T00:35:05Z","timestamp":1768005305575,"version":"3.49.0"},"reference-count":44,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2010,7]]},"abstract":"<jats:p>Increased expression of the facilitative glucose transporter, GLUT1, leads to glomerulopathy that resembles diabetic nephropathy, whereas prevention of enhanced GLUT1 expression retards nephropathy. While many of the GLUT1-mediated effects are likely due to mesangial cell effects, we hypothesized that increased GLUT1 expression in podocytes also contributes to the progression of diabetic nephropathy. Therefore, we generated two podocyte-specific GLUT1 transgenic mouse lines (driven by a podocin promoter) on a db\/m C57BLKS background. Progeny of the two founders were used to generate diabetic db\/db and control db\/m littermate mice. Immunoblots of glomerular lysates showed that transgenic mice had a 3.5-fold ( line 1) and 2.1-fold ( line 2) increase in GLUT1 content compared with wild-type mice. Both lines showed similar increases in fasting blood glucose and body weights at 24 wk of age compared with wild-type mice. Mesangial index (percent PAS-positive material in the mesangial tuft) increased 88% ( line 1) and 75% ( line 2) in the wild-type diabetic mice but only 48% ( line 1) and 39% ( line 2) in the diabetic transgenic mice ( P &lt; 0.05, transgenic vs. wild-type mice). This reduction in mesangial expansion was accompanied by a reduction in fibronectin accumulation, and vascular endothelial growth factor (VEGF) levels increased only half as much in the transgenic diabetic mice as in wild-type diabetic mice. Levels of nephrin, neph1, CD2AP, podocin, and GLUT4 were not significantly different in transgenic compared with wild-type mice. Taken together, increased podocyte GLUT1 expression in diabetic mice does not contribute to early diabetic nephropathy; surprisingly, it protects against mesangial expansion and fibronectin accumulation possibly by blunting podocyte VEGF increases.<\/jats:p>","DOI":"10.1152\/ajprenal.00021.2010","type":"journal-article","created":{"date-parts":[[2010,4,8]],"date-time":"2010-04-08T00:55:22Z","timestamp":1270688122000},"page":"F91-F98","source":"Crossref","is-referenced-by-count":41,"title":["Podocyte-specific overexpression of GLUT1 surprisingly reduces mesangial matrix expansion in diabetic nephropathy in mice"],"prefix":"10.1152","volume":"299","author":[{"given":"Hongyu","family":"Zhang","sequence":"first","affiliation":[{"name":"Departments of 1Internal Medicine and"}]},{"given":"MaryLee","family":"Schin","sequence":"additional","affiliation":[{"name":"Departments of 1Internal Medicine and"}]},{"given":"Jharna","family":"Saha","sequence":"additional","affiliation":[{"name":"Departments of 1Internal Medicine and"}]},{"given":"Kathleen","family":"Burke","sequence":"additional","affiliation":[{"name":"Departments of 1Internal Medicine and"}]},{"given":"Lawrence B.","family":"Holzman","sequence":"additional","affiliation":[{"name":"Departments of 1Internal Medicine and"}]},{"given":"Wanda","family":"Filipiak","sequence":"additional","affiliation":[{"name":"Molecular and Integrative Physiology, University of Michigan Medical School, Ann Arbor, Michigan; and"}]},{"given":"Thomas","family":"Saunders","sequence":"additional","affiliation":[{"name":"Departments of 1Internal Medicine and"}]},{"given":"Minghui","family":"Xiang","sequence":"additional","affiliation":[{"name":"the 3Department of Internal Medicine, University of Florida College of Medicine, Jacksonville, Florida"}]},{"given":"Charles W.","family":"Heilig","sequence":"additional","affiliation":[{"name":"the 3Department of Internal Medicine, University of Florida College of Medicine, Jacksonville, Florida"}]},{"suffix":"III","given":"Frank C.","family":"Brosius","sequence":"additional","affiliation":[{"name":"Departments of 1Internal Medicine and"},{"name":"Molecular and Integrative Physiology, University of Michigan Medical School, Ann Arbor, Michigan; and"}]}],"member":"24","reference":[{"key":"B1","unstructured":"American Registry of Pathology.Manual of Histologic Staining Methods of the Armed Forces Institute of Pathology. New York: McGraw-Hill, 1968."},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1023\/A:1022166921766"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004080648"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1992.391"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-004-1748-x"},{"key":"B6","first-page":"581A","volume":"14","author":"Chen SHK","year":"2003","journal-title":"J Am Soc Nephrol"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1053\/snep.2002.34724"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.2337\/db06-0693"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.54.11.3095"},{"key":"B10","doi-asserted-by":"crossref","first-page":"993","DOI":"10.1681\/ASN.V125993","volume":"12","author":"de Vriese AS","year":"2001","journal-title":"J Am Soc Nephrol"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005090921"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1007\/s11248-006-9002-x"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.51.10.3090"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1007\/s00210-007-0147-9"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.00948-07"},{"key":"B16","first-page":"674","volume":"73","author":"Heilig C","year":"1995","journal-title":"Lab Invest"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1017\/S1462399406010490"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118226"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.4.F657"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.2337\/diab.46.6.1030"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.1.F97"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1038\/nm1667"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1038\/377151a0"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00377.2009"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.2337\/db08-0647"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.3349\/ymj.2007.48.2.301"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1007\/s00125-009-1423-7"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1159\/000080889"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.267.5.F816"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1007\/s001250051447"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1002\/gene.10164"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119163"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000089829.45296.7C"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5001620"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00234.2004"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.5.F658"},{"key":"B38","doi-asserted-by":"crossref","first-page":"1998","DOI":"10.1681\/ASN.V1481998","volume":"14","author":"Shigehara T","year":"2003","journal-title":"J Am Soc Nephrol"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1186\/1471-2369-7-6"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.55.01.06.db05-0894"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.00044.2003"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.52.2.527"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005010055"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.54.6.1626"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90208.2008"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00021.2010","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,10,25]],"date-time":"2021-10-25T17:20:55Z","timestamp":1635182455000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00021.2010"}},"issued":{"date-parts":[[2010,7]]},"references-count":44,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2010,7]]}},"alternative-id":["10.1152\/ajprenal.00021.2010"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00021.2010","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2010,7]]}},{"indexed":{"date-parts":[[2026,1,13]],"date-time":"2026-01-13T16:09:22Z","timestamp":1768320562458,"version":"3.49.0"},"reference-count":54,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2008,1]]},"abstract":"<jats:p>Maleate injection causes dose-dependent injury in proximal tubular cells. This study sought to better define underlying pathogenic mechanisms and to test whether maleate toxicity recapitulates critical components of the hypoxic\/ischemic renal injury cascade. CD-1 mice were injected with maleate or used as a source for proximal tubule segments (PTS) for in vitro studies. Maleate induced dose-dependent PTS injury [lactate deydrogenase (LDH) release, ATP reductions, nonesterified fatty acid (NEFA) accumulation]. These changes were partially dependent on maleate metabolism (protection conferred by metabolic inhibitors: succinate, acetoacetate). Maleate toxicity reproduced critical characteristics of the hypoxia\/ATP depletion-induced injury cascade: 1) glutathione (GSH) conferred protection, but due to its glycine, not cysteine (antioxidant), content; 2) ATP reductions reflected decreased production, not Na-K-ATPase-driven increased consumption; 3) cell death was completely blocked by extracellular acidosis (pH 6.6); 4) intracellular Ca<jats:sup>2+<\/jats:sup>chelation (BAPTA) mitigated cell death; 5) maleate and hypoxia each caused plasma membrane cholesterol shedding and in both instances, this was completely glycine suppressible; 6) maleate + hypoxia caused neither additive NEFA accumulation nor LDH release, implying shared pathogenic pathways; and 7) maleate, like ischemia, induced renal cortical cholesterol loading; increased HMG CoA reductase (HMGCR) activity (statin inhibitable), increased HMGCR mRNA levels, and increased RNA polymerase II recruitment to the HMGCR locus (chromatin immunoprecipitation, ChIP, assay) were involved. These results further define critical determinants of maleate nephrotoxicity and suggest that it can serve as a useful adjunct for studies of ischemia\/ATP depletion-induced, proximal tubule-specific, cell death.<\/jats:p>","DOI":"10.1152\/ajprenal.00434.2007","type":"journal-article","created":{"date-parts":[[2007,10,18]],"date-time":"2007-10-18T01:04:53Z","timestamp":1192669493000},"page":"F187-F197","source":"Crossref","is-referenced-by-count":45,"title":["Maleate nephrotoxicity: mechanisms of injury and correlates with ischemic\/hypoxic tubular cell death"],"prefix":"10.1152","volume":"294","author":[{"given":"Richard A.","family":"Zager","sequence":"first","affiliation":[]},{"given":"Ali C. M.","family":"Johnson","sequence":"additional","affiliation":[]},{"given":"Masayo","family":"Naito","sequence":"additional","affiliation":[]},{"given":"Karol","family":"Bomsztyk","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.89"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1399-6576.2006.01102.x"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1172\/JCI108386"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.4.F908"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1991.138"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00476.2006"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00305.2005"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1016\/0006-2952(83)90404-5"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M703467200"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1172\/JCI116787"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1097\/01.TP.0000158355.83327.62"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1172\/JCI22832"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.2000.278.6.Ha1"},{"key":"R14","doi-asserted-by":"crossref","unstructured":"Lochhead KM, Kharasch ED, Zager RA.Anesthetic effects on the glycerol model of rhabdomyolysis induced acute renal failure in rats.J Am Soc Nephrol9: 305\u2013309, 1998.","DOI":"10.1681\/ASN.V92305"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00022.x"},{"key":"R16","doi-asserted-by":"crossref","unstructured":"Lu CY, Hartono J, Senitko M, Chen J.The inflammatory response to ischemic acute kidney injury: a result of the \u201cright stuff\u201d in the \u201cwrong place\u201d?Curr Opin Nephrol Hypertens6: 83\u201389, 2007.","DOI":"10.1097\/MNH.0b013e3280403c4e"},{"key":"R17","unstructured":"Mason J, Joeris B, Welsch J, Kriz W.Vascular congestion in ischemic renal failure: the role of cell swelling.Miner Electrolyte Metab15: 114\u2013124, 1989."},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1987.10"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.3109\/08860229709047723"},{"key":"R20","doi-asserted-by":"crossref","unstructured":"Nath KA, Ngo EO, Hebbel RP, Croat AJ, Nutter LM.Alpha ketoacids scavenge H2O2in vitro and in vivo and reduce menadione-induced DNA injury and cytotoxicity.Am J Physiol Cell Physiol268: C227\u2013C236, 1995.","DOI":"10.1152\/ajpcell.1995.268.1.C227"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115847"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1038\/nprot.2006.27"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.97"},{"key":"R24","doi-asserted-by":"crossref","unstructured":"Pacanis A, Rogulski J.Studies on chemical and enzymatic synthesis of maleyl-CoA.J Biol Chem256: 13030\u201313034, 1981.","DOI":"10.1016\/S0021-9258(18)43000-1"},{"key":"R25","doi-asserted-by":"crossref","unstructured":"Pacanis A, Strzelecki T, Rogliski J.Effects of maleate on the content of CoA and its derivatives in rat kidney mitochondria.J Biol Chem256: 13035\u201313038, 1981.","DOI":"10.1016\/S0021-9258(18)43001-3"},{"key":"R26","unstructured":"Pacanis A, Rogulski J.Substrate specificity of succinyl-CoA transferase from rat kidney mitochondria.Acta Biochim Pol24: 3\u201311, 1977."},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00230.2005"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1126\/science.185.4147.277"},{"key":"R29","unstructured":"Rogulski J, Pacanis A.Effects of maleate on CoA metabolism in rat kidney.Curr Probl Clin Biochem8: 406\u2013415, 1977."},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1007\/s004240000297"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.384"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1980.239.1.F50"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1016\/S0009-2797(00)00180-0"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006080894"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1978.87"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1172\/JCI113380"},{"key":"R37","doi-asserted-by":"crossref","unstructured":"Weinberg JM, Davis JA, Roeser NF, Venkatachalam MA.Role of intracellular pH during cytoprotection of proximal tubule cells by glycine or acidosis.J Am Soc Nephrol5: 1314\u20131323, 1994.","DOI":"10.1681\/ASN.V561314"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1172\/JCI113224"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115033"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119584"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.168.3.1286"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00745.x"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)64224-1"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00071.x"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1053\/ajkd.2000.8967"},{"key":"R46","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00238.x"},{"key":"R47","unstructured":"Zager RA, Conrad DS, Burkhart K.Phospholipase A2: a potentially important determinant of adenosine triphosphate levels during hypoxic-reoxygenation tubular injury.J Am Soc Nephrol7: 2327\u20132339, 1996."},{"key":"R48","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)64613-5"},{"key":"R49","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.72.4.837"},{"key":"R50","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.90.17.8297"},{"key":"R51","unstructured":"Zager RA, Gmur DJ, Bredl CR, Eng MJ.Temperature effects on ischemic and hypoxic renal proximal tubule injury.Lab Invest64: 766\u2013776, 1991."},{"key":"R52","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.68.1.185"},{"key":"R53","doi-asserted-by":"publisher","DOI":"10.1016\/0304-4165(90)90169-W"},{"key":"R54","unstructured":"Zager RA.Partial aortic ligation: a hypoperfusion model of ischemic acute renal failure and a comparison with renal artery occlusion.J Lab Clin Med110: 396\u2013405, 1987."}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00434.2007","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,8,25]],"date-time":"2021-08-25T22:12:34Z","timestamp":1629929554000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00434.2007"}},"issued":{"date-parts":[[2008,1]]},"references-count":54,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2008,1]]}},"alternative-id":["10.1152\/ajprenal.00434.2007"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00434.2007","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2008,1]]}},{"indexed":{"date-parts":[[2026,2,8]],"date-time":"2026-02-08T00:31:14Z","timestamp":1770510674799,"version":"3.49.0"},"reference-count":49,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,3,1]]},"abstract":"<jats:p>This study examined the effect of substitution of a 2.4-megabase pair (Mbp) region of Brown Norway (BN) rat chromosome 1 (RNO1) between 258.8 and 261.2 Mbp onto the genetic background of fawn-hooded hypertensive (FHH) rats on autoregulation of renal blood flow (RBF), myogenic response of renal afferent arterioles (AF-art), K<jats:sup>+<\/jats:sup>channel activity in renal vascular smooth muscle cells (VSMCs), and development of proteinuria and renal injury. FHH rats exhibited poor autoregulation of RBF, while FHH.1BN congenic strains with the 2.4-Mbp BN region exhibited nearly perfect autoregulation of RBF. The diameter of AF-art from FHH rats increased in response to pressure but decreased in congenic strains containing the 2.4-Mbp BN region. Protein excretion and glomerular and interstitial damage were significantly higher in FHH rats than in congenic strains containing the 2.4-Mbp BN region. K<jats:sup>+<\/jats:sup>channel current was fivefold greater in VSMCs from renal arterioles of FHH rats than cells obtained from congenic strains containing the 2.4-Mbp region. Sequence analysis of the known and predicted genes in the 2.4-Mbp region of FHH rats revealed amino acid-altering variants in the exons of three genes: Add3, Rbm20, and Soc-2. Quantitative PCR studies indicated that Mxi1 and Rbm20 were differentially expressed in the renal vasculature of FHH and FHH.1BN congenic strain F. These data indicate that transfer of this 2.4-Mbp region from BN to FHH rats restores the myogenic response of AF-art and autoregulation of RBF, decreases K<jats:sup>+<\/jats:sup>current, and slows the progression of proteinuria and renal injury.<\/jats:p>","DOI":"10.1152\/ajprenal.00404.2012","type":"journal-article","created":{"date-parts":[[2012,12,6]],"date-time":"2012-12-06T05:50:05Z","timestamp":1354773005000},"page":"F565-F577","source":"Crossref","is-referenced-by-count":29,"title":["Genetic basis of the impaired renal myogenic response in FHH rats"],"prefix":"10.1152","volume":"304","author":[{"given":"Marilyn","family":"Burke","sequence":"first","affiliation":[{"name":"Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi;"}]},{"given":"Malikarjuna","family":"Pabbidi","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi;"}]},{"given":"Fan","family":"Fan","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi;"}]},{"given":"Ying","family":"Ge","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi;"}]},{"given":"Ruisheng","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Mississippi Medical Center, Jackson, Mississippi;"}]},{"given":"Jan Michael","family":"Williams","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi;"}]},{"given":"Allison","family":"Sarkis","sequence":"additional","affiliation":[{"name":"Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin"}]},{"given":"Jozef","family":"Lazar","sequence":"additional","affiliation":[{"name":"Human and Molecular Genetics Center, Medical College of Wisconsin, Milwaukee, Wisconsin;"},{"name":"Department of Dermatology, Medical College of Wisconsin, Milwaukee, Wisconsin; and"}]},{"given":"Howard J.","family":"Jacob","sequence":"additional","affiliation":[{"name":"Human and Molecular Genetics Center, Medical College of Wisconsin, Milwaukee, Wisconsin;"},{"name":"Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin"}]},{"given":"Richard J.","family":"Roman","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-199715120-00057"},{"key":"B2","first-page":"763","volume":"10","author":"Bianchi G","year":"1995","journal-title":"Nephrol Dial Transplant"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.91.9.3999"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/ng0196-44"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.3109\/08860229809045128"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1988.254.2.F291"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119657"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1055\/s-0037-1613405"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1999.79.2.387"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010060606"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.43.25534"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1998.78.1.53"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1999.277.4.H1338"},{"key":"B14","doi-asserted-by":"crossref","first-page":"12792","DOI":"10.1016\/S0021-9258(18)45276-3","volume":"262","author":"Fowler VM","year":"1987","journal-title":"J Biol Chem"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0036469"},{"key":"B16","doi-asserted-by":"crossref","first-page":"1339","DOI":"10.1016\/S0021-9258(17)36096-9","volume":"261","author":"Gardner K","year":"1986","journal-title":"J Biol Chem"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1038\/nm.2693"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2002.kid557.x"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000070078.66465.55"},{"key":"B20","doi-asserted-by":"crossref","first-page":"13130","DOI":"10.1016\/S0021-9258(19)38276-6","volume":"265","author":"Joshi R","year":"1990","journal-title":"J Biol Chem"},{"key":"B21","first-page":"637","volume":"92","author":"Kreisberg JI","year":"1978","journal-title":"Am J Pathol"},{"key":"B22","first-page":"181","volume":"65","author":"Kuijpers MH","year":"1984","journal-title":"Br J Exp Pathol"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/physiolgenomics.00288.2005"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00335.2005"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00012.2007"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00374.2004"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/0047-6374(87)90113-8"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000085193.25617.78"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00275.x"},{"key":"B30","first-page":"S2","volume":"45","author":"Provoost AP","year":"1994","journal-title":"Kidney Int Suppl"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/gkf493"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005010029"},{"key":"B33","first-page":"389","volume":"32","author":"Rudofsky UH","year":"1982","journal-title":"Lab Anim Sci"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1002\/ajh.21427"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00234.2006"},{"key":"B36","doi-asserted-by":"crossref","first-page":"2068","DOI":"10.1681\/ASN.V11112068","volume":"11","author":"Shiozawa M","year":"2000","journal-title":"J Am Soc Nephrol"},{"key":"B37","doi-asserted-by":"crossref","first-page":"1775","DOI":"10.1681\/ASN.V3111775","volume":"3","author":"Simons JL","year":"1993","journal-title":"J Am Soc Nephrol"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1991.260.6.H1779"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/gkl988"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1999.276.1.R189"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/15.9.1337"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1016\/S0895-7061(97)00163-5"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1999.276.3.R855"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/13.4.893"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1053\/ajkd.2001.29205"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.6.F962"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.4.F706"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00261.2010"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.266.2.F275"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00404.2012","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,2,2]],"date-time":"2022-02-02T16:48:58Z","timestamp":1643820538000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00404.2012"}},"issued":{"date-parts":[[2013,3,1]]},"references-count":49,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2013,3,1]]}},"alternative-id":["10.1152\/ajprenal.00404.2012"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00404.2012","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2013,3,1]]}},{"indexed":{"date-parts":[[2025,10,11]],"date-time":"2025-10-11T21:19:47Z","timestamp":1760217587566},"reference-count":36,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,9,1]]},"abstract":"<jats:p>In the present study, the role of 5-HT<jats:sub>3<\/jats:sub>receptors in pudendal neuromodulation of bladder activity and its interaction with opioid receptors were investigated in anesthetized cats. The bladder was distended with either saline to induce normal bladder activity or with 0.25% acetic acid (AA) to induce bladder overactivity. Pudendal afferent nerves were activated by 5-Hz stimulation at multiples of the threshold (T) intensity for the induction of anal twitching. AA irritation significantly reduced bladder capacity to 16.5 \u00b1 3.3% of saline control capacity, whereas pudendal nerve stimulation (PNS) at 1.5\u20132 and 3\u20134 T restored the capacity to 82.0 \u00b1 12% ( P = 0.0001) and 98.6 \u00b1 15% ( P &lt; 0.0001), respectively. Cumulative doses (1\u20133 mg\/kg iv) of ondansetron, a 5-HT<jats:sub>3<\/jats:sub>receptor antagonist, eliminated low-intensity (1.5\u20132 T) PNS inhibition and reduced high-intensity (3\u20134 T) PNS inhibition of bladder overactivity. During saline distention, PNS at 1.5\u20132 and 3\u20134 T significantly increased bladder capacity to 173.2 \u00b1 26.4% ( P = 0.036) and 193.2 \u00b1 22.5% ( P = 0.008), respectively, of saline control capacity, but ondansetron (0.003\u20133 mg\/kg iv) did not alter PNS inhibition. Ondansetron (0.1\u20133 mg\/kg) also significantly ( P &lt; 0.05) increased control bladder capacity (50\u2013200%) during either AA irritation or saline distention. In both conditions, the effects of low- and high-intensity PNS were not significantly different. After ondansetron (3 mg\/kg) treatment, naloxone (1 mg\/kg iv) significantly ( P &lt; 0.05) decreased control bladder capacity (40\u201370%) during either AA irritation or saline distention but failed to affect PNS inhibition. This study revealed that activation of 5-HT<jats:sub>3<\/jats:sub>receptors has a role in PNS inhibition of bladder overactivity. It also indicated that 5-HT<jats:sub>3<\/jats:sub>receptor antagonists might be useful for the treatment of overactive bladder symptoms.<\/jats:p>","DOI":"10.1152\/ajprenal.00105.2013","type":"journal-article","created":{"date-parts":[[2013,7,4]],"date-time":"2013-07-04T08:28:15Z","timestamp":1372926495000},"page":"F663-F671","source":"Crossref","is-referenced-by-count":25,"title":["Involvement of 5-HT<sub>3<\/sub>receptors in pudendal inhibition of bladder overactivity in cats"],"prefix":"10.1152","volume":"305","author":[{"given":"Zeyad","family":"Schwen","sequence":"first","affiliation":[{"name":"Department of Urology, University of Pittsburgh, Pittsburgh, Pennsylvania; and"}]},{"given":"Yosuke","family":"Matsuta","sequence":"additional","affiliation":[{"name":"Department of Urology, University of Pittsburgh, Pittsburgh, Pennsylvania; and"}]},{"given":"Bing","family":"Shen","sequence":"additional","affiliation":[{"name":"Department of Urology, University of Pittsburgh, Pittsburgh, Pennsylvania; and"}]},{"given":"Jicheng","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Urology, University of Pittsburgh, Pittsburgh, Pennsylvania; and"}]},{"given":"James R.","family":"Roppolo","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Chemical Biology, University of Pittsburgh, Pittsburgh, Pennsylvania"}]},{"given":"William C.","family":"de Groat","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Chemical Biology, University of Pittsburgh, Pittsburgh, Pennsylvania"}]},{"given":"Changfeng","family":"Tai","sequence":"additional","affiliation":[{"name":"Department of Urology, University of Pittsburgh, Pittsburgh, Pennsylvania; and"},{"name":"Department of Pharmacology and Chemical Biology, University of Pittsburgh, Pittsburgh, Pennsylvania"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/j.urology.2003.10.005"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1124\/pr.56.4.4"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2036.1999.00610.x"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/j.expneurol.2010.04.003"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1111\/j.1526-4610.1991.hed3105296.x"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/S0090-4295(01)01636-3"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1016\/0014-2999(95)00614-1"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-8993(98)00401-6"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejphar.2007.01.028"},{"key":"B11","first-page":"1","volume":"21","author":"Farber L","year":"2001","journal-title":"Int J Clin Pharmacol Res"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1038\/nrn2401"},{"key":"B13","volume-title":"Zofran Prescribing Information","author":"GlaxoSmithKline","year":"2002"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1002\/nau.10043"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2011.215657"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1590\/S1677-55382006000600002"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/j.juro.2012.09.095"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199003223221205"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1046\/j.1464-410x.2001.02228.x"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1126\/science.6154313"},{"key":"B21","first-page":"S90","volume":"15","author":"Onukwugha E","year":"2009","journal-title":"Am J Manag Care"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1111\/j.1464-410X.2007.07082.x"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1002\/nau.20174"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1016\/S0936-6555(05)80790-3"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1016\/S0304-3959(03)00207-0"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0706504"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1097\/00001756-199010000-00005"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(81)90578-3"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/j.apmr.2006.04.023"},{"key":"B30","doi-asserted-by":"crossref","first-page":"327","DOI":"10.1007\/s00345-002-0301-4","volume":"20","author":"Stewart WF","year":"2003","journal-title":"World J Urol"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1016\/j.juro.2011.04.023"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00609.2011"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1046\/j.1464-410x.2001.02038.x"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1016\/j.juro.2007.07.032"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1016\/0304-3959(88)90011-5"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.22-03-01010.2002"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00107.2012"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00105.2013","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2020,7,29]],"date-time":"2020-07-29T19:06:54Z","timestamp":1596049614000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00105.2013"}},"issued":{"date-parts":[[2013,9,1]]},"references-count":36,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2013,9,1]]}},"alternative-id":["10.1152\/ajprenal.00105.2013"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00105.2013","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2013,9,1]]}},{"indexed":{"date-parts":[[2025,10,10]],"date-time":"2025-10-10T12:57:13Z","timestamp":1760101033189},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1984,9,1]]},"abstract":"<jats:p> Recent studies have shown that in situ PCO2 in rat renal cortical structures far exceeds systemic arterial PCO2. These results were opposite to previous assumptions that renal proximal tubule fluid PCO2 approximated arterial PCO2. The present studies examined the species and organ specificity of the elevated PCO2 in 39 New Zealand White rabbits studied under normal acid-base conditions. In situ PCO2 was measured in renal cortex, superficial hepatic parenchyma, skeletal muscle, superficial cerebral cortex, and femoral nerve, artery, and vein. The results showed rabbit renal cortical PCO2 (57.2 +\/- 1.2 mmHg) to be higher than both systemic arterial (39.1 +\/- 2.0 mmHg) and venous PCO2 (45.4 +\/- 2.1 mmHg). Similarly, liver PCO2 (64.1 +\/- 3.5 mmHg) was found to be significantly higher than systemic arterial and venous PCO2 and also higher than portal and hepatic vein PCO2. Skeletal muscle, cerebral cortex, and femoral nerve PCO2 levels were usually greater than systemic arterial PCO2 but less than systemic venous PCO2. These observations show that in situ PCO2 is significantly elevated above afferent and efferent blood PCO2 in the kidney and liver but not in muscle or brain. A possible explanation for these findings in the former two organs may be high CO2 production and\/or trapping of CO2 by their vascular systems. <\/jats:p>","DOI":"10.1152\/ajprenal.1984.247.3.f491","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T11:17:14Z","timestamp":1513941434000},"page":"F491-F498","source":"Crossref","is-referenced-by-count":1,"title":["In situ PCO2 in the renal cortex, liver, muscle, and brain of the New Zealand white rabbit"],"prefix":"10.1152","volume":"247","author":[{"given":"R. J.","family":"Hogg","sequence":"first","affiliation":[]},{"given":"L. R.","family":"Pucacco","sequence":"additional","affiliation":[]},{"given":"N. W.","family":"Carter","sequence":"additional","affiliation":[]},{"given":"A. R.","family":"Laptook","sequence":"additional","affiliation":[]},{"given":"J. P.","family":"Kokko","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1984.247.3.F491","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T14:31:00Z","timestamp":1567953060000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1984.247.3.F491"}},"issued":{"date-parts":[[1984,9,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1984,9,1]]}},"alternative-id":["10.1152\/ajprenal.1984.247.3.F491"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1984.247.3.f491","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[1984,9,1]]}},{"indexed":{"date-parts":[[2025,10,12]],"date-time":"2025-10-12T19:03:48Z","timestamp":1760295828228,"version":"3.37.3"},"reference-count":55,"publisher":"American Physiological Society","issue":"4","funder":[{"DOI":"10.13039\/100005713","name":"DOD | Office of the Secretary of Defense (OSD)","doi-asserted-by":"publisher","award":["W81XWH-16-1-0640"],"award-info":[{"award-number":["W81XWH-16-1-0640"]}],"id":[{"id":"10.13039\/100005713","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Centers of Biomedical Research Excellence, NIH","award":["P20 RR017677"],"award-info":[{"award-number":["P20 RR017677"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2018,4,1]]},"abstract":"<jats:p>The development of nephritis is a leading cause of morbidity and mortality in lupus patients. Although the general pathophysiological progression of lupus nephritis is known, the molecular mediators and mechanisms are incompletely understood. Previously, we demonstrated that the glycosphingolipid (GSL) catabolic pathway is elevated in the kidneys of MRL\/lpr lupus mice and human lupus patients with nephritis. Specifically, the activity of neuraminidase (NEU) and expression of Neu1, an enzyme in the GSL catabolic pathway is significantly increased. To better understand the role and mechanisms by which this pathway contributes to the progression of LN, we analyzed the expression and effects of NEU activity on the function of MRL\/lpr lupus-prone mesangial cells (MCs). We demonstrate that NEU1 and NEU3 promote IL-6 production in MES13 MCs. Neu1 expression, NEU activity, and IL-6 production are significantly increased in stimulated primary MRL\/lpr lupus-prone MCs, and blocking NEU activity inhibits IL-6 production. NEU1 and NEU3 expression overlaps IgG deposits in MCs in vitro and in renal sections from nephritic MRL\/lpr mice. Together, our results suggest that NEU activity mediates IL-6 production in lupus-prone MCs possibly through an IgG-receptor complex signaling pathway.<\/jats:p>","DOI":"10.1152\/ajprenal.00421.2017","type":"journal-article","created":{"date-parts":[[2018,1,8]],"date-time":"2018-01-08T18:33:31Z","timestamp":1515436411000},"page":"F630-F642","source":"Crossref","is-referenced-by-count":24,"title":["Neuraminidase activity mediates IL-6 production by activated lupus-prone mesangial cells"],"prefix":"10.1152","volume":"314","author":[{"given":"Kamala","family":"Sundararaj","sequence":"first","affiliation":[{"name":"Division of Rheumatology and Immunology, Department of Medicine, Medical University of South Carolina, Charleston, South Carolina"}]},{"given":"Jessalyn I.","family":"Rodgers","sequence":"additional","affiliation":[{"name":"Division of Rheumatology and Immunology, Department of Medicine, Medical University of South Carolina, Charleston, South Carolina"}]},{"given":"Subathra","family":"Marimuthu","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, James Graham Brown Cancer Center, University of Louisville, Louisville, Kentucky"}]},{"given":"Leah J.","family":"Siskind","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, James Graham Brown Cancer Center, University of Louisville, Louisville, Kentucky"}]},{"given":"Evelyn","family":"Bruner","sequence":"additional","affiliation":[{"name":"Division of Pathology and Laboratory Medicine, Department of Medicine, Medical University of South Carolina, Charleston, South Carolina"}]},{"given":"Tamara K.","family":"Nowling","sequence":"additional","affiliation":[{"name":"Division of Rheumatology and Immunology, Department of Medicine, Medical University of South Carolina, Charleston, South Carolina"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M111.237578"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/j.cellsig.2013.06.010"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/j.cellsig.2014.02.015"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.3791\/2142"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1186\/ar4166"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1093\/glycob\/cwq010"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1101\/gad.10.24.3156"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M109.031419"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.3899\/jrheum.090194"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.7554\/eLife.04066"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.2337\/db12-1825"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1089\/jir.2015.0082"},{"key":"B13","first-page":"61","volume":"65","author":"Fukatsu A","year":"1991","journal-title":"Lab Invest"},{"key":"B14","doi-asserted-by":"crossref","first-page":"5247","DOI":"10.4049\/jimmunol.153.11.5247","volume":"153","author":"G\u00f3mez-Guerrero C","year":"1994","journal-title":"J Immunol"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1128\/AAC.00344-08"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1191\/096120398678919949"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2008.071081"},{"key":"B18","first-page":"16","volume":"40","author":"Iwano M","year":"1993","journal-title":"Clin Nephrol"},{"key":"B19","doi-asserted-by":"crossref","first-page":"58","DOI":"10.1681\/ASN.V4158","volume":"4","author":"Kiberd BA","year":"1993","journal-title":"J Am Soc Nephrol"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/j.lfs.2005.01.034"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.0803219"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2567.2006.02433.x"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M605633200"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.177.10.6880"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M104547200"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/j.bmcl.2007.11.084"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1002\/art.10813"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1016\/j.ygeno.2003.08.019"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1042\/bj3490343"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1093\/glycob\/9.12.1313"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.178.5.2651"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1016\/j.molmed.2017.05.006"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1189\/jlb.1105692"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014050508"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfl336"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1177\/096120339600500603"},{"key":"B37","doi-asserted-by":"crossref","first-page":"1281","DOI":"10.4049\/jimmunol.153.3.1281","volume":"153","author":"Radeke HH","year":"1994","journal-title":"J Immunol"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M200419200"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1990.193"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1021\/bi200449j"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1038\/nmeth.2089"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M109.055475"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0106320"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0603912103"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1016\/j.molimm.2013.05.219"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1007\/BF00191429"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1084\/jem.190.12.1813"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1159\/000045663"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/17.6.1588"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0096801"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-61779-367-7_13"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1042\/BJ20050017"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.173.10.6481"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1021\/jm301892f"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1093\/rheumatology\/kew427"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00421.2017","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,8,30]],"date-time":"2023-08-30T13:37:31Z","timestamp":1693402651000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00421.2017"}},"issued":{"date-parts":[[2018,4,1]]},"references-count":55,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2018,4,1]]}},"alternative-id":["10.1152\/ajprenal.00421.2017"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00421.2017","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2018,4,1]]}},{"indexed":{"date-parts":[[2025,10,12]],"date-time":"2025-10-12T19:04:04Z","timestamp":1760295844477,"version":"3.41.0"},"reference-count":33,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2000,7,1]]},"abstract":"<jats:p>The cellular distribution of Ca<jats:sup>2+<\/jats:sup>-inhibitable adenylyl cyclase (AC) type 5 and type 6 mRNAs in rat outer medullary collecting duct (OMCD) was performed by in situ hybridization. Kidney sections were also stained with specific antibodies against either collecting duct intercalated cells or principal cells. The localization of type 5 AC in H<jats:sup>+<\/jats:sup>-ATPase-, but not aquaporin-3-, positive cells demonstrated that type 5 AC mRNA is expressed only in intercalated cells. In contrast, type 6 AC mRNA was observed in both intercalated and principal cells. In microdissected OMCDs, the simultaneous superfusion of carbachol and PGE<jats:sub>2<\/jats:sub>elicited an additive increase in the intracellular Ca<jats:sup>2+<\/jats:sup>concentration, suggesting that the Ca<jats:sup>2+<\/jats:sup>-dependent regulation of these agents occurs in different cell types. Glucagon-dependent cAMP synthesis was inhibited by both a pertussis toxin-sensitive PGE<jats:sub>2<\/jats:sub>pathway (63.7 \u00b1 4.6% inhibition, n = 5) and a Ca<jats:sup>2+<\/jats:sup>-dependent carbachol pathway (48.6 \u00b1 3.3%, n = 5). The simultaneous addition of both agents induced a cumulative inhibition of glucagon-dependent cAMP synthesis (78.2 \u00b1 3.3%, n = 5). The results demonstrate a distinct cellular localization of type 5 and type 6 AC mRNAs in OMCD and the functional expression of these Ca<jats:sup>2+<\/jats:sup>-inhibitable enzymes in intercalated cells.<\/jats:p>","DOI":"10.1152\/ajprenal.2000.279.1.f185","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T12:43:17Z","timestamp":1514032997000},"page":"F185-F194","source":"Crossref","is-referenced-by-count":28,"title":["Cellular localization of type 5 and type 6 ACs in collecting duct and regulation of cAMP synthesis"],"prefix":"10.1152","volume":"279","author":[{"given":"C\u00e9cile","family":"H\u00e9li\u00e8s-Toussaint","sequence":"first","affiliation":[{"name":"Service de Biologie Cellulaire, Commissariat \u00e0l'\u00c9nergie Atomique\/Saclay, 91191 Gif-sur-Yvette, and"}]},{"given":"Lotfi","family":"Aarab","sequence":"additional","affiliation":[{"name":"Service de Biologie Cellulaire, Commissariat \u00e0l'\u00c9nergie Atomique\/Saclay, 91191 Gif-sur-Yvette, and"}]},{"given":"Jean-Marie","family":"Gasc","sequence":"additional","affiliation":[{"name":"Laboratoire de M\u00e9decine Exp\u00e9rimentale, Coll\u00e8ge de France, 75005 Paris, France"}]},{"given":"Jean-Marc","family":"Verbavatz","sequence":"additional","affiliation":[{"name":"Service de Biologie Cellulaire, Commissariat \u00e0l'\u00c9nergie Atomique\/Saclay, 91191 Gif-sur-Yvette, and"}]},{"given":"Danielle","family":"Chabard\u00e8s","sequence":"additional","affiliation":[{"name":"Service de Biologie Cellulaire, Commissariat \u00e0l'\u00c9nergie Atomique\/Saclay, 91191 Gif-sur-Yvette, and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1007\/BF00374933"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1007\/BF00374867"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0702390"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/361315a0"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.1993.Supplement_17.8"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.32.19264"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/S0898-6568(99)00031-5"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1016\/0303-7207(84)90096-0"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/0303-7207(90)90124-Q"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1007\/s002329900194"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.3.1149"},{"key":"B12","doi-asserted-by":"crossref","first-page":"205","DOI":"10.1016\/S0031-6997(25)06784-5","volume":"46","author":"Coleman RA","year":"1994","journal-title":"Pharmacol Rev"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1016\/0898-6568(94)90016-7"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.24.15192"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1096\/fasebj.9.8.7768353"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/0006-2952(90)90678-E"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/S0968-0004(97)01050-5"},{"key":"B18","doi-asserted-by":"crossref","first-page":"24858","DOI":"10.1016\/S0021-9258(18)35842-3","volume":"267","author":"Krupinski J","year":"1992","journal-title":"J Biol Chem"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1985.249.6.F956"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1007\/BF00382690"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.257.6.F1003"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1986.66.2.377"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.89.20.9809"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.3.F611"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.94.7.2915"},{"key":"B26","first-page":"586","volume":"73","author":"Sibony M","year":"1995","journal-title":"Lab Invest"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.267.3.F354"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1007\/s002329900265"},{"key":"B29","doi-asserted-by":"crossref","first-page":"6093","DOI":"10.1016\/S0021-9258(17)37574-9","volume":"269","author":"Taussig R","year":"1994","journal-title":"J Biol Chem"},{"key":"B30","first-page":"310","volume":"316","author":"Verkman AS.","year":"1998","journal-title":"Am J Med Sci"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(94)80279-3"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.272.6.F751"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.89.15.6716"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.2000.279.1.F185","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,6,29]],"date-time":"2025-06-29T04:36:38Z","timestamp":1751171798000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.2000.279.1.F185"}},"issued":{"date-parts":[[2000,7,1]]},"references-count":33,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2000,7,1]]}},"alternative-id":["10.1152\/ajprenal.2000.279.1.F185"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.2000.279.1.f185","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2000,7,1]]}},{"indexed":{"date-parts":[[2025,10,18]],"date-time":"2025-10-18T10:46:21Z","timestamp":1760784381080,"version":"3.41.0"},"reference-count":30,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2001,7,1]]},"abstract":"<jats:p>Our present study has investigated the effect of cyclooxygenase-2 (COX-2) inhibition on prostaglandin E<jats:sub>2<\/jats:sub>(PGE<jats:sub>2<\/jats:sub>) receptor expression in M-1 cortical collecting duct cells and measured their response to PGE<jats:sub>2<\/jats:sub>. Using a semiquantitative titration analysis method, we show that following the addition of the COX-2-specific inhibitor NS-398, E-prostanoid receptor subtype (EP<jats:sub>3<\/jats:sub>and EP<jats:sub>4<\/jats:sub>) mRNA expression was found to increase threefold each vs. the vehicle-treated control. We also observed that EP<jats:sub>1<\/jats:sub>but not EP<jats:sub>2<\/jats:sub>is expressed in M-1 cells and EP<jats:sub>2<\/jats:sub>levels are not induced by NS-398. To determine the status of the PGE<jats:sub>2<\/jats:sub>response on exposure to NS-398, we measured cAMP levels in cells after stimulation with varying concentrations of PGE<jats:sub>2<\/jats:sub>, then pretreated the cells with 10 \u03bcM NS-398 before PGE<jats:sub>2<\/jats:sub>exposure and found a significant rise in the stimulatory effect of PGE<jats:sub>2<\/jats:sub>on cAMP production. Finally, Western blot analysis of the levels of the EP<jats:sub>4<\/jats:sub>receptor protein in control vs. NS-398-treated cells revealed an induction in protein levels in these cells, correlating with the induction in EP<jats:sub>4<\/jats:sub>mRNA. We conclude that NS-398 upregulates the expression of EP<jats:sub>3<\/jats:sub>and EP<jats:sub>4<\/jats:sub>mRNA in M-1 cells. Also, EP<jats:sub>4<\/jats:sub>protein levels are increased, resulting in an increased stimulation of cAMP production by PGE<jats:sub>2<\/jats:sub>.<\/jats:p>","DOI":"10.1152\/ajprenal.2001.281.1.f123","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T14:16:05Z","timestamp":1514038565000},"page":"F123-F132","source":"Crossref","is-referenced-by-count":26,"title":["Effect of COX-2 inhibitor NS-398 on expression of PGE<sub>2<\/sub>receptor subtypes in M-1 mouse CCD cells"],"prefix":"10.1152","volume":"281","author":[{"given":"Rania","family":"Nasrallah","sequence":"first","affiliation":[{"name":"Departments of Cellular and Molecular Medicine and Kidney Research Centre and of"}]},{"given":"Odette","family":"Laneuville","sequence":"additional","affiliation":[{"name":"Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, Ontario, Canada K1H 8M5"}]},{"given":"Shawn","family":"Ferguson","sequence":"additional","affiliation":[{"name":"Departments of Cellular and Molecular Medicine and Kidney Research Centre and of"}]},{"given":"Richard L.","family":"H\u00e9bert","sequence":"additional","affiliation":[{"name":"Departments of Cellular and Molecular Medicine and Kidney Research Centre and of"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.47.29569"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1996.1469"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.26.15792"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.22.15719"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.253.3.F377"},{"key":"B6","first-page":"588","volume":"67","author":"Breyer MD","year":"1998","journal-title":"Kidney Int"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199106133242407"},{"key":"B8","doi-asserted-by":"crossref","first-page":"205","DOI":"10.1016\/S0031-6997(25)06784-5","volume":"46","author":"Coleman RA","year":"1994","journal-title":"Pharmacol Rev"},{"key":"B9","doi-asserted-by":"crossref","first-page":"625","DOI":"10.1016\/S0026-895X(24)23023-6","volume":"55","author":"DeWitt DL.","year":"1999","journal-title":"Mol Pharmacol"},{"key":"B10","doi-asserted-by":"crossref","first-page":"2261","DOI":"10.1681\/ASN.V10112261","volume":"10","author":"Ferguson S","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1172\/JCI2872"},{"key":"B12","first-page":"1888","volume":"39","author":"Hardy P","year":"1998","journal-title":"Invest Ophthalmol Vis Sci"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115227"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.268.1.F145"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1111\/j.1432-1033.1993.tb18248.x"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(95)00966-D"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1084\/jem.187.4.517"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1993.265.2.C349"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1997.273.4.R1283"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(95)90125-6"},{"key":"B21","first-page":"F229","volume":"31","author":"Nadler SP","year":"1992","journal-title":"Am J Physiol"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1172\/JCI116013"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1016\/S0079-6123(08)61091-2"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1999.79.4.1193"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.2.F266"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/S0009-9236(99)70056-1"},{"key":"B27","doi-asserted-by":"crossref","first-page":"8479","DOI":"10.1016\/S0021-9258(19)38913-6","volume":"265","author":"Sonnenburg WK","year":"1990","journal-title":"J Biol Chem"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1991.148"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.263.1.F1"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.266.5.F823"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.2001.281.1.F123","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,6,29]],"date-time":"2025-06-29T04:38:07Z","timestamp":1751171887000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.2001.281.1.F123"}},"issued":{"date-parts":[[2001,7,1]]},"references-count":30,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2001,7,1]]}},"alternative-id":["10.1152\/ajprenal.2001.281.1.F123"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.2001.281.1.f123","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2001,7,1]]}},{"indexed":{"date-parts":[[2025,10,14]],"date-time":"2025-10-14T01:18:53Z","timestamp":1760404733820},"reference-count":99,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1999,4,1]]},"abstract":"<jats:p>Recent data suggests that the number of nephrons in normal adult human kidneys ranges from \u223c300,000 to more than 1 million. There is increasing evidence that reduced nephron number, either inherited or acquired, is associated with the development of essential hypertension, chronic renal failure, renal disease in transitional indigenous populations, and possibly the long-term success of renal allografts. Three processes ultimately govern the number of nephrons formed during the development of the permanent kidney (metanephros): branching of the ureteric duct in the metanephric mesenchyme; condensation of mesenchymal cells at the tips of the ureteric branches; and conversion of the mesenchymal condensates into epithelium. This epithelium then grows and differentiates to form nephrons. In recent years, we have learned a great deal about the molecular regulation of these three central processes and hence the molecular regulation of nephron endowment. Data has come from studies on cell lines, isolated ureteric duct epithelial cells, isolated metanephric mesenchyme, and whole metanephric organ culture, as well as from studies of heterozygous and homozygous null mutant mice. With accurate and precise methods now available for estimating the total number of nephrons in kidneys, more advances in our understanding of the molecular regulation of nephron endowment can be expected in the near future.<\/jats:p>","DOI":"10.1152\/ajprenal.1999.276.4.f485","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T18:10:57Z","timestamp":1514052657000},"page":"F485-F497","source":"Crossref","is-referenced-by-count":15,"title":["Molecular regulation of nephron endowment"],"prefix":"10.1152","volume":"276","author":[{"given":"Amander T.","family":"Clark","sequence":"first","affiliation":[{"name":"Department of Anatomy and Cell Biology, University of Melbourne, Parkville, Victoria 3168, Australia"}]},{"given":"John F.","family":"Bertram","sequence":"additional","affiliation":[{"name":"Department of Anatomy and Cell Biology, University of Melbourne, Parkville, Victoria 3168, Australia"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/0925-4773(93)90090-K"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.10.4412"},{"key":"B3","doi-asserted-by":"crossref","first-page":"1693","DOI":"10.1242\/dev.122.6.1693","volume":"122","author":"Bellusci S.","year":"1996","journal-title":"Development"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/S0074-7696(08)62497-3"},{"key":"B5","first-page":"1594","volume":"7","author":"Bertram J. F.","year":"1996","journal-title":"J. Am. Soc. Nephrol."},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1007\/BF00381877"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(12)80967-X"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1093\/ajh\/1.4.335"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/0272-6386(93)70097-I"},{"key":"B10","first-page":"421","volume":"98","author":"Briere N.","year":"1991","journal-title":"Comp. Biochem. Biophysiol. Acta"},{"issue":"42","key":"B11","first-page":"F386","volume":"273","author":"Choi M. E.","year":"1997","journal-title":"Am. J. Physiol."},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1797.1995.tb00054.x"},{"key":"B13","doi-asserted-by":"crossref","first-page":"1594","DOI":"10.1681\/ASN.V781223","volume":"7","author":"Clark A. T.","year":"1996","journal-title":"J. Am. Soc. Nephrol."},{"key":"B14","first-page":"21","volume":"16","author":"Clark A. T.","year":"1997","journal-title":"Proc. Aust. NZ Soc. Cell Dev. Biol."},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1038\/icb.1995.92"},{"key":"B16","first-page":"S73","volume":"50","author":"Daniel T. O.","year":"1996","journal-title":"Kidney Int."},{"key":"B17","doi-asserted-by":"crossref","first-page":"1507","DOI":"10.1242\/dev.121.5.1507","volume":"121","author":"Davies J. A.","year":"1995","journal-title":"Development"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.89.4.1179"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1101\/gad.9.22.2795"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1097-0177(199703)208:3<349::AID-AJA6>3.0.CO;2-I"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1006\/dbio.1997.8664"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/381789a0"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.91.1.1"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(90)90748-4"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.89.2.276"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/0300-483X(87)90089-8"},{"key":"B27","first-page":"656","volume":"70","author":"Gilbert T.","year":"1994","journal-title":"Lab. Invest."},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.377"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1101\/gad.10.12.1467"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.1993.Supplement_17.9"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1006\/dbio.1994.1360"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.3109\/15513819309048221"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-0528.1992.tb13726.x"},{"key":"B34","first-page":"777","volume":"64","author":"Hinchliffe S. A.","year":"1991","journal-title":"Lab. Invest."},{"issue":"39","key":"B35","first-page":"F886","volume":"270","author":"Hyink D. P.","year":"1996","journal-title":"Am. J. Physiol."},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1006\/excr.1996.3411"},{"key":"B37","doi-asserted-by":"crossref","first-page":"4159","DOI":"10.1242\/dev.122.12.4159","volume":"122","author":"Karavanova I.","year":"1996","journal-title":"Development"},{"key":"B38","doi-asserted-by":"crossref","first-page":"4225","DOI":"10.1242\/dev.125.21.4225","volume":"125","author":"Kispert A.","year":"1998","journal-title":"Development"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1097-0177(199605)206:1<59::AID-AJA6>3.0.CO;2-#"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(93)90515-R"},{"key":"B41","first-page":"3","volume":"143","author":"Kulkarni A. B.","year":"1993","journal-title":"Am. J. Pathol."},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1016\/S0925-4773(97)00667-9"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1987.238"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.136.6.1363"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1006\/dbio.1996.0204"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1007\/s004670050374"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1101\/gad.9.22.2808"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117571"},{"key":"B49","first-page":"229","volume":"5","author":"Mallie J. P.","year":"1986","journal-title":"Pediatr. Pharmacol."},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1007\/BF00865473"},{"key":"B51","first-page":"19","volume":"26","author":"Merlet-Benichou C.","year":"1997","journal-title":"Adv. Nephrol. Necker Hosp."},{"key":"B52","doi-asserted-by":"crossref","first-page":"1653","DOI":"10.1242\/dev.124.9.1653","volume":"124","author":"Miyamoto N.","year":"1997","journal-title":"Development"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(91)90115-F"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(91)90363-4"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1038\/382076a0"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)81903-0"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1006\/mvre.1993.1022"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1002\/ar.1092320205"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1006\/dbio.1996.0259"},{"key":"B60","first-page":"290","volume":"76","author":"Osathanondh V.","year":"1966","journal-title":"Arch. Pathol."},{"key":"B61","first-page":"277","volume":"76","author":"Osathanondh V.","year":"1966","journal-title":"Arch. Pathol."},{"key":"B62","doi-asserted-by":"crossref","first-page":"1005","DOI":"10.1242\/dev.119.4.1005","volume":"119","author":"Pachnis V.","year":"1993","journal-title":"Development"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1016\/0012-1606(87)90117-5"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1006\/dbio.1997.8745"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.10.4696"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1006\/dbio.1993.1129"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1038\/382073a0"},{"issue":"42","key":"B68","first-page":"F961","volume":"273","author":"Piscione T. D.","year":"1997","journal-title":"Am. J. Physiol."},{"key":"B69","doi-asserted-by":"crossref","first-page":"3207","DOI":"10.1242\/dev.121.10.3207","volume":"121","author":"Qiao J.","year":"1995","journal-title":"Development"},{"key":"B70","doi-asserted-by":"publisher","DOI":"10.1016\/0925-4773(94)00342-K"},{"issue":"31","key":"B71","first-page":"F533","volume":"262","author":"Rogers S. A.","year":"1992","journal-title":"Am. J. Physiol."},{"issue":"33","key":"B72","first-page":"F996","volume":"264","author":"Rogers S. A.","year":"1993","journal-title":"Am. J. Physiol."},{"key":"B73","doi-asserted-by":"crossref","first-page":"711","DOI":"10.1242\/dev.119.3.711","volume":"119","author":"Rothenpieler U. W.","year":"1993","journal-title":"Development"},{"key":"B74","first-page":"S17","volume":"45","author":"Ruoslahti E.","year":"1994","journal-title":"Kidney Int."},{"key":"B75","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.133.5.1095"},{"key":"B76","doi-asserted-by":"crossref","first-page":"4077","DOI":"10.1242\/dev.124.20.4077","volume":"124","author":"Sainio K.","year":"1997","journal-title":"Development"},{"key":"B77","doi-asserted-by":"crossref","first-page":"1293","DOI":"10.1242\/dev.124.7.1293","volume":"124","author":"Sainio K.","year":"1997","journal-title":"Development"},{"key":"B78","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.94.12.6279"},{"issue":"41","key":"B79","first-page":"F139","volume":"272","author":"Sakurai H.","year":"1997","journal-title":"Am. J. Physiol."},{"key":"B80","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00969.x"},{"key":"B81","doi-asserted-by":"publisher","DOI":"10.1038\/382070a0"},{"key":"B82","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.94.12.6238"},{"key":"B83","doi-asserted-by":"publisher","DOI":"10.1006\/dbio.1993.1308"},{"key":"B85","doi-asserted-by":"publisher","DOI":"10.1038\/367380a0"},{"key":"B86","doi-asserted-by":"crossref","first-page":"1919","DOI":"10.1242\/dev.122.6.1919","volume":"122","author":"Schuchardt A.","year":"1996","journal-title":"Development"},{"key":"B87","doi-asserted-by":"publisher","DOI":"10.1002\/j.1460-2075.1992.tb05319.x"},{"key":"B88","doi-asserted-by":"crossref","first-page":"207","DOI":"10.1242\/jcs.96.2.207","volume":"96","author":"Sonnenberg A.","year":"1990","journal-title":"J. Cell Sci."},{"key":"B89","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.111.3.1265"},{"key":"B90","doi-asserted-by":"publisher","DOI":"10.1038\/372679a0"},{"key":"B91","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2818.1984.tb02501.x"},{"key":"B92","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.125.3.681"},{"key":"B93","doi-asserted-by":"crossref","first-page":"4057","DOI":"10.1242\/dev.121.12.4057","volume":"121","author":"Torres M.","year":"1995","journal-title":"Development"},{"key":"B94","doi-asserted-by":"publisher","DOI":"10.1038\/373702a0"},{"key":"B95","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.208"},{"key":"B96","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(87)90664-7"},{"key":"B97","doi-asserted-by":"publisher","DOI":"10.1101\/gad.9.17.2105"},{"key":"B98","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.128.1.171"},{"key":"B99","doi-asserted-by":"publisher","DOI":"10.1159\/000020500"},{"key":"B100","doi-asserted-by":"crossref","first-page":"2977","DOI":"10.1242\/dev.122.10.2977","volume":"122","author":"Zhang H.","year":"1996","journal-title":"Development"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1999.276.4.F485","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:55:18Z","timestamp":1660190118000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1999.276.4.F485"}},"issued":{"date-parts":[[1999,4,1]]},"references-count":99,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1999,4,1]]}},"alternative-id":["10.1152\/ajprenal.1999.276.4.F485"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1999.276.4.f485","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1999,4,1]]}},{"indexed":{"date-parts":[[2025,10,16]],"date-time":"2025-10-16T20:05:55Z","timestamp":1760645155643},"reference-count":49,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2006,5]]},"abstract":"<jats:p>Oxygen consumed by the kidney (Q<jats:sub>O<jats:sub>2<\/jats:sub><\/jats:sub>) is primarily obligated to sodium reabsorption (T<jats:sub>Na<\/jats:sub>). The relationship of Q<jats:sub>O<jats:sub>2<\/jats:sub><\/jats:sub>to T<jats:sub>Na<\/jats:sub>(Q<jats:sub>O<jats:sub>2<\/jats:sub><\/jats:sub>\/T<jats:sub>Na<\/jats:sub>) may be altered by hormones and autacoids. To examine whether Q<jats:sub>O<jats:sub>2<\/jats:sub><\/jats:sub>\/T<jats:sub>Na<\/jats:sub>depends on the mechanism of sodium reabsorption, we first evaluated the effects on Q<jats:sub>O<jats:sub>2<\/jats:sub><\/jats:sub>and Q<jats:sub>O<jats:sub>2<\/jats:sub><\/jats:sub>\/T<jats:sub>Na<\/jats:sub>of benzolamide (BNZ), a proximal diuretic that works by inhibiting membrane carbonic anhydrase. During BNZ infusion in anesthetized rats, Q<jats:sub>O<jats:sub>2<\/jats:sub><\/jats:sub>increased by 50% despite a 25% decline in T<jats:sub>Na<\/jats:sub>. However, BNZ failed to increase Q<jats:sub>O<jats:sub>2<\/jats:sub><\/jats:sub>\/T<jats:sub>Na<\/jats:sub>when given along with the adenosine A1 receptor blocker, DPCPX, which inhibits basolateral Na-bicarbonate cotransport (NBC1), or EIPA, which inhibits sodium-hydrogen exchange (NHE). Incubating freshly harvested rat proximal tubules with BNZ also caused Q<jats:sub>O<jats:sub>2<\/jats:sub><\/jats:sub>to increase by 62%, an effect that was prevented by blocking the apical NHE3 with S3226. Blocking NBC1 or NHE3 in the proximal tubule will have opposite effects on cell pH, but both maneuvers should reduce active chloride transport. In conclusion, inhibiting membrane carbonic anhydrase in the proximal tubule increases Q<jats:sub>O<jats:sub>2<\/jats:sub><\/jats:sub>and reduces the energy efficiency of sodium reabsorption by the kidney. This is not purely due to shifting the burden of reabsorption to a more expensive site downstream from the proximal tubule. Instead, increased cost may be incurred within the proximal tubule as the result of increased active chloride transport.<\/jats:p>","DOI":"10.1152\/ajprenal.00343.2005","type":"journal-article","created":{"date-parts":[[2005,12,14]],"date-time":"2005-12-14T02:38:47Z","timestamp":1134527927000},"page":"F1009-F1015","source":"Crossref","is-referenced-by-count":20,"title":["Kidney oxygen consumption, carbonic anhydrase, and proton secretion"],"prefix":"10.1152","volume":"290","author":[{"given":"Aihua","family":"Deng","sequence":"first","affiliation":[]},{"given":"Cynthia M.","family":"Miracle","sequence":"additional","affiliation":[]},{"given":"Mark","family":"Lortie","sequence":"additional","affiliation":[]},{"given":"Joseph","family":"Satriano","sequence":"additional","affiliation":[]},{"given":"Francis B.","family":"Gabbai","sequence":"additional","affiliation":[]},{"given":"Karen A.","family":"Munger","sequence":"additional","affiliation":[]},{"given":"Scott C.","family":"Thomson","sequence":"additional","affiliation":[]},{"given":"Roland C.","family":"Blantz","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1985.248.2.F272"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1385\/CBB:36:2-3:147"},{"key":"R3","doi-asserted-by":"crossref","unstructured":"Aronson PSand Giebisch G.Mechanisms of chloride transport in the proximal tubule.Am J Physiol Renal Physiol273: F179\u2013F192, 1997.","DOI":"10.1152\/ajprenal.1997.273.2.F179"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfh097"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.092259799"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200401000-00010"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115316"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1172\/JCI21851"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1982.242.3.F274"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00682.x"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00450.x"},{"key":"R12","unstructured":"Deng A, Munger KA, Miracle CM, Satriano J, Lortie M, Gabbai F, Thomson SC, and Blantz RCM.Inhibition of proximal reabsorption and renal O2consumption in vivo and in vitro (Abstract).J Am Soc NephrolIn press."},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00701.x"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1989.257.2.C333"},{"key":"R15","unstructured":"DuBose TD Jr, Pucacco LR, and Carter NW.Determination of disequilibrium pH in the rat kidney in vivo: evidence for hydrogen secretion.Am J Physiol Renal Fluid Electrolyte Physiol140: F138\u2013F146, 1981."},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1979.82"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1007\/BF00586045"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1016\/S0167-0115(00)00136-1"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000035087.11758.ED"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-201X.2003.01058.x"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000092145.90389.65"},{"key":"R22","unstructured":"Klahr S, Hamm LL, Hammerman MR, and Mandel LJ.Renal metabolism: integrated responses. In:Handbook of Physiology, Renal Physiology. Bethesda, MD: Am Physiol Soc, 1989, vol. II, sect. 8, p. 2264\u20132333."},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.141241098"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.1993.tb13564.x"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00474.x"},{"key":"R26","unstructured":"Kost CK Jr, Herzer WA, Rominski BR, Mi Z, and Jackson EK.Diuretic response to adenosine A1 receptor blockade in normotensive and spontaneously hypertensive rats: role of pertussis toxin-sensitive G-proteins.J Pharmacol Exp Ther292: 752\u2013760, 2000."},{"key":"R27","unstructured":"Langberg H, Hartmann A, and Kiil F.Inhibitory effect of acetazolamide on renal tubular reabsorption of NaHCO3and NaCl in dogs varies inversely with plasma pH.J Pharmacol Exp Ther234: 747\u2013753, 1985."},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.82.12.1263"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1172\/JCI113638"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1980.238.3.F175"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1007\/s004240050411"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1989.tb08738.x"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-004-1309-y"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1983.244.5.F461"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.259.6.F910"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1007\/s004240050704"},{"key":"R37","doi-asserted-by":"crossref","unstructured":"Sejersted OM, Mathisen O, and Kiil F.Oxygen requirement of renal Na-K-ATPase-dependent sodium reabsorption.Am J Physiol232: 152\u2013158, 1977.","DOI":"10.1152\/ajprenal.1977.232.2.F152"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.171317998"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.265.4.F511"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1172\/JCI8761"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.3181\/00379727-106-26451"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1172\/JCI109229"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-004-1239-8"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1981.241.4.F403"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.281.2.F288"},{"key":"R46","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1986.250.5.F860"},{"key":"R47","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1984.247.1.F151"},{"key":"R48","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00729.x"},{"key":"R49","doi-asserted-by":"crossref","unstructured":"Wilcox CS, Welch WJ, Schreiner GF, and Belardinelli L.Natriuretic and diuretic actions of a highly selective adenosine A1 receptor antagonist.J Am Soc Nephrol10: 714\u2013720, 1999.","DOI":"10.1681\/ASN.V104714"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00343.2005","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,7,21]],"date-time":"2021-07-21T12:38:23Z","timestamp":1626871103000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00343.2005"}},"issued":{"date-parts":[[2006,5]]},"references-count":49,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2006,5]]}},"alternative-id":["10.1152\/ajprenal.00343.2005"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00343.2005","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2006,5]]}},{"indexed":{"date-parts":[[2025,10,27]],"date-time":"2025-10-27T10:30:38Z","timestamp":1761561038663,"version":"3.32.0"},"reference-count":69,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2006,8]]},"abstract":"<jats:p>Chronic upregulation of the renal betaine\/GABA transporter (BGT1) by hypertonic stress has been well documented, but it is not known whether BGT1 can be regulated acutely after insertion in the basolateral plasma membrane. Related transporters, such as the rat brain GABA transporter, can be rapidly removed from the plasma membrane through activation of G protein-coupled receptors. The goal of the present study was to determine whether acute changes in extracellular and\/or intracellular Ca<jats:sup>2+<\/jats:sup>will regulate BGT1 transport activity at the plasma membrane level in Madin-Darby canine kidney cells subjected to 24-h hypertonic stress. After brief pretreatment with a Ca<jats:sup>2+<\/jats:sup>-free solution, the addition of extracellular Ca<jats:sup>2+<\/jats:sup>in the transport assay produced dose-dependent inhibition of Na<jats:sup>+<\/jats:sup>-GABA cotransport. Maximum inhibition was 49% at 2 mM Ca<jats:sup>2+<\/jats:sup>( P &lt; 0.05). Fura 2 imaging confirmed that addition of 2 mM Ca<jats:sup>2+<\/jats:sup>produced a transient increase in intracellular Ca<jats:sup>2+<\/jats:sup>that preceded transport inhibition. Acute inhibition of Na<jats:sup>+<\/jats:sup>-GABA cotransport was reproduced by addition of thapsigargin (5 \u03bcM) and ionomycin (10 \u03bcM). Amino acid transport system A, assayed as a control, was not inhibited. Brief treatment with phorbol esters reproduced the specific inhibition of Na<jats:sup>+<\/jats:sup>-GABA cotransport, and the inhibition was blocked by staurosporine. Surface biotinylation confirmed that the response to phorbol esters was accompanied by loss of BGT1 protein from the plasma membrane, and immunohistochemistry showed a shift to an intracellular distribution. We conclude that BGT1 can be inhibited acutely by extracellular Ca<jats:sup>2+<\/jats:sup>through a mechanism involving BGT1 protein internalization, and protein kinase C may play a role.<\/jats:p>","DOI":"10.1152\/ajprenal.00428.2005","type":"journal-article","created":{"date-parts":[[2006,3,9]],"date-time":"2006-03-09T02:14:19Z","timestamp":1141870459000},"page":"F305-F313","source":"Crossref","is-referenced-by-count":9,"title":["Inhibition of the renal betaine transporter by calcium ions"],"prefix":"10.1152","volume":"291","author":[{"given":"Stephen A.","family":"Kempson","sequence":"first","affiliation":[]},{"given":"Jason M.","family":"Edwards","sequence":"additional","affiliation":[]},{"given":"Michael","family":"Sturek","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.12.6917"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.273.1.F129"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.2000.3226"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00733.x"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.19-01-00001.1999"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00289.2002"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1042\/bj20021056"},{"key":"R8","unstructured":"Brown EM, Chattopadhyay N, Vassilev PM, and Hebert SC.The calcium-sensing receptor (CaR) permits Ca2+to function as a versatile extracellular first messenger.Recent Prog Horm Res53: 257\u2013280, 1998."},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1034\/j.1600-0854.2000.010205.x"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1096\/fasebj.10.14.9002551"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1359\/jbmr.1997.12.4.568"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.270.3.F419"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-003-1064-5"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1093\/ajcp\/45.3.290"},{"key":"R15","doi-asserted-by":"crossref","unstructured":"Dmitrieva NI, Burg MB, and Ferraris JD.DNA damage and osmotic regulation in the kidney.Am J Physiol Renal Physiol289: F2\u2013F7, 2005.","DOI":"10.1152\/ajprenal.00041.2005"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfg455"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00984.x"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.1999.0327t.x"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2736(94)00284-V"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1053\/j.semnephrol.2003.08.017"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00161.2003"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.060002408.x"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.121.1.61"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.2000.00435.x"},{"key":"R24A","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-5793(99)01389-7"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.108.2.389"},{"key":"R26","unstructured":"Hill BJ, Katwa LC, Wamhoff BR, and Sturek M.Enhanced endothelinAreceptor-mediated calcium mobilization and contraction in organ cultured porcine coronary arteries.J Pharmacol Exp Ther295: 484\u2013491, 2000."},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1038\/nrm1154"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1997.272.3.C804"},{"key":"R29","doi-asserted-by":"crossref","unstructured":"Jan CRand Tseng CJ.MK-886, a leukotriene biosynthesis inhibitor, as an activator of Ca2+mobilization in Madin-Darby canine kidney (MDCK) cells.J Pharmacol Exp Ther294: 96\u2013102, 2000.","DOI":"10.1016\/S0022-3565(24)39044-5"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1016\/S0091-679X(08)61114-0"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1016\/S0005-2736(98)00051-0"},{"key":"R32","unstructured":"Kempson SAand Montrose MH.Osmotic regulation of renal betaine transport: transcription and beyond.Pfl\u00fcgers Arch449: 227\u2013234, 2004."},{"key":"R33","doi-asserted-by":"crossref","unstructured":"Kempson SA, Parikh V, Xi L, Chu S, and Montrose M.Subcellular distribution of the renal betaine transporter during hypertonic stress.Am J Physiol Cell Physiol285: C1091\u2013C1100, 2003.","DOI":"10.1152\/ajpcell.00021.2003"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1016\/S1095-6433(01)00440-8"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1995.2224"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1002\/cbf.1241"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1998.78.1.247"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1016\/0003-9861(84)90278-9"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-5793(00)01532-5"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.86.15.6007"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M412668200"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.24.16709"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.5.2538"},{"key":"R44","doi-asserted-by":"crossref","unstructured":"Nemeth EFand Scarpa A.Rapid mobilization of cellular Ca2+in bovine parathyroid cells evoked by extracellular divalent cations. Evidence for a cell surface calcium receptor.J Biol Chem262: 5188\u20135196, 1987.","DOI":"10.1016\/B978-0-12-521040-9.50009-7"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00216.2002"},{"key":"R46","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00993.x"},{"key":"R47","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00121.2003"},{"key":"R48","doi-asserted-by":"crossref","unstructured":"Preston A, Yamauchi A, Kwon H, and Handler J.Activators of protein kinase A and of protein kinase C inhibit MDCK cell myo-inositol and betaine uptake.J Am Soc Nephrol6: 1559\u20131564, 1995.","DOI":"10.1681\/ASN.V661559"},{"key":"R49","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.66036.x"},{"key":"R50","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.3.F611"},{"key":"R51","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119299"},{"key":"R52","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.267.1.F28"},{"key":"R53","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0705213"},{"key":"R54","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00284.2003"},{"key":"R55","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-8993(01)02802-5"},{"key":"R56","doi-asserted-by":"publisher","DOI":"10.1021\/bi00552a018"},{"key":"R57","doi-asserted-by":"publisher","DOI":"10.1172\/JCI116367"},{"key":"R58","doi-asserted-by":"publisher","DOI":"10.1034\/j.1600-0854.2000.010606.x"},{"key":"R59","doi-asserted-by":"publisher","DOI":"10.1007\/s10254-003-0009-x"},{"key":"R60","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000079040.55124.25"},{"key":"R61","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-002-0849-2"},{"key":"R62","doi-asserted-by":"publisher","DOI":"10.1007\/s00232-001-0149-3"},{"key":"R63","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00135.2004"},{"key":"R64","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.261.1.F197"},{"key":"R65","doi-asserted-by":"crossref","unstructured":"Yamauchi A, Uchida S, Kwon HM, Preston AS, Robey RB, Garcia-Perez A, Burg MB, and Handler JS.Cloning of a Na+- and Cl\u2212-dependent betaine transporter that is regulated by hypertonicity.J Biol Chem267: 649\u2013652, 1992.","DOI":"10.1016\/S0021-9258(18)48543-2"},{"key":"R66","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.275.13.9612"},{"key":"R67","doi-asserted-by":"publisher","DOI":"10.1006\/mgme.2000.3110"},{"key":"R68","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0402961101"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00428.2005","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,1,7]],"date-time":"2025-01-07T23:32:22Z","timestamp":1736292742000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00428.2005"}},"issued":{"date-parts":[[2006,8]]},"references-count":69,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2006,8]]}},"alternative-id":["10.1152\/ajprenal.00428.2005"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00428.2005","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2006,8]]}},{"indexed":{"date-parts":[[2025,10,27]],"date-time":"2025-10-27T10:46:01Z","timestamp":1761561961389},"reference-count":43,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2002,8,1]]},"abstract":"<jats:p>The human nongastric H<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-ATPase, ATP1AL1, shown to reabsorb K<jats:sup>+<\/jats:sup>in exchange for H<jats:sup>+<\/jats:sup>or Na<jats:sup>+<\/jats:sup>, is localized in the luminal plasma membrane of renal epithelial cells. It is presumed that renal H<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-ATPases can be regulated by endocytosis. However, little is known about the molecular mechanisms that control plasma membrane expression of renal H<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-ATPases. In our study, activation of protein kinase C (PKC) using phorbol esters (phorbol 12-myristate 13-acetate) leads to clathrin-dependent internalization and intracellular accumulation of the ion pump in stably transfected Madin-Darby canine kidney cells. Functional inactivation of the H<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-ATPase by PKC activation is shown by intracellular pH measurements. Proton extrusion capacity of ATP1AL1-transfected cells is drastically reduced after phorbol 12-myristate 13-acetate incubation and can be prevented with the PKC blocker bisindolylmaleimide. Ion pump internalization and inactivation are specifically mediated by the PKC pathway, whereas activation of the protein kinase A pathway has no influence. Our results show that the nongastric H<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-ATPase is a specific target for the PKC pathway. Therefore, PKC-mediated phosphorylation is a potential regulatory mechanism for apical nongastric H<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-ATPase plasma membrane expression.<\/jats:p>","DOI":"10.1152\/ajprenal.00226.2001","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:35:38Z","timestamp":1425414938000},"page":"F335-F343","source":"Crossref","is-referenced-by-count":13,"title":["Stimulation of protein kinase C pathway mediates endocytosis of human nongastric H<sup>+<\/sup>-K<sup>+<\/sup>-ATPase, ATP1AL1"],"prefix":"10.1152","volume":"283","author":[{"given":"J.","family":"Reinhardt","sequence":"first","affiliation":[{"name":"Institute of Physiology and"}]},{"given":"M.","family":"Kosch","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of M\u00fcnster, D-48149 M\u00fcnster, Germany"}]},{"given":"M.","family":"Lerner","sequence":"additional","affiliation":[{"name":"Institute of Physiology and"}]},{"given":"H.","family":"Bertram","sequence":"additional","affiliation":[{"name":"Institute of Physiology and"}]},{"given":"D.","family":"Lemke","sequence":"additional","affiliation":[{"name":"Institute of Physiology and"}]},{"given":"H.","family":"Oberleithner","sequence":"additional","affiliation":[{"name":"Institute of Physiology and"}]}],"member":"24","reference":[{"key":"B1","first-page":"396","volume":"22","author":"Bastani B","year":"1996","journal-title":"Miner Electrolyte Metab"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.115.1.151"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.1997.272.6.G1304"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.124.5.717"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1997.273.5.C1458"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.4.1920"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.15.8814"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.47.29759"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.11.6516"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1007\/s004410050799"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.253.3.F418"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1021\/bi0007831"},{"key":"B13","doi-asserted-by":"crossref","first-page":"18607","DOI":"10.1016\/S0021-9258(17)32353-0","volume":"269","author":"Eker P","year":"1994","journal-title":"J Biol Chem"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.2001.81.1.345"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1007\/s004240000411"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.23.14072"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.1999.0327t.x"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.268.2.F285"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.3.F539"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.43.27772"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.25.14740"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1006\/excr.1995.1075"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.6.F812"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.123.6.1421"},{"key":"B25","doi-asserted-by":"crossref","first-page":"4116","DOI":"10.1016\/S0021-9258(17)41751-0","volume":"269","author":"Kaplan DL","year":"1994","journal-title":"J Biol Chem"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.270.3.F548"},{"key":"B27","first-page":"349","volume":"22","author":"Kone BC.","year":"1996","journal-title":"Miner Electrolyte Metab"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.5.2543"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118247"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1995.269.4.C992"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1007\/BF00382687"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.97.7.3242"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1998.274.4.C1017"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.3.F417"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1996.76.4.949"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1997.272.2.C685"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.6.F799"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.2000.279.3.C541"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1021\/bi00578a012"},{"key":"B40","doi-asserted-by":"crossref","first-page":"15771","DOI":"10.1016\/S0021-9258(18)98476-0","volume":"266","author":"Toullec D","year":"1991","journal-title":"J Biol Chem"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.275.5.F818"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.256.5.F957"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1172\/JCI114165"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00226.2001","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,5,1]],"date-time":"2022-05-01T09:34:54Z","timestamp":1651397694000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00226.2001"}},"issued":{"date-parts":[[2002,8,1]]},"references-count":43,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2002,8,1]]}},"alternative-id":["10.1152\/ajprenal.00226.2001"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00226.2001","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2002,8,1]]}},{"indexed":{"date-parts":[[2025,10,27]],"date-time":"2025-10-27T20:44:50Z","timestamp":1761597890333},"reference-count":57,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2001,7,1]]},"abstract":"<jats:p>Development of micro- and macrovascular disease in diabetes mellitus (DM) warrants a thorough investigation into the repertoire of endothelial cell (EC) responses to diabetic environmental cues. Using human umbilical vein EC (HUVEC) cultured in three-dimensional (3-D) native collagen I (NC) or glycated collagen I (GC), we observed capillary cord formation that showed a significant reduction in branching when cells were cultured in GC. To gain insight into the molecular determinants of this phenomenon, HUVEC subjected to GC vs. NC were studied using a PCR-selected subtraction approach. Nine different genes were identified as up- or downregulated in response to GC; among those, plasminogen activator inhibitor-1 (PAI-1) mRNA was found to be upregulated by GC. Western blot analysis of HUVEC cultured on GC showed an increase in PAI-1 expression. The addition of a neutralizing anti-PAI-1 antibody to HUVEC cultured in GC restored the branching pattern of formed capillary cords. In contrast, supplementation of culture medium with the constitutively active PAI-1 reproduced defective branching patterns in HUVEC cultured in NC. Ex vivo capillary sprouting in GC was unaffected in PAI-1 knockout mice but was inhibited in wild-type mice. This difference persisted in diabetic mice. In conclusion, the PCR-selected subtraction technique identified PAI-1 as one of the genes characterizing an early response of HUVEC to the diabetic-like interstitial environment modeled by GC and responsible for the defective branching of endothelial cells. We propose that an upregulation of PAI-1 is causatively linked to the defective formation of capillary networks during wound healing and eventual vascular dropout characteristic of diabetic nephropathy.<\/jats:p>","DOI":"10.1152\/ajprenal.2001.281.1.f71","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T14:16:05Z","timestamp":1514038565000},"page":"F71-F80","source":"Crossref","is-referenced-by-count":22,"title":["Delayed branching of endothelial capillary-like cords in glycated collagen I is mediated by early induction of PAI-1"],"prefix":"10.1152","volume":"281","author":[{"given":"Jun","family":"Chen","sequence":"first","affiliation":[{"name":"Departments of Medicine and Physiology and Biophysics, State University of New York, Stony Brook, New York 11794-8152;"}]},{"given":"Sergey","family":"Brodsky","sequence":"additional","affiliation":[{"name":"Departments of Medicine and Physiology and Biophysics, State University of New York, Stony Brook, New York 11794-8152;"}]},{"given":"Hong","family":"Li","sequence":"additional","affiliation":[{"name":"Departments of Medicine and Physiology and Biophysics, State University of New York, Stony Brook, New York 11794-8152;"}]},{"given":"Dierk J.","family":"Hampel","sequence":"additional","affiliation":[{"name":"Departments of Medicine and Physiology and Biophysics, State University of New York, Stony Brook, New York 11794-8152;"}]},{"given":"Toshio","family":"Miyata","sequence":"additional","affiliation":[{"name":"Tokai University School of Medicine, Kanagawa, Japan;"}]},{"given":"Talia","family":"Weinstein","sequence":"additional","affiliation":[{"name":"Department of Medicine, Tel Aviv University, Israel; and"}]},{"given":"Uzi","family":"Gafter","sequence":"additional","affiliation":[{"name":"Department of Medicine, Tel Aviv University, Israel; and"}]},{"given":"Jill T.","family":"Norman","sequence":"additional","affiliation":[{"name":"Department of Medicine, University College London, London, United Kingdom"}]},{"given":"Leon G.","family":"Fine","sequence":"additional","affiliation":[{"name":"Department of Medicine, University College London, London, United Kingdom"}]},{"given":"Michael S.","family":"Goligorsky","sequence":"additional","affiliation":[{"name":"Departments of Medicine and Physiology and Biophysics, State University of New York, Stony Brook, New York 11794-8152;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"crossref","first-page":"1165","DOI":"10.1681\/ASN.V551165","volume":"5","author":"Adler S.","year":"1994","journal-title":"J Am Soc Nephrol"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI116929"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119089"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.150"},{"key":"B5","first-page":"595","volume":"240","author":"Bobbink IW","year":"1997","journal-title":"Biochem J"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1007\/BF01747747"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.me.42.020191.001111"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-101-4-527"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1038\/368419a0"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1172\/JCI116893"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.134.6.1563"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/S0378-1119(98)00577-0"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1021\/bi00219a007"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118396"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117786"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.80.4.490"},{"key":"B17","first-page":"2358","volume":"36","author":"Kalfa TA","year":"1995","journal-title":"Invest Ophthalmol Vis Sci"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00139.x"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1006\/excr.1997.3540"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1993.95"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.7"},{"key":"B22","doi-asserted-by":"crossref","first-page":"5","DOI":"10.1111\/j.0954-6820.1963.tb12557.x","volume":"174","author":"Ljundquist A.","year":"1963","journal-title":"Acta Med Scand"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.2337\/diab.41.8.1009"},{"key":"B24","doi-asserted-by":"crossref","first-page":"5133","DOI":"10.1016\/S0021-9258(18)42741-X","volume":"267","author":"Makita Z","year":"1992","journal-title":"J Biol Chem"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00093.x"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.81.2.583"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM198602133140702"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.97.5.1648"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.9.5830"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1007\/BF02810077"},{"key":"B31","first-page":"78","volume":"128","author":"Nicosia RF","year":"1987","journal-title":"Am J Pathol"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.3.1747"},{"key":"B33","doi-asserted-by":"crossref","first-page":"513","DOI":"10.1242\/jcs.92.3.513","volume":"92","author":"Oliver MH","year":"1989","journal-title":"J Cell Sci"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.377"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1038\/nm0396-287"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.272.1.F139"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119180"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118175"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1096\/fasebj.14.1.145"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00157.x"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/5.10.889"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.129.2.335"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1038\/383441a0"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1007\/s001250050972"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1993.1677"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.78"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115405"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1093\/oxfordjournals.ndt.a027265"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.2337\/diab.46.2.S19"},{"key":"B50","first-page":"138","volume":"70","author":"Vlassara H","year":"1994","journal-title":"Lab Invest"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.89.24.12043"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1126\/science.273.5281.1551"},{"key":"B53","doi-asserted-by":"crossref","first-page":"1563","DOI":"10.1093\/clinchem\/43.9.1563","volume":"43","author":"Wrobel K","year":"1997","journal-title":"Clin Chem"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1007\/s001250051089"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.13.8723"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.46.29393"},{"key":"B57","first-page":"10","volume":"54","author":"Ziyadeh FN.","year":"1996","journal-title":"Kidney Int"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.2001.281.1.F71","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,6,30]],"date-time":"2024-06-30T01:59:20Z","timestamp":1719712760000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.2001.281.1.F71"}},"issued":{"date-parts":[[2001,7,1]]},"references-count":57,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2001,7,1]]}},"alternative-id":["10.1152\/ajprenal.2001.281.1.F71"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.2001.281.1.f71","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2001,7,1]]}},{"indexed":{"date-parts":[[2025,10,28]],"date-time":"2025-10-28T18:40:10Z","timestamp":1761676810344},"reference-count":48,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2020,3,1]]},"abstract":"<jats:p>Little is known about changes in parathyroid cells when calcimimetics are withdrawn. We examined the response of parathyroid glands to cinacalcet (Cina) withdrawal in uremic Sprague-Dawley rats fed a high-phosphate diet to develop secondary hyperparathyroidism and divided into groups treated with vehicle (UC), Cina, and Cina and maxacalcitol (Maxa), a vitamin D receptor activator (CiNa + Maxa). After 2 wk of treatment, vehicle and Cina were withdrawn and Maxa was continued. Rats were analyzed immediately ( day 0) and 7 days ( day 7) after withdrawal. The Cina and CiNa + Maxa groups had significantly lower parathyroid hormone (PTH) than the UC group on day 0, although PTH in the Cina group reached UC levels on day 7. On day 0, there were significantly more proliferating cell nuclear antigen-positive cells in the UC group compared with normal controls, and this increase was significantly suppressed in the Cina and CiNa + Maxa groups. On day 7, the Cina group, but not the CiNa + Maxa group, showed a significant increase in proliferating cell nuclear antigen-positive cells compared with the UC group. This increase was related to parathyroid cell diameter regression to UC levels, whereas combination treatment maintained diameter suppression. These results indicate that parathyroid growth activity is stimulated by Cina withdrawal, although the PTH level was not further increased. Continuous administration of Cina may be required for optimal control of secondary hyperparathyroidism, and simultaneous use of a vitamin D receptor activator may be advisable during Cina withdrawal.<\/jats:p>","DOI":"10.1152\/ajprenal.00479.2019","type":"journal-article","created":{"date-parts":[[2020,1,21]],"date-time":"2020-01-21T18:20:12Z","timestamp":1579630812000},"page":"F639-F646","source":"Crossref","is-referenced-by-count":1,"title":["Early response of the parathyroid gland to withdrawal of a calcimimetic compound in uremic rats"],"prefix":"10.1152","volume":"318","author":[{"given":"Masahide","family":"Mizobuchi","sequence":"first","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Showa University School of Medicine, Tokyo, Japan"}]},{"given":"Hiroaki","family":"Ogata","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Showa University Northern Yokohama Hospital, Yokohama, Japan"}]},{"given":"Fumihiko","family":"Koiwa","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Showa University Fujigaoka Hospital, Yokohama, Japan"}]},{"given":"Hirokazu","family":"Honda","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Showa University School of Medicine, Tokyo, Japan"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI32409"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/ncpendmet0394"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-199307000-00004"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfp616"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009040427"},{"key":"B6","doi-asserted-by":"crossref","first-page":"903","DOI":"10.1681\/ASN.V115903","volume":"11","author":"Chin J","year":"2000","journal-title":"J Am Soc Nephrol"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.67103.x"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.06040710"},{"key":"B9","doi-asserted-by":"crossref","first-page":"1141","DOI":"10.1681\/ASN.V1161141","volume":"11","author":"Dr\u00fceke TB","year":"2000","journal-title":"J Am Soc Nephrol"},{"key":"B10","volume-title":"Endotext","author":"Dr\u00fceke TB","year":"2000"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1159\/000188261"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1172\/JCI116720"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1186\/1741-7007-7-17"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000037676.54018.CB"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfr668"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfg296"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1046\/j.0001-6772.2003.01238.x"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.407"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2017.04.006"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2009.188"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1113\/JP273774"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2009.466"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2009.414"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1159\/000274483"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000024439.38838.03"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1111\/j.1525-139X.2006.00161.x"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90272.2008"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfr589"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000141016.20133.33"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2007.07.177"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1254\/jphs.FMJ04007X6"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(03)00905-3"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90625.2008"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1007\/s00223-015-0052-z"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.103.057273"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2014.09.005"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00027.x"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1359\/jbmr.2002.17.12.2206"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00538.x"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1210\/endo-119-6-2864"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.82.12.4270"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.07304.x"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/11.supp3.130"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1007\/s002689900113"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2010.02.340"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119851"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00837.x"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1210\/endo.137.11.8895317"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00479.2019","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,10,12]],"date-time":"2022-10-12T05:58:54Z","timestamp":1665554334000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00479.2019"}},"issued":{"date-parts":[[2020,3,1]]},"references-count":48,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2020,3,1]]}},"alternative-id":["10.1152\/ajprenal.00479.2019"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00479.2019","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2020,3,1]]}},{"indexed":{"date-parts":[[2025,10,29]],"date-time":"2025-10-29T03:43:43Z","timestamp":1761709423844},"reference-count":51,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1999,10,1]]},"abstract":"<jats:p>The integrity of the tight junction (TJ), which is responsible for the permeability barrier of the polarized epithelium, is disrupted during ischemic injury and must be reestablished for recovery. Recently, with the use of an ATP depletion-repletion model for ischemia and reperfusion injury in Madin-Darby canine kidney cells, TJ proteins such as zonula occludens-1 (ZO-1) were shown to reversibly form large complexes and associate with cytoskeletal proteins (T. Tsukamoto and S. K. Nigam, J. Biol. Chem. 272: 16133\u201316139, 1997). In this study, we examined the role of intracellular calcium in TJ reassembly after ATP depletion-repletion by employing the cell-permeant calcium chelator 1,2-bis(2-aminophenoxy)ethane- N, N, N\u2032, N\u2032-tetraacetic acid-AM (BAPTA-AM). Lowering intracellular calcium during ATP depletion is associated with significant inhibition of the reestablishment of the permeability barrier following ATP repletion as measured by transepithelial electrical resistance and mannitol flux, marked alterations in the subcellular localization of occludin by immunofluorescent analysis, and decreased solubility of ZO-1 and other TJ proteins by Triton X-100 extraction assay, suggesting that lowering intracellular calcium potentiates the interaction of TJ proteins with the cytoskeleton. Coimmunoprecipitation studies indicated that decreased solubility may partly result from the stabilization of large TJ protein-containing complexes with fodrin. Although ionic detergents (SDS and deoxycholate) appeared to cause a dissociation of ZO-1-containing complexes from the cytoskeleton, sucrose gradient analyses of the solubilized proteins suggested that calcium chelation leads to self-association of these complexes. Together, these results raise the possibility that intracellular calcium plays an important facilitatory role in the reassembly of the TJ damaged by ischemic insults. Calcium appears to be necessary for the dissociation of TJ-cytoskeletal complexes, thus permitting functional TJ reassembly and paracellular permeability barrier recovery.<\/jats:p>","DOI":"10.1152\/ajprenal.1999.277.4.f524","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T12:29:22Z","timestamp":1514032162000},"page":"F524-F532","source":"Crossref","is-referenced-by-count":22,"title":["A role for intracellular calcium in tight junction reassembly after ATP depletion-repletion"],"prefix":"10.1152","volume":"277","author":[{"given":"Jiuming","family":"Ye","sequence":"first","affiliation":[{"name":"Renal Division, Department of Medicine, Brigham and Women\u2019s Hospital and Harvard Medical School, Boston, Massachusetts 02115; and"}]},{"given":"Tatsuo","family":"Tsukamoto","sequence":"additional","affiliation":[{"name":"Renal Division, Department of Medicine, Brigham and Women\u2019s Hospital and Harvard Medical School, Boston, Massachusetts 02115; and"}]},{"given":"Adam","family":"Sun","sequence":"additional","affiliation":[{"name":"Renal Division, Rhode Island Hospital, Brown University School of Medicine, Providence, Rhode Island 02903"}]},{"given":"Sanjay K.","family":"Nigam","sequence":"additional","affiliation":[{"name":"Renal Division, Department of Medicine, Brigham and Women\u2019s Hospital and Harvard Medical School, Boston, Massachusetts 02115; and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.123.2.293"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.134.4.1031"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1996.270.5.C1263"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1990.70.4.1029"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1038\/333272a0"},{"issue":"43","key":"B6","first-page":"F1","volume":"274","author":"Denker B. M.","year":"1998","journal-title":"Am. J. Physiol."},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.42.25750"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)81278-7"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.98.6.1973"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199406023302207"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.141.7.1539"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.123.6.1777"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.127.6.1617"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1998.275.3.C798"},{"key":"B15","doi-asserted-by":"crossref","first-page":"3440","DOI":"10.1016\/S0021-9258(19)83641-4","volume":"260","author":"Grynkiewicz G.","year":"1985","journal-title":"J. Biol. Chem."},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.88.8.3460"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.141.1.199"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.95.1.249"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.138.1.181"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.121.3.491"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.124.6.949"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.142.1.101"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.134.4.1003"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.93.16.8584"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1172\/JCI772"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1987.253.1.C171"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1038\/361552a0"},{"key":"B28","doi-asserted-by":"crossref","first-page":"3315","DOI":"10.1242\/jcs.107.12.3315","volume":"107","author":"Mandel L. J.","year":"1994","journal-title":"J. Cell Sci."},{"key":"B29","doi-asserted-by":"crossref","first-page":"2287","DOI":"10.1242\/jcs.109.9.2287","volume":"109","author":"McCarthy K. M.","year":"1996","journal-title":"J. Cell Sci."},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.60.1.121"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1172\/JCI114427"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.108.3.893"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.89.13.6162"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1126\/science.2672330"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.141.2.397"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.137.6.1393"},{"issue":"34","key":"B37","first-page":"F342","volume":"265","author":"Sheridan A. M.","year":"1993","journal-title":"Am. J. Physiol."},{"key":"B38","doi-asserted-by":"crossref","first-page":"367","DOI":"10.1242\/jcs.107.3.367","volume":"107","author":"Stevenson B. R.","year":"1994","journal-title":"J. Cell Sci."},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.103.3.755"},{"key":"B40","first-page":"315","volume":"15","author":"Stuart R. O.","year":"1995","journal-title":"Semin. Nephrol."},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.13.6072"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.23.13636"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.1041590306"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.21.12725"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.26.16133"},{"issue":"45","key":"B45a","first-page":"F737","volume":"276","author":"Tsukamoto T.","year":"1999","journal-title":"Am. J. Physiol."},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.275"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115033"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119584"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.139.3.785"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.120.2.477"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1999.277.4.F524","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:39:15Z","timestamp":1660189155000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1999.277.4.F524"}},"issued":{"date-parts":[[1999,10,1]]},"references-count":51,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1999,10,1]]}},"alternative-id":["10.1152\/ajprenal.1999.277.4.F524"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1999.277.4.f524","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[1999,10,1]]}},{"indexed":{"date-parts":[[2025,10,29]],"date-time":"2025-10-29T13:10:32Z","timestamp":1761743432432},"reference-count":53,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2011,4]]},"abstract":"<jats:p>The effects of Na<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-2Cl<jats:sup>\u2212<\/jats:sup>cotransporter type 2 (NKCC2) isoforms on the regulation of nuclear factor of activated T cells isoform 5 (NFAT5) were determined in mouse medullary thick ascending limb (mTAL) cells exposed to high NaCl concentration. Primary cultures of mTAL cells and freshly isolated mTAL tubules, both derived from the outer medulla (outer stripe&gt;inner stripe), express NKCC2 isoforms A and F. The relative expression of NKCC2A mRNA was approximately twofold greater than NKCC2F in these preparations. The abundance of NKCC2A mRNA, but not NKCC2F mRNA, increased approximately twofold when mTAL cells were exposed for 2 h to a change in osmolality from 300 to 500 mosmol\/kgH<jats:sub>2<\/jats:sub>O, produced with NaCl. Total NKCC2 protein expression also increased. Moreover, a 2.5-fold increase in NFAT5 mRNA accumulation was observed after cells were exposed to 500 mosmol\/kgH<jats:sub>2<\/jats:sub>O for 4 h. Laser-scanning cytometry detected a twofold increase in endogenous NFAT5 protein expression in response to high NaCl concentration. Pretreatment with the loop diuretic bumetanide dramatically reduced transcriptional activity of the NFAT5-specific reporter construct TonE-Luc in mTAL cells exposed to high NaCl. Transient transfection of mTAL cells with shRNA vectors targeting NKCC2A prevented increases in NFAT5 mRNA abundance and protein expression and inhibited NFAT5 transcriptional activity in response to hypertonic stress. Silencing of NKCC2F mRNA did not affect NFAT5 mRNA accumulation but partially inhibited NFAT5 transcriptional activity. These findings suggest that NKCC2A and NKCC2F exhibit differential effects on NFAT5 expression and transcriptional activity in response to hypertonicity produced by high NaCl concentration.<\/jats:p>","DOI":"10.1152\/ajprenal.00408.2010","type":"journal-article","created":{"date-parts":[[2011,1,13]],"date-time":"2011-01-13T03:21:43Z","timestamp":1294888903000},"page":"F966-F975","source":"Crossref","is-referenced-by-count":23,"title":["Differential regulation of NFAT5 by NKCC2 isoforms in medullary thick ascending limb (mTAL) cells"],"prefix":"10.1152","volume":"300","author":[{"given":"Shoujin","family":"Hao","sequence":"first","affiliation":[{"name":"Departments of 1Pharmacology and"}]},{"given":"Hong","family":"Zhao","sequence":"additional","affiliation":[{"name":"Pathology, New York Medical College, Valhalla, New York"}]},{"given":"Zbigniew","family":"Darzynkiewicz","sequence":"additional","affiliation":[{"name":"Pathology, New York Medical College, Valhalla, New York"}]},{"given":"Sailaja","family":"Battula","sequence":"additional","affiliation":[{"name":"Departments of 1Pharmacology and"}]},{"given":"Nicholas R.","family":"Ferreri","sequence":"additional","affiliation":[{"name":"Departments of 1Pharmacology and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00223.2005"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00056.2006"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00448.2004"},{"key":"B4","doi-asserted-by":"crossref","first-page":"327","DOI":"10.1111\/j.1748-1716.2010.02099.x","volume":"199","author":"Carota I","year":"2010","journal-title":"Acta Physiol (Oxf)"},{"key":"B5","first-page":"385","volume":"86","author":"Carroll MA","year":"2003","journal-title":"Methods Mol Med"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00455.2004"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00106.2008"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1097-0320(19981101)33:3<376::AID-CYTO13>3.0.CO;2-Q"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/11.5.1475"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.1.F46"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00426.2006"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1994.266.6.C1568"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/gki701"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/S0076-6879(07)28016-4"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.241637298"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00262.2002"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00011.2004"},{"key":"B18","doi-asserted-by":"crossref","first-page":"17713","DOI":"10.1016\/S0021-9258(17)32499-7","volume":"269","author":"Gamba G","year":"1994","journal-title":"J Biol Chem"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1021\/bi061126x"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M610780200"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.C200021200"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90436.2008"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1984.246.6.F745"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.3.F405"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.39.24556"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.112.5.549"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.12.7179"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.18.11295"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.2006.01551.x"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00145.2006"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1006\/meth.2001.1262"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0308703100"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.13.7214"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1995.269.6.C1496"},{"key":"B35","doi-asserted-by":"crossref","first-page":"25428","DOI":"10.1016\/S0021-9258(19)74059-9","volume":"267","author":"Lytle C","year":"1992","journal-title":"J Biol Chem"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.250"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1016\/S0167-4781(99)00122-0"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.5.2538"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00410.2005"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.3.F347"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.275.6.F885"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006040384"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006091070"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1006\/cyto.1998.0426"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.91.10.4544"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/29.9.e45"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M110442200"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.601"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1038\/ng0696-183"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.090091297"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.165.9.4884"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1086\/301872"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00108.2002"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00408.2010","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,4,3]],"date-time":"2024-04-03T00:21:31Z","timestamp":1712103691000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00408.2010"}},"issued":{"date-parts":[[2011,4]]},"references-count":53,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2011,4]]}},"alternative-id":["10.1152\/ajprenal.00408.2010"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00408.2010","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2011,4]]}},{"indexed":{"date-parts":[[2025,10,28]],"date-time":"2025-10-28T14:57:53Z","timestamp":1761663473289,"version":"3.37.3"},"reference-count":24,"publisher":"American Physiological Society","issue":"11","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2016,6,1]]},"abstract":"<jats:p> Structural studies of the glomerulus, largely undertaken in animal models, have informed our understanding of the progression of chronic kidney disease (CKD) for decades. A fundamental tenet of that understanding is that a loss of podocytes underlies progression in many or most cases of progressive CKD. Recent attempts have been made to reconcile earlier findings from glomerular physiology (the primacy of glomerular capillary hypertension in causation of secondary glomerular sclerosis) with structural findings and have suggested a more detailed model of the mechanisms underlying podocyte detachment as viable cells. A new appreciation of the main locus of mechanical challenges to the podocyte (in the filtration slit) may both explain the renoprotective action of some current therapies and help to suggest novel therapeutic strategies. <\/jats:p>","DOI":"10.1152\/ajprenal.00099.2016","type":"journal-article","created":{"date-parts":[[2016,5,3]],"date-time":"2016-05-03T13:56:33Z","timestamp":1462283793000},"page":"F1385-F1388","source":"Crossref","is-referenced-by-count":23,"title":["Glomerular pathology and the progression of chronic kidney disease"],"prefix":"10.1152","volume":"310","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8342-5458","authenticated-orcid":false,"given":"Kevin V.","family":"Lemley","sequence":"first","affiliation":[{"name":"Department of Pediatrics, University of Southern California Keck School of Medicine, Los Angeles, California; and"},{"name":"Division of Nephrology, Children's Hospital Los Angeles, Los Angeles, California"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI112013"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00223.2013"},{"key":"B3","doi-asserted-by":"crossref","first-page":"556","DOI":"10.1152\/ajplegacy.1974.227.3.556","volume":"227","author":"Deen WM","year":"1974","journal-title":"Am J Physiol"},{"key":"B4","doi-asserted-by":"crossref","first-page":"1178","DOI":"10.1152\/ajplegacy.1972.223.5.1178","volume":"223","author":"Deen WM","year":"1972","journal-title":"Am J Physiol"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.266.1.F1"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2012.06.004"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1038\/nm.1857"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00196.2005"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2012030271"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2011.306"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.01470506"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1097\/01.mnh.0000165884.85803.e1"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00044.x"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014030278"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-016-3358-9."},{"key":"B16a","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00478.2012"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00269.x"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.2337\/db13-0399"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1987.62"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1159\/000188546"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00723.x"},{"key":"B22","first-page":"509","volume":"426","author":"Tenschert S","year":"1995","journal-title":"Virchows Arch"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00404.2002"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1038\/labinvest.2015.118"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00099.2016","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:37:30Z","timestamp":1567975050000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00099.2016"}},"issued":{"date-parts":[[2016,6,1]]},"references-count":24,"journal-issue":{"issue":"11","published-print":{"date-parts":[[2016,6,1]]}},"alternative-id":["10.1152\/ajprenal.00099.2016"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00099.2016","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2016,6,1]]}},{"indexed":{"date-parts":[[2025,10,28]],"date-time":"2025-10-28T05:53:31Z","timestamp":1761630811706},"reference-count":31,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1997,10,1]]},"abstract":"<jats:p>We describe a simplified method for the isolation of large numbers of nephron segments from rat and rabbit kidneys. In contrast to most previous protocols, the kidneys are not perfused. After removal from the animal, the kidney is sliced and torn in pieces that are subsequently digested in culture medium containing 0.5 mg\/ml of collagenase at 37\u00b0C. If the preparation is agitated only very gently and infrequently, then the tissue gradually falls apart into a suspension containing long nephron fragments, often consisting of multiple connected segments. These are easily sorted into homogeneous segment populations that can be used for enzyme assays, protein extraction for immunoblotting, and RNA extraction for reverse transcription-polymerase chain reaction, all of which have been done successfully in our laboratory. For comparison, we have also examined cortical collecting tubule segments and cells prepared by the more rigorous protocol described previously (E. Schlatter, U. Fr\u00f6be, and R. Greger. Pfl\u00fcgers Arch. 421: 381\u2013387, 1992). Even after the isolation of single cells in a Ca<jats:sup>2+<\/jats:sup>-free medium, the cells maintain their normal architecture and a distinct separation of apical and basolateral membranes.<\/jats:p>","DOI":"10.1152\/ajprenal.1997.273.4.f650","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T14:56:01Z","timestamp":1514040961000},"page":"F650-F657","source":"Crossref","is-referenced-by-count":33,"title":["A simplified method for isolation of large numbers of defined nephron segments"],"prefix":"10.1152","volume":"273","author":[{"given":"J. A.","family":"Schafer","sequence":"first","affiliation":[{"name":"Department of Physiology and Biophysics, University of Alabama at Birmingham, Birmingham, Alabama 35294-0005;"}]},{"given":"M. L.","family":"Watkins","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, University of Alabama at Birmingham, Birmingham, Alabama 35294-0005;"}]},{"given":"L.","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, University of Alabama at Birmingham, Birmingham, Alabama 35294-0005;"}]},{"given":"P.","family":"Herter","sequence":"additional","affiliation":[{"name":"Max-Planck Institut f\u00fcr Molekulare Physiologie, 44026 Dortmund; and"}]},{"given":"S.","family":"Haxelmans","sequence":"additional","affiliation":[{"name":"Westf\u00e4lische-Wilhelms-Universit\u00e4t M\u00fcnster, Medizinische Poliklinik, Experimentelle Nephrologie, 48149 M\u00fcnster, Germany"}]},{"given":"E.","family":"Schlatter","sequence":"additional","affiliation":[{"name":"Westf\u00e4lische-Wilhelms-Universit\u00e4t M\u00fcnster, Medizinische Poliklinik, Experimentelle Nephrologie, 48149 M\u00fcnster, Germany"}]}],"member":"24","reference":[{"key":"B1","first-page":"R123","volume":"429","author":"Ankorina I.","year":"1995","journal-title":"Pfl\u00fcgers Arch."},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/S0143-4160(97)90040-3"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1007\/BF00374789"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1007\/BF00374149"},{"key":"B5","doi-asserted-by":"crossref","first-page":"1293","DOI":"10.1152\/ajplegacy.1966.210.6.1293","volume":"210","author":"Burg M.","year":"1966","journal-title":"Am. J. Physiol."},{"key":"B6","doi-asserted-by":"crossref","first-page":"327","DOI":"10.1152\/ajplegacy.1962.203.2.327","volume":"203","author":"Burg M. B.","year":"1962","journal-title":"Am. J. Physiol."},{"key":"B7","doi-asserted-by":"crossref","first-page":"482","DOI":"10.1152\/ajplegacy.1938.123.2.482","volume":"123","author":"Cameron G.","year":"1938","journal-title":"Am. J. Physiol."},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.1030030203"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1042\/bj1300525"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1983.244.3.C211"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1515\/bchm2.1971.352.2.1319"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1007\/BF00374910"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1007\/BF00374148"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.64"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1007\/BF00584645"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1210\/endo-102-4-1254"},{"key":"B17","first-page":"9","volume":"11","author":"Li L.","year":"1997","journal-title":"FASEB J."},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1994.267.4.C901"},{"issue":"9","key":"B19","first-page":"F159","volume":"240","author":"Morel F.","year":"1981","journal-title":"Am. J. Physiol."},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1976.29"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1042\/bj2230353"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1985.227"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1159\/000174042"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1007\/BF00374227"},{"key":"B26","doi-asserted-by":"crossref","first-page":"1223","DOI":"10.1681\/ASN.V641223","volume":"6","author":"Schlatter E.","year":"1995","journal-title":"J. Am. Soc. Nephrol."},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1007\/BF00374587"},{"issue":"40","key":"B28","first-page":"F1158","volume":"271","author":"Schlatter E.","year":"1996","journal-title":"Am. J. Physiol."},{"key":"B29","first-page":"8","volume":"11","author":"Sun D.","year":"1997","journal-title":"FASEB J."},{"key":"B30","first-page":"745","volume":"1","author":"Terada Y.","year":"1990","journal-title":"J. Am. Soc. Nephrol."},{"issue":"39","key":"B31","first-page":"F766","volume":"270","author":"Wilborn T. W.","year":"1996","journal-title":"Am. J. Physiol."},{"key":"B32","doi-asserted-by":"crossref","first-page":"248","DOI":"10.1096\/fasebj.11.4.9068613","volume":"11","author":"Wilborn T. W.","year":"1997","journal-title":"FASEB J."}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1997.273.4.F650","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:47:46Z","timestamp":1660189666000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1997.273.4.F650"}},"issued":{"date-parts":[[1997,10,1]]},"references-count":31,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1997,10,1]]}},"alternative-id":["10.1152\/ajprenal.1997.273.4.F650"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1997.273.4.f650","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1997,10,1]]}},{"indexed":{"date-parts":[[2025,10,29]],"date-time":"2025-10-29T03:44:45Z","timestamp":1761709485277,"version":"3.37.3"},"reference-count":58,"publisher":"American Physiological Society","issue":"3","funder":[{"DOI":"10.13039\/100000062","name":"NIDDK","doi-asserted-by":"crossref","award":["DK64324"],"award-info":[{"award-number":["DK64324"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000041","name":"American Diabetes Association (ADA)","doi-asserted-by":"publisher","award":["4-15-CKD-56"],"award-info":[{"award-number":["4-15-CKD-56"]}],"id":[{"id":"10.13039\/100000041","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2018,9,1]]},"abstract":"<jats:p> The prorenin receptor (PRR) was originally proposed to be a member of the renin-angiotensin system (RAS); however, recent work questioned their association. The present paper describes a functional link between the PRR and RAS in the renal juxtaglomerular apparatus (JGA), a classic anatomical site of the RAS. PRR expression was found in the sensory cells of the JGA, the macula densa (MD), and immunohistochemistry-localized PRR to the MD basolateral cell membrane in mouse, rat, and human kidneys. MD cell PRR activation led to MAP kinase ERK1\/2 signaling and stimulation of PGE<jats:sub>2<\/jats:sub> release, the classic pathway of MD-mediated renin release. Exogenous renin or prorenin added to the in vitro microperfused JGA-induced acute renin release, which was inhibited by removing the MD or by the administration of a PRR decoy peptide. To test the function of MD PRR in vivo, we established a new mouse model with inducible conditional knockout (cKO) of the PRR in MD cells based on neural nitric oxide synthase-driven Cre-lox recombination. Deletion of the MD PRR significantly reduced blood pressure and plasma renin. Challenging the RAS by low-salt diet + captopril treatment caused further significant reductions in blood pressure, renal renin, cyclooxygenase-2, and microsomal PGE synthase expression in cKO vs. wild-type mice. These results suggest that the MD PRR is essential in a novel JGA short-loop feedback mechanism, which is integrated within the classic MD mechanism to control renin synthesis and release and to maintain blood pressure. <\/jats:p>","DOI":"10.1152\/ajprenal.00029.2018","type":"journal-article","created":{"date-parts":[[2018,4,18]],"date-time":"2018-04-18T10:21:50Z","timestamp":1524046910000},"page":"F521-F534","source":"Crossref","is-referenced-by-count":42,"title":["The macula densa prorenin receptor is essential in renin release and blood pressure control"],"prefix":"10.1152","volume":"315","author":[{"given":"Anne D. M.","family":"Riquier-Brison","sequence":"first","affiliation":[{"name":"Departments of Physiology and Neuroscience, and Medicine, Zilkha Neurogenetic Institute, University of Southern California, Los Angeles, California"}]},{"given":"Arnold","family":"Sipos","sequence":"additional","affiliation":[{"name":"Departments of Physiology and Neuroscience, and Medicine, Zilkha Neurogenetic Institute, University of Southern California, Los Angeles, California"}]},{"given":"\u00c1gnes","family":"Pr\u00f3kai","sequence":"additional","affiliation":[{"name":"Departments of Physiology and Neuroscience, and Medicine, Zilkha Neurogenetic Institute, University of Southern California, Los Angeles, California"}]},{"given":"Sarah L.","family":"Vargas","sequence":"additional","affiliation":[{"name":"Departments of Physiology and Neuroscience, and Medicine, Zilkha Neurogenetic Institute, University of Southern California, Los Angeles, California"}]},{"given":"lldik\u00f3","family":"Toma","sequence":"additional","affiliation":[{"name":"Departments of Physiology and Neuroscience, and Medicine, Zilkha Neurogenetic Institute, University of Southern California, Los Angeles, California"}]},{"given":"Elliott J.","family":"Meer","sequence":"additional","affiliation":[{"name":"Departments of Physiology and Neuroscience, and Medicine, Zilkha Neurogenetic Institute, University of Southern California, Los Angeles, California"}]},{"given":"Karie G.","family":"Villanueva","sequence":"additional","affiliation":[{"name":"Departments of Physiology and Neuroscience, and Medicine, Zilkha Neurogenetic Institute, University of Southern California, Los Angeles, California"}]},{"given":"Jennifer C. M.","family":"Chen","sequence":"additional","affiliation":[{"name":"Departments of Physiology and Neuroscience, and Medicine, Zilkha Neurogenetic Institute, University of Southern California, Los Angeles, California"}]},{"given":"Georgina","family":"Gyarmati","sequence":"additional","affiliation":[{"name":"Departments of Physiology and Neuroscience, and Medicine, Zilkha Neurogenetic Institute, University of Southern California, Los Angeles, California"}]},{"given":"Christopher","family":"Yih","sequence":"additional","affiliation":[{"name":"Departments of Physiology and Neuroscience, and Medicine, Zilkha Neurogenetic Institute, University of Southern California, Los Angeles, California"}]},{"given":"Elaine","family":"Tang","sequence":"additional","affiliation":[{"name":"Departments of Physiology and Neuroscience, and Medicine, Zilkha Neurogenetic Institute, University of Southern California, Los Angeles, California"}]},{"given":"Bahram","family":"Nadim","sequence":"additional","affiliation":[{"name":"Departments of Physiology and Neuroscience, and Medicine, Zilkha Neurogenetic Institute, University of Southern California, Los Angeles, California"}]},{"given":"Sujith","family":"Pendekanti","sequence":"additional","affiliation":[{"name":"Departments of Physiology and Neuroscience, and Medicine, Zilkha Neurogenetic Institute, University of Southern California, Los Angeles, California"}]},{"given":"Ingrid M.","family":"Garrelds","sequence":"additional","affiliation":[{"name":"Division of Vascular Medicine and Pharmacology, Department of Internal Medicine, Erasmus MC, Rotterdam, The Netherlands"}]},{"given":"Genevieve","family":"Nguyen","sequence":"additional","affiliation":[{"name":"Centre for Interdisciplinary Research in Biology, UMR INSERM U1050, Coll\u00e8ge de France, Paris, France"}]},{"given":"A. H. Jan","family":"Danser","sequence":"additional","affiliation":[{"name":"Division of Vascular Medicine and Pharmacology, Department of Internal Medicine, Erasmus MC, Rotterdam, The Netherlands"}]},{"given":"J\u00e1nos","family":"Peti-Peterdi","sequence":"additional","affiliation":[{"name":"Departments of Physiology and Neuroscience, and Medicine, Zilkha Neurogenetic Institute, University of Southern California, Los Angeles, California"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.109.128645"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.268.5.F885"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1979.237.5.F333"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.111.180737"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1172\/JCI71702"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00011.2009"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1126\/science.1179802"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.29.6.1240"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007091030"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00433.2002"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00267.2014"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.110.167957"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.112.196303"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1097\/MAJ.0000000000000335"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1172\/JCI65460"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1038\/nm.3405"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.111.186056"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000011"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1172\/JCI21398"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000215838.48170.0b"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006010029"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.3.F659"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5001627"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00521.2005"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00492.2015"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1602397113"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00204.2012"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1992.382"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1002\/dvg.20335"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5001723"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1172\/JCI0214276"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00178.2016"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00425.2005"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00420.2003"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009070759"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1172\/JCI200318018"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1215927110"},{"key":"B38","first-page":"26","volume":"13","author":"Prieto MC","year":"2013","journal-title":"Ochsner J"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00152.2017"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00476.2016"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00126.2015"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00088.2016"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2011020200"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.275.1.F46"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.115.07012"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1016\/j.amjms.2017.05.018"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1167\/iovs.06-0534"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2010.151"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008101099"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1016\/j.ydbio.2015.11.024"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1016\/j.phrs.2017.05.016"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuron.2011.07.026"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1159\/000090622"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1172\/JCI33293"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2015080915"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008070740"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2017030295"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1186\/s12916-015-0514-1"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00029.2018","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,24]],"date-time":"2019-09-24T10:22:56Z","timestamp":1569320576000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00029.2018"}},"issued":{"date-parts":[[2018,9,1]]},"references-count":58,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2018,9,1]]}},"alternative-id":["10.1152\/ajprenal.00029.2018"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00029.2018","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2018,9,1]]}},{"indexed":{"date-parts":[[2025,10,29]],"date-time":"2025-10-29T03:36:51Z","timestamp":1761709011418,"version":"3.40.4"},"reference-count":53,"publisher":"American Physiological Society","issue":"12","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2014,12,15]]},"abstract":"<jats:p>Hyperfiltration subjects podocytes to increased tensile stress and fluid flow shear stress (FFSS). We showed a 1.5- to 2.0-fold increase in FFSS in uninephrectomized animals and altered podocyte actin cytoskeleton and increased synthesis of prostaglandin E<jats:sub>2<\/jats:sub>(PGE<jats:sub>2<\/jats:sub>) following in vitro application of FFSS. We hypothesized that increased FFSS mediates cellular changes through specific receptors of PGE<jats:sub>2<\/jats:sub>. Presently, we studied the effect of FFSS on cultured podocytes and decapsulated isolated glomeruli in vitro, and on solitary kidney in uninephrectomized sv129 mice. In cultured podocytes, FFSS resulted in increased gene and protein expression of cyclooxygenase (COX)-2 but not COX-1, prostanoid receptor EP2 but not EP4, and increased synthesis and secretion of PGE<jats:sub>2<\/jats:sub>, which were effectively blocked by indomethacin. Next, we developed a special flow chamber for applying FFSS to isolated glomeruli to determine its effect on an intact glomerular filtration barrier by measuring change in albumin permeability ( P<jats:sub>alb<\/jats:sub>) in vitro. FFSS caused an increase in P<jats:sub>alb<\/jats:sub>that was blocked by indomethacin ( P &lt; 0.001). Finally, we show that unilateral nephrectomy in sv129 mice resulted in glomerular hypertrophy ( P = 0.006), increased glomerular expression of COX-2 ( P &lt; 0.001) and EP2 ( P = 0.039), and increased urinary albumin excretion ( P = 0.001). Activation of the COX-2-PGE<jats:sub>2<\/jats:sub>-EP2 axis appears to be a specific response to FFSS in podocytes and provides a mechanistic basis for alteration in podocyte structure and the glomerular filtration barrier, leading to albuminuria in hyperfiltration-mediated kidney injury. The COX-2-PGE<jats:sub>2<\/jats:sub>-EP2 axis is a potential target for developing specific interventions to ameliorate the effects of hyperfiltration-mediated kidney injury in the progression of chronic kidney disease.<\/jats:p>","DOI":"10.1152\/ajprenal.00335.2014","type":"journal-article","created":{"date-parts":[[2014,9,19]],"date-time":"2014-09-19T04:46:29Z","timestamp":1411101989000},"page":"F1323-F1333","source":"Crossref","is-referenced-by-count":27,"title":["Cyclooxygenase-2, prostaglandin E<sub>2<\/sub>, and prostanoid receptor EP2 in fluid flow shear stress-mediated injury in the solitary kidney"],"prefix":"10.1152","volume":"307","author":[{"given":"Tarak","family":"Srivastava","sequence":"first","affiliation":[{"name":"Section of Nephrology, Children's Mercy Hospital and University of Missouri-Kansas City, Kansas City, Missouri;"},{"name":"Renal Research Laboratory, Research and Development, Kansas City Veterans Affairs Medical Center, Kansas City, Missouri;"}]},{"given":"Uri S.","family":"Alon","sequence":"additional","affiliation":[{"name":"Section of Nephrology, Children's Mercy Hospital and University of Missouri-Kansas City, Kansas City, Missouri;"}]},{"given":"Patricia A.","family":"Cudmore","sequence":"additional","affiliation":[{"name":"Section of Nephrology, Children's Mercy Hospital and University of Missouri-Kansas City, Kansas City, Missouri;"}]},{"given":"Belal","family":"Tarakji","sequence":"additional","affiliation":[{"name":"Section of Nephrology, Children's Mercy Hospital and University of Missouri-Kansas City, Kansas City, Missouri;"}]},{"given":"Alexander","family":"Kats","sequence":"additional","affiliation":[{"name":"Department of Pathology and Laboratory Medicine, Children's Mercy Hospital and University of Missouri-Kansas City, Kansas City, Missouri;"}]},{"given":"Robert E.","family":"Garola","sequence":"additional","affiliation":[{"name":"Department of Pathology and Laboratory Medicine, Children's Mercy Hospital and University of Missouri-Kansas City, Kansas City, Missouri;"}]},{"given":"R. Scott","family":"Duncan","sequence":"additional","affiliation":[{"name":"Section of Infectious Diseases, Children's Mercy Hospital and University of Missouri-Kansas City, Kansas City, Missouri;"}]},{"given":"Ellen T.","family":"McCarthy","sequence":"additional","affiliation":[{"name":"Kidney Institute, University of Kansas Medical Center, Kansas City, Kansas;"}]},{"given":"Ram","family":"Sharma","sequence":"additional","affiliation":[{"name":"Renal Research Laboratory, Research and Development, Kansas City Veterans Affairs Medical Center, Kansas City, Missouri;"}]},{"given":"Mark L.","family":"Johnson","sequence":"additional","affiliation":[{"name":"Department of Oral Biology, University of Missouri-Kansas City School of Dentistry, Kansas City, Missouri; and"}]},{"given":"Lynda F.","family":"Bonewald","sequence":"additional","affiliation":[{"name":"Department of Oral Biology, University of Missouri-Kansas City School of Dentistry, Kansas City, Missouri; and"}]},{"given":"Ashraf","family":"El-Meanawy","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Medical College of Wisconsin, Milwaukee, Wisconsin"}]},{"given":"Virginia J.","family":"Savin","sequence":"additional","affiliation":[{"name":"Kidney Institute, University of Kansas Medical Center, Kansas City, Kansas;"},{"name":"Renal Research Laboratory, Research and Development, Kansas City Veterans Affairs Medical Center, Kansas City, Missouri;"}]},{"given":"Mukut","family":"Sharma","sequence":"additional","affiliation":[{"name":"Kidney Institute, University of Kansas Medical Center, Kansas City, Kansas;"},{"name":"Renal Research Laboratory, Research and Development, Kansas City Veterans Affairs Medical Center, Kansas City, Missouri;"}]}],"member":"24","reference":[{"key":"B1","first-page":"S124","author":"Brenner BM","year":"1997","journal-title":"Kidney Int"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.270.5.F912"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00634.2013"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1007\/BF00858530"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1991.tb09109.x"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1210\/endo.142.8.8338"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M302993200"},{"key":"B8","first-page":"451","volume":"20","author":"Christinasen JS","year":"1981","journal-title":"Diabetlogia"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000153791.89776.43"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00362.x"},{"key":"B11","doi-asserted-by":"crossref","first-page":"413","DOI":"10.1681\/ASN.V123413","volume":"12","author":"Endlich N","year":"2001","journal-title":"J Am Soc Nephrol"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/j.cellsig.2008.08.007"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1016\/j.cellsig.2010.03.014"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1172\/JCI0216044"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00169.2012"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1002\/jbmr.5650111112"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00196.2005"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.166.7.4689"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1998.9540"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa020549"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1002\/jbmr.168"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.272.4.F460"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00327.2013"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00067.2003"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00331.2003"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00172.x"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1096\/fj.04-2210fje"},{"key":"B28","doi-asserted-by":"crossref","first-page":"1851","DOI":"10.1681\/ASN.V1091851","volume":"10","author":"Morath R","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1999.79.4.1193"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.252.5.F829"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(12)70174-9"},{"key":"B32","doi-asserted-by":"crossref","first-page":"1031","DOI":"10.1016\/S0026-895X(25)09407-6","volume":"50","author":"Nishigaki N","year":"1996","journal-title":"Mol Pharmacol"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005010029"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2009.220"},{"key":"B35","doi-asserted-by":"crossref","first-page":"1260","DOI":"10.1681\/ASN.V361260","volume":"3","author":"Savin VJ","year":"1992","journal-title":"J Am Soc Nephrol"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199604043341402"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1177\/153537020623100112"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1177\/153537020422900111"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.2741\/1853"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gft387"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1007\/s12079-010-0088-9"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1016\/j.prostaglandins.2012.11.001"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1159\/000183676"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009121234"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1016\/S0025-6196(12)60980-X"},{"key":"B46","first-page":"105","volume":"25","author":"Vriesendorp R","year":"1986","journal-title":"Clin Nephrol"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1016\/0002-9343(86)90910-1"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00093.x"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.275.4.F613"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000158434.69180.2D"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1542\/peds.2012-2088"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfq844"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gft012"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00335.2014","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,5,4]],"date-time":"2025-05-04T18:28:02Z","timestamp":1746383282000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00335.2014"}},"issued":{"date-parts":[[2014,12,15]]},"references-count":53,"journal-issue":{"issue":"12","published-print":{"date-parts":[[2014,12,15]]}},"alternative-id":["10.1152\/ajprenal.00335.2014"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00335.2014","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2014,12,15]]}},{"indexed":{"date-parts":[[2025,10,29]],"date-time":"2025-10-29T03:25:17Z","timestamp":1761708317846},"reference-count":13,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2009,4]]},"DOI":"10.1152\/ajprenal.00007.2009","type":"journal-article","created":{"date-parts":[[2009,2,5]],"date-time":"2009-02-05T01:55:59Z","timestamp":1233798959000},"page":"F689-F690","source":"Crossref","is-referenced-by-count":18,"title":["PiT-2 Coming Out of the Pits"],"prefix":"10.1152","volume":"296","author":[{"given":"Orson W.","family":"Moe","sequence":"first","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2006.07.001"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1007\/s002329900394"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1983.245.2.F175"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-003-1088-x"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1210\/jc.2004-1039"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1007\/s00774-007-0779-3"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.91.15.7071"},{"key":"R8","doi-asserted-by":"crossref","unstructured":"Miller DG, Miller AD.A family of retroviruses that utilize related phosphate transporters for cell entry.J Virol68: 8270\u20138276, 1994.","DOI":"10.1128\/JVI.68.12.8270-8276.1994"},{"key":"R9","unstructured":"Moe OW, Palacin M, Wright S.Renal organic solute transport. In:Brenner and Rector's The Kidney, edited by Brenner BM. Philadelphia, PA: Saunders Elsevier, 2007, p. 214\u2013247."},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002000"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00064.2007"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90623.2008"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00228.2007"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00007.2009","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2020,5,15]],"date-time":"2020-05-15T10:45:34Z","timestamp":1589539534000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00007.2009"}},"issued":{"date-parts":[[2009,4]]},"references-count":13,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2009,4]]}},"alternative-id":["10.1152\/ajprenal.00007.2009"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00007.2009","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2009,4]]}},{"indexed":{"date-parts":[[2025,12,13]],"date-time":"2025-12-13T07:06:52Z","timestamp":1765609612194},"reference-count":47,"publisher":"American Physiological Society","issue":"11","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2014,6,1]]},"abstract":"<jats:p>A mathematical model of renal hemodynamics was used to assess the individual contributions of the tubuloglomerular feedback (TGF) mechanism and the myogenic response to glomerular filtration rate regulation in the rat kidney. The model represents an afferent arteriole segment, glomerular filtration, and a short loop of Henle. The afferent arteriole model exhibits myogenic response, which is activated by hydrostatic pressure variations to induce changes in membrane potential and vascular muscle tone. The tubule model predicts tubular fluid and Cl<jats:sup>\u2212<\/jats:sup>transport. Macula densa Cl<jats:sup>\u2212<\/jats:sup>concentration is sensed as the signal for TGF, which acts to constrict or dilate the afferent arteriole. With this configuration, the model afferent arteriole maintains stable glomerular filtration rate within a physiologic range of perfusion pressure (80\u2013180 mmHg). The contribution of TGF to overall autoregulation is significant only within a narrow band of perfusion pressure values (80\u2013110 mmHg). Model simulations of ramp-like perfusion pressure perturbations agree well with findings by Flemming et al. (Flemming B, Arenz N, Seeliger E, Wronski T, Steer K, Persson PB. J Am Soc Nephrol 12: 2253\u20132262, 2001), which indicate that changes in vascular conductance are markedly sensitive to pressure velocity. That asymmetric response is attributed to the rate-dependent kinetics of the myogenic mechanism. Moreover, simulations of renal autoregulation in diabetes mellitus predict that, due to the impairment of the voltage-gated Ca<jats:sup>2+<\/jats:sup>channels of the afferent arteriole smooth muscle cells, the perfusion pressure range in which single-nephron glomerular filtration rate remains stable is reduced by \u223c70% and that TGF gain is reduced by nearly 40%, consistent with experimental findings.<\/jats:p>","DOI":"10.1152\/ajprenal.00649.2013","type":"journal-article","created":{"date-parts":[[2014,3,13]],"date-time":"2014-03-13T04:09:24Z","timestamp":1394683764000},"page":"F1357-F1371","source":"Crossref","is-referenced-by-count":46,"title":["Theoretical assessment of renal autoregulatory mechanisms"],"prefix":"10.1152","volume":"306","author":[{"given":"Ioannis","family":"Sgouralis","sequence":"first","affiliation":[{"name":"Department of Mathematics, Duke University, Durham, North Carolina"}]},{"given":"Anita T.","family":"Layton","sequence":"additional","affiliation":[{"name":"Department of Mathematics, Duke University, Durham, North Carolina"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00261.2008"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1985.248.2.F163"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1172\/JCI114700"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.256.6.F1000"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.109.133777"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00262.2008"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1080\/10739680590934745"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.258.1.F94"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119075"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00382.2010"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1172\/JCI107422"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.259.4.F715"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00194.2006"},{"key":"B14","doi-asserted-by":"crossref","first-page":"1178","DOI":"10.1152\/ajplegacy.1972.223.5.1178","volume":"223","author":"Deen WM","year":"1972","journal-title":"Am J Physiol"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.4.F581"},{"key":"B16","doi-asserted-by":"crossref","first-page":"2253","DOI":"10.1681\/ASN.V12112253","volume":"12","author":"Flemming B","year":"2001","journal-title":"J Am Soc Nephrol"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1990.95"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-8703(99)70312-1"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1007\/BF00585066"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.261.5.F880"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1994.74.3.637"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00417.2010"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00332.2006"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1002\/cnm.1475"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.261.5.F904"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.268.1.F163"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-201X.2004.01312.x"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000024262.11534.18"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00402.2005"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00539.2004"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00540.2004"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90669.2008"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1007\/BF02460464"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1978.234.5.F357"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002190"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00589.2011"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1007\/s11538-013-9907-5"},{"key":"B38","doi-asserted-by":"crossref","first-page":"676","DOI":"10.1152\/ajplegacy.1951.167.3.676","volume":"167","author":"Shipley RE","year":"1951","journal-title":"Am J Physiol"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00114.2009"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1172\/JCI10963"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.06713.x"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007121326"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00809.2010"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.6.F876"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1146\/annurev-physiol-020911-153333"},{"key":"B46","first-page":"F855","volume":"276","author":"van Dokkum RP","year":"1999","journal-title":"Am J Physiol Renal Physiol"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00490.2007"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00649.2013","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,3,29]],"date-time":"2022-03-29T21:36:54Z","timestamp":1648589814000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00649.2013"}},"issued":{"date-parts":[[2014,6,1]]},"references-count":47,"journal-issue":{"issue":"11","published-print":{"date-parts":[[2014,6,1]]}},"alternative-id":["10.1152\/ajprenal.00649.2013"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00649.2013","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2014,6,1]]}},{"indexed":{"date-parts":[[2025,12,23]],"date-time":"2025-12-23T05:25:42Z","timestamp":1766467542668,"version":"3.37.3"},"reference-count":44,"publisher":"American Physiological Society","issue":"7","funder":[{"DOI":"10.13039\/501100003725","name":"National Research Foundation of Korea (NRF)","doi-asserted-by":"publisher","award":["2010-0019393","2013R1A1A2007266","2014R1A5A2009242"],"award-info":[{"award-number":["2010-0019393","2013R1A1A2007266","2014R1A5A2009242"]}],"id":[{"id":"10.13039\/501100003725","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2015,4,1]]},"abstract":"<jats:p>Kidney collecting duct cells are continuously exposed to the changes of extracellular pH (pH<jats:sub>e<\/jats:sub>). We aimed to study the effects of altered pH<jats:sub>e<\/jats:sub>on desmopressin (dDAVP)-induced phosphorylation (Ser<jats:sup>256<\/jats:sup>, Ser<jats:sup>261<\/jats:sup>, Ser<jats:sup>264<\/jats:sup>, and Ser<jats:sup>269<\/jats:sup>) and apical targeting of aquaporin-2 (AQP2) in rat kidney inner medullary collecting duct (IMCD) cells. When freshly prepared IMCD tubule suspensions exposed to HEPES buffer with pH 5.4, 6.4, 7.4, or 8.4 for 1 h were stimulated with dDAVP (10<jats:sup>\u221210<\/jats:sup>M, 3 min), AQP2 phosphorylation at Ser<jats:sup>256<\/jats:sup>, Ser<jats:sup>264<\/jats:sup>, and Ser<jats:sup>269<\/jats:sup>was significantly attenuated under acidic conditions. Next, IMCD cells primary cultured in transwell chambers were exposed to a transepithelial pH gradient for 1 h (apical pH 6.4, 7.4, or 8.4 vs. basolateral pH 7.4 and vice versa). Immunocytochemistry and cell surface biotinylation assay revealed that exposure to either apical pH 6.4 or basolateral pH 6.4 for 1 h was associated with decreased dDAVP (10<jats:sup>\u22129<\/jats:sup>M, 15 min, basolateral)-induced apical targeting of AQP2 and surface expression of AQP2. Fluorescence resonance energy transfer analysis revealed that the dDAVP (10<jats:sup>\u22129<\/jats:sup>M)-induced increase of PKA activity was significantly attenuated when LLC-PK1 cells were exposed to pH<jats:sub>e<\/jats:sub>6.4 compared with pH<jats:sub>e<\/jats:sub>7.4 and 8.4. In contrast, forskolin (10<jats:sup>\u22127<\/jats:sup>M)-induced PKA activation and dDAVP (10<jats:sup>\u22129<\/jats:sup>M)-induced increases of intracellular Ca<jats:sup>2+<\/jats:sup>were not affected. Taken together, dDAVP-induced phosphorylation and apical targeting of AQP2 are attenuated in IMCD cells under acidic pH<jats:sub>e<\/jats:sub>, likely via an inhibition of vasopressin V2 receptor-G protein-cAMP-PKA actions.<\/jats:p>","DOI":"10.1152\/ajprenal.00376.2014","type":"journal-article","created":{"date-parts":[[2015,1,29]],"date-time":"2015-01-29T05:31:17Z","timestamp":1422509477000},"page":"F737-F748","source":"Crossref","is-referenced-by-count":24,"title":["Extracellular pH affects phosphorylation and intracellular trafficking of AQP2 in inner medullary collecting duct cells"],"prefix":"10.1152","volume":"308","author":[{"given":"Hyo-Jung","family":"Choi","sequence":"first","affiliation":[{"name":"Department of Biochemistry and Cell Biology, School of Medicine, Kyungpook National University, Taegu, Korea; and"},{"name":"BK21 Plus KNU Biomedical Convergence Program, Department of Biomedical Science, Kyungpook National University, Taegu, Korea"}]},{"given":"Hyun Jun","family":"Jung","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Cell Biology, School of Medicine, Kyungpook National University, Taegu, Korea; and"}]},{"given":"Tae-Hwan","family":"Kwon","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Cell Biology, School of Medicine, Kyungpook National University, Taegu, Korea; and"},{"name":"BK21 Plus KNU Biomedical Convergence Program, Department of Biomedical Science, Kyungpook National University, Taegu, Korea"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1996.sp021396"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-008-0498-1"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1988.255.6.C844"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1979.66"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M408565200"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M005552200"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.23.14800"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/361549a0"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00249.2013"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M803074200"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00284.2006"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0600895103"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.262.5.F784"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1039\/C0IB00018C"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00519.2010"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00270.2012"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.E11-01-0072"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbagen.2013.12.002"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.275.5.F724"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/j.krcp.2013.07.005"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1007\/978-3-540-79885-9_5"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1007\/s00240-013-0546-y"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00117.2011"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00090.2006"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1038\/sj.embor.embor711"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1983.245.2.F188"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-012-1129-4"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1038\/hr.2009.19"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0400417101"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1007\/978-3-540-79885-9_6"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00024.2001"},{"key":"B32","doi-asserted-by":"crossref","first-page":"647","DOI":"10.1681\/ASN.V103647","volume":"10","author":"Nielsen S","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1983.244.6.F712"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00469.2012"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.253.2.F251"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00257.2001"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1177\/0192623309332990"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1007\/s004240100590"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2006.09.004"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118044"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1210\/en.2005-0868"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.272.4.F443"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.90650.2007"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.412"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00376.2014","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,4,27]],"date-time":"2022-04-27T22:21:26Z","timestamp":1651098086000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00376.2014"}},"issued":{"date-parts":[[2015,4,1]]},"references-count":44,"journal-issue":{"issue":"7","published-print":{"date-parts":[[2015,4,1]]}},"alternative-id":["10.1152\/ajprenal.00376.2014"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00376.2014","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2015,4,1]]}},{"indexed":{"date-parts":[[2025,12,26]],"date-time":"2025-12-26T22:09:06Z","timestamp":1766786946342},"reference-count":72,"publisher":"American Physiological Society","issue":"4","funder":[{"name":"European Union's Seventh Framework Program","award":["317246"],"award-info":[{"award-number":["317246"]}]},{"name":"Dutch Technology Foundation Stichting Technische Wetenschappen","award":["11823"],"award-info":[{"award-number":["11823"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2017,4,1]]},"abstract":"<jats:p> Polycystic kidney disease (PKD) is a major cause of end-stage renal disease. The disease mechanisms are not well understood and the pathogenesis toward renal failure remains elusive. In this study, we present the first RNASeq analysis of a Pkd1-mutant mouse model in a combined meta-analysis with other published PKD expression profiles. We introduce the PKD Signature, a set of 1,515 genes that are commonly dysregulated in PKD studies. We show that the signature genes include many known and novel PKD-related genes and functions. Moreover, genes with a role in injury repair, as evidenced by expression data and\/or automated literature analysis, were significantly enriched in the PKD Signature, with 35% of the PKD Signature genes being directly implicated in injury repair. NF-\u03baB signaling, epithelial-mesenchymal transition, inflammatory response, hypoxia, and metabolism were among the most prominent injury or repair-related biological processes with a role in the PKD etiology. Novel PKD genes with a role in PKD and in injury were confirmed in another Pkd1-mutant mouse model as well as in animals treated with a nephrotoxic agent. We propose that compounds that can modulate the injury-repair response could be valuable drug candidates for PKD treatment. <\/jats:p>","DOI":"10.1152\/ajprenal.00653.2016","type":"journal-article","created":{"date-parts":[[2017,2,2]],"date-time":"2017-02-02T01:20:16Z","timestamp":1485998416000},"page":"F806-F817","source":"Crossref","is-referenced-by-count":29,"title":["Meta-analysis of polycystic kidney disease expression profiles defines strong involvement of injury repair processes"],"prefix":"10.1152","volume":"312","author":[{"given":"Tareq B.","family":"Malas","sequence":"first","affiliation":[{"name":"Department of Human Genetics, Leiden University Medical Center, Leiden, The Netherlands; and"}]},{"given":"Chiara","family":"Formica","sequence":"additional","affiliation":[{"name":"Department of Human Genetics, Leiden University Medical Center, Leiden, The Netherlands; and"}]},{"given":"Wouter N.","family":"Leonhard","sequence":"additional","affiliation":[{"name":"Department of Human Genetics, Leiden University Medical Center, Leiden, The Netherlands; and"}]},{"given":"Pooja","family":"Rao","sequence":"additional","affiliation":[{"name":"GenomeScan, Leiden, The Netherlands"}]},{"given":"Zoraide","family":"Granchi","sequence":"additional","affiliation":[{"name":"GenomeScan, Leiden, The Netherlands"}]},{"given":"Marco","family":"Roos","sequence":"additional","affiliation":[{"name":"Department of Human Genetics, Leiden University Medical Center, Leiden, The Netherlands; and"}]},{"given":"Dorien J. M.","family":"Peters","sequence":"additional","affiliation":[{"name":"Department of Human Genetics, Leiden University Medical Center, Leiden, The Netherlands; and"}]},{"given":"Peter A. C.","family":"'t Hoen","sequence":"additional","affiliation":[{"name":"Department of Human Genetics, Leiden University Medical Center, Leiden, The Netherlands; and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/j.ccr.2011.09.006"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2011.217"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1093\/bioinformatics\/btu638"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(95)90339-9"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1007\/BF02536384"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010050526"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.18632\/aging.100900"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.3349\/ymj.2009.50.1.105"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/j.freeradbiomed.2010.12.025"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1186\/1756-0500-1-131"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014111138"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0049569"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.15586\/codon.pkd.2015.ch7"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/j.matbio.2011.07.004"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1186\/gb-2004-5-10-r80"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/ddp190"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1002\/path.2734"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.12688\/f1000research.4830.1"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/gkn923"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1038\/nprot.2008.211"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/j.ygeno.2004.03.009"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1186\/gb-2008-9-6-r96"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.14670\/HH-25.1481"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1093\/bioinformatics\/btp354"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00783.x"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1186\/gb-2013-14-4-r36"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.01722-07"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/gku1057"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2011-02-338061"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00470.2010"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1038\/nmeth.1923"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/ddm299"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013080864"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1016\/j.cels.2015.12.004"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1172\/JCI72126"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M111.279836"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1002\/wsbm.1289"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1016\/j.ebiom.2016.01.027"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pgen.1003053"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1126\/science.272.5266.1339"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1093\/bioinformatics\/btn654"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2011040340"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/physiolgenomics.00187.2011"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1186\/1752-0509-5-56"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1159\/000315859"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1186\/1471-2369-8-12"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/ddn045"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.520"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1016\/j.ccr.2007.02.005"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1172\/JCI36150"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000309"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/gkv007"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1038\/nm.3092"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfl071"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0509694103"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/ddp165"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0126622"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1093\/bioinformatics\/btm369"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0506580102"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2012.446"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1111\/nep.12045"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/ddp147"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1159\/000354057"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbadis.2011.01.011"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa1205511"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.pharmtox.48.113006.094615"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1038\/ng833"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.1038\/nature01262"},{"key":"B69","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00275.2007"},{"key":"B70","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(12)80338-6"},{"key":"B71","doi-asserted-by":"publisher","DOI":"10.1159\/000324407"},{"key":"B72","doi-asserted-by":"publisher","DOI":"10.1152\/physiolgenomics.00223.2005"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00653.2016","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T06:09:06Z","timestamp":1568009346000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00653.2016"}},"issued":{"date-parts":[[2017,4,1]]},"references-count":72,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2017,4,1]]}},"alternative-id":["10.1152\/ajprenal.00653.2016"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00653.2016","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2017,4,1]]}},{"indexed":{"date-parts":[[2025,12,24]],"date-time":"2025-12-24T20:54:40Z","timestamp":1766609680476},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1985,4,1]]},"abstract":"<jats:p> Metabolism of glutamine results in the net production of ATP; however, cells cannot sustain an ATP production rate greater than their rate of ATP utilization. The purpose of these studies was to determine whether the rate of ATP turnover in the kidney could set an upper limit on renal glutamine metabolism and thereby renal ammoniagenesis. The acidotic dog kidneys extracted glutamine, lactate, citrate, and oxygen from the arterial blood and added ammonium and alanine to the venous blood. Renal glutamine metabolism was responsible for almost all the ammonium production. Renal ATP production was estimated from the rate of oxygen consumption and appeared to be derived roughly equally from the oxidation of glutamine and lactate. There was no apparent renal glucose production from ATP balance calculations and this impression was supported when the inhibitor of gluconeogenesis, 3-mercaptopicolinate, did not inhibit ammoniagenesis. Approximately 90% of the ATP synthesized was utilized to reabsorb sodium. When the amount of ATP utilized for sodium reabsorption in the proximal convoluted tubule (assumed to be 60% of filtered sodium) was compared with the amount of ATP produced from glutamine metabolism, the values were similar despite the fact that the glomerular filtration rate in individual dogs varied more than fourfold. When the quantity of ATP expended for sodium reabsorption was decreased by the infusion of ouabain or by the constriction of one renal artery without reducing glutamine delivery, the kidney lowered its rate of ammoniagenesis to a quantitatively predictable amount.(ABSTRACT TRUNCATED AT 250 WORDS) <\/jats:p>","DOI":"10.1152\/ajprenal.1985.248.4.f607","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T19:30:23Z","timestamp":1513971023000},"page":"F607-F615","source":"Crossref","is-referenced-by-count":5,"title":["Regulation of the maximum rate of renal ammoniagenesis in the acidotic dog"],"prefix":"10.1152","volume":"248","author":[{"given":"M. L.","family":"Halperin","sequence":"first","affiliation":[]},{"given":"P.","family":"Vinay","sequence":"additional","affiliation":[]},{"given":"A.","family":"Gougoux","sequence":"additional","affiliation":[]},{"given":"C.","family":"Pichette","sequence":"additional","affiliation":[]},{"given":"R. L.","family":"Jungas","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1985.248.4.F607","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:32:01Z","timestamp":1567956721000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1985.248.4.F607"}},"issued":{"date-parts":[[1985,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1985,4,1]]}},"alternative-id":["10.1152\/ajprenal.1985.248.4.F607"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1985.248.4.f607","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1985,4,1]]}},{"indexed":{"date-parts":[[2025,12,29]],"date-time":"2025-12-29T11:27:31Z","timestamp":1767007651938},"reference-count":21,"publisher":"American Physiological Society","issue":"12","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2012,6,15]]},"abstract":"<jats:p>Urea functions as a key osmolyte in the urinary concentrating mechanism of the inner medulla. The urea transporter UT-A1 is upregulated by antidiuretic hormone, facilitating faster equilibration of urea between the lumen and interstitium of the inner medullary collecting duct, resulting in the formation of more highly concentrated urine. New methods in dynamic nuclear polarization, providing \u223c50,000-fold enhancement of nuclear magnetic resonance signals in the liquid state, offer a novel means to monitor this process in vivo using magnetic resonance imaging. In this study, we detected significant signal differences in the rat kidney between acute diuretic and antidiuretic states, using dynamic<jats:sup>13<\/jats:sup>C magnetic resonance imaging following a bolus infusion of hyperpolarized [<jats:sup>13<\/jats:sup>C]urea. More rapid medullary enhancement was observed under antidiuresis, consistent with known upregulation of UT-A1.<\/jats:p>","DOI":"10.1152\/ajprenal.00640.2011","type":"journal-article","created":{"date-parts":[[2012,4,5]],"date-time":"2012-04-05T04:32:39Z","timestamp":1333600359000},"page":"F1658-F1662","source":"Crossref","is-referenced-by-count":46,"title":["Monitoring urea transport in rat kidney in vivo using hyperpolarized<sup>13<\/sup>C magnetic resonance imaging"],"prefix":"10.1152","volume":"302","author":[{"given":"Cornelius","family":"von Morze","sequence":"first","affiliation":[{"name":"Department of Radiology and Biomedical Imaging, University of California, San Francisco, San Francisco, California; and"}]},{"given":"Robert A.","family":"Bok","sequence":"additional","affiliation":[{"name":"Department of Radiology and Biomedical Imaging, University of California, San Francisco, San Francisco, California; and"}]},{"given":"Jeff M.","family":"Sands","sequence":"additional","affiliation":[{"name":"Department of Medicine, Renal Division, Emory University, Atlanta, Georgia"}]},{"given":"John","family":"Kurhanewicz","sequence":"additional","affiliation":[{"name":"Department of Radiology and Biomedical Imaging, University of California, San Francisco, San Francisco, California; and"}]},{"given":"Daniel B.","family":"Vigneron","sequence":"additional","affiliation":[{"name":"Department of Radiology and Biomedical Imaging, University of California, San Francisco, San Francisco, California; and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1733835100"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.2967\/jnumed.110.075895"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00424.2009"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0401704101"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.1970.tb12899.x"},{"key":"B6","doi-asserted-by":"crossref","first-page":"424","DOI":"10.1681\/ASN.V73424","volume":"7","author":"Fransen R","year":"1996","journal-title":"J Am Soc Nephrol"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1733836100"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0601319103"},{"key":"B9","unstructured":"Haacke EM, Brown RW, Thompson MR, Venkatesan R.Magnetic resonance imaging: physical principles and sequence design. New York: Wiley, 1999, p. 876."},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.1.F62"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006030246"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00210.x"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1148\/radiol.2423061640"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1593\/neo.101102"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1096\/fj.06-6979com"},{"key":"B16","first-page":"177","volume":"7","author":"McCullough PA","year":"2006","journal-title":"Rev Cardiovasc Med"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1172\/JCI105387"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2009.03.008"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1007\/BF00581179"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1002\/jmri.22484"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.0054.2001"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00640.2011","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,1,12]],"date-time":"2022-01-12T06:27:53Z","timestamp":1641968873000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00640.2011"}},"issued":{"date-parts":[[2012,6,15]]},"references-count":21,"journal-issue":{"issue":"12","published-print":{"date-parts":[[2012,6,15]]}},"alternative-id":["10.1152\/ajprenal.00640.2011"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00640.2011","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2012,6,15]]}},{"indexed":{"date-parts":[[2026,1,2]],"date-time":"2026-01-02T17:25:34Z","timestamp":1767374734949,"version":"3.35.0"},"reference-count":46,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2008,9]]},"abstract":"<jats:p>The present study was performed to test the hypothesis that under normal physiological conditions and\/or during augmentation of kinin levels, intrarenal kinins act on medullary bradykinin B<jats:sub>2<\/jats:sub>(BKB<jats:sub>2<\/jats:sub>) receptors to acutely increase papillary blood flow (PBF) and therefore Na<jats:sup>+<\/jats:sup>excretion. We determined the effect of acute inner medullary interstitial (IMI) BKB<jats:sub>2<\/jats:sub>receptor blockade on renal hemodynamics and excretory function in rats fed either a normal (0.23%)- or a low (0.08%)-NaCl diet. For each NaCl diet, two groups of rats were studied. Baseline renal hemodynamic and excretory function were determined during IMI infusion of 0.9% NaCl into the left kidney. The infusion was then either changed to HOE-140 (100 \u03bcg\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7h<jats:sup>\u22121<\/jats:sup>, treated group) or maintained with 0.9% NaCl (time control group), and the parameters were again determined. In rats fed a normal-salt diet, HOE-140 infusion decreased left kidney Na<jats:sup>+<\/jats:sup>excretion (urinary Na<jats:sup>+<\/jats:sup>extraction rate) and fractional Na<jats:sup>+<\/jats:sup>excretion by 40 \u00b1 5% and 40 \u00b1 4%, respectively ( P &lt; 0.01), but did not alter glomerular filtration rate, inner medullary blood flow (PBF), or cortical blood flow. In rats fed a low-salt diet, HOE-140 infusion did not alter renal regional hemodynamics or excretory function. We conclude that in rats fed a normal-salt diet, kinins act tonically via medullary BKB<jats:sub>2<\/jats:sub>receptors to increase Na<jats:sup>+<\/jats:sup>excretion independent of changes in inner medullary blood flow.<\/jats:p>","DOI":"10.1152\/ajprenal.90225.2008","type":"journal-article","created":{"date-parts":[[2008,7,17]],"date-time":"2008-07-17T00:54:15Z","timestamp":1216256055000},"page":"F811-F817","source":"Crossref","is-referenced-by-count":20,"title":["Blockade of renal medullary bradykinin B<sub>2<\/sub>receptors increases tubular sodium reabsorption in rats fed a normal-salt diet"],"prefix":"10.1152","volume":"295","author":[{"given":"Sema-Hayriye","family":"Sivritas","sequence":"first","affiliation":[]},{"given":"David W.","family":"Ploth","sequence":"additional","affiliation":[]},{"given":"Wayne R.","family":"Fitzgibbon","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.29.1.483"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1988.254.4.F484"},{"key":"R3","unstructured":"Bhoola KD, Figueroa CD, Worthy K.Bioregulation of kinins: kallikreins, kininogens, and kininases.Pharmacol Rev44: 1\u201380, 1992."},{"key":"R4","doi-asserted-by":"crossref","unstructured":"Campbell DJ, Anastasopoulos F, Duncan AM, James GM, Kladis A, Briscoe TA.Effects of neutral endopeptidase inhibition and combined angiotensin converting enzyme and neutral endopeptidase inhibition on angiotensin and bradykinin peptides in rats.J Pharmacol Exp Ther287: 567\u2013577, 2003.","DOI":"10.1016\/S0022-3565(24)37829-2"},{"key":"R5","doi-asserted-by":"crossref","unstructured":"Carretero OA, Scili AG.Local hormonal factors (intracrine, autocrine, and paracrine) in hypertension.Hypertension18,SupplI: I-58\u2013I-69, 1991.","DOI":"10.1161\/01.HYP.18.3_Suppl.I58"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1016\/0304-4165(88)90033-5"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-199212007-00020"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1985.249.3.F439"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1992.263.5.R1136"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1177\/32.1.6558105"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1177\/43.2.7822771"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1007\/BF00492599"},{"key":"R13","unstructured":"Fitzgibbon WR, Ploth DW.Luminal injection of a bradykinin B2receptor antagonist (HOE 140) increases distal nephron22Na absorption in rats (Abstract).Proceedings of the 16th International Conference on the Kallikrein-Kinin System (Kinins 2002), Charleston SC, 2002."},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1016\/0024-3205(85)90503-X"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1007\/BF01473295"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0703749"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.1993.tb12856.x"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1038\/ncpneph0444"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.23.5.646"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.22.5.705"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.256.5.F909"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.pa.29.040189.002015"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.21.6.961"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.260.5.F670"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1996.271.2.R352"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0701797"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1016\/S0008-6363(98)00194-1"},{"key":"R28","unstructured":"Nishimura M, Margolius HS.A kinin receptor antagonist affects renal function of Dahl salt-resistant (SR\/Jr) rats (Abstract).Hypertension20: 402, 1992."},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1983.244.5.F510"},{"key":"R30","doi-asserted-by":"crossref","unstructured":"Proud D, Perkins M, Pierce JV, Yates KN, Highet PF, Herring PL, Mangkornkanok\/Mark M, Bahu R, Carone F, Pisano JJ.Characterization and localization of human renal kininogen.J Biol Chem256: 10634\u201310639, 1981.","DOI":"10.1016\/S0021-9258(19)68671-0"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1988.255.4.F690"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.260.1.F86"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.25.5.1008"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1985.249.5.F645"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.1993.265.4.E648"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.23.6.1068"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1984.246.5.F732"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1172\/JCI112268"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1172\/JCI111935"},{"key":"R40","doi-asserted-by":"crossref","unstructured":"Tomiyama H, Scicli AG, Scicli GM, Carretero OA.Renal effects of Fab fragments of kinin antibodies on deoxycorticosterone acetate-salt-treated rats.Hypertension15: 761\u2013766, 1989.","DOI":"10.1161\/01.HYP.15.6.761"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.86.5.589"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.19.2_Suppl.II10"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1016\/0162-3109(96)00031-8"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1093\/ajh\/1.1.76"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.258.6.F1584"},{"key":"R46","doi-asserted-by":"publisher","DOI":"10.1046\/j.1440-1681.2000.03277.x"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.90225.2008","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,1,31]],"date-time":"2025-01-31T01:40:15Z","timestamp":1738287615000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.90225.2008"}},"issued":{"date-parts":[[2008,9]]},"references-count":46,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2008,9]]}},"alternative-id":["10.1152\/ajprenal.90225.2008"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.90225.2008","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2008,9]]}},{"indexed":{"date-parts":[[2026,1,9]],"date-time":"2026-01-09T15:37:09Z","timestamp":1767973029133,"version":"3.49.0"},"reference-count":40,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2001,8,1]]},"abstract":"<jats:p>The aim of this study was to determine whether expressing aquaporin (AQP)-1 could affect transport of NH<jats:sub>3<\/jats:sub>. Using ion-selective microelectrodes, the experiments were conducted on frog oocytes (cells characterized by low NH<jats:sub>3<\/jats:sub>permeability) expressing AQP1. In H<jats:sub>2<\/jats:sub>O-injected oocytes, exposure to NH<jats:sub>3<\/jats:sub>\/NH[Formula: see text] (20 mM, pH 7.5) caused a sustained cell acidification and no initial increase in pH<jats:sub>i<\/jats:sub>(as expected from NH<jats:sub>3<\/jats:sub>influx), and the cell depolarized to near 0 mV. The absence of Na<jats:sup>+<\/jats:sup>, the presence of Ba<jats:sup>2+<\/jats:sup>, or raising bath pH (pH<jats:sub>B<\/jats:sub>) did not inhibit the magnitude of the pH<jats:sub>i<\/jats:sub>decrease or result in an initial increase in pH<jats:sub>i<\/jats:sub>when NH<jats:sub>3<\/jats:sub>\/NH[Formula: see text] was added. However, after the cell was acidified (because of NH<jats:sub>3<\/jats:sub>\/NH[Formula: see text]), raising pH<jats:sub>B<\/jats:sub>to 8.0 caused a slow increase in pH<jats:sub>i<\/jats:sub>but had no effect on membrane potential. The changes in pH<jats:sub>i<\/jats:sub>with raising pH<jats:sub>B<\/jats:sub>did not occur in the absence of NH<jats:sub>3<\/jats:sub>\/NH[Formula: see text]. In AQP1 oocytes, exposure to NH<jats:sub>3<\/jats:sub>\/NH[Formula: see text]usually resulted in little or no change in pH<jats:sub>i<\/jats:sub>, and in the absence of Na<jats:sup>+<\/jats:sup>there was a small increase in pH<jats:sub>i<\/jats:sub>(the cell still depolarized to near 0 mV). However, after exposure to NH<jats:sub>3<\/jats:sub>\/NH[Formula: see text], raising pH<jats:sub>B<\/jats:sub>to 8.0 caused pH<jats:sub>i<\/jats:sub>to increase more than two times faster than in control oocytes. This increase in pH<jats:sub>i<\/jats:sub>is likely the result of increased NH<jats:sub>3<\/jats:sub>entry and not the result of NH[Formula: see text] transport. These results indicate that 1) the oocyte membrane, although highly permeable to NH[Formula: see text], has a significant NH<jats:sub>3<\/jats:sub>permeability and 2) NH<jats:sub>3<\/jats:sub>permeability is enhanced by AQP1.<\/jats:p>","DOI":"10.1152\/ajprenal.2001.281.2.f255","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T14:08:31Z","timestamp":1514038111000},"page":"F255-F263","source":"Crossref","is-referenced-by-count":83,"title":["Transport of NH<sub>3<\/sub>\/NH 4 + in oocytes expressing aquaporin-1"],"prefix":"10.1152","volume":"281","author":[{"given":"Nazih L.","family":"Nakhoul","sequence":"first","affiliation":[{"name":"Section of Nephrology, Departments of Medicine and Physiology, Tulane University School of Medicine, and Veterans Affairs Medical Center, New Orleans, Louisiana 70112"}]},{"given":"Kathleen S.","family":"Hering-Smith","sequence":"additional","affiliation":[{"name":"Section of Nephrology, Departments of Medicine and Physiology, Tulane University School of Medicine, and Veterans Affairs Medical Center, New Orleans, Louisiana 70112"}]},{"given":"Solange M.","family":"Abdulnour-Nakhoul","sequence":"additional","affiliation":[{"name":"Section of Nephrology, Departments of Medicine and Physiology, Tulane University School of Medicine, and Veterans Affairs Medical Center, New Orleans, Louisiana 70112"}]},{"given":"L. Lee","family":"Hamm","sequence":"additional","affiliation":[{"name":"Section of Nephrology, Departments of Medicine and Physiology, Tulane University School of Medicine, and Veterans Affairs Medical Center, New Orleans, Louisiana 70112"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1007\/BF00373921"},{"key":"B2","doi-asserted-by":"crossref","first-page":"764","DOI":"10.1681\/ASN.V114764","volume":"11","author":"Agre P","year":"2000","journal-title":"J Am Soc Nephrol"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/S0076-6879(99)94032-6"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1021\/ac00237a031"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.biochem.68.1.425"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.67.1.91"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1007\/s004240050401"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1007\/BF00378645"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1007\/BF00374144"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1998.275.6.C1481"},{"key":"B11","first-page":"L26","volume":"13","author":"Cooper GJ","year":"1999","journal-title":"FASEB J"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1007\/BF02191917"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1988.255.1.F78"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1985.248.4.F459"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1984.247.1.F35"},{"key":"B16","first-page":"367A","volume":"29","author":"Hamm LL.","year":"1986","journal-title":"Kidney Int"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(89)80197-0"},{"key":"B18","first-page":"283","volume":"16","author":"Hamm LL","year":"1990","journal-title":"Miner Electrolyte Metab"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1172\/JCI111723"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1006\/jmbi.1999.3413"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1038\/339478a0"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1989.69.1.179"},{"key":"B23","first-page":"41A","volume":"10","author":"Nakhoul NL","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1998.274.2.C543"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.92.3.369"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.50.33123"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.88.24.11110"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1126\/science.256.5055.385"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1021\/bi00061a002"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1981.241.1.F39"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1016\/0167-4889(92)90098-V"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.25.11573"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1007\/BF01869332"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.1.F13"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1038\/368332a0"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.267.4.F660"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.275.4.2686"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.10.5808"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1021\/bi00172a042"},{"key":"B41","first-page":"155","volume":"13","author":"Zeidel M","year":"1993","journal-title":"Semin Nephrol"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.2001.281.2.F255","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:44:22Z","timestamp":1660189462000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.2001.281.2.F255"}},"issued":{"date-parts":[[2001,8,1]]},"references-count":40,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2001,8,1]]}},"alternative-id":["10.1152\/ajprenal.2001.281.2.F255"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.2001.281.2.f255","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2001,8,1]]}},{"indexed":{"date-parts":[[2026,1,9]],"date-time":"2026-01-09T17:58:09Z","timestamp":1767981489974,"version":"3.49.0"},"reference-count":60,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2008,11]]},"abstract":"<jats:p>Progressive renal enlargement due to the growth of innumerable fluid-filled cysts is a central pathophysiological feature of autosomal dominant polycystic kidney disease (ADPKD). These epithelial neoplasms enlarge slowly and damage noncystic parenchyma by mechanisms that have not been clearly defined. In a microarray analysis of cultured human ADPKD cyst epithelial cells, periostin mRNA was overexpressed 15-fold compared with normal human kidney (NHK) cells. Periostin, initially identified in osteoblasts, is not expressed in normal adult kidneys but is expressed transiently during renal development. We found periostin in cyst-lining cells in situ in the extracellular matrix adjacent to the cysts and within cyst fluid. ADPKD cells secreted periostin across luminal and basolateral plasma membranes. Periostin increased proliferation of cyst epithelial cells 27.9 \u00b1 3.1% ( P &lt; 0.001) above baseline and augmented in vitro cyst growth but did not affect proliferation of normal renal cells. Expression of \u03b1<jats:sub>V<\/jats:sub>-integrin, a periostin receptor, was ninefold higher in ADPKD cells compared with NHK cells, and antibodies that block \u03b1<jats:sub>V<\/jats:sub>-integrin inhibited periostin-induced cell proliferation. We conclude that periostin is a novel autocrine mitogen secreted by mural epithelial cells with the potential to accelerate cyst growth and promote interstitial remodeling in ADPKD.<\/jats:p>","DOI":"10.1152\/ajprenal.90266.2008","type":"journal-article","created":{"date-parts":[[2008,8,28]],"date-time":"2008-08-28T00:44:32Z","timestamp":1219884272000},"page":"F1463-F1471","source":"Crossref","is-referenced-by-count":71,"title":["Periostin induces proliferation of human autosomal dominant polycystic kidney cells through \u03b1<sub>V<\/sub>-integrin receptor"],"prefix":"10.1152","volume":"295","author":[{"given":"Darren P.","family":"Wallace","sequence":"first","affiliation":[]},{"given":"Megan T.","family":"Quante","sequence":"additional","affiliation":[]},{"given":"Gail A.","family":"Reif","sequence":"additional","affiliation":[]},{"given":"Emily","family":"Nivens","sequence":"additional","affiliation":[]},{"given":"Farhana","family":"Ahmed","sequence":"additional","affiliation":[]},{"given":"Scott J.","family":"Hempson","sequence":"additional","affiliation":[]},{"given":"Gustavo","family":"Blanco","sequence":"additional","affiliation":[]},{"given":"Tamio","family":"Yamaguchi","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1016\/S1535-6108(04)00081-9"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00843.x"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00768.x"},{"key":"R4","unstructured":"Calvet JP.Molecular genetics of polycystic kidney disease.J Nephrol11: 24\u201334, 1998."},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1096\/fasebj.13.1.81"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00065.x"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1206347"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1980.43"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1002\/jez.1402700208"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.304"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.4161\/cc.4.11.2185"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1038\/nm935"},{"key":"R13","unstructured":"Gillan L, Matei D, Fishman DA, Gerbin CS, Karlan BY, Chang DD.Periostin secreted by epithelial ovarian carcinoma is a ligand for alpha(V)beta(3) and alpha(V)beta(5) integrins and promotes cell motility.Cancer Res62: 5358\u20135364, 2002."},{"key":"R14","unstructured":"Grantham JJ.1992 Homer Smith Award. Fluid secretion, cellular proliferation, and the pathogenesis of renal epithelial cysts.J Am Soc Nephrol3: 1841\u20131857, 1993."},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00242.x"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1983.244.1.F3"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2007.060158"},{"key":"R18","doi-asserted-by":"crossref","unstructured":"Hanaoka K, Guggino WB.cAMP regulates cell proliferation and cyst formation in autosomal polycystic kidney disease cells.J Am Soc Nephrol11: 1179\u20131187, 2000.","DOI":"10.1681\/ASN.V1171179"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1359\/jbmr.1999.14.7.1239"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00533.x"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)63539-0"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M207055200"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1161\/01.ATV.0000149141.81230.c6"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)63486-4"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006030295"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1126\/science.272.5266.1339"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006030251"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002629"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00755.x"},{"key":"R30","doi-asserted-by":"crossref","unstructured":"Nakamura T, Ebihara I, Nagaoka I, Tomino Y, Nagao S, Takahashi H, Koide H.Growth factor gene expression in kidney of murine polycystic kidney disease.J Am Soc Nephrol3: 1378\u20131386, 1993.","DOI":"10.1681\/ASN.V371378"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1992.184"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006010086"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1038\/emm.2004.29"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002229"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/ddn045"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006111218"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1086\/316939"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0706793104"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1002\/1097-0142(20010815)92:4<843::AID-CNCR1391>3.0.CO;2-P"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1023\/A:1021899904332"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfl071"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.24.9.3992-4003.2004"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1111\/ocr.1999.2.1.42"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1089\/dna.1992.11.511"},{"key":"R45","doi-asserted-by":"crossref","unstructured":"Sullivan LP, Wallace DP, Grantham JJ.Chloride and fluid secretion in polycystic kidney disease.J Am Soc Nephrol9: 903\u2013916, 1998.","DOI":"10.1681\/ASN.V95903"},{"key":"R46","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1998.78.4.1165"},{"key":"R47","doi-asserted-by":"publisher","DOI":"10.1093\/carcin\/bgi034"},{"key":"R48","doi-asserted-by":"publisher","DOI":"10.1042\/bj2940271"},{"key":"R49","doi-asserted-by":"publisher","DOI":"10.1038\/nm1004"},{"key":"R50","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.445"},{"key":"R51","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007060688"},{"key":"R52","unstructured":"Watnick T, Germino GG.Molecular basis of autosomal dominant polycystic kidney disease.Semin Nephrol19: 327\u2013343, 1999."},{"key":"R53","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.1041500220"},{"key":"R54","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006080912"},{"key":"R55","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00023.x"},{"key":"R56","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00991.x"},{"key":"R57","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M405079200"},{"key":"R58","doi-asserted-by":"crossref","unstructured":"Ye M, Grant M, Sharma M, Elzinga L, Swan S, Torres VE, Grantham JJ.Cyst fluid from human autosomal dominant polycystic kidneys promotes cyst formation and expansion by renal epithelial cells in vitro.J Am Soc Nephrol3: 984\u2013994, 1992.","DOI":"10.1681\/ASN.V34984"},{"key":"R59","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199307293290503"},{"key":"R60","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000088720.61783.19"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.90266.2008","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,9,15]],"date-time":"2021-09-15T16:19:18Z","timestamp":1631722758000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.90266.2008"}},"issued":{"date-parts":[[2008,11]]},"references-count":60,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2008,11]]}},"alternative-id":["10.1152\/ajprenal.90266.2008"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.90266.2008","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2008,11]]}},{"indexed":{"date-parts":[[2026,1,8]],"date-time":"2026-01-08T02:56:38Z","timestamp":1767840998335,"version":"3.49.0"},"reference-count":35,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2011,7]]},"abstract":"<jats:p>Renal tubular cell apoptosis is a significant component of obstruction-induced renal injury, and it results in a progressive loss in renal parenchymal mass during renal obstruction. Although IL-18 is an important mediator of inflammatory renal disease and renal fibrosis, its role in obstruction-induced renal tubular cell apoptosis remains unclear. To study this, male C57BL6 wild-type mice and C57BL6 mice transgenic for human IL-18-binding protein (IL-18BP Tg) were subjected to renal obstruction vs. sham operation. The kidneys were harvested after 1 or 2 wk and analyzed for IL-18 production, apoptosis, caspase activity, and Fas\/Fas Ligand (FasL) expression. HK-2 cells were similarly analyzed for apoptosis and proapoptotic signaling following 3 days of direct exposure to IL-18 vs. control media. Renal obstruction induced a significant increase in IL-18 production, renal tubular cell apoptosis, caspase activation, and FasL expression. IL-18 neutralization, on the other hand, significantly reduced obstruction-induced apoptosis, caspase-8 and caspase-3 activity, and FasL expression. In vitro experiments similarly demonstrate that IL-18 stimulation induces apoptosis, FasL expression, and increases active caspase-8 and caspase-3 expression in a dose-dependent fashion. siRNA knockdown of FasL gene expression, however, significantly reduced IL-18-induced apoptosis. This study reveals that IL-18 is a significant mediator of obstruction-induced tubular cell apoptosis, and it demonstrates that IL-18 stimulates proapoptotic signaling through a FasL-dependent mechanism.<\/jats:p>","DOI":"10.1152\/ajprenal.00339.2010","type":"journal-article","created":{"date-parts":[[2011,4,21]],"date-time":"2011-04-21T02:14:18Z","timestamp":1303352058000},"page":"F171-F178","source":"Crossref","is-referenced-by-count":29,"title":["IL-18 mediates proapoptotic signaling in renal tubular cells through a Fas ligand-dependent mechanism"],"prefix":"10.1152","volume":"301","author":[{"given":"Hongji","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Urology, Indiana University School of Medicine, Indianapolis, Indiana"}]},{"given":"Karen L.","family":"Hile","sequence":"additional","affiliation":[{"name":"Department of Urology, Indiana University School of Medicine, Indianapolis, Indiana"}]},{"given":"Hiroshi","family":"Asanuma","sequence":"additional","affiliation":[{"name":"Department of Urology, Indiana University School of Medicine, Indianapolis, Indiana"}]},{"given":"Brian","family":"Vanderbrink","sequence":"additional","affiliation":[{"name":"Department of Urology, Indiana University School of Medicine, Indianapolis, Indiana"}]},{"given":"Ethan I.","family":"Franke","sequence":"additional","affiliation":[{"name":"Department of Urology, Indiana University School of Medicine, Indianapolis, Indiana"}]},{"given":"Matthew T.","family":"Campbell","sequence":"additional","affiliation":[{"name":"Department of Urology, Indiana University School of Medicine, Indianapolis, Indiana"}]},{"given":"Kirstan K.","family":"Meldrum","sequence":"additional","affiliation":[{"name":"Department of Urology, Indiana University School of Medicine, Indianapolis, Indiana"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2009.216"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M313980200"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1159\/000020657"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00310.x"},{"key":"B5","doi-asserted-by":"crossref","first-page":"5506","DOI":"10.4049\/jimmunol.162.9.5506","volume":"162","author":"Daemen MA","year":"1999","journal-title":"J Immunol"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/S0091-6749(99)70518-X"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1002\/jlb.63.6.658"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00045.2005"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1189\/jlb.0503230"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1002\/art.10563"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1136\/gut.2003.018572"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1038\/386619a0"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2249.2004.02475.x"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0406421101"},{"key":"B15","doi-asserted-by":"crossref","first-page":"583","DOI":"10.4049\/jimmunol.163.2.583","volume":"163","author":"Hashimoto W","year":"1999","journal-title":"J Immunol"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000444"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00777.2002"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/j.jss.2007.03.037"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1797.2006.00737.x"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/S1043-4666(03)00150-9"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.2001.281.2.C563"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1172\/JCI12089"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1172\/JCI0215623"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00099.2004"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1016\/j.jss.2004.02.016"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00414.x"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.164.5.2644"},{"key":"B28","first-page":"3253","volume":"17","author":"Ohtsuki T","year":"1997","journal-title":"Anticancer Res"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.2174\/1568005310202020181"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005030236"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2003.10.040"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1016\/S0031-6865(99)00038-2"},{"key":"B33","first-page":"641","volume":"18","author":"Truong LD","year":"1998","journal-title":"Semin Nephrol"},{"key":"B34","doi-asserted-by":"crossref","first-page":"3961","DOI":"10.4049\/jimmunol.159.8.3961","volume":"159","author":"Tsutsui H","year":"1997","journal-title":"J Immunol"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-6143.2006.01536.x"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00339.2010","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,4,6]],"date-time":"2024-04-06T08:18:06Z","timestamp":1712391486000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00339.2010"}},"issued":{"date-parts":[[2011,7]]},"references-count":35,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2011,7]]}},"alternative-id":["10.1152\/ajprenal.00339.2010"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00339.2010","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2011,7]]}},{"indexed":{"date-parts":[[2026,1,8]],"date-time":"2026-01-08T02:33:46Z","timestamp":1767839626075,"version":"3.49.0"},"reference-count":51,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2006,12]]},"abstract":"<jats:p>Aging is associated with alterations in Ca<jats:sup>2+<\/jats:sup>homeostasis, which predisposes elder people to hyperparathyroidism and osteoporosis. Intestinal Ca<jats:sup>2+<\/jats:sup>absorption decreases with aging and, in particular, active transport of Ca<jats:sup>2+<\/jats:sup>by the duodenum. In addition, there are age-related changes in renal Ca<jats:sup>2+<\/jats:sup>handling. To examine age-related changes in expression of the renal and intestinal epithelial Ca<jats:sup>2+<\/jats:sup>channels, control (TRPV5<jats:sup>+\/+<\/jats:sup>) and TRPV5 knockout (TRPV5<jats:sup>\u2212\/\u2212<\/jats:sup>) mice aged 10, 30, and 52 wk were studied. Aging of TRPV5<jats:sup>+\/+<\/jats:sup>mice resulted in a tendency toward increased renal Ca<jats:sup>2+<\/jats:sup>excretion and significantly decreased intestinal Ca<jats:sup>2+<\/jats:sup>absorption, which was accompanied by reduced expression of TRPV5 and TRPV6, respectively, despite increased serum 1,25(OH)<jats:sub>2<\/jats:sub>D<jats:sub>3<\/jats:sub>levels. Similarly, in TRPV5<jats:sup>\u2212\/\u2212<\/jats:sup>mice the existing renal Ca<jats:sup>2+<\/jats:sup>loss was more pronounced in elder animals, whereas the compensatory intestinal Ca<jats:sup>2+<\/jats:sup>absorption and TRPV6 expression declined with aging. In both mice strains, aging resulted in a resistance to 1,25(OH)<jats:sub>2<\/jats:sub>D<jats:sub>3<\/jats:sub>and diminished renal vitamin D receptor mRNA levels, whereas serum Ca<jats:sup>2+<\/jats:sup>levels remained constant. Furthermore, 52-wk-old TRPV5<jats:sup>\u2212\/\u2212<\/jats:sup>mice showed severe hyperparathyroidism, whereas PTH levels in elder TRPV5<jats:sup>+\/+<\/jats:sup>mice remained normal. In 52-wk-old TRPV5<jats:sup>\u2212\/\u2212<\/jats:sup>mice, serum osteocalcin levels were increased in accordance with the elevated PTH levels, suggesting an increased bone turnover in these mice. In conclusion, downregulation of TRPV5 and TRPV6 is likely involved in the impaired Ca<jats:sup>2+<\/jats:sup>(re)absorption during aging. Moreover, TRPV5<jats:sup>\u2212\/\u2212<\/jats:sup>mice likely develop age-related hyperparathyroidism and osteoporotic characteristics before TRPV5<jats:sup>+\/+<\/jats:sup>mice, demonstrating the importance of the epithelial Ca<jats:sup>2+<\/jats:sup>channels in Ca<jats:sup>2+<\/jats:sup>homeostasis.<\/jats:p>","DOI":"10.1152\/ajprenal.00038.2006","type":"journal-article","created":{"date-parts":[[2006,5,17]],"date-time":"2006-05-17T01:43:10Z","timestamp":1147830190000},"page":"F1177-F1183","source":"Crossref","is-referenced-by-count":51,"title":["Age-dependent alterations in Ca<sup>2+<\/sup>homeostasis: role of TRPV5 and TRPV6"],"prefix":"10.1152","volume":"291","author":[{"given":"Monique","family":"van Abel","sequence":"first","affiliation":[]},{"given":"Sylvie","family":"Huybers","sequence":"additional","affiliation":[]},{"given":"Joost G. J.","family":"Hoenderop","sequence":"additional","affiliation":[]},{"given":"Annemiete W. C. M.","family":"van der Kemp","sequence":"additional","affiliation":[]},{"given":"Johannes P. T. M.","family":"van Leeuwen","sequence":"additional","affiliation":[]},{"given":"Ren\u00e9 J. M.","family":"Bindels","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"crossref","unstructured":"Agus ZS, Gardner LB, Beck LH, and Goldberg M.Effects of parathyroid hormone on renal tubular reabsorption of calcium, sodium, and phosphate.Am J Physiol224: 1143\u20131148, 1973.","DOI":"10.1152\/ajplegacy.1973.224.5.1143"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1210\/endo-125-6-2950"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1016\/j.abb.2003.09.025"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.1999.277.1.G41"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.1984.246.3.E266"},{"key":"R6","doi-asserted-by":"crossref","unstructured":"Armbrecht HJ, Zenser TV, Bruns MEH, and Davis BB.Effect of age on intestinal calcium absorption and adaptation to dietary calcium.Am J Physiol Endocrinol Metab Gastrointest Physiol236: E769\u2013E774, 1979.","DOI":"10.1152\/ajpendo.1979.236.6.E769"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.1980.239.5.E322"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.9.5372"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.261.5.F799"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.266.4.F620"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1016\/j.abb.2005.02.007"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1093\/geronj\/38.1.19"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1359\/jbmr.1999.14.1.57"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1172\/JCI109516"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1002\/jcb.10472"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.259.3.F444"},{"key":"R17","doi-asserted-by":"crossref","unstructured":"Hanai H, Ishida M, Liang CT, and Sacktor B.Parathyroid hormone increases sodium\/calcium exchange activity in renal cells and the blunting of the response in aging.J Biol Chem261: 5419\u20135425, 1986.","DOI":"10.1016\/S0021-9258(19)57232-5"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1172\/JCI113869"},{"key":"R19","doi-asserted-by":"crossref","unstructured":"Hoenderop JG, Hartog A, Stuiver M, Doucet A, Willems PH, and Bindels RJ.Localization of the epithelial Ca2+channel in rabbit kidney and intestine.J Am Soc Nephrol11: 1171\u20131178, 2000.","DOI":"10.1681\/ASN.V1171171"},{"key":"R20","doi-asserted-by":"crossref","unstructured":"Hoenderop JG, Muller D, Van Der Kemp AW, Hartog A, Suzuki M, Ishibashi K, Imai M, Sweep F, Willems PH, Van Os CH, and Bindels RJ.Calcitriol controls the epithelial calcium channel in kidney.J Am Soc Nephrol12: 1342\u20131349, 2001.","DOI":"10.1681\/ASN.V1271342"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.64.081501.155921"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.13.8375"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1172\/JCI200319826"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1096\/fj.02-0225com"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1210\/endo-126-2-1053"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1016\/0531-5565(95)00014-3"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1159\/000177664"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.2001.281.3.E558"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1016\/0531-5565(94)90049-3"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1097-4652(200003)182:3<429::AID-JCP14>3.0.CO;2-S"},{"key":"R31","doi-asserted-by":"crossref","unstructured":"Melton L Jr, Atkinson EJ, O'Fallon WM, Wahner HW, and Riggs BL.Long-term fracture prediction by bone mineral assessed at different skeletal sites.J Bone Miner Res8: 1227\u20131233, 1993.","DOI":"10.1002\/jbmr.5650081010"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1016\/S1097-2765(02)00448-3"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118224"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000094081.78893.E8"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2265.1994.tb03782.x"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1210\/jcem-63-6-1262"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1002\/jcb.240550308"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.32.22739"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1997.273.4.C1349"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005060632"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1016\/8756-3282(95)00088-U"},{"key":"R42","doi-asserted-by":"crossref","unstructured":"Sherman SS, Tobin JD, Hollis BW, Gundberg CM, Roy TA, and Plato CC.Biochemical parameters associated with low bone density in healthy men and women.J Bone Miner Res7: 1123\u20131130, 1992.","DOI":"10.1002\/jbmr.5650071003"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1016\/0304-4165(90)90148-P"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1126\/science.289.5484.1504"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.00036.2003"},{"key":"R46","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000022423.34922.2A"},{"key":"R47","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00587.x"},{"key":"R48","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.5.F985"},{"key":"R49","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.231474698"},{"key":"R50","doi-asserted-by":"publisher","DOI":"10.1677\/joe.0.1200143"},{"key":"R51","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.272.6.F751"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00038.2006","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,7,27]],"date-time":"2021-07-27T09:02:32Z","timestamp":1627376552000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00038.2006"}},"issued":{"date-parts":[[2006,12]]},"references-count":51,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2006,12]]}},"alternative-id":["10.1152\/ajprenal.00038.2006"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00038.2006","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2006,12]]}},{"indexed":{"date-parts":[[2026,1,8]],"date-time":"2026-01-08T09:07:44Z","timestamp":1767863264223,"version":"3.49.0"},"reference-count":28,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2006,6]]},"abstract":"<jats:p>The small GTPase p21 Ras and its downstream effectors play a central role in the control of cell survival and apoptosis. We studied the effects of Ras\/ERK1\/2 signaling inhibition on oxidative damage in cultured renal and endothelial cells and on renal ischemia-reperfusion injury in the rat. Primary human renal tubular and human endothelial ECV304 cells underwent significant cell death when subjected to oxidative stress. This type of stress induced robustly ERK1\/2 and phosphoinositide 3-kinase (PI3-kinase) signaling. Inhibition of Ras\/ERK1\/2 with a farnesyl transferase inhibitor, chaetomellic acid A (S-FTI), or with PD-98059, an inhibitor of MEK, a kinase upstream ERK1\/2, significantly reduced the fraction of dead cells. The inhibitor of the PI3-kinase\/Akt pathway, LY-294002, failed to exert a protective effect. We have translated these data in a rat model of renal ischemic injury in vivo. In uninephrectomized animals, anesthetized with pentobarbital sodium (Nembutal, 50 mg\/kg ip), 24 h after an acute ischemic renal insult (45-min occlusion of left renal artery) a significant fraction of kidney cells succumbed to cell death resulting in renal failure [glomerular filtration rate (GFR) 0.17 \u00b1 0.1 vs. 0.90 \u00b1 0.4 ml\u00b7min<jats:sup>\u22121<\/jats:sup>\u00b7100 g body wt<jats:sup>\u22121<\/jats:sup>in normal rats]. Rats treated with S-FTI maintained the renal function (GFR 0.50 \u00b1 0.1 ml\u00b7min<jats:sup>\u22121<\/jats:sup>\u00b7100 g body wt<jats:sup>\u22121<\/jats:sup>), and the kidneys showed a significant reduction of tubular necrosis. Reduction of ischemic damage in kidney and tubular cells paralleled Ha-Ras inhibition, assayed by cytosolic translocation of the protein. These data demonstrate that inhibition of farnesylation and consequently of Ras\/ERK1\/2 signaling significantly reduces acute postischemic renal injury.<\/jats:p>","DOI":"10.1152\/ajprenal.00304.2005","type":"journal-article","created":{"date-parts":[[2006,1,25]],"date-time":"2006-01-25T03:08:42Z","timestamp":1138158522000},"page":"F1408-F1415","source":"Crossref","is-referenced-by-count":44,"title":["Inhibition of Ras\/ERK1\/2 signaling protects against postischemic renal injury"],"prefix":"10.1152","volume":"290","author":[{"given":"Massimo","family":"Sabbatini","sequence":"first","affiliation":[]},{"given":"Mariarosaria","family":"Santillo","sequence":"additional","affiliation":[]},{"given":"Antonio","family":"Pisani","sequence":"additional","affiliation":[]},{"given":"Roberto","family":"Patern\u00f2","sequence":"additional","affiliation":[]},{"given":"Francesco","family":"Uccello","sequence":"additional","affiliation":[]},{"given":"Rosalba","family":"Ser\u00f9","sequence":"additional","affiliation":[]},{"given":"Gianfranco","family":"Matrone","sequence":"additional","affiliation":[]},{"given":"Gianrico","family":"Spagnuolo","sequence":"additional","affiliation":[]},{"given":"Michele","family":"Andreucci","sequence":"additional","affiliation":[]},{"given":"Vittorio","family":"Serio","sequence":"additional","affiliation":[]},{"given":"Pasquale","family":"Esposito","sequence":"additional","affiliation":[]},{"given":"Bruno","family":"Cianciaruso","sequence":"additional","affiliation":[]},{"given":"Giorgio","family":"Fuiano","sequence":"additional","affiliation":[]},{"given":"Enrico V.","family":"Avvedimento","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.457"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.761_2.x"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1161\/hc0802.104324"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1172\/JCI6974"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1984.28"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00567.x"},{"key":"R7","unstructured":"Du Bose TD Jr, Warnock DG, Meht RL, Bonventre JV, Hammerman MR, Molitoris BA, Paller MS, Siegel NJ, Scherbenske J, and Striker GE.Acute renal failure in the 21st century: recommendations for management and outcomes assessment.Am J Kidney Dis29: 793\u2013799, 1998."},{"key":"R8","doi-asserted-by":"crossref","unstructured":"Fischer MA, Gransier TJ, Beckers LM, Bekers O, Bast A, and Haenen GR.Determination of the antioxidant capacity in blood.Clin Chem Lab Med43: 735\u2013740, 2005.","DOI":"10.1515\/CCLM.2005.125"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.11.6221"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1172\/JCI13018"},{"key":"R11","doi-asserted-by":"crossref","unstructured":"Lowry OH, Rosbrough NJ, Farr AL, and Randall RJ.Protein measurement with the Folin-phenol reagents.J Biol Chem193: 265\u2013275, 1951.","DOI":"10.1016\/S0021-9258(19)52451-6"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00491.x"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)80601-7"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1016\/S0955-0674(96)80066-4"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000074239.22357.06"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1097\/00007890-199706150-00015"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1172\/JCI111524"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000119573.01290.AE"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.177"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1016\/S0960-9822(01)00159-2"},{"key":"R21","doi-asserted-by":"crossref","unstructured":"Sebti SMand Adjei AA.Farnesyltransferase inhibitors.Semin Oncol29: 3\u201339, 2004.","DOI":"10.1053\/j.seminoncol.2003.12.012"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-4159.2004.02754.x"},{"key":"R23","doi-asserted-by":"crossref","unstructured":"Svegliati S, Cancello R, Sambo P, Luchetti M, Paroncini P, Orlandini G, Discepoli G, Paterno R, Santillo M, Cuozzo C, Cassano S, Avvedimento EV, and Gabrielli A.Platelet-derived growth factor and reactive oxygen species (ROS) regulate Ras protein levels in primary human fibroblasts via ERK1\/2. Amplification of ROS and Ras in systemic sclerosis fibroblasts.J Biol Chem280: 36474\u201336482.","DOI":"10.1074\/jbc.M502851200"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199605303342207"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000075552.97794.8C"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00724.x"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.7.4391"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1016\/0955-0674(95)80063-8"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00304.2005","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,7,23]],"date-time":"2021-07-23T03:03:57Z","timestamp":1627009437000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00304.2005"}},"issued":{"date-parts":[[2006,6]]},"references-count":28,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2006,6]]}},"alternative-id":["10.1152\/ajprenal.00304.2005"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00304.2005","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2006,6]]}},{"indexed":{"date-parts":[[2026,1,8]],"date-time":"2026-01-08T07:32:50Z","timestamp":1767857570384,"version":"3.49.0"},"reference-count":62,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2010,2]]},"abstract":"<jats:p>An intact genome is essential for kidney growth and differentiation, but less is known about whether, and how, an altered fetal milieu modifies these processes. Maternal low-protein diets perturb growth of the metanephros, the precursor of the mature kidney. Fetal corticosteroid overexposure may, in part, mediate this, because such diets downregulate placental 11\u03b2-hydroxysteroid dehydrogenase-2, which degrades maternal corticosteroids. We report that glucocorticoid and mineralocorticoid receptors are expressed in mouse metanephric epithelia. Metanephroi maintained in organ culture with hydrocortisone (1.4 or 14 \u03bcM) underwent a dose-dependant deceleration of overall growth accompanied by cyst formation. Dexamethasone, a glucocorticoid, reproduced these outcomes, but aldosterone, a mineralocorticoid, did not. Hydrocortisone upregulated transcripts levels of cadherin-11 and downregulated prospero-related homeobox-1, hence mimicking reported effects of maternal low-protein diet. Hydrocortisone also upregulated transcripts encoding Na<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-ATPase subunits and ligands for the epidermal growth factor receptor, all previously implicated in renal cyst growth. The most upregulated transcript, however, was indian hedgehog, and the encoded protein was immunodetected in metanephric cysts. Furthermore, in the presence of hydrocortisone, cystogenesis, but not whole organ growth, was significantly reduced by cyclopamine, a drug downregulating hedgehog signaling. Finally, both glucocorticoid receptor and indian hedgehog proteins were detected by immunohistochemistry in cystic tubules within human dysplastic kidneys, consistent with the hypothesis that these molecules modify the severity of this congenital malformation. Collectively, our observations raise the possibility that enhanced hedgehog signaling is an important stimulus for renal cyst formation. Furthermore, pharmacological inhibition of this pathway should be explored as a potential therapy for renal cystic diseases, starting with relevant animal models.<\/jats:p>","DOI":"10.1152\/ajprenal.00574.2009","type":"journal-article","created":{"date-parts":[[2009,12,10]],"date-time":"2009-12-10T02:37:43Z","timestamp":1260412663000},"page":"F346-F356","source":"Crossref","is-referenced-by-count":53,"title":["Corticosteroid-induced kidney dysmorphogenesis is associated with deregulated expression of known cystogenic molecules, as well as indian hedgehog"],"prefix":"10.1152","volume":"298","author":[{"given":"Shun-Kai","family":"Chan","sequence":"first","affiliation":[{"name":"Nephro-Urology,"}]},{"given":"Paul R.","family":"Riley","sequence":"additional","affiliation":[{"name":"Molecular Medicine, and"}]},{"given":"Karen L.","family":"Price","sequence":"additional","affiliation":[{"name":"Nephro-Urology,"}]},{"given":"Fiona","family":"McElduff","sequence":"additional","affiliation":[{"name":"Biostatistics and Epidemiology Units, University College London Institute of Child Health, London; and"}]},{"given":"Paul J.","family":"Winyard","sequence":"additional","affiliation":[{"name":"Nephro-Urology,"}]},{"given":"Simon J. M.","family":"Welham","sequence":"additional","affiliation":[{"name":"Division of Nutritional Sciences, University of Nottingham, Nottingham, United Kingdom"}]},{"given":"Adrian S.","family":"Woolf","sequence":"additional","affiliation":[{"name":"Nephro-Urology,"}]},{"given":"David A.","family":"Long","sequence":"additional","affiliation":[{"name":"Nephro-Urology,"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008060633"},{"key":"B2","first-page":"208","volume":"50","author":"Avner ED","year":"1984","journal-title":"Lab Invest"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1985.151"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/ncpneph0344"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0605789103"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.3.F391"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1242\/dev.022442"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1203\/00006450-199809000-00009"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2006.060245"},{"key":"B10","doi-asserted-by":"crossref","first-page":"803","DOI":"10.1242\/dev.125.5.803","volume":"125","author":"Cho EA","year":"1998","journal-title":"Development"},{"key":"B11","first-page":"2244","volume":"83","author":"Dave-Sharma S","year":"1998","journal-title":"J Clin Endocrinol Metab"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/ddl459"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1995.269.2.C487"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/0022-4731(86)90352-3"},{"key":"B16","first-page":"267","volume":"119","author":"Heine VM","year":"2009","journal-title":"J Clin Invest"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.03291006"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.4464-05.2006"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1242\/dev.02220"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1038\/nature02061"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1983.245.2.F232"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/nrg1969"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa020549"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1038\/ncpneph0807"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1016\/j.mod.2007.01.002"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1002\/dvdy.1170"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/S0143-4004(96)80010-5"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1530\/EJE-07-0410"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1038\/ng1874"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1983.244.5.F504"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00382.2005"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1998.8768"},{"key":"B33","doi-asserted-by":"crossref","first-page":"2018","DOI":"10.1111\/j.1523-1755.2004.00623.x","volume":"65","author":"MacRae Dell K","year":"2004","journal-title":"Kidney Int"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1242\/dev.00520"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00225.x"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7580.2006.00670.x"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1096\/fj.08-127696"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1016\/S0925-4773(02)00291-5"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1038\/ng1076"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1210\/mend.13.12.0396"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.4324\/9780203450437"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1990.111"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0b013e3283262ab0"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1999.276.6.R1825"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-4419-0318-1"},{"key":"B46","unstructured":"Potter EL . Normal and abnormal development of the kidney. Chicago, IL: Year Book Medical, 1972."},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1152\/physiolgenomics.00147.2006"},{"key":"B48","first-page":"1149","volume-title":"Heptinstall's Pathology of the Kidney","author":"Risdon RA","year":"1998","edition":"5"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1111\/j.1432-0436.2007.00187.x"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00156.2007"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1016\/j.jsbmb.2003.12.014"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2009.128"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.13.8466"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007020252"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1994.267.2.C450"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006111282"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1152\/physiolgenomics.00167.2004"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00264.x"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.260.3.F420"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.128.1.171"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1007\/978-3-540-76341-3_1"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)61678-1"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1016\/j.gde.2004.07.009"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00574.2009","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,10,15]],"date-time":"2021-10-15T21:16:37Z","timestamp":1634332597000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00574.2009"}},"issued":{"date-parts":[[2010,2]]},"references-count":62,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2010,2]]}},"alternative-id":["10.1152\/ajprenal.00574.2009"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00574.2009","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2010,2]]}},{"indexed":{"date-parts":[[2026,1,9]],"date-time":"2026-01-09T20:59:14Z","timestamp":1767992354435,"version":"3.49.0"},"reference-count":96,"publisher":"American Physiological Society","issue":"3","funder":[{"DOI":"10.13039\/100006955","name":"Office of Extramural Research, National Institutes of Health","doi-asserted-by":"publisher","award":["2R01DK083785"],"award-info":[{"award-number":["2R01DK083785"]}],"id":[{"id":"10.13039\/100006955","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Canada 150 Research Chair"},{"name":"NSERC Discovery Program"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2020,9,1]]},"abstract":"<jats:p>Each day, ~1.7 kg of NaCl and 180 liters of water are reabsorbed by nephron segments in humans, with urinary excretion fine tuned to meet homeostatic requirements. These tasks are coordinated by a spectrum of renal Na<jats:sup>+<\/jats:sup>transporters and channels. The goal of the present study was to investigate the extent to which inhibitors of transepithelial Na<jats:sup>+<\/jats:sup>transport (T<jats:sub>Na<\/jats:sub>) along the nephron alter urinary solute excretion and how those effects may vary between male and female subjects. To accomplish that goal, we developed sex-specific multinephron models that represent detailed transcellular and paracellular transport processes along the nephrons of male and female rat kidneys. We simulated inhibition of Na<jats:sup>+<\/jats:sup>\/H<jats:sup>+<\/jats:sup>exchanger 3 (NHE3), bumetanide-sensitive Na<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-2Cl<jats:sup>\u2212<\/jats:sup>cotransporter (NKCC2), Na<jats:sup>+<\/jats:sup>-Cl<jats:sup>\u2212<\/jats:sup>cotransporter (NCC), and amiloride-sensitive epithelial Na<jats:sup>+<\/jats:sup>channel (ENaC). NHE3 inhibition simulations predicted a substantially reduced proximal tubule T<jats:sub>Na<\/jats:sub>, and NKCC2 inhibition substantially reduced thick ascending limb T<jats:sub>Na<\/jats:sub>. Both gave rise to diuresis, natriuresis, and kaliuresis, with those effects stronger in female rats. While NCC inhibition was predicted to have only minor impact on renal T<jats:sub>Na<\/jats:sub>, it nonetheless had a notable effect of enhancing excretion of Na<jats:sup>+<\/jats:sup>, K<jats:sup>+<\/jats:sup>, and Cl<jats:sup>\u2212<\/jats:sup>, particularly in female rats. Inhibition of ENaC was predicted to have opposite effects on the excretion of Na<jats:sup>+<\/jats:sup>(increased) and K<jats:sup>+<\/jats:sup>(decreased) and to have only a minor impact on whole kidney T<jats:sub>Na<\/jats:sub>. Unlike inhibition of other transporters, ENaC inhibition induced stronger natriuresis and diuresis in male rats than female rats. Overall, model predictions agreed well with measured changes in Na<jats:sup>+<\/jats:sup>and K<jats:sup>+<\/jats:sup>excretion in response to diuretics and Na<jats:sup>+<\/jats:sup>transporter mutations.<\/jats:p>","DOI":"10.1152\/ajprenal.00240.2020","type":"journal-article","created":{"date-parts":[[2020,8,3]],"date-time":"2020-08-03T09:19:04Z","timestamp":1596446344000},"page":"F487-F505","source":"Crossref","is-referenced-by-count":70,"title":["Sex differences in solute transport along the nephrons: effects of Na<sup>+<\/sup>transport inhibition"],"prefix":"10.1152","volume":"319","author":[{"given":"Rui","family":"Hu","sequence":"first","affiliation":[{"name":"Department of Applied Mathematics, University of Waterloo, Waterloo, Ontario, Canada"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0459-469X","authenticated-orcid":false,"given":"Alicia A.","family":"McDonough","sequence":"additional","affiliation":[{"name":"Department of Physiology and Neuroscience, Keck School of Medicine, University of Southern California, Los Angeles, California"}]},{"given":"Anita T.","family":"Layton","sequence":"additional","affiliation":[{"name":"Department of Applied Mathematics, University of Waterloo, Waterloo, Ontario, Canada"},{"name":"Department of Biology, Cheriton School of Computer Science, and School of Pharmacology, University of Waterloo, Waterloo, Ontario, Canada"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00396.2011"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00415.2012"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1161\/CIR.0000000000000659"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-008-0595-1"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1159\/000074675"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00174.2014"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.ph.49.030187.001343"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/367463a0"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.275.3.F379"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1038\/ng0396-248"},{"key":"B10a","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00572.2009"},{"key":"B11","doi-asserted-by":"crossref","first-page":"1112","DOI":"10.1681\/ASN.V541112","volume":"5","author":"Chen Z","year":"1994","journal-title":"J Am Soc Nephrol"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1172\/JCI9260"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1985.248.4.F527"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.64.081501.155847"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00577.2014"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00129.2015"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2017.02.001"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.350"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00334.2015"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00600.2014"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00149.2014"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1172\/JCI8609"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00055.2017"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1097\/00000441-200001000-00005"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1987.39"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.2337\/dc11-s246"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00039.2013"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1042\/CS20150654"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200309000-00008"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M804322200"},{"key":"B31","first-page":"457","volume":"27","author":"Higgins BA","year":"1964","journal-title":"Clin Sci"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00044.2018"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1985.154"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00352.2019"},{"key":"B35","first-page":"523","volume":"14","author":"Johnston PA","year":"1992","journal-title":"Methods Find Exp Clin Pharmacol"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(05)17741-1"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1111\/j.1472-8206.2010.00854.x"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1172\/JCI108105"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00203.2010"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00204.2010"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00263.2011"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00294.2016"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00249.2009"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00398.2003"},{"key":"B44a","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00551.2017"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00363.2018"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00657.2016"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1016\/j.compbiomed.2018.11.002"},{"key":"B47a","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00171.2018"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00087.2017"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.3.F447"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1038\/ng.2218"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00002.2010"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00056.2003"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00288.2014"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1159\/000179741"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1988.254.2.F223"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1016\/j.steroids.2010.05.014"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00183.2013"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006091070"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.12391213"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.05760513"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1988.206"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00354.2015"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1006\/phrs.1998.0311"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1152\/physiol.00026.2016"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1016\/j.cbpb.2003.10.006"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-007-0308-1"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00450.2011"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.1113\/expphysiol.2003.002652"},{"key":"B69","doi-asserted-by":"publisher","DOI":"10.1186\/2042-6410-3-7"},{"key":"B70","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2019080790"},{"key":"B71","doi-asserted-by":"publisher","DOI":"10.1038\/969"},{"key":"B72","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00649.2013"},{"key":"B73","doi-asserted-by":"publisher","DOI":"10.1530\/JOE-16-0669"},{"key":"B74","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.119.13887"},{"key":"B75","doi-asserted-by":"publisher","DOI":"10.1016\/0272-6386(95)90119-1"},{"key":"B76","doi-asserted-by":"publisher","DOI":"10.1038\/ng0196-24"},{"key":"B77","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2015070734"},{"key":"B78","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00060.2019"},{"key":"B79","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1987.117"},{"key":"B80","doi-asserted-by":"publisher","DOI":"10.1001\/jama.1976.03260470017018"},{"key":"B81","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.05920613"},{"key":"B82","doi-asserted-by":"publisher","DOI":"10.1007\/s002329900297"},{"key":"B83","doi-asserted-by":"publisher","DOI":"10.1139\/y05-012"},{"key":"B84","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00031.2005"},{"key":"B85","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00236.2011"},{"key":"B86","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00030.2009"},{"key":"B87","doi-asserted-by":"publisher","DOI":"10.1126\/science.109.2837.489"},{"key":"B88","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2017030295"},{"key":"B89","doi-asserted-by":"publisher","DOI":"10.1111\/apha.13448"},{"key":"B90","doi-asserted-by":"publisher","DOI":"10.1016\/j.coph.2014.12.012"},{"key":"B91","doi-asserted-by":"publisher","DOI":"10.1016\/0895-7061(95)00216-2"},{"key":"B92","doi-asserted-by":"publisher","DOI":"10.1126\/science.1062844"},{"key":"B93","doi-asserted-by":"publisher","DOI":"10.1172\/JCI107721"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00240.2020","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,11,5]],"date-time":"2022-11-05T13:58:55Z","timestamp":1667656735000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00240.2020"}},"issued":{"date-parts":[[2020,9,1]]},"references-count":96,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2020,9,1]]}},"alternative-id":["10.1152\/ajprenal.00240.2020"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00240.2020","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2020,9,1]]}},{"indexed":{"date-parts":[[2026,2,11]],"date-time":"2026-02-11T16:18:13Z","timestamp":1770826693842,"version":"3.50.1"},"reference-count":52,"publisher":"American Physiological Society","issue":"2","funder":[{"DOI":"10.13039\/100000049","name":"HHS | NIH | National Institute on Aging","doi-asserted-by":"publisher","award":["R01 AG062515-S1"],"award-info":[{"award-number":["R01 AG062515-S1"]}],"id":[{"id":"10.13039\/100000049","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000049","name":"HHS | NIH | National Institute on Aging","doi-asserted-by":"publisher","award":["AG062515-S1"],"award-info":[{"award-number":["AG062515-S1"]}],"id":[{"id":"10.13039\/100000049","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Hevolution Foundation","award":["HF-GRO-23-1199246-43"],"award-info":[{"award-number":["HF-GRO-23-1199246-43"]}]},{"DOI":"10.13039\/100000050","name":"HHS | NIH | National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["R01 HL139867"],"award-info":[{"award-number":["R01 HL139867"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"HHS | NIH | National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["R01 141406"],"award-info":[{"award-number":["R01 141406"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000049","name":"HHS | NIH | National Institute on Aging","doi-asserted-by":"publisher","award":["R01 AG062515"],"award-info":[{"award-number":["R01 AG062515"]}],"id":[{"id":"10.13039\/100000049","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2024,8,1]]},"abstract":"<jats:p> NCC regulation is sex dependent. In normotensive male and female Sprague-Dawley and Dahl salt-resistant rats, which exhibit dietary Na<jats:sup>+<\/jats:sup>-evoked NCC suppression, male rats exhibit decreased WNK4 expression and decreased SPAK and OxSR1 levels, whereas female rats only suppress SPAK and OxSR1. In hypertensive Dahl salt-sensitive rats, the ability of females to suppress NCC (in opposition to males) via a SPAK\/OxSR1 mechanism likely contributes to their lower magnitude of salt-sensitive hypertension. <\/jats:p>","DOI":"10.1152\/ajprenal.00150.2023","type":"journal-article","created":{"date-parts":[[2024,5,30]],"date-time":"2024-05-30T08:03:07Z","timestamp":1717056187000},"page":"F277-F289","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":8,"title":["Sex differences in dietary sodium evoked NCC regulation and blood pressure in male and female Sprague-Dawley, Dahl salt-resistant, and Dahl salt-sensitive rats"],"prefix":"10.1152","volume":"327","author":[{"given":"Kiyoung","family":"Kim","sequence":"first","affiliation":[{"name":"Department of Pharmacology and Experimental Therapeutics, Whitaker Cardiovascular Institute, Boston University Chobanian and Avedisian School of Medicine, Boston, Massachusetts, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1597-7530","authenticated-orcid":false,"given":"Kayla M.","family":"Nist","sequence":"additional","affiliation":[{"name":"Department of Anatomy and Neurobiology, Boston University Chobanian and Avedisian School of Medicine, Boston, Massachusetts, United States"}]},{"given":"Franco","family":"Puleo","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Experimental Therapeutics, Whitaker Cardiovascular Institute, Boston University Chobanian and Avedisian School of Medicine, Boston, Massachusetts, United States"}]},{"suffix":"3rd","given":"James","family":"McKenna","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2830-5618","authenticated-orcid":false,"given":"Richard D.","family":"Wainford","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Experimental Therapeutics, Whitaker Cardiovascular Institute, Boston University Chobanian and Avedisian School of Medicine, Boston, Massachusetts, United States"},{"name":"Division of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia, United States"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(14)60685-1"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2013.07.024"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(12)61766-8"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1161\/HYP.0000000000000066"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.3390\/nu11091970"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1161\/CIR.0b013e31820d0793"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(97)05189-1"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1093\/nutrit\/nuw028"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1001\/jama.2017.0947"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1038\/s41371-022-00690-0"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1016\/s0092-8674(01)00241-0"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1001\/jama.1996.03530440061038"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1172\/JCI72274"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00508.2012"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-013-1407-9"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.2007.04846.x"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00514.2014"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.3389\/fphys.2022.1081261"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-015-1708-2"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2017.01.007"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1146\/annurev-physiol-021115-105431"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00264.2019"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.3389\/fphys.2021.784957"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.120.15928"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.114.04036"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2014.12.006"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1172\/JCI601"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2017030295"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.111.00014"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.114.04463"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1111\/apha.12610"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1097\/HJH.0b013e32835ebd54"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1113\/EP087924"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1113\/EP087700"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0036311"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.119.13777"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00216.2019"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1016\/j.jpain.2019.05.005"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-021-02611-5"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00447.2014"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.33549\/physiolres.934334"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90341.2008"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00263.2011"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1038\/nm.2337"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.114.03335"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1161\/01.hyp.0000022062.70639.1c"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.23.24.9208-9221.2003"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1097\/01.asn.0000089830.97681.3b"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00280.2005"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/ddq525"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1006128107"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00145.2018"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00150.2023","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,8,5]],"date-time":"2024-08-05T13:19:32Z","timestamp":1722863972000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00150.2023"}},"issued":{"date-parts":[[2024,8,1]]},"references-count":52,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2024,8,1]]}},"alternative-id":["10.1152\/ajprenal.00150.2023"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00150.2023","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2024,8,1]]},"assertion":[{"value":"2023-05-31","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2024-05-07","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2024-05-15","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2024-08-05","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,2,12]],"date-time":"2026-02-12T11:04:53Z","timestamp":1770894293845,"version":"3.50.1"},"reference-count":42,"publisher":"American Physiological Society","issue":"1","funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81741033"],"award-info":[{"award-number":["81741033"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100007219","name":"Natural Science Foundation of Shanghai","doi-asserted-by":"publisher","award":["15ZR1404400"],"award-info":[{"award-number":["15ZR1404400"]}],"id":[{"id":"10.13039\/100007219","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100003399","name":"Science and Technology Commission of Shanghai Municipality","doi-asserted-by":"publisher","award":["16140904000"],"award-info":[{"award-number":["16140904000"]}],"id":[{"id":"10.13039\/501100003399","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2020,1,1]]},"abstract":"<jats:p> The offspring of Robo2 mutant mice usually present with variable phenotypes of congenital anomalies of the kidney and urinary tract (CAKUT). An intrauterine low-protein diet can also cause CAKUT in offspring, dominated by the duplicated collecting system phenotype. A single genetic or environment factor can only partially explain the pathogenesis of CAKUT. The present study aimed to establish an intrauterine low-protein diet roundabout 2 ( Robo2) mutant mouse model and found that the intrauterine low-protein diet led to significantly increased CAKUT phenotypes in Robo2<jats:sup>PB\/+<\/jats:sup> mice offspring, dominant by a duplicated collecting system. At the same time, more ectopic and lower located ureteric buds (UBs) were observed in the intrauterine low-protein diet-fed Robo2 mutant mouse model, and the number of UB branches was reduced in the serum-free culture. During UB protrusion, intrauterine low-protein diet reduced the expression of Slit2\/Robo2 in Robo2 mutant mice and affected the expression of glial cell-derived neurotrophic factor\/Ret, which is a key molecule for metanephric development, with increasing phospho-Akt and phospho-cAMP responsive element-binding protein 3 activity and a reduction of apoptotic cells in embryonic day 11.5 UB tissues. The mechanism by which an intrauterine low-protein diet aggravates CAKUT in Robo2 mutant mice may be related to the disruption of Akt\/cAMP responsive element-binding protein 3 signaling and a reduction in apoptosis in UB tissue. <\/jats:p>","DOI":"10.1152\/ajprenal.00405.2019","type":"journal-article","created":{"date-parts":[[2019,10,21]],"date-time":"2019-10-21T04:17:17Z","timestamp":1571631437000},"page":"F43-F52","source":"Crossref","is-referenced-by-count":9,"title":["Intrauterine low-protein diet aggravates developmental abnormalities of the urinary system via the Akt\/Creb3 pathway in <i>Robo2<\/i> mutant mice"],"prefix":"10.1152","volume":"318","author":[{"given":"Minghui","family":"Yu","sequence":"first","affiliation":[{"name":"Department of Nephrology, Children\u2019s Hospital of Fudan University, Shanghai Kidney Development and Pediatric Kidney Disease Research Center, Shanghai, China"}]},{"given":"Lihong","family":"Tan","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Children\u2019s Hospital of Fudan University, Shanghai Kidney Development and Pediatric Kidney Disease Research Center, Shanghai, China"}]},{"given":"Yaxin","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Children\u2019s Hospital of Fudan University, Shanghai Kidney Development and Pediatric Kidney Disease Research Center, Shanghai, China"}]},{"given":"Jing","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Children\u2019s Hospital of Fudan University, Shanghai Kidney Development and Pediatric Kidney Disease Research Center, Shanghai, China"}]},{"given":"Yihui","family":"Zhai","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Children\u2019s Hospital of Fudan University, Shanghai Kidney Development and Pediatric Kidney Disease Research Center, Shanghai, China"}]},{"given":"Jia","family":"Rao","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Children\u2019s Hospital of Fudan University, Shanghai Kidney Development and Pediatric Kidney Disease Research Center, Shanghai, China"}]},{"given":"Xiaoyan","family":"Fang","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Children\u2019s Hospital of Fudan University, Shanghai Kidney Development and Pediatric Kidney Disease Research Center, Shanghai, China"}]},{"given":"Xiaohui","family":"Wu","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Children\u2019s Hospital of Fudan University, Shanghai Kidney Development and Pediatric Kidney Disease Research Center, Shanghai, China"},{"name":"State Key Laboratory of Genetic Engineering and National Center for International Research of Development and Disease, Institute of Developmental Biology and Molecular Medicine, Collaborative Innovation Center of Genetics and Development, School of Life Sciences, Fudan University, Shanghai, China"}]},{"given":"Hong","family":"Xu","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Children\u2019s Hospital of Fudan University, Shanghai Kidney Development and Pediatric Kidney Disease Research Center, Shanghai, China"}]},{"given":"Qian","family":"Shen","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Children\u2019s Hospital of Fudan University, Shanghai Kidney Development and Pediatric Kidney Disease Research Center, Shanghai, China"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-009-1432-2"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/j.ydbio.2006.08.051"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007060692"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMc1802894"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-014-2962-9"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-014-2884-6"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-013-2606-5"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2013.100"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.cellbio.22.010305.104340"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/0012-1606(81)90373-0"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1016\/S1534-5807(04)00108-X"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.14715\/cmb\/2018.64.5.6"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(10)60236-X"},{"key":"B14","first-page":"565","volume":"89","author":"Hilliard SA","year":"2016","journal-title":"Yale J Biol Med"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0058243"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2017040380"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2013.508"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00188.x"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1172\/JCI41619"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.4161\/org.5.4.10048"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1515\/prilozi-2017-0007"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2012.04.029"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.10221012"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1186\/s12882-016-0308-5"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1002\/bdra.20778"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1086\/512735"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-016-3543-x"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1038\/pr.2016.51"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0084155"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1002\/bdra.23475"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1097\/MD.0b013e31819cf5da"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1097\/MD.0000000000002659"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1247\/csf.16023"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-011-1826-9"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2014.03.111"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1172\/JCI37196"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1111\/j.1399-0004.2009.01175.x"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1055\/s-0035-1558423"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2017121265"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006030277"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2014.394"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2019.04.057"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00405.2019","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,12,18]],"date-time":"2019-12-18T09:01:01Z","timestamp":1576659661000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00405.2019"}},"issued":{"date-parts":[[2020,1,1]]},"references-count":42,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2020,1,1]]}},"alternative-id":["10.1152\/ajprenal.00405.2019"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00405.2019","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2020,1,1]]}},{"indexed":{"date-parts":[[2026,2,8]],"date-time":"2026-02-08T18:49:48Z","timestamp":1770576588180,"version":"3.49.0"},"reference-count":71,"publisher":"American Physiological Society","issue":"3","funder":[{"DOI":"10.13039\/100018694","name":"EC | Horizon Europe | Excellent Science | HORIZON EUROPE Marie Sklodowska-Curie Actions","doi-asserted-by":"publisher","award":["745513"],"award-info":[{"award-number":["745513"]}],"id":[{"id":"10.13039\/100018694","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100009708","name":"Novo Nordisk Fonden","doi-asserted-by":"publisher","award":["NNF18OC0031686"],"award-info":[{"award-number":["NNF18OC0031686"]}],"id":[{"id":"10.13039\/501100009708","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100009708","name":"Novo Nordisk Fonden","doi-asserted-by":"publisher","award":["NNF21OC0067647"],"award-info":[{"award-number":["NNF21OC0067647"]}],"id":[{"id":"10.13039\/501100009708","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2024,9,1]]},"abstract":"<jats:p> The prostanoid EP3 receptor is proposed to play a key role in the kidney tubule and antagonize the effects of vasopressin on aquaporin-mediated water reabsorption. Here, we phenotyped a kidney tubule-specific inducible knockout mouse model of the EP3 receptor. Our major finding is that, even under physiological stress, tubular EP3 plays no detectable role in renal water or solute handling. This suggests that other EP receptors must be important for renal salt and water handling. <\/jats:p>","DOI":"10.1152\/ajprenal.00146.2024","type":"journal-article","created":{"date-parts":[[2024,7,4]],"date-time":"2024-07-04T08:14:38Z","timestamp":1720080878000},"page":"F504-F518","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":4,"title":["Inducible deletion of the prostaglandin EP3 receptor in kidney tubules of male and female mice has no major effect on water homeostasis"],"prefix":"10.1152","volume":"327","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7364-3865","authenticated-orcid":false,"given":"Cristina","family":"Esteva-Font","sequence":"first","affiliation":[{"name":"Department of Biomedicine, Aarhus University, Aarhus, Denmark"}]},{"given":"Frank","family":"Geurts","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Transplantation, Department of Internal Medicine, Erasmus Medical Center, University Medical Center Rotterdam, Rotterdam, The Netherlands"}]},{"given":"Toke P. K.","family":"Hansen","sequence":"additional","affiliation":[{"name":"Department of Biomedicine, Aarhus University, Aarhus, Denmark"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8738-3571","authenticated-orcid":false,"given":"Ewout J.","family":"Hoorn","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Transplantation, Department of Internal Medicine, Erasmus Medical Center, University Medical Center Rotterdam, Rotterdam, The Netherlands"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1623-199X","authenticated-orcid":false,"given":"Robert A.","family":"Fenton","sequence":"additional","affiliation":[{"name":"Department of Biomedicine, Aarhus University, Aarhus, Denmark"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1002\/ijc.31007"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/S0021-9258(19)45905-X"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.3390\/metabo12080721"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1161\/JAHA.123.032835"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2012020217"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00634.2011"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/j.krcp.2015.10.004"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.0000000000000269"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.06718.x"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00307.2023"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00564.x"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.270.5.F912"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.266.5.F823"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.R600038200"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.275.6.F955"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1042\/CS20070089"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1038\/labinvest.2017.133"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00414.2021"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1990.251"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.265.5.F643"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.262.2.F229"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.2.F257"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.259.2.F318"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1139\/y95-026"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.63.1.579"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1038\/s41581-021-00447-x"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.00640"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00204.2014"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1007\/s00125-016-3916-5"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00589.2015"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.pharmtox.41.1.661"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1124\/mol.110.068569"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1974.115"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1172\/JCI107207"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1038\/nm.1865"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0148055"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00072.2023"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90253.2008"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00088.2017"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1016\/j.ajpath.2012.09.014"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00049.2024"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00347.2023"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.150680"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.3389\/fnut.2016.00046"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2013.14"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.505"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00276.2006"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00129.2015"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00427.2021"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00123.2022"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00093.2015"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.3.F481"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.3390\/ijms18122539"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.2001.280.1.H327"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1016\/s0304-3940(02)00174-x"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2020101406"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1993.1904"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1993.391"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1016\/j.jmoldx.2011.08.002"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1111\/j.1432-1033.1993.tb18248.x"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1038\/26233"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1016\/s0016-5085(99)70398-7"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00197.2023"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1038\/5583"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1172\/JCI2872"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.3389\/fphys.2021.787598"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00183.2005"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00250.2022"},{"key":"B69","doi-asserted-by":"publisher","DOI":"10.2337\/db16-0773"},{"key":"B70","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.118.11694"},{"key":"B71","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2015050528"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00146.2024","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,8,20]],"date-time":"2024-08-20T18:53:08Z","timestamp":1724179988000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00146.2024"}},"issued":{"date-parts":[[2024,9,1]]},"references-count":71,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2024,9,1]]}},"alternative-id":["10.1152\/ajprenal.00146.2024"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00146.2024","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2024,9,1]]},"assertion":[{"value":"2024-05-14","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2024-06-20","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2024-06-21","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2024-08-20","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,2,10]],"date-time":"2026-02-10T12:27:24Z","timestamp":1770726444767,"version":"3.49.0"},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1996,9,1]]},"abstract":"<jats:p> Conflicting reports claim that circulating interleukin (IL)-6 promotes or suppresses renal disease. Although autoimmune MRL-lpr mice have an increase in serum IL-6, and kidneys can produce IL-6, the relevance of systemic and local exposure remains undefined. To investigate the impact of IL-6 on kidney disease, we constructed a gene transfer approach to deliver sustained, stable IL-6 into the kidney and circulation. We infused syngeneic genetically modified tubular epithelial cells (IL-6-TEC) under the renal capsule of autoimmune and nonautoimmune mice. IL-6-TEC did not incite renal injury in any strain. Furthermore, serum IL-6 levels, which were increased three- to fivefold by IL-6-TEC, did not alter the contralateral kidney. Therefore, neither local nor systemic exposure to IL-6 promoted renal injury. As opposed to IL-6, we previously established that granulocyte macrophage (GM)-colony-stimulating factor (CSF) initiates renal injury in autoimmune mice. To determine whether IL-6 could suppress GM-CSF-incited damage, we infused GM-CSF-TEC TEC along with IL-6-TEC. Local production of IL-6 into the kidney did not alter the tempo or severity of GM-CSF-induced injury. Thus neither local nor systemic delivery of IL-6 promotes or suppresses kidney disease. <\/jats:p>","DOI":"10.1152\/ajprenal.1996.271.3.f603","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T01:31:13Z","timestamp":1513992673000},"page":"F603-F609","source":"Crossref","is-referenced-by-count":0,"title":["A gene transfer system establishes interleukin-6 neither promotes nor suppresses renal injury"],"prefix":"10.1152","volume":"271","author":[{"given":"T.","family":"Naito","sequence":"first","affiliation":[{"name":"Laboratory of Immunogenetics and Transplantation, Brigham and Women'sHospital, Boston 02115, USA."}]},{"given":"H.","family":"Yokoyama","sequence":"additional","affiliation":[{"name":"Laboratory of Immunogenetics and Transplantation, Brigham and Women'sHospital, Boston 02115, USA."}]},{"given":"K. J.","family":"Moore","sequence":"additional","affiliation":[{"name":"Laboratory of Immunogenetics and Transplantation, Brigham and Women'sHospital, Boston 02115, USA."}]},{"given":"G.","family":"Dranoff","sequence":"additional","affiliation":[{"name":"Laboratory of Immunogenetics and Transplantation, Brigham and Women'sHospital, Boston 02115, USA."}]},{"given":"R. C.","family":"Mulligan","sequence":"additional","affiliation":[{"name":"Laboratory of Immunogenetics and Transplantation, Brigham and Women'sHospital, Boston 02115, USA."}]},{"given":"V. R.","family":"Kelley","sequence":"additional","affiliation":[{"name":"Laboratory of Immunogenetics and Transplantation, Brigham and Women'sHospital, Boston 02115, USA."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1996.271.3.F603","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:05:54Z","timestamp":1567958754000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1996.271.3.F603"}},"issued":{"date-parts":[[1996,9,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1996,9,1]]}},"alternative-id":["10.1152\/ajprenal.1996.271.3.F603"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1996.271.3.f603","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1996,9,1]]}},{"indexed":{"date-parts":[[2026,1,22]],"date-time":"2026-01-22T20:59:41Z","timestamp":1769115581824,"version":"3.49.0"},"reference-count":30,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1998,2,1]]},"abstract":"<jats:p>To gain insight into the mechanisms in the development of glomerulosclerosis in juxtamedullary cortex, the degree of glomerulosclerosis, glomerular tuft diameter, glomerular capillary pressure (P<jats:sub>gc<\/jats:sub>), and local renal blood flow (RBF) autoregulation were measured in superficial and juxtamedullary cortex of 10- and 70-wk-old spontaneously hypertensive rat (SHR), using aged matched Wistar-Kyoto (WKY) rats as controls. P<jats:sub>gc<\/jats:sub>was measured after corticotomy by direct micropuncture of glomeruli in superficial and juxtamedullary cortex. Total RBF was measured by a transit-time flowmeter (Transonic) and local blood flow by use of laser-Doppler flowmetry. The degree of glomerulosclerosis measured by a semiquantitative histological technique was significantly increased in juxtamedullary compared with superficial cortex in all groups. The difference was most pronounced in the juxtamedullary cortex of 70-wk-old SHR. P<jats:sub>gc<\/jats:sub>was significantly increased in juxtamedullary cortex compared with superficial cortex in 70-wk SHR (57.1 \u00b1 2.7 vs. 46.5 \u00b1 0.5 mmHg, P &lt; 0.01). The corresponding data set from 70-wk WKY was 45.5 \u00b1 0.43 vs. 41.6 \u00b1 1.5 ( P &lt; 0.05). The P<jats:sub>gc<\/jats:sub>in juxtamedullary cortex of 10-wk SHR was slightly higher than in superficial cortex (45.1 \u00b1 2.3 vs. 50.1 \u00b1 1.2 mmHg, P = 0.05), whereas there was no difference in 10-wk WKY. Glomerular diameter was larger in juxtamedullary cortex in old animals but not significantly different in 10-wk WKY rats and 10-wk SHR. Total RBF was reset to higher perfusion pressures in hypertensive rats. Juxtamedullary and superficial blood flow autoregulation were not significantly different from total RBF autoregulation in all groups. These results suggest that hypertrophy as well as increased P<jats:sub>gc<\/jats:sub>might contribute to the development of manifest glomerulosclerosis. Changes in local blood flow autoregulation do not seem to play a major role in the development of glomerulosclerosis.<\/jats:p>","DOI":"10.1152\/ajprenal.1998.274.2.f365","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T14:28:38Z","timestamp":1514039318000},"page":"F365-F373","source":"Crossref","is-referenced-by-count":17,"title":["Increased glomerular capillary pressure and size mediate glomerulosclerosis in SHR juxtamedullary cortex"],"prefix":"10.1152","volume":"274","author":[{"given":"Bjarne M.","family":"Iversen","sequence":"first","affiliation":[{"name":"Renal Research Group, Medical Department A, University of Bergen, N-5021 Haukeland, Norway; and"}]},{"given":"Kerstin","family":"Amann","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Heidelberg, Heidelberg, Germany"}]},{"given":"Fred I.","family":"Kvam","sequence":"additional","affiliation":[{"name":"Renal Research Group, Medical Department A, University of Bergen, N-5021 Haukeland, Norway; and"}]},{"given":"Xuemei","family":"Wang","sequence":"additional","affiliation":[{"name":"Renal Research Group, Medical Department A, University of Bergen, N-5021 Haukeland, Norway; and"}]},{"given":"Jarle","family":"Ofstad","sequence":"additional","affiliation":[{"name":"Renal Research Group, Medical Department A, University of Bergen, N-5021 Haukeland, Norway; and"}]}],"member":"24","reference":[{"issue":"36","key":"B1","first-page":"F35","volume":"267","author":"Anderson S.","year":"1994","journal-title":"Am. J. Physiol."},{"issue":"5","key":"B2","first-page":"F246","volume":"236","author":"Arendshorst W. J.","year":"1979","journal-title":"Am. J. Physiol."},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1977.tb06025.x"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1042\/cs0560203"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1983.143"},{"issue":"21","key":"B6","first-page":"F1003","volume":"252","author":"Bidani A.","year":"1987","journal-title":"Am. J. Physiol."},{"issue":"34","key":"B7","first-page":"F391","volume":"265","author":"Bidani A. K.","year":"1993","journal-title":"Am. J. Physiol."},{"issue":"27","key":"B8","first-page":"F1479","volume":"258","author":"Daniels F. H.","year":"1990","journal-title":"Am. J. Physiol."},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1172\/JCI113590"},{"issue":"31","key":"B10","first-page":"R947","volume":"262","author":"Fujihara C. K.","year":"1992","journal-title":"Am. J. Physiol."},{"issue":"20","key":"B11","first-page":"F25","volume":"251","author":"G\u00f8ranson A.","year":"1986","journal-title":"Am. J. Physiol."},{"key":"B12","first-page":"77","volume":"54","author":"Grond J.","year":"1986","journal-title":"Lab. Invest."},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1987.142"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/0026-2862(70)90009-9"},{"issue":"31","key":"B15","first-page":"F361","volume":"262","author":"Iversen B. M.","year":"1992","journal-title":"Am. J. Physiol."},{"issue":"23","key":"B16","first-page":"F284","volume":"254","author":"Iversen B. M.","year":"1988","journal-title":"Am. J. Physiol."},{"issue":"21","key":"B17","first-page":"F480","volume":"252","author":"Iversen B. M.","year":"1987","journal-title":"Am. J. Physiol."},{"issue":"33","key":"B18","first-page":"R578","volume":"264","author":"Mattson D. L.","year":"1993","journal-title":"Am. J. Physiol."},{"issue":"3","key":"B19","first-page":"F357","volume":"234","author":"Navar L. G.","year":"1978","journal-title":"Am. J. Physiol."},{"key":"B20","first-page":"S8","volume":"41","author":"Ofstad J.","year":"1992","journal-title":"Kidney Int."},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1986.76"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1984.147"},{"key":"B23","doi-asserted-by":"crossref","first-page":"1775","DOI":"10.1681\/ASN.V3111775","volume":"3","author":"Simons J. L.","year":"1993","journal-title":"J. Am. Soc. Nephrol."},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1994.tb09782.x"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1979.tb06376.x"},{"issue":"38","key":"B26","first-page":"F515","volume":"269","author":"Wang X.","year":"1995","journal-title":"Am. J. Physiol."},{"key":"B27","first-page":"237","volume":"3","author":"Weibel E. R.","year":"1973","journal-title":"Principles of Techniques of Electron Microscopy"},{"key":"B28","doi-asserted-by":"crossref","first-page":"173","DOI":"10.1152\/ajplegacy.1964.207.1.173","volume":"207","author":"Wiederhjelm C. A.","year":"1964","journal-title":"Am. J. Physiol."},{"key":"B29","doi-asserted-by":"crossref","first-page":"327","DOI":"10.1038\/ki.1988.77","volume":"33","author":"Yoshida Y.","year":"1988","journal-title":"Kidney Int."},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1989.35"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1998.274.2.F365","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:46:46Z","timestamp":1660189606000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1998.274.2.F365"}},"issued":{"date-parts":[[1998,2,1]]},"references-count":30,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1998,2,1]]}},"alternative-id":["10.1152\/ajprenal.1998.274.2.F365"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1998.274.2.f365","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1998,2,1]]}},{"indexed":{"date-parts":[[2026,1,22]],"date-time":"2026-01-22T20:21:32Z","timestamp":1769113292709,"version":"3.49.0"},"reference-count":45,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,8,15]]},"abstract":"<jats:p> Increasing evidence indicates that vitamin D deficiency exacerbates chronic kidney injury, but its effects on renal enlargement in polycystic kidney disease (PKD) are not known. In this study, male Lewis polycystic kidney disease (LPK) rats received a normal diet (ND; AIN-93G) supplemented with or without cholecalciferol (vitamin D-deficient diet, VDD; both 0.5% calcium), commenced at either postnatal week 3 (until weeks 10\u201320; study 1) or from week 10 (until week 20; study 2). Levels of 25-hydroxy vitamin D were reduced in groups receiving the VDD (12 \u00b1 1 nmol\/l vs. 116 \u00b1 5 in ND; P &lt; 0.001). In study 1, food intake and weight gain increased by \u223c25% in LPK rats receiving the VDD ad libitum, and at week 20 this was associated with a mild reduction in the corrected serum calcium (SCa<jats:sup>2+<\/jats:sup>, 7.4%) and TKW:BW ratio (8.8%), and exacerbation of proteinuria (87%) and hypertension (19%; all P &lt; 0.05 vs. ND). When LPK rats were pair-fed for weeks 3\u201310, there was a further reduction in the SCa<jats:sup>2+<\/jats:sup> (25%) and TKW:BW ratio (22%) in the VDD group ( P &lt; 0.05 vs. ND). In study 2, the VDD did not alter food intake and body weight, reduced SCa<jats:sup>2+<\/jats:sup> (7.7%), worsened proteinuria (41.9%), interstitial monocyte accumulation (26.4%), renal dysfunction (21.4%), and cardiac enlargement (13.2%, all P &lt; 0.05), but there was a trend for a reduction in the TKW:BW ratio (13%, P = 0.09). These data suggest that chronic vitamin D deficiency has adverse long-term actions on proteinuria, interstitial inflammation, renal function, and cardiovascular disease in PKD, and these negate its mild inhibitory effect on kidney enlargement. <\/jats:p>","DOI":"10.1152\/ajprenal.00411.2012","type":"journal-article","created":{"date-parts":[[2013,5,23]],"date-time":"2013-05-23T02:06:57Z","timestamp":1369274817000},"page":"F574-F582","source":"Crossref","is-referenced-by-count":18,"title":["Chronic effects of dietary vitamin D deficiency without increased calcium supplementation on the progression of experimental polycystic kidney disease"],"prefix":"10.1152","volume":"305","author":[{"given":"Gopala K.","family":"Rangan","sequence":"first","affiliation":[{"name":"Michael Stern Translational Laboratory for Polycystic Kidney Disease, Centre for Transplant and Renal Research, Westmead Millennium Institute, The University of Sydney, Sydney, Australia;"},{"name":"Department of Renal Medicine, Westmead Hospital, Western Sydney Local Health District, Sydney, Australia;"}]},{"given":"Kristina G.","family":"Schwensen","sequence":"additional","affiliation":[{"name":"Michael Stern Translational Laboratory for Polycystic Kidney Disease, Centre for Transplant and Renal Research, Westmead Millennium Institute, The University of Sydney, Sydney, Australia;"}]},{"given":"Sheryl L.","family":"Foster","sequence":"additional","affiliation":[{"name":"Department of Magnetic Resonance Imaging, Westmead Hospital and The University of Sydney, Sydney, Australia; and"}]},{"given":"Mayuresh S.","family":"Korgaonkar","sequence":"additional","affiliation":[{"name":"Brain Dynamics Centre, Westmead Millennium Institute, The University of Sydney, Sydney, Australia"}]},{"given":"Anthony","family":"Peduto","sequence":"additional","affiliation":[{"name":"Department of Magnetic Resonance Imaging, Westmead Hospital and The University of Sydney, Sydney, Australia; and"}]},{"given":"David C.","family":"Harris","sequence":"additional","affiliation":[{"name":"Michael Stern Translational Laboratory for Polycystic Kidney Disease, Centre for Transplant and Renal Research, Westmead Millennium Institute, The University of Sydney, Sydney, Australia;"},{"name":"Department of Renal Medicine, Westmead Hospital, Western Sydney Local Health District, Sydney, Australia;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbadis.2010.09.016"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.02010309"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1210\/jc.2008-1454"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1097\/01.pap.0000201831.77472.d3"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-004-1665-z"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1210\/er.2008-0004"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1093\/jn\/114.8.1377"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.2174\/157489011795933800"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2007.04.015"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.419"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1093\/ajcn\/80.6.1689S"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(10)61032-X"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1210\/endo.133.2.8393775"},{"key":"B14","first-page":"529A","volume":"21","author":"Gitomer B","year":"2010","journal-title":"J Am Soc Nephrol"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMcp0804458"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00195.2003"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2010.18"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1038\/nrendo.2010.234"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/j.transproceed.2011.08.081"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/j.jacc.2008.08.050"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002009"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-007-0641-9"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfs138"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1186\/1471-2164-13-393"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002629"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00362.2007"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1515\/jpem.2011.107"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007040490"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1159\/000101828"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1586\/erc.10.142"},{"key":"B31","first-page":"A403","volume":"10","author":"Rangan GK","year":"2005","journal-title":"Nephrology (Carlton)"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.501"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfr744"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1111\/j.1753-4887.2008.00094.x"},{"key":"B35","first-page":"e93","volume":"117","author":"Schwensen KG","year":"2011","journal-title":"Nephron"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006020136"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006090985"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfl595"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2011.196"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.108.115220"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-010-1585-z"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1126\/science.280.5368.1378"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005060645"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.453"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1007\/s001090050221"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00411.2012","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T23:47:51Z","timestamp":1567986471000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00411.2012"}},"issued":{"date-parts":[[2013,8,15]]},"references-count":45,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2013,8,15]]}},"alternative-id":["10.1152\/ajprenal.00411.2012"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00411.2012","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2013,8,15]]}},{"indexed":{"date-parts":[[2026,1,19]],"date-time":"2026-01-19T04:04:34Z","timestamp":1768795474159,"version":"3.49.0"},"reference-count":52,"publisher":"American Physiological Society","issue":"5","funder":[{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["R01 DK101484"],"award-info":[{"award-number":["R01 DK101484"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["R01 DK100357"],"award-info":[{"award-number":["R01 DK100357"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["R01 DK098204"],"award-info":[{"award-number":["R01 DK098204"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["P30 DK079307"],"award-info":[{"award-number":["P30 DK079307"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["R01 118726"],"award-info":[{"award-number":["R01 118726"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["R01 DK098204"],"award-info":[{"award-number":["R01 DK098204"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["P30 DK079307"],"award-info":[{"award-number":["P30 DK079307"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100004543","name":"China Scholarship Council","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100004543","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100008392","name":"Danish Medical Research Council","doi-asserted-by":"crossref","award":["DFF 12-132499"],"award-info":[{"award-number":["DFF 12-132499"]}],"id":[{"id":"10.13039\/100008392","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100008392","name":"Danish Medical Research Council","doi-asserted-by":"crossref","award":["DFF 4183-00014B"],"award-info":[{"award-number":["DFF 4183-00014B"]}],"id":[{"id":"10.13039\/100008392","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/501100002739","name":"Aarhus University Research Foundation","doi-asserted-by":"crossref","award":["AUFF-E-2017-7-25"],"award-info":[{"award-number":["AUFF-E-2017-7-25"]}],"id":[{"id":"10.13039\/501100002739","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2020,5,1]]},"abstract":"<jats:p>Proximal tubule (PT) cells express a single saturable albumin-binding site whose affinity matches the estimated tubular concentration of albumin; however, albumin uptake capacity is greatly increased under nephrotic conditions. Deciphering the individual contributions of megalin and cubilin to the uptake of normal and nephrotic levels of albumin is impossible in vivo, as knockout of megalin in mice globally disrupts PT endocytic uptake. We quantified concentration-dependent albumin uptake in an optimized opossum kidney cell culture model and fit the kinetic profiles to identify albumin-binding affinities and uptake capacities. Mathematical deconvolution fit best to a three-component model that included saturable high- and low-affinity uptake sites for albumin and underlying nonsaturable uptake consistent with passive uptake of albumin in the fluid phase. Knockdown of cubilin or its chaperone amnionless selectively reduced the binding capacity of the high-affinity site, whereas knockdown of megalin impacted the low-affinity site. Knockdown of disabled-2 decreased the capacities of both binding sites. Additionally, knockdown of megalin or disabled-2 profoundly inhibited the uptake of a fluid phase marker, with cubilin knockdown having a more modest effect. We propose a novel model for albumin retrieval along the PT in which cubilin and megalin receptors have different functions in recovering filtered albumin in proximal tubule cells. Cubilin binding to albumin is tuned to capture normally filtered levels of the protein. In contrast, megalin binding to albumin is of lower affinity, and its expression is also essential for enabling the recovery of high concentrations of albumin in the fluid phase.<\/jats:p>","DOI":"10.1152\/ajprenal.00030.2020","type":"journal-article","created":{"date-parts":[[2020,3,23]],"date-time":"2020-03-23T09:00:28Z","timestamp":1584954028000},"page":"F1284-F1294","source":"Crossref","is-referenced-by-count":46,"title":["Distinct functions of megalin and cubilin receptors in recovery of normal and nephrotic levels of filtered albumin"],"prefix":"10.1152","volume":"318","author":[{"given":"Qidong","family":"Ren","sequence":"first","affiliation":[{"name":"School of Medicine, Tsinghua University, Beijing, China"},{"name":"Renal-Electrolyte Division, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania"}]},{"given":"Kathrin","family":"Weyer","sequence":"additional","affiliation":[{"name":"Department of Biomedicine, Aarhus University, Aarhus, Denmark"}]},{"given":"Youssef","family":"Rbaibi","sequence":"additional","affiliation":[{"name":"Renal-Electrolyte Division, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania"}]},{"given":"Kimberly R.","family":"Long","sequence":"additional","affiliation":[{"name":"Renal-Electrolyte Division, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1012-1722","authenticated-orcid":false,"given":"Roderick J.","family":"Tan","sequence":"additional","affiliation":[{"name":"Renal-Electrolyte Division, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania"}]},{"given":"Rikke","family":"Nielsen","sequence":"additional","affiliation":[{"name":"Department of Biomedicine, Aarhus University, Aarhus, Denmark"}]},{"given":"Erik I.","family":"Christensen","sequence":"additional","affiliation":[{"name":"Department of Biomedicine, Aarhus University, Aarhus, Denmark"}]},{"given":"Catherine J.","family":"Baty","sequence":"additional","affiliation":[{"name":"Renal-Electrolyte Division, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania"}]},{"given":"Ossama B.","family":"Kashlan","sequence":"additional","affiliation":[{"name":"Renal-Electrolyte Division, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania"}]},{"given":"Ora A.","family":"Weisz","sequence":"additional","affiliation":[{"name":"Renal-Electrolyte Division, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1042\/BJ20070919"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010050492"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1172\/JCI129937"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.264.2.F239"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1172\/JCI8862"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1111\/j.1742-4658.2005.04857.x"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/physiol.00022.2012"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1979.132"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfs565"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004110925"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.4.F900"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1002\/ar.a.10123"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-012-2335-1"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00228.2017"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1146\/annurev-physiol-022516-034234"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1210\/me.2005-0209"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.2.F286"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00164.2005"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00243.2004"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/j.febslet.2004.12.031"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0178796"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.14814\/phy2.12086"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.01090.2003"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2015020190"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1038\/s41467-018-07468-4"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014111067"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)65238-8"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.e17-04-0211"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1979.128"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.9.5235"},{"key":"B31","doi-asserted-by":"crossref","first-page":"16564","DOI":"10.1016\/S0021-9258(19)85456-X","volume":"268","author":"Moestrup SK","year":"1993","journal-title":"J Biol Chem"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009040379"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/21.7.1555"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00292.2004"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2013.218"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.241516998"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1172\/JCI111270"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1016\/j.devcel.2019.08.001"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-0854.2010.01042.x"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00459.2019"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1111\/tra.12648"},{"key":"B42","first-page":"1654","volume":"142","author":"Sahali D","year":"1993","journal-title":"Am J Pathol"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2018050522"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1007\/BF00550876"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1159\/000321161"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1242\/dev.01341"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.263.4.F601"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014111107"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2017.07.024"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfr525"},{"key":"B51","first-page":"387","volume":"48","author":"Zaias J","year":"2009","journal-title":"J Am Assoc Lab Anim Sci"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M405608200"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00030.2020","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,3,5]],"date-time":"2021-03-05T16:09:55Z","timestamp":1614960595000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00030.2020"}},"issued":{"date-parts":[[2020,5,1]]},"references-count":52,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2020,5,1]]}},"alternative-id":["10.1152\/ajprenal.00030.2020"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00030.2020","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2020,5,1]]}},{"indexed":{"date-parts":[[2026,1,23]],"date-time":"2026-01-23T09:49:22Z","timestamp":1769161762965,"version":"3.49.0"},"reference-count":38,"publisher":"American Physiological Society","issue":"11","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2012,6,1]]},"abstract":"<jats:p>Loss of functional nephrons associated with chronic kidney disease induces glomerular hyperfiltration and compensatory renal hypertrophy. We hypothesized that the endothelial nitric oxide synthase (eNOS) [soluble guanylate cyclase (sGC)] protein kinase G (PKG) pathway plays an important role in compensatory renal hypertrophy after unilateral nephrectomy. Analysis of mice subjected to unilateral nephrectomy showed increases in kidney weight-to-body weight and total protein-to-DNA ratios in wild-type but not eNOS knockout (eNOSKO) mice. Serum creatinine and blood urea nitrogen increased after nephrectomy in eNOSKO but not in wild-type mice. Furthermore, Bay 41\u20132272, an sGC stimulator, induced compensatory renal hypertrophy in eNOSKO mice and rescued renal function. The NO donor S-nitrosoglutathione (GSNO) and Bay 41\u20132272 stimulated PKG activity and induced phosphorylation of Akt protein in human proximal tubular cells. GSNO also induced phosphorylation of eukaryotic initiation factor 4E-binding protein and ribosomal protein S6. Our results highlight the importance of the eNOS-NO-PKG pathway in compensatory renal hypertrophy and suggest that reduced eNOS-NO bioavailability due to endothelial dysfunction is the underlying mechanism of failure of compensatory hypertrophy and acceleration of progressive renal dysfunction.<\/jats:p>","DOI":"10.1152\/ajprenal.00459.2011","type":"journal-article","created":{"date-parts":[[2012,3,1]],"date-time":"2012-03-01T04:15:15Z","timestamp":1330575315000},"page":"F1402-F1408","source":"Crossref","is-referenced-by-count":31,"title":["Endothelial dysfunction promotes the transition from compensatory renal hypertrophy to kidney injury after unilateral nephrectomy in mice"],"prefix":"10.1152","volume":"302","author":[{"given":"Hajime","family":"Nagasu","sequence":"first","affiliation":[{"name":"Department of Nephrology and Hypertension, Kawasaki Medical School, Kurashiki, Okayama, Japan; and"}]},{"given":"Minoru","family":"Satoh","sequence":"additional","affiliation":[{"name":"Department of Nephrology and Hypertension, Kawasaki Medical School, Kurashiki, Okayama, Japan; and"}]},{"given":"Kengo","family":"Kidokoro","sequence":"additional","affiliation":[{"name":"Department of Nephrology and Hypertension, Kawasaki Medical School, Kurashiki, Okayama, Japan; and"}]},{"given":"Yuko","family":"Nishi","sequence":"additional","affiliation":[{"name":"Department of Nephrology and Hypertension, Kawasaki Medical School, Kurashiki, Okayama, Japan; and"}]},{"given":"Keith M.","family":"Channon","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular Medicine, University of Oxford, Oxford, United Kingdom"}]},{"given":"Tamaki","family":"Sasaki","sequence":"additional","affiliation":[{"name":"Department of Nephrology and Hypertension, Kawasaki Medical School, Kurashiki, Okayama, Japan; and"}]},{"given":"Naoki","family":"Kashihara","sequence":"additional","affiliation":[{"name":"Department of Nephrology and Hypertension, Kawasaki Medical School, Kurashiki, Okayama, Japan; and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M110508200"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.265"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00186.2009"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1055\/s-0029-1220752"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1001\/jama.298.17.2038"},{"key":"B5a","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1986.45"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/0026-0495(95)90223-6"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1183\/09059180.00003809"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.110.167015"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0611079104"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1983.64"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1042\/BA20090130"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1097\/00005344-199912000-00016"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.23.16.5726-5737.2003"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1007\/s10157-007-0011-8"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00414.2002"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1253\/circj.CJ-10-0910"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(02)01254-0"},{"key":"B18","first-page":"289","volume":"40","author":"Mattart M","year":"2003","journal-title":"Biorheology"},{"key":"B18a","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0502236102"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2011.02.089"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfq139"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90450.2008"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1172\/JCI4394"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1007\/s12576-009-0048-4"},{"key":"B24","doi-asserted-by":"crossref","first-page":"S17","DOI":"10.33549\/physiolres.930000.55.S1.17","volume":"55","author":"Pechanova O","year":"2006","journal-title":"Physiol Res"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.110.940932"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.106.108878"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00669.x"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00828.x"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1038\/hr.2009.190"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M710269200"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000130563.67384.81"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000237669.64066.c5"},{"key":"B33","first-page":"730","volume":"3","author":"Triggle CR","journal-title":"Front Biosci (Schol Ed)"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1999.276.6.R1718"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1936024100"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-6143.2008.02339.x"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00459.2011","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,6,20]],"date-time":"2023-06-20T21:12:53Z","timestamp":1687295573000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00459.2011"}},"issued":{"date-parts":[[2012,6,1]]},"references-count":38,"journal-issue":{"issue":"11","published-print":{"date-parts":[[2012,6,1]]}},"alternative-id":["10.1152\/ajprenal.00459.2011"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00459.2011","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2012,6,1]]}},{"indexed":{"date-parts":[[2026,2,19]],"date-time":"2026-02-19T02:06:33Z","timestamp":1771466793566,"version":"3.50.1"},"reference-count":48,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2008,3]]},"abstract":"<jats:p> This study revealed that in awake chronic spinal cord-injured (SCI) cats reflexes from perigenital skin area to the bladder can be either inhibitory or excitatory. Electrical perigenital stimulation at frequencies between 5 and 7 Hz significantly inhibited large-amplitude rhythmic reflex bladder activity, whereas frequencies between 20 and 40 Hz induced large-amplitude bladder contractions even at low bladder volumes when reflex bladder activity was absent. Both inhibitory and excitatory effects were enhanced as the stimulation intensity increased (5\u201330 V, 0.2-ms pulse width). During cystometrograms, the inhibitory stimulation (7 Hz) significantly increased the micturition volume threshold 35 \u00b1 13% above the control volume, while the excitatory stimulation (30 Hz) significantly reduced the threshold 21 \u00b1 3%. Mechanical perigenital stimulation applied by repeated light stroking of the perigenital skin with a cotton swab only induced an excitatory effect on the bladder. Both electrical and mechanical perigenital stimuli induced large-amplitude (&gt;30 cmH<jats:sub>2<\/jats:sub>O) bladder contractions that were relatively consistent over a range of bladder volumes (10\u201390% of the capacity). However, the excitatory electrical stimulation only induced bladder contractions lasting on average 42.2 \u00b1 3.9 s, but the mechanical stimulation induced bladder contractions that lasted as long as the stimulation continued (2\u20133 min). Excitatory electrical or mechanical perigenital stimulation also induced poststimulus voiding. The ability to either inhibit or excite the bladder by noninvasive methods could significantly transform the current clinical management of bladder function after SCI. <\/jats:p>","DOI":"10.1152\/ajprenal.00443.2007","type":"journal-article","created":{"date-parts":[[2007,12,26]],"date-time":"2007-12-26T20:44:18Z","timestamp":1198701858000},"page":"F591-F602","source":"Crossref","is-referenced-by-count":35,"title":["Inhibitory and excitatory perigenital-to-bladder spinal reflexes in the cat"],"prefix":"10.1152","volume":"294","author":[{"given":"Changfeng","family":"Tai","sequence":"first","affiliation":[]},{"given":"Bing","family":"Shen","sequence":"additional","affiliation":[]},{"given":"Jicheng","family":"Wang","sequence":"additional","affiliation":[]},{"given":"Michael B.","family":"Chancellor","sequence":"additional","affiliation":[]},{"given":"James R.","family":"Roppolo","sequence":"additional","affiliation":[]},{"given":"William C.","family":"de Groat","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1002\/nau.10134"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.17-21-08402.1997"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(17)54147-6"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1152\/jn.00978.2004"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2006.111815"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1038\/sc.1994.126"},{"key":"R7","unstructured":"Cardenas DD, Kelly E, Mayo ME. Manual stimulation of reflex voiding after spinal cord injury. Arch Phys Med Rehabil 66: 459\u2013462, 1985."},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1097\/00005392-199907000-00002"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1999.277.3.R786"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(70)90137-X"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(71)90125-9"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(75)90417-5"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1976.sp011381"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1016\/S0031-9384(02)00919-8"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1016\/S0166-4328(97)00185-X"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(75)90884-7"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1016\/0165-1838(90)90105-R"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1972.sp009985"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1968.sp008524"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1969.sp008683"},{"key":"R22","unstructured":"Fall M, Erlandson BE, Carlsson CA, Lindstrom S. The effect of intravaginal electrical stimulation on the feline urethra and urinary bladder: neuronal mechanisms. Scand J Urol Nephrol 44: 19\u201330, 1978."},{"key":"R23","unstructured":"Fall M, Lindstrom S. Electrical stimulation: a physiologic approach to the treatment of urinary incontinence. Urol Clin North Am 18: 393\u2013407, 1991."},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1097\/01.ju.0000158160.11083.1b"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1038\/sj.sc.3101132"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.1999.0599t.x"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(94)90054-X"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1038\/sj.sc.3101177"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1006\/exnr.1994.1010"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(17)52127-8"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1002\/ar.1091800104"},{"key":"R32","unstructured":"Mazieres L, Jiang C, Lindstrom S. Bladder parasympathetic response to electrical stimulation of urethral afferents in the cat. Neurourol Urodyn 16: 471\u2013472, 1997."},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.1998.531bb.x"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2006.112995"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1088\/1741-2560\/4\/4\/002"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1038\/sj.sc.3100440"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1038\/sc.1996.17"},{"key":"R38","unstructured":"Rodriquez AA, Awad E. Detrusor muscle and sphincter response to anorectal stimulation in spinal cord injury. Arch Phys Med Rehabil 60: 269\u2013272, 1979."},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1016\/S0304-3940(98)00155-4"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1016\/j.expneurol.2006.01.007"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1016\/j.expneurol.2005.09.013"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1002\/nau.20374"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(17)51984-9"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1038\/sj.sc.3101519"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1002\/nau.1930050404"},{"key":"R46","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(17)40632-X"},{"key":"R47","doi-asserted-by":"publisher","DOI":"10.1002\/nau.1930120306"},{"key":"R48","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(17)37145-8"},{"key":"R49","doi-asserted-by":"publisher","DOI":"10.1097\/00019052-200012000-00011"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00443.2007","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:52:16Z","timestamp":1567968736000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00443.2007"}},"issued":{"date-parts":[[2008,3]]},"references-count":48,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2008,3]]}},"alternative-id":["10.1152\/ajprenal.00443.2007"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00443.2007","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2008,3]]}},{"indexed":{"date-parts":[[2026,3,18]],"date-time":"2026-03-18T11:25:42Z","timestamp":1773833142589,"version":"3.50.1"},"reference-count":48,"publisher":"American Physiological Society","issue":"1","funder":[{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK063114"],"award-info":[{"award-number":["DK063114"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100006733","name":"Indiana University","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100006733","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100019592","name":"Veterans Administration Medical Center","doi-asserted-by":"publisher","award":["BX001736-01A1"],"award-info":[{"award-number":["BX001736-01A1"]}],"id":[{"id":"10.13039\/100019592","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2024,1,1]]},"abstract":"<jats:p> Despite the apparent recovery of renal filtration function following acute kidney injury (AKI) in rats, the renal hemodynamic reserve response is significantly attenuated, suggesting that clinical evaluation of this parameter may provide information on the potential development of chronic kidney disease. Treatments such as hydrodynamic isotonic fluid delivery, or other treatments in the early post-AKI period, could minimize chronic inflammation or loss of microvessels with the potential to promote a more favorable outcome on long-term function. <\/jats:p>","DOI":"10.1152\/ajprenal.00204.2023","type":"journal-article","created":{"date-parts":[[2023,10,26]],"date-time":"2023-10-26T08:00:23Z","timestamp":1698307223000},"page":"F86-F94","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":4,"title":["Impaired hemodynamic renal reserve response following recovery from established acute kidney injury and improvement by hydrodynamic isotonic fluid delivery"],"prefix":"10.1152","volume":"326","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5712-6750","authenticated-orcid":false,"given":"Md Mahbub","family":"Ullah","sequence":"first","affiliation":[{"name":"Department of Anatomy, Cell Biology and Physiology, Indiana University School of Medicine, Indianapolis, Indiana, United States"}]},{"given":"Jason A.","family":"Collett","sequence":"additional","affiliation":[{"name":"Department of Anatomy, Cell Biology and Physiology, Indiana University School of Medicine, Indianapolis, Indiana, United States"}]},{"given":"Robert L.","family":"Bacallao","sequence":"additional","affiliation":[{"name":"Department of Anatomy, Cell Biology and Physiology, Indiana University School of Medicine, Indianapolis, Indiana, United States"},{"name":"Division of Nephrology, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana, United States"},{"name":"Roudebush Veterans Affairs Medical Center, Indianapolis, Indiana, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4649-3464","authenticated-orcid":false,"given":"David P.","family":"Basile","sequence":"additional","affiliation":[{"name":"Department of Anatomy, Cell Biology and Physiology, Indiana University School of Medicine, Indianapolis, Indiana, United States"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1002\/cphy.c110041"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1002\/ar.24260"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2017060675"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.281.5.F887"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.426"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2022.10.006"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.761_5.x"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2011.16"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1159\/000477181"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010040430"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2019.10.006"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0143961"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013101110"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00462.2016"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00821.2007"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2011.149"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/0306-9877(95)90221-x"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1159\/000449511"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.11070821"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2016.11.028"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1159\/000363721"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00237.2020"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2016040404"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1111\/1440-1681.13301"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00546.2010"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1999.277.5.H1985"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2019111179"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1038\/s41467-019-12872-5"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1111\/jcmm.13071"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00169.2002"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.91022.2008"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2015030309"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra1214243"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.12101112"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2015.3"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2017.06.030"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.2005477117"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfy227"},{"key":"B39","first-page":"349","volume":"49","author":"Fagugli RM","year":"1998","journal-title":"Clin Nephrol"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00691.2011"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1991.226"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.2337\/diab.41.3.267"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.257.6.F1140"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00871.2007"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00386.2004"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1172\/JCI126108"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.3389\/fphys.2023.1194803"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2015020204"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00204.2023","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,2,7]],"date-time":"2024-02-07T14:06:50Z","timestamp":1707314810000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00204.2023"}},"issued":{"date-parts":[[2024,1,1]]},"references-count":48,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2024,1,1]]}},"alternative-id":["10.1152\/ajprenal.00204.2023"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00204.2023","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2024,1,1]]},"assertion":[{"value":"2023-07-18","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2023-10-04","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2023-10-18","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2023-12-20","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,3,19]],"date-time":"2026-03-19T17:57:56Z","timestamp":1773943076531,"version":"3.50.1"},"reference-count":50,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2014,9,1]]},"abstract":"<jats:p> Emerging data have suggested that acute kidney injury (AKI) is often incompletely repaired and can lead to chronic kidney disease (CKD), which is characterized by tubulointerstitial inflammation and fibrosis. However, the underlying mechanisms linking AKI to CKD remain obscure. The present study aimed to investigate the role of cysteine-rich protein 61 (Cyr61) after unilateral kidney ischemia-reperfusion injury (IRI) in mice. After IRI, increased expression of Cyr61 was detected, predominately in the proximal tubular epithelium. This was confirmed by in vitro experiments, which showed that hypoxia stimulated Cyr61 expression in cultured proximal tubular epithelial cells. The proinflammatory property of Cyr61 was indicated by its ability to upregulate monocyte chemoattractant protein-1 and IL-6. Additionally, we found elevated urinary Cyr61 excretion in patients with AKI. Notably, treatment of mice with an anti-Cyr61 antibody attenuated the upregulation of kidney monocyte chemoattractant protein-1, IL-6, IL-1\u03b2, and macrophage inflammatory protein-2 and reduced the infiltration of F4\/80-positive macrophages on days 7 and 14 after IRI. In addition, blockade of Cyr61 reduced the mRNA expression of collagen, transforming growth factor-\u03b2, and plasminogen activator inhibitor-I as well as the degree of collagen fibril accumulation, as evaluated by picrosirius red staining, and levels of \u03b1-smooth muscle actin proteins by day 14. Concurrently, in the treated group, peritubular microvascular density was more preserved on day 14. We conclude that Cyr61 blockade inhibits the triad of inflammation, interstitial fibrosis, and capillary rarefaction after severe ischemic AKI. The results of this study expand the knowledge of the mechanisms underlying the AKI-to-CKD transition and suggest that Cyr61 is a potential therapeutic target. <\/jats:p>","DOI":"10.1152\/ajprenal.00670.2013","type":"journal-article","created":{"date-parts":[[2014,6,12]],"date-time":"2014-06-12T07:37:22Z","timestamp":1402558642000},"page":"F581-F592","source":"Crossref","is-referenced-by-count":42,"title":["Blockade of cysteine-rich protein 61 attenuates renal inflammation and fibrosis after ischemic kidney injury"],"prefix":"10.1152","volume":"307","author":[{"given":"Chun-Fu","family":"Lai","sequence":"first","affiliation":[{"name":"Graduate Institute of Clinical Medicine, National Taiwan University College of Medicine, Taipei, Taiwan;"},{"name":"Department of Internal Medicine, National Taiwan University Hospital and College of Medicine, Taipei, Taiwan;"}]},{"given":"Shuei-Liong","family":"Lin","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, National Taiwan University Hospital and College of Medicine, Taipei, Taiwan;"},{"name":"Graduate Institute of Physiology, National Taiwan University College of Medicine, Taipei, Taiwan;"}]},{"given":"Wen-Chih","family":"Chiang","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, National Taiwan University Hospital and College of Medicine, Taipei, Taiwan;"}]},{"given":"Yung-Ming","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, National Taiwan University Hospital and College of Medicine, Taipei, Taiwan;"},{"name":"Department of Internal Medicine, National Taiwan University Hospital Yun-Lin Branch, Douliou City, Taiwan;"}]},{"given":"Vin-Cent","family":"Wu","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, National Taiwan University Hospital and College of Medicine, Taipei, Taiwan;"}]},{"given":"Guang-Huar","family":"Young","sequence":"additional","affiliation":[{"name":"Department of Surgery, National Taiwan University Hospital and College of Medicine, Taipei, Taiwan; and"}]},{"given":"Wen-Jo","family":"Ko","sequence":"additional","affiliation":[{"name":"Department of Surgery, National Taiwan University Hospital and College of Medicine, Taipei, Taiwan; and"}]},{"given":"Min-Liang","family":"Kuo","sequence":"additional","affiliation":[{"name":"Institute of Biochemical Sciences, National Taiwan University College of Life Science, Taipei, Taiwan"}]},{"given":"Tun-Jun","family":"Tsai","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, National Taiwan University Hospital and College of Medicine, Taipei, Taiwan;"}]},{"given":"Kwan-Dun","family":"Wu","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, National Taiwan University Hospital and College of Medicine, Taipei, Taiwan;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000182903.16652.d7"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.0902792"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002312"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00596.2007"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00546.2010"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1038\/nbt0510-436"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1172\/JCI45161"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1126\/scitranslmed.3000111"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/j.biocel.2008.07.025"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M107666200"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1002\/jcb.21194"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00766.x"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004090740"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2009.86"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2010.03.003"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1186\/cc12824"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2009.080295"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2012.20"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/j.jtcvs.2009.07.007"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002715"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010050553"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/ncb2070"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.00049-13"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfm694"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00619.2009"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/j.biochi.2010.11.010"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0056481"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1186\/cc11419"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2012.463"},{"key":"B30","first-page":"5","volume":"27","author":"Li PK","year":"2013","journal-title":"Acta Nephrologica"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006030221"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1016\/j.ajpath.2010.10.012"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005040435"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000034909.10994.8A"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2008.080433"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0912228107"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2009.289"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1007\/s00018-012-0981-x"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.2741\/3361"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00633.x"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1242\/dev.012187"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.110.945261"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200603176"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1038\/labinvest.2010.45"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)63946-6"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00017.2010"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1001\/jama.2009.1322"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1016\/j.ajpath.2012.09.009"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2011.259"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1038\/nm.2144"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00670.2013","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T01:01:56Z","timestamp":1567990916000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00670.2013"}},"issued":{"date-parts":[[2014,9,1]]},"references-count":50,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2014,9,1]]}},"alternative-id":["10.1152\/ajprenal.00670.2013"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00670.2013","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2014,9,1]]}},{"indexed":{"date-parts":[[2026,3,25]],"date-time":"2026-03-25T22:16:26Z","timestamp":1774476986394,"version":"3.50.1"},"reference-count":54,"publisher":"American Physiological Society","issue":"7","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,10,1]]},"abstract":"<jats:p>In the present study, we examine the hypothesis that the nitric oxide (NO) produced by endothelial NO synthase (eNOS) plays a protective role in the development of ANG II-induced hypertension and renal injury by minimizing oxidative stress and the inflammation induced by TNF-\u03b1. Systolic blood pressure (SBP) and renal injury responses to chronic infusions of ANG II (via implanted minipumps) were evaluated for 2 wk in wild-type (WT) and in eNOS knockout mice (KO) cotreated with or without a superoxide (O<jats:sub>2<\/jats:sub><jats:sup>\u2212<\/jats:sup>) scavenger, tempol (400 mg\/l in the drinking water), or a TNF-\u03b1 receptor blocker, etanercept (5 mg\/kg\/day ip). In study 1, when ANG II was given at a dose of 25 ng\/min, it increased mean SBP in WT mice (\u039436 \u00b1 3 mmHg; n = 7), and this effect was attenuated in mice pretreated with tempol (\u039424 \u00b1 3 mmHg; n = 6). In KO mice ( n = 9), this dose of ANG II resulted in severe renal injury associated with high mortality. To avoid this high mortality in KO, study 2 was conducted with a lower dose of ANG II (10 ng\/min) that increased SBP slightly in WT (\u039417 \u00b1 7 mmHg; n = 6) but exaggeratedly in KO (\u039448 \u00b1 12 mmHg, n = 6) associated with severe renal injury. Cotreatment with either tempol ( n = 6) or etanercept ( n = 6) ameliorated the hypertensive, as well as the renal injury responses in KO compared with WT. These data demonstrate a protective role for eNOS activity in preventing renal inflammatory injury and hypertension induced by chronic increases in ANG II.<\/jats:p>","DOI":"10.1152\/ajprenal.00024.2013","type":"journal-article","created":{"date-parts":[[2013,8,8]],"date-time":"2013-08-08T06:22:30Z","timestamp":1375942950000},"page":"F1031-F1041","source":"Crossref","is-referenced-by-count":20,"title":["Protective role of the endothelial isoform of nitric oxide synthase in ANG II-induced inflammatory responses in the kidney"],"prefix":"10.1152","volume":"305","author":[{"given":"Curtis","family":"Whiting","sequence":"first","affiliation":[{"name":"Department of Physiology, Hypertension and Renal Center of Excellence, Tulane University Health Sciences Center, New Orleans, Louisiana"}]},{"given":"Alexander","family":"Castillo","sequence":"additional","affiliation":[{"name":"Department of Physiology, Hypertension and Renal Center of Excellence, Tulane University Health Sciences Center, New Orleans, Louisiana"}]},{"given":"Mohammed Z.","family":"Haque","sequence":"additional","affiliation":[{"name":"Department of Physiology, Hypertension and Renal Center of Excellence, Tulane University Health Sciences Center, New Orleans, Louisiana"}]},{"given":"Dewan S. A.","family":"Majid","sequence":"additional","affiliation":[{"name":"Department of Physiology, Hypertension and Renal Center of Excellence, Tulane University Health Sciences Center, New Orleans, Louisiana"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1089\/ars.2011.3967"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1399-302X.2006.00304.x"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1097\/01.mnh.0000191912.65281.e9"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1097\/SHK.0b013e3181cdc327"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000143630.14515.7C"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200501000-00011"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2249.2002.01918.x"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.5.F797"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.5.F876"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00298.2009"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00466.2007"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000198545.01860.90"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.1.F148"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00138.x"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1291\/hypres.31.305"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000066143.02832.5E"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00153.2006"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20070657"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(94)00531-1"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1038\/ajh.2010.173"},{"key":"B21","first-page":"A1030.7","volume":"25","author":"Islam MT","year":"2011","journal-title":"FASEB J"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000015603.84788.47"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1034\/j.1399-6576.1999.430307.x"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004080676"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00090.2005"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00047.2010"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1097\/HJH.0b013e3282efb195"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.509"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000101968.09376.79"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-4419-6612-4_48"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.2007.04642.x"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00294.2004"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00073.2004"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000228320.23697.29"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.35.2.587"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.055003877.x"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.38.3.655"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00150.2007"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00482.2007"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1016\/j.amjhyper.2005.11.008"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00491.2002"},{"key":"B42","first-page":"1440","volume":"10","author":"Rodr\u00edguez-Iturbe B","year":"2011","journal-title":"Clin Exp Pharmacol Physiol"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.62.s82.4.x"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90297.2008"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00611.2009"},{"key":"B46","doi-asserted-by":"crossref","first-page":"A182","DOI":"10.1161\/hyp.60.suppl_1.A182","volume":"60","author":"Singh P","year":"2012","journal-title":"Hypertension"},{"key":"B47","first-page":"A392","volume":"484","author":"Singh P","year":"2013","journal-title":"J Invest Med"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.107.102152"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00481.2007"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1165\/ajrcmb.17.3.2998m"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1007\/s11010-008-9725-5"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1161\/hh0901.089987"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000250468.02084.ce"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1016\/j.vph.2008.01.004"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00024.2013","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,7,3]],"date-time":"2023-07-03T19:02:23Z","timestamp":1688410943000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00024.2013"}},"issued":{"date-parts":[[2013,10,1]]},"references-count":54,"journal-issue":{"issue":"7","published-print":{"date-parts":[[2013,10,1]]}},"alternative-id":["10.1152\/ajprenal.00024.2013"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00024.2013","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2013,10,1]]}},{"indexed":{"date-parts":[[2026,3,23]],"date-time":"2026-03-23T15:46:16Z","timestamp":1774280776236,"version":"3.50.1"},"reference-count":92,"publisher":"American Physiological Society","issue":"6","funder":[{"DOI":"10.13039\/100000066","name":"HHS | NIH | National Institute of Environmental Health Sciences","doi-asserted-by":"publisher","award":["T32-5T32ES007091-40"],"award-info":[{"award-number":["T32-5T32ES007091-40"]}],"id":[{"id":"10.13039\/100000066","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000738","name":"U.S. Department of Veterans Affairs","doi-asserted-by":"publisher","award":["BX005218"],"award-info":[{"award-number":["BX005218"]}],"id":[{"id":"10.13039\/100000738","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000738","name":"U.S. Department of Veterans Affairs","doi-asserted-by":"publisher","award":["BX000851-09A1"],"award-info":[{"award-number":["BX000851-09A1"]}],"id":[{"id":"10.13039\/100000738","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2025,12,1]]},"abstract":"<jats:p>In the present study, we confirmed that lasmiditan-induced renal recovery following moderate-severe bilateral ischemia\/reperfusion-induced acute kidney injury (I\/R-AKI) in mice is dependent on the HTR1F expression. Furthermore, lasmiditan treatment ameliorated acute tubular injury, mitochondrial dysfunction, tubulointerstitial fibrosis, and renal cortical vascular rarefaction postinjury, likely contributing to this enhanced recovery. Interestingly, we also found that mice lacking the HTR1F display decreased innate renal cortical vasculature, exacerbated rarefaction, and exhibit markedly increased mortality following moderate-severe I\/R-AKI.<\/jats:p>","DOI":"10.1152\/ajprenal.00307.2025","type":"journal-article","created":{"date-parts":[[2025,10,8]],"date-time":"2025-10-08T16:21:43Z","timestamp":1759940503000},"page":"F834-F852","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["5-Hydroxytryptamine 1F receptor loss reduces renal vasculature and prevents lasmiditan-induced recovery following moderate-severe acute kidney injury in mice"],"prefix":"10.1152","volume":"329","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4643-3229","authenticated-orcid":false,"given":"Austin D.","family":"Thompson","sequence":"first","affiliation":[{"name":"University of Arizona","place":["United States"]},{"name":"Southern Arizona VA Health Care System","place":["United States"]},{"name":"University of Arizona","place":["United States"]}]},{"ORCID":"https:\/\/orcid.org\/0009-0009-2059-1008","authenticated-orcid":false,"given":"Kai W.","family":"McAlister","sequence":"additional","affiliation":[{"name":"University of Arizona","place":["United States"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1234-5482","authenticated-orcid":false,"given":"Natalie E.","family":"Scholpa","sequence":"additional","affiliation":[{"name":"University of Arizona","place":["United States"]},{"name":"Southern Arizona VA Health Care System","place":["United States"]}]},{"given":"Jaroslav","family":"Janda","sequence":"additional","affiliation":[{"name":"University of Arizona","place":["United States"]}]},{"given":"John","family":"Hortareas","sequence":"additional","affiliation":[{"name":"University of Arizona","place":["United States"]}]},{"given":"Teodora G.","family":"Georgieva","sequence":"additional","affiliation":[{"name":"The University of Arizona BIO5 Institute","place":["United States"]},{"name":"The University of Arizona Cancer Center","place":["United States"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6226-6064","authenticated-orcid":false,"given":"Rick G.","family":"Schnellmann","sequence":"additional","affiliation":[{"name":"University of Arizona","place":["United States"]},{"name":"Southern Arizona VA Health Care System","place":["United States"]},{"name":"University of Arizona","place":["United States"]},{"name":"University of Arizona","place":["United States"]}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/j.kisu.2021.11.003"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(20)30045-3"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1038\/s41581-024-00820-6"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2019.07.012"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2015.25"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1038\/s41572-024-00589-9"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2017.06.030"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/s41581-021-00410-w"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2021.06.028"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.3390\/futurepharmacol2030017"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2017.12.026"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1111\/bph.17440"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00116.2025"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00249.2022"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2015.3"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.3389\/fcvm.2023.1114726"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2018.11.028"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2024.12.020"},{"key":"B19","first-page":"184","volume":"43","author":"Mousleh R","year":"2018","journal-title":"Iran J Med Sci"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00254.2023"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2019.03.023"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90609.2008"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.14814\/phy2.14556"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2016.07.042"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.3389\/fncel.2024.1365158"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/j.bcp.2019.113644"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00077.2018"},{"key":"B28","volume-title":"Guide for the Care and Use of Laboratory Animals","author":"National Research Council","year":"2010"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pbio.3000410"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00035.2011"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M116.754762"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1007\/s00018-019-03391-z"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2022.05.032"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1038\/s41419-021-03693-w"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00324.2017"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.04810908"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1016\/j.taap.2013.09.026"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2015010006"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1016\/j.bcp.2023.115855"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.109.161992"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1021\/acsptsci.4c00246"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.2005477117"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1007\/164_2016_6"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.3389\/fcell.2021.603802"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1093\/ckj\/sfx133"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.07270520"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.3390\/ijms21218255"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1097\/MCO.0b013e32833cc93d"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1002\/mds.29286"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-018-23663-1"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2016.07.038"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002312"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013101121"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2021.06.018"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfw308"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1016\/j.bioactmat.2022.08.022"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2023.02.010"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1016\/j.biocel.2023.106391"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00533.2019"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2017.107"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1021\/acs.jmedchem.6b00669"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00427.2020"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1124\/pharmrev.122.000560"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.3389\/fcell.2021.706832"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.114.214700"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfv317"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1186\/s10194-020-01132-3"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.1016\/j.heliyon.2024.e41485"},{"key":"B69","doi-asserted-by":"publisher","DOI":"10.14814\/phy2.14078"},{"key":"B70","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M117.809897"},{"key":"B71","doi-asserted-by":"publisher","DOI":"10.3791\/50495"},{"key":"B72","doi-asserted-by":"publisher","DOI":"10.3390\/ijms241814019"},{"key":"B73","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00285.2020"},{"key":"B74","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0045870"},{"key":"B75","doi-asserted-by":"publisher","DOI":"10.2741\/3204"},{"key":"B76","doi-asserted-by":"publisher","DOI":"10.3389\/fphar.2023.1095487"},{"key":"B77","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2009.080983"},{"key":"B78","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2017.01.013"},{"key":"B79","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-013-2430-y"},{"key":"B80","doi-asserted-by":"publisher","DOI":"10.1186\/s12860-014-0040-6"},{"key":"B81","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.0000000000000488"},{"key":"B82","doi-asserted-by":"publisher","DOI":"10.1007\/s10456-023-09883-8"},{"key":"B83","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2015111219"},{"key":"B84","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2013.06.022"},{"key":"B85","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbi.2008.09.001"},{"key":"B86","doi-asserted-by":"publisher","DOI":"10.1016\/s0959-4388(99)00061-6"},{"key":"B87","doi-asserted-by":"publisher","DOI":"10.3389\/fphys.2021.685064"},{"key":"B88","doi-asserted-by":"publisher","DOI":"10.1016\/j.genrep.2023.101834"},{"key":"B89","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1797.2006.00566.x"},{"key":"B90","doi-asserted-by":"publisher","DOI":"10.1301\/nr2004.jun243-246"},{"key":"B91","doi-asserted-by":"publisher","DOI":"10.5625\/lar.2018.34.4.147"},{"key":"B92","doi-asserted-by":"publisher","DOI":"10.1016\/j.vph.2023.107241"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00307.2025","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,11,18]],"date-time":"2025-11-18T18:46:59Z","timestamp":1763491619000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00307.2025"}},"issued":{"date-parts":[[2025,12,1]]},"references-count":92,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2025,12,1]]}},"alternative-id":["10.1152\/ajprenal.00307.2025"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00307.2025","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2025,12,1]]},"assertion":[{"value":"2025-08-20","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2025-09-08","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2025-10-02","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2025-11-18","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,3,24]],"date-time":"2026-03-24T04:04:44Z","timestamp":1774325084448,"version":"3.50.1"},"reference-count":40,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2006,6]]},"abstract":"<jats:p>Epithelial Na<jats:sup>+<\/jats:sup>channels (ENaC) are inhibited by extracellular Na<jats:sup>+<\/jats:sup>, a process referred to as Na<jats:sup>+<\/jats:sup>self-inhibition. We previously demonstrated that mutation of key residues within two furin cleavage consensus sites in \u03b1, or one site in \u03b3, blocked subunit proteolysis and inhibited channel activity when mutant channels were expressed in Xenopus laevis oocytes (Hughey RP, Bruns JB, Kinlough CL, Harkleroad KL, Tong Q, Carattino MD, Johnson JP, Stockand JD, and Kleyman TR. J Biol Chem 279: 18111\u201318114, 2004). Cleavage of subunits was also blocked by these mutations when expressed in Madin-Darby canine kidney cells, and both subunit cleavage and channel activity were blocked when wild-type subunits were expressed in furin-deficient Chinese hamster ovary cells. We now report that channels with mutant \u03b1-subunits lacking either one or both furin cleavage sites exhibited a marked enhancement of the Na<jats:sup>+<\/jats:sup>self-inhibition response, while channels with a mutant \u03b3-subunit showed a modestly enhanced Na<jats:sup>+<\/jats:sup>self-inhibition response. Analysis of Na<jats:sup>+<\/jats:sup>self-inhibition at varying [Na<jats:sup>+<\/jats:sup>] indicates that channels containing mutant \u03b1-subunits exhibit an increased Na<jats:sup>+<\/jats:sup>affinity. At the single-channel level, channels with a mutant \u03b1-subunit had a low open probability ( P<jats:sub>o<\/jats:sub>) in the presence of a high external [Na<jats:sup>+<\/jats:sup>] in the patch pipette. P<jats:sub>o<\/jats:sub>dramatically increased when trypsin was also present, or when a low external [Na<jats:sup>+<\/jats:sup>] was in the patch pipette. Our results suggest that furin cleavage of ENaC subunits activates the channels by relieving Na<jats:sup>+<\/jats:sup>self-inhibition and that activation requires that the \u03b1-subunit be cleaved twice. Moreover, we demonstrate for the first time a clear relationship between ENaC P<jats:sub>o<\/jats:sub>and extracellular [Na<jats:sup>+<\/jats:sup>], supporting the notion that Na<jats:sup>+<\/jats:sup>self-inhibition reflects a P<jats:sub>o<\/jats:sub>reduction due to high extracellular [Na<jats:sup>+<\/jats:sup>].<\/jats:p>","DOI":"10.1152\/ajprenal.00439.2005","type":"journal-article","created":{"date-parts":[[2006,2,1]],"date-time":"2006-02-01T03:43:31Z","timestamp":1138765411000},"page":"F1488-F1496","source":"Crossref","is-referenced-by-count":138,"title":["Furin cleavage activates the epithelial Na<sup>+<\/sup>channel by relieving Na<sup>+<\/sup>self-inhibition"],"prefix":"10.1152","volume":"290","author":[{"given":"Shaohu","family":"Sheng","sequence":"first","affiliation":[]},{"given":"Marcelo D.","family":"Carattino","sequence":"additional","affiliation":[]},{"given":"James B.","family":"Bruns","sequence":"additional","affiliation":[]},{"given":"Rebecca P.","family":"Hughey","sequence":"additional","affiliation":[]},{"given":"Thomas R.","family":"Kleyman","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"crossref","unstructured":"Adachi M, Kitamura K, Miyoshi T, Narikiyo T, Iwashita K, Shiraishi N, Nonoguchi H, and Tomita K.Activation of epithelial sodium channels by prostasin inXenopusoocytes.J Am Soc Nephrol12: 1114\u20131121, 2001.","DOI":"10.1681\/ASN.V1261114"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M301315200"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M105208200"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1016\/S0896-6273(02)00687-6"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1152\/ajplung.00435.2004"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00342.2003"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-003-1178-9"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.20028612"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.111.1.127"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M304441200"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-005-1385-7"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-5793(01)02081-6"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/17.2.344"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1016\/S0960-9822(95)00085-6"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1988.68.2.309"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1997.77.2.359"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.20-07-02575.2000"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1159\/000076406"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.C400080200"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.C400460200"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M307003200"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1007\/s11906-003-0005-1"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00094.2003"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.22.13469"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.64.082101.143243"},{"key":"R26","doi-asserted-by":"crossref","unstructured":"Schulz AR.Enzyme Kinetics: From Disease to Multi-Enzyme Systems. Cambridge, UK: Cambridge Univ. Press, 1994, p. 38\u201341.","DOI":"10.1017\/CBO9780511608438"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M311952200"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M209975200"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M405224200"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1210\/edrv.23.2.0458"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.2.681"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1529\/biophysj.104.056804"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M404169200"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.2165\/00129785-200404030-00003"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200409000-00010"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1991.71.2.429"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1038\/39329"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1038\/282519a0"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1985.65.4.833"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1096\/fasebj.11.11.9285481"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00439.2005","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,7,23]],"date-time":"2021-07-23T11:03:09Z","timestamp":1627038189000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00439.2005"}},"issued":{"date-parts":[[2006,6]]},"references-count":40,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2006,6]]}},"alternative-id":["10.1152\/ajprenal.00439.2005"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00439.2005","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2006,6]]}},{"indexed":{"date-parts":[[2026,3,24]],"date-time":"2026-03-24T03:46:13Z","timestamp":1774323973214,"version":"3.50.1"},"reference-count":54,"publisher":"American Physiological Society","issue":"12","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2014,12,15]]},"abstract":"<jats:p>Urea transporters (UT) play an important role in the urine concentration mechanism by mediating intrarenal urea recycling, suggesting that UT inhibitors could have therapeutic use as a novel class of diuretic. Recently, we found a thienoquinolin UT inhibitor, PU-14, that exhibited diuretic activity. The purpose of this study was to identify more potent UT inhibitors that strongly inhibit UT-A isoforms in the inner medullary collecting duct (IMCD). Efficient thienoquinolin UT inhibitors were identified by structure-activity relationship analysis. Urea transport inhibition activity was assayed in perfused rat terminal IMCDs. Diuretic activity of the compound was determined in rats and mice using metabolic cages. The results show that the compound PU-48 exhibited potent UT-A inhibition activity. The inhibition was 69.5% with an IC<jats:sub>50<\/jats:sub>of 0.32 \u03bcM. PU-48 significantly inhibited urea transport in perfused rat terminal IMCDs. PU-48 caused significant diuresis in UT-B null mice, which indicates that UT-A is the target of PU-48. The diuresis caused by PU-48 did not change blood Na<jats:sup>+<\/jats:sup>, K<jats:sup>+<\/jats:sup>, or Cl<jats:sup>\u2212<\/jats:sup>levels or nonurea solute excretion in rats and mice. No toxicity was detected in cells or animals treated with PU-48. The results indicate that thienoquinolin UT inhibitors induce a diuresis by inhibiting UT-A in the IMCD. This suggests that they may have the potential to be developed as a novel class of diuretics with fewer side effects than classical diuretics.<\/jats:p>","DOI":"10.1152\/ajprenal.00421.2014","type":"journal-article","created":{"date-parts":[[2014,10,9]],"date-time":"2014-10-09T00:24:21Z","timestamp":1412814261000},"page":"F1363-F1372","source":"Crossref","is-referenced-by-count":23,"title":["Thienoquinolins exert diuresis by strongly inhibiting UT-A urea transporters"],"prefix":"10.1152","volume":"307","author":[{"given":"Huiwen","family":"Ren","sequence":"first","affiliation":[{"name":"State Key Laboratory of Natural and Biomimetic Drugs, Department of Pharmacology, School of Basic Medical Sciences, Peking University, Beijing, China;"}]},{"given":"Yanhua","family":"Wang","sequence":"additional","affiliation":[{"name":"Renal Division, Departments of Medicine and Physiology, Emory University School of Medicine, Atlanta, Georgia;"}]},{"given":"Yongning","family":"Xing","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Natural and Biomimetic Drugs, Department of Pharmacology, School of Basic Medical Sciences, Peking University, Beijing, China;"}]},{"given":"Jianhua","family":"Ran","sequence":"additional","affiliation":[{"name":"Department of Anatomy, Neuroscience Research Center, Basic Medical College, Chongqing Medical University, Chongqing, China; and"}]},{"given":"Ming","family":"Liu","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Natural and Biomimetic Drugs, Department of Pharmacology, School of Basic Medical Sciences, Peking University, Beijing, China;"}]},{"given":"Tianluo","family":"Lei","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Natural and Biomimetic Drugs, Department of Pharmacology, School of Basic Medical Sciences, Peking University, Beijing, China;"}]},{"given":"Hong","family":"Zhou","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Natural and Biomimetic Drugs, Department of Pharmacology, School of Basic Medical Sciences, Peking University, Beijing, China;"}]},{"given":"Runtao","family":"Li","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Natural and Biomimetic Drugs, Department of Pharmacology, School of Basic Medical Sciences, Peking University, Beijing, China;"}]},{"given":"Jeff M.","family":"Sands","sequence":"additional","affiliation":[{"name":"Renal Division, Departments of Medicine and Physiology, Emory University School of Medicine, Atlanta, Georgia;"}]},{"given":"Baoxue","family":"Yang","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Natural and Biomimetic Drugs, Department of Pharmacology, School of Basic Medical Sciences, Peking University, Beijing, China;"},{"name":"Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, Beijing, China"}]}],"member":"24","reference":[{"key":"B1","first-page":"23","volume":"91","author":"Ames R","year":"1998","journal-title":"Arch Mal Coeur Vaiss"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1002\/ardp.200500982"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00260.2002"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.281.3.F400"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90228.2008"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00197.2007"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00690.2009"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1080\/08037050310019418"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/j.chembiol.2013.08.005"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0401704101"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00567.2001"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00263.2001"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00349.2007"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00499.2003"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-827X(00)00051-3"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1128\/AAC.01112-08"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00617.2009"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/j.jacc.2010.06.034"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/j.bmcl.2013.02.038"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1038\/sj.jhh.1001513"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00682.2009"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-012-1157-0"},{"key":"B23","doi-asserted-by":"crossref","first-page":"699","DOI":"10.1002\/cphy.c100030","volume":"1","author":"Klein JD","year":"2011","journal-title":"Compr Physiol"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006030246"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2013.94"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/j.bmcl.2012.01.096"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejmech.2005.11.005"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00404.2011"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1096\/fj.06-6979com"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2013.62"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.080499597"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.8.4296"},{"key":"B33","first-page":"26","volume":"29","author":"Mohamed BG","year":"2006","journal-title":"Arch Pharm (Weinheim)"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1001\/archinternmed.2009.342"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.93.11.5495"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.5414\/CNP69450"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1016\/j.jmgm.2009.11.002"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1016\/j.chembiol.2013.10.003"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.253.5.F823"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1983.244.5.F472"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1016\/j.mam.2012.12.003"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-003-1124-x"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.3.F487"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1111\/j.1524-6175.2004.03789.x"},{"key":"B45","first-page":"419","volume":"6","author":"Soleimani M","year":"2012","journal-title":"Iran J Kidney Dis"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00334.2003"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1038\/nchembio.435"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1016\/j.toxlet.2005.08.007"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00322.2010"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00367.2004"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M200207200"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M008216200"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2011070751"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.0054.2001"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00421.2014","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,4,19]],"date-time":"2022-04-19T16:03:51Z","timestamp":1650384231000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00421.2014"}},"issued":{"date-parts":[[2014,12,15]]},"references-count":54,"journal-issue":{"issue":"12","published-print":{"date-parts":[[2014,12,15]]}},"alternative-id":["10.1152\/ajprenal.00421.2014"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00421.2014","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2014,12,15]]}},{"indexed":{"date-parts":[[2026,3,24]],"date-time":"2026-03-24T02:58:58Z","timestamp":1774321138401,"version":"3.50.1"},"reference-count":23,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2019,12,1]]},"abstract":"<jats:p> Renal fibrosis is a key pathological phenomenon of chronic kidney disease (CKD) contributing to the progressive loss of renal function. UK383,367 is a procollagen C proteinase inhibitor that has been selected as a candidate for dermal antiscarring agents, whereas its role in renal fibrosis is unclear. In the present study, UK383,367 was applied to a CKD mouse model of unilateral ureteral obstruction (UUO) and cell lines of renal tubular epithelial cells (mouse proximal tubular cells) and renal fibroblast cells (NRK-49F cells) challenged by transforming growth factor-\u03b2<jats:sub>1<\/jats:sub>. In vivo, bone morphogenetic protein 1, the target of UK383,367, was significantly enhanced in UUO mouse kidneys and renal biopsies from patients with CKD. Strikingly, UK383,367 administration ameliorated tubulointerstitial fibrosis as shown by Masson\u2019s trichrome staining in line with the blocked expression of collagen type I\/III, fibronectin, and \u03b1-smooth muscle actin in the kidneys from UUO mice. Similarly, the enhanced inflammatory factors in obstructed kidneys were also blunted. In vitro, UK383,367 pretreatment inhibited the induction of collagen type I\/III, fibronectin, and \u03b1-smooth muscle actin in both mouse proximal tubular cells and NRK-49F cells treated with transforming growth factor-\u03b2<jats:sub>1<\/jats:sub>. Taken together, these findings indicate that the bone morphogenetic protein 1 inhibitor UK383,367 could serve as a potential drug in antagonizing CKD renal fibrosis by acting on the maturation and deposition of collagen and the subsequent profibrotic response and inflammation. <\/jats:p>","DOI":"10.1152\/ajprenal.00230.2019","type":"journal-article","created":{"date-parts":[[2019,9,23]],"date-time":"2019-09-23T18:52:41Z","timestamp":1569264761000},"page":"F1430-F1438","source":"Crossref","is-referenced-by-count":20,"title":["BMP1 inhibitor UK383,367 attenuates renal fibrosis and inflammation in CKD"],"prefix":"10.1152","volume":"317","author":[{"given":"Mi","family":"Bai","sequence":"first","affiliation":[{"name":"Department of Nephrology, State Key Laboratory of Reproductive Medicine, Children's Hospital of Nanjing Medical University, Nanjing, China"},{"name":"Jiangsu Key Laboratory of Pediatrics, Nanjing Medical University, Nanjing, China"},{"name":"Nanjing Key Lab of Pediatrics, Children\u2019s Hospital of Nanjing Medical University, Nanjing, China"}]},{"given":"Juan","family":"Lei","sequence":"additional","affiliation":[{"name":"Department of Nephrology, State Key Laboratory of Reproductive Medicine, Children's Hospital of Nanjing Medical University, Nanjing, China"},{"name":"Jiangsu Key Laboratory of Pediatrics, Nanjing Medical University, Nanjing, China"}]},{"given":"Shuqin","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Nephrology, State Key Laboratory of Reproductive Medicine, Children's Hospital of Nanjing Medical University, Nanjing, China"},{"name":"Jiangsu Key Laboratory of Pediatrics, Nanjing Medical University, Nanjing, China"}]},{"given":"Dan","family":"Ding","sequence":"additional","affiliation":[{"name":"Department of Nephrology, State Key Laboratory of Reproductive Medicine, Children's Hospital of Nanjing Medical University, Nanjing, China"},{"name":"Jiangsu Key Laboratory of Pediatrics, Nanjing Medical University, Nanjing, China"}]},{"given":"Xiaowen","family":"Yu","sequence":"additional","affiliation":[{"name":"Department of Nephrology, State Key Laboratory of Reproductive Medicine, Children's Hospital of Nanjing Medical University, Nanjing, China"},{"name":"Jiangsu Key Laboratory of Pediatrics, Nanjing Medical University, Nanjing, China"},{"name":"Nanjing Key Lab of Pediatrics, Children\u2019s Hospital of Nanjing Medical University, Nanjing, China"}]},{"given":"Yan","family":"Guo","sequence":"additional","affiliation":[{"name":"Department of Nephrology, State Key Laboratory of Reproductive Medicine, Children's Hospital of Nanjing Medical University, Nanjing, China"},{"name":"Jiangsu Key Laboratory of Pediatrics, Nanjing Medical University, Nanjing, China"},{"name":"Nanjing Key Lab of Pediatrics, Children\u2019s Hospital of Nanjing Medical University, Nanjing, China"}]},{"given":"Shuang","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Nephrology, State Key Laboratory of Reproductive Medicine, Children's Hospital of Nanjing Medical University, Nanjing, China"},{"name":"Jiangsu Key Laboratory of Pediatrics, Nanjing Medical University, Nanjing, China"}]},{"given":"Yang","family":"Du","sequence":"additional","affiliation":[{"name":"Department of Nephrology, State Key Laboratory of Reproductive Medicine, Children's Hospital of Nanjing Medical University, Nanjing, China"},{"name":"Jiangsu Key Laboratory of Pediatrics, Nanjing Medical University, Nanjing, China"}]},{"given":"Deyi","family":"Li","sequence":"additional","affiliation":[{"name":"School of Life Sciences and Biopharmaceutics, Shenyang Pharmaceutical University, Shenyang, China"}]},{"given":"Yue","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Nephrology, State Key Laboratory of Reproductive Medicine, Children's Hospital of Nanjing Medical University, Nanjing, China"},{"name":"Jiangsu Key Laboratory of Pediatrics, Nanjing Medical University, Nanjing, China"}]},{"given":"Songming","family":"Huang","sequence":"additional","affiliation":[{"name":"Department of Nephrology, State Key Laboratory of Reproductive Medicine, Children's Hospital of Nanjing Medical University, Nanjing, China"},{"name":"Jiangsu Key Laboratory of Pediatrics, Nanjing Medical University, Nanjing, China"}]},{"given":"Zhanjun","family":"Jia","sequence":"additional","affiliation":[{"name":"Department of Nephrology, State Key Laboratory of Reproductive Medicine, Children's Hospital of Nanjing Medical University, Nanjing, China"},{"name":"Jiangsu Key Laboratory of Pediatrics, Nanjing Medical University, Nanjing, China"},{"name":"Nanjing Key Lab of Pediatrics, Children\u2019s Hospital of Nanjing Medical University, Nanjing, China"}]},{"given":"Aihua","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Nephrology, State Key Laboratory of Reproductive Medicine, Children's Hospital of Nanjing Medical University, Nanjing, China"},{"name":"Jiangsu Key Laboratory of Pediatrics, Nanjing Medical University, Nanjing, China"},{"name":"Nanjing Key Lab of Pediatrics, Children\u2019s Hospital of Nanjing Medical University, Nanjing, China"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1080\/00498250600618177"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/j.bmcl.2008.10.036"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1001\/jama.2017.4046"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/j.intimp.2017.11.043"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/j.mehy.2014.09.011"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1021\/jm061010z"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1002\/bdrc.20060"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1080\/08977194.2018.1428966"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010070722"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/j.matbio.2007.05.004"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1021\/acsmedchemlett.8b00173"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1126\/science.271.5247.360"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00362.2001"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(17)30788-2"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.93.10.5127"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2011.149"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.21873\/invivo.11019"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/17.3.363"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/0888-7543(91)90254-C"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1038\/s41581-019-0110-2"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(16)32064-5"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.12688\/f1000research.6970.1"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00328.2012"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00230.2019","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,12,2]],"date-time":"2019-12-02T09:52:39Z","timestamp":1575280359000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00230.2019"}},"issued":{"date-parts":[[2019,12,1]]},"references-count":23,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2019,12,1]]}},"alternative-id":["10.1152\/ajprenal.00230.2019"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00230.2019","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2019,12,1]]}},{"indexed":{"date-parts":[[2026,3,22]],"date-time":"2026-03-22T08:02:57Z","timestamp":1774166577769,"version":"3.50.1"},"reference-count":61,"publisher":"American Physiological Society","issue":"7","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2014,4,1]]},"abstract":"<jats:p>Using patch clamp, we induced depolarization of descending vasa recta (DVR) pericytes or endothelia and tested whether it was conducted to distant cells. Membrane potential was measured with the fluorescent voltage dye di-8-ANEPPS or with a second patch-clamp electrode. Depolarization of an endothelial cell induced responses in other endothelia within a millisecond and was slowed by gap junction blockade with heptanol. Endothelial response to pericyte depolarization was poor, implying high-resistance myo-endothelial coupling. In contrast, dual patch clamp of neighboring pericytes revealed syncytial coupling. At high sampling rate, the spread of depolarization between pericytes and endothelia occurred in 9 \u00b1 2 or 12 \u00b1 2 \u03bcs, respectively. Heptanol (2 mM) increased the overall input resistance of the pericyte layer to current flow and prevented transmission of depolarization between neighboring cells. The fluorescent tracer Lucifer yellow (LY), when introduced through ruptured patches, spread between neighboring endothelia in 1 to 7 s, depending on location of the flanking cell. LY diffused to endothelial cells on the ipsilateral but not contralateral side of the DVR wall and minimally between pericytes. We conclude that both DVR pericytes and endothelia are part of individual syncytia. The rate of conduction of membrane potential exceeds that for diffusion of hydrophilic molecules by orders of magnitude. Gap junction coupling of adjacent endothelial cells may be spatially oriented to favor longitudinal transmission along the DVR axis.<\/jats:p>","DOI":"10.1152\/ajprenal.00470.2013","type":"journal-article","created":{"date-parts":[[2014,1,1]],"date-time":"2014-01-01T03:30:44Z","timestamp":1388547044000},"page":"F751-F763","source":"Crossref","is-referenced-by-count":7,"title":["Descending vasa recta endothelial cells and pericytes form mural syncytia"],"prefix":"10.1152","volume":"306","author":[{"given":"Zhong","family":"Zhang","sequence":"first","affiliation":[{"name":"Division of Nephrology, Department of Medicine, University of Maryland School of Medicine, Baltimore, Maryland"}]},{"given":"Hai","family":"Lin","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, University of Maryland School of Medicine, Baltimore, Maryland"}]},{"given":"Chunhua","family":"Cao","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, University of Maryland School of Medicine, Baltimore, Maryland"}]},{"given":"Kristie","family":"Payne","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, University of Maryland School of Medicine, Baltimore, Maryland"}]},{"given":"Thomas L.","family":"Pallone","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, University of Maryland School of Medicine, Baltimore, Maryland"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2002.031823"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.2010.02244.x"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1139\/y92-098"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00112.2010"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00877.2005"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00278.2007"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1984.246.3.F349"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1159\/000339110"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.2011.02310.x"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.3389\/fphys.2013.00307"},{"key":"B11","first-page":"148","volume":"19","author":"De Wit C","year":"2004","journal-title":"News Physiol Sci"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000035243.66189.92"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1007\/BF00519727"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000144465.56360.ad"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.2004.04003.x"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1097\/01.hjh.0000133744.85490.9d"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/physiol.00008.2004"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1007\/BF01900104"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/S0008-6363(99)00174-1"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00808.2009"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1161\/hh1901.097126"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/j.pbiomolbio.2007.03.011"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1172\/JCI113612"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00417.2010"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.92.2.145"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1977.118"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00732.2010"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00070.2006"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.76.3.498"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90669.2008"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1002\/psc.1005"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1167\/iovs.11-8176"},{"key":"B33","doi-asserted-by":"crossref","first-page":"1981","DOI":"10.1002\/cphy.c110051","volume":"2","author":"Nielsen MS","year":"2012","journal-title":"Compr Physiol"},{"key":"B34","first-page":"443","volume":"86","author":"Pallone TL","year":"2003","journal-title":"Methods Mol Med"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.266.6.F850"},{"key":"B36","doi-asserted-by":"crossref","first-page":"97","DOI":"10.1002\/cphy.c100036","volume":"2","author":"Pallone TL","year":"2012","journal-title":"Compr Physiol"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00306.2001"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1990.70.3.885"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.2000.278.4.H1248"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00657.2002"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1172\/JCI116948"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.257.4.F547"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00304.2002"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0b013e32835b4e6e"},{"key":"B45","first-page":"1659","volume":"33","author":"Pucihar G","year":"2009","journal-title":"J Vis Exp"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1080\/10739680601072099"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-3495(90)82406-1"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00065.2002"},{"key":"B49","first-page":"68","volume":"60","author":"Schmidt VJ","year":"2008","journal-title":"Pharmacol Rep"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00002.2013"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000186193.22438.6c"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1111\/j.1549-8719.2011.00149.x"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00453.2010"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00261.2006"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00493.2007"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2010.202937"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2005.091538"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.2001.280.6.R1878"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00321.2010"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00394.2003"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00220.2013"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00470.2013","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,3,21]],"date-time":"2022-03-21T03:11:10Z","timestamp":1647832270000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00470.2013"}},"issued":{"date-parts":[[2014,4,1]]},"references-count":61,"journal-issue":{"issue":"7","published-print":{"date-parts":[[2014,4,1]]}},"alternative-id":["10.1152\/ajprenal.00470.2013"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00470.2013","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2014,4,1]]}},{"indexed":{"date-parts":[[2026,3,22]],"date-time":"2026-03-22T07:47:25Z","timestamp":1774165645629,"version":"3.50.1"},"reference-count":48,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2019,9,1]]},"abstract":"<jats:p> Diabetic nephropathy (DN) has become the main cause of end-stage renal disease worldwide, but the efficacy of current therapeutic strategies on DN remains unsatisfactory. Recent research has reported the involvement of metabolic rearrangement in the pathological process of DN, and of all the disturbances in metabolism, mitochondria serve as key regulatory hubs. In the present study, high-resolution mass spectrometry-based nontarget metabolomics was used to uncover the metabolic characteristics of the early diabetic kidney with or without the inhibition of mitochondrial activity. At first, we observed a moderate enhancement of mitochondrial complex-1 activity in the diabetic kidney, which was completely normalized by the specific mitochondrial complex-1 inhibitor rotenone (ROT). Meanwhile, metabolomics data indicated an overactivated pentose phosphate pathway, purine and pyrimidine metabolism, hexosamine biosynthetic pathway, and tricarboxylic acid cycle, which were strikingly corrected by ROT. In addition, ROT also strikingly corrected imbalanced redox homeostasis, possibly by increasing the ratio of antioxidant metabolites glutathione and NADPH against their oxidative form. In agreement with the improved metabolic status and oxidative response, ROT attenuated glomerular and tubular injury efficiently. Fibrotic markers (fibronectin, \u03b1-smooth muscle actin, collagen type I, and collagen type III), inflammatory factors (TNF-\u03b1, IL-1\u03b2, and ICAM-1), and oxidative stress were all markedly blocked by ROT. In vitro, ROT dose dependently attenuated high glucose-induced proliferation and extracellular matrix production in mesangial cells. Collectively, these findings revealed that the overactivation of mitochondrial activity in the kidney could contribute to metabolic disorders and the pathogenesis of early DN. <\/jats:p>","DOI":"10.1152\/ajprenal.00076.2019","type":"journal-article","created":{"date-parts":[[2019,7,3]],"date-time":"2019-07-03T13:45:26Z","timestamp":1562161526000},"page":"F593-F605","source":"Crossref","is-referenced-by-count":36,"title":["Mitochondrial activity contributes to impaired renal metabolic homeostasis and renal pathology in STZ-induced diabetic mice"],"prefix":"10.1152","volume":"317","author":[{"given":"Mengqiu","family":"Wu","sequence":"first","affiliation":[{"name":"Department of Nephrology, Children\u2019s Hospital of Nanjing Medical University, Nanjing, China"},{"name":"Jiangsu Key Laboratory of Pediatrics, Nanjing Medical University, Nanjing,China"},{"name":"Nanjing Key Laboratory of Pediatrics, Children\u2019s Hospital of Nanjing Medical University, Nanjing, China"},{"name":"State Key Laboratory of Kidney Diseases, Beijing, China"}]},{"given":"Shuzhen","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Children\u2019s Hospital of Nanjing Medical University, Nanjing, China"},{"name":"Jiangsu Key Laboratory of Pediatrics, Nanjing Medical University, Nanjing,China"},{"name":"Nanjing Key Laboratory of Pediatrics, Children\u2019s Hospital of Nanjing Medical University, Nanjing, China"}]},{"given":"Xiaowen","family":"Yu","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Children\u2019s Hospital of Nanjing Medical University, Nanjing, China"},{"name":"Jiangsu Key Laboratory of Pediatrics, Nanjing Medical University, Nanjing,China"},{"name":"Nanjing Key Laboratory of Pediatrics, Children\u2019s Hospital of Nanjing Medical University, Nanjing, China"}]},{"given":"Weiyi","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Children\u2019s Hospital of Nanjing Medical University, Nanjing, China"},{"name":"Jiangsu Key Laboratory of Pediatrics, Nanjing Medical University, Nanjing,China"},{"name":"Nanjing Key Laboratory of Pediatrics, Children\u2019s Hospital of Nanjing Medical University, Nanjing, China"}]},{"given":"Haoyang","family":"Ma","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Children\u2019s Hospital of Nanjing Medical University, Nanjing, China"},{"name":"Jiangsu Key Laboratory of Pediatrics, Nanjing Medical University, Nanjing,China"},{"name":"Nanjing Key Laboratory of Pediatrics, Children\u2019s Hospital of Nanjing Medical University, Nanjing, China"}]},{"given":"Chang","family":"Shao","sequence":"additional","affiliation":[{"name":"College of Pharmacy, China Pharmaceutical University, Nanjing, China"}]},{"given":"Yue","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Children\u2019s Hospital of Nanjing Medical University, Nanjing, China"},{"name":"Jiangsu Key Laboratory of Pediatrics, Nanjing Medical University, Nanjing,China"},{"name":"Nanjing Key Laboratory of Pediatrics, Children\u2019s Hospital of Nanjing Medical University, Nanjing, China"}]},{"given":"Aihua","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Children\u2019s Hospital of Nanjing Medical University, Nanjing, China"},{"name":"Jiangsu Key Laboratory of Pediatrics, Nanjing Medical University, Nanjing,China"},{"name":"Nanjing Key Laboratory of Pediatrics, Children\u2019s Hospital of Nanjing Medical University, Nanjing, China"}]},{"given":"Songming","family":"Huang","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Children\u2019s Hospital of Nanjing Medical University, Nanjing, China"},{"name":"Jiangsu Key Laboratory of Pediatrics, Nanjing Medical University, Nanjing,China"},{"name":"Nanjing Key Laboratory of Pediatrics, Children\u2019s Hospital of Nanjing Medical University, Nanjing, China"}]},{"given":"Zhanjun","family":"Jia","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Children\u2019s Hospital of Nanjing Medical University, Nanjing, China"},{"name":"Jiangsu Key Laboratory of Pediatrics, Nanjing Medical University, Nanjing,China"},{"name":"Nanjing Key Laboratory of Pediatrics, Children\u2019s Hospital of Nanjing Medical University, Nanjing, China"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1038\/nrd.2016.67"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.54.6.1615"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1007\/s00125-011-2099-3"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1042\/CS20150838"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008050514"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/j.ebiom.2015.04.002"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.12659\/MSM.895945"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1172\/JCI18127"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.07702.x"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1172\/JCI57935"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2018.9"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2017.05.034"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1016\/j.yjmcc.2016.01.009"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1007\/s11892-016-0748-0"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2017.30"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1111\/jcmm.13432"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1159\/000492589"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1053\/j.ackd.2014.03.008"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2016.08.021"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1038\/ni0311-199"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1007\/s11892-015-0685-3"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1096\/fasebj.13.12.1601"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.2337\/dc17-1954"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00536.2012"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1172\/JCI87927"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1053\/j.gastro.2018.06.083"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2018.02.003"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1038\/35008121"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.3390\/biom5010194"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1186\/s12933-016-0397-2"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.3109\/10409238.2015.1135102"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1038\/s41569-018-0059-z"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1038\/nm.4328"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1172\/JCI72271"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1172\/jci.insight.86976"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.07703.x"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.4.F676"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.2337\/diab.34.5.485"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1155\/2014\/670106"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00591.2009"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1797.2007.00796.x"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.00016.2018"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1021\/acs.jproteome.7b00111"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2015030302"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1038\/nprot.2012.024"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2012.188"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2014.274"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.18632\/oncotarget.24733"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00076.2019","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:14:56Z","timestamp":1567973696000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00076.2019"}},"issued":{"date-parts":[[2019,9,1]]},"references-count":48,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2019,9,1]]}},"alternative-id":["10.1152\/ajprenal.00076.2019"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00076.2019","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2019,9,1]]}},{"indexed":{"date-parts":[[2026,3,26]],"date-time":"2026-03-26T04:01:04Z","timestamp":1774497664740,"version":"3.50.1"},"reference-count":41,"publisher":"American Physiological Society","issue":"12","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,6,15]]},"abstract":"<jats:p>\n                    The precise roles of hypoxia in the initiation and progression of kidney disease remain unresolved. A major technical limitation has been the absence of methods allowing long-term measurement of kidney tissue oxygen tension (Po\n                    <jats:sub>2<\/jats:sub>\n                    ) in unrestrained animals. We developed a telemetric method for the measurement of kidney tissue Po\n                    <jats:sub>2<\/jats:sub>\n                    in unrestrained rats, using carbon paste electrodes (CPEs). After acute implantation in anesthetized rats, tissue Po\n                    <jats:sub>2<\/jats:sub>\n                    measured by CPE-telemetry in the inner cortex and medulla was in close agreement with that provided by the \u201cgold standard\u201d Clark electrode. The CPE-telemetry system could detect small changes in renal tissue Po\n                    <jats:sub>2<\/jats:sub>\n                    evoked by mild hypoxemia. In unanesthetized rats, CPE-telemetry provided stable measurements of medullary tissue Po\n                    <jats:sub>2<\/jats:sub>\n                    over days 5\u2212 19 after implantation. It also provided reproducible responses to systemic hypoxia and hyperoxia over this time period. There was little evidence of fibrosis or scarring after 3 wk of electrode implantation. However, because medullary Po\n                    <jats:sub>2<\/jats:sub>\n                    measured by CPE-telemetry was greater than that documented from previous studies in anesthetized animals, this method is presently best suited for monitoring relative changes rather than absolute values. Nevertheless, this new technology provides, for the first time, the opportunity to examine the temporal relationships between tissue hypoxia and the progression of renal disease.\n                  <\/jats:p>","DOI":"10.1152\/ajprenal.00662.2012","type":"journal-article","created":{"date-parts":[[2013,4,10]],"date-time":"2013-04-10T23:20:34Z","timestamp":1365636034000},"page":"F1471-F1480","source":"Crossref","is-referenced-by-count":20,"title":["Telemetry-based oxygen sensor for continuous monitoring of kidney oxygenation in conscious rats"],"prefix":"10.1152","volume":"304","author":[{"given":"Maarten P.","family":"Koeners","sequence":"first","affiliation":[{"name":"Department of Physiology, Auckland Bioengineering Institute, University of Auckland, Auckland, New Zealand;"},{"name":"Nephrology, University Medical Centre Utrecht, Utrecht, Netherlands;"}]},{"given":"Connie P. C.","family":"Ow","sequence":"additional","affiliation":[{"name":"Department of Physiology, Monash University, Melbourne, Australia;"}]},{"given":"David M.","family":"Russell","sequence":"additional","affiliation":[{"name":"Department of Physiology, Auckland Bioengineering Institute, University of Auckland, Auckland, New Zealand;"},{"name":"Millar Instruments, Auckland, New Zealand; and"}]},{"given":"Amany","family":"Abdelkader","sequence":"additional","affiliation":[{"name":"Department of Physiology, Monash University, Melbourne, Australia;"}]},{"given":"Gabriela A.","family":"Eppel","sequence":"additional","affiliation":[{"name":"Department of Physiology, Monash University, Melbourne, Australia;"}]},{"given":"John","family":"Ludbrook","sequence":"additional","affiliation":[{"name":"Department of Surgery, University of Melbourne, Melbourne, Australia"}]},{"given":"Simon C.","family":"Malpas","sequence":"additional","affiliation":[{"name":"Department of Physiology, Auckland Bioengineering Institute, University of Auckland, Auckland, New Zealand;"},{"name":"Millar Instruments, Auckland, New Zealand; and"}]},{"given":"Roger G.","family":"Evans","sequence":"additional","affiliation":[{"name":"Department of Physiology, Monash University, Melbourne, Australia;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1021\/cr900396q"},{"key":"B2","unstructured":"Bard AJ , Faulkner LR.\n                      Electrochemical Methods: Fundamentals and Applications\n                      . New York: Wiley, 2001, p. xxi."},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1021\/cr60242a003"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1039\/c1an15324b"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/j.jneumeth.2010.11.013"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.3390\/s5110473"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115316"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.00105.2006"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.1994.tb55706.x"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90230.2008"},{"key":"B11","doi-asserted-by":"crossref","first-page":"1405","DOI":"10.1111\/j.1440-1681.2008.05023.x","volume":"35","author":"Evans RG","year":"2008","journal-title":"Clin Exp Pharmacol Physiol"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00552.2010"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1111\/1440-1681.12031"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.57.s75.12.x"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1991.255"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1159\/000146075"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1038\/hr.2009.224"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.01315.2005"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1039\/a806942e"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00067.2002"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90371.2008"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.2119\/2008-00006.Legrand"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1007\/s004240050455"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1016\/S0165-0270(96)00140-9"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1997.sp021875"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuroimage.2010.04.187"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.49"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.2010.05376.x"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.1991.tb01468.x"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1093\/cvr\/28.3.303"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005070757"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1016\/j.vascn.2010.01.007"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.2006.04475.x"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1039\/AN9931800433"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1159\/000090610"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.2006.04472.x"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1016\/j.jneumeth.2011.11.019"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1046\/j.1440-1681.2003.03810.x"},{"key":"B40","first-page":"195","volume":"41","author":"Saheb JL","year":"1977","journal-title":"Can J Comp Med"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1093\/gerona\/61.8.795"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuroscience.2010.03.042"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00662.2012","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:40:42Z","timestamp":1567971642000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00662.2012"}},"issued":{"date-parts":[[2013,6,15]]},"references-count":41,"journal-issue":{"issue":"12","published-print":{"date-parts":[[2013,6,15]]}},"alternative-id":["10.1152\/ajprenal.00662.2012"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00662.2012","relation":{"has-review":[{"id-type":"doi","id":"10.3410\/f.718352050.793493823","asserted-by":"object"}]},"ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2013,6,15]]}},{"indexed":{"date-parts":[[2026,3,26]],"date-time":"2026-03-26T14:53:32Z","timestamp":1774536812454,"version":"3.50.1"},"reference-count":67,"publisher":"American Physiological Society","issue":"3","license":[{"start":{"date-parts":[[2026,1,19]],"date-time":"2026-01-19T00:00:00Z","timestamp":1768780800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0"}],"funder":[{"DOI":"10.13039\/501100002997","name":"Nierstichting","doi-asserted-by":"publisher","award":["21OK022"],"award-info":[{"award-number":["21OK022"]}],"id":[{"id":"10.13039\/501100002997","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100002997","name":"Nierstichting","doi-asserted-by":"publisher","award":["23OK2065"],"award-info":[{"award-number":["23OK2065"]}],"id":[{"id":"10.13039\/501100002997","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000781","name":"EC | European Research Council","doi-asserted-by":"publisher","award":["101040682"],"award-info":[{"award-number":["101040682"]}],"id":[{"id":"10.13039\/501100000781","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000781","name":"EC | European Research Council","doi-asserted-by":"publisher","award":["IN-THE-KIDNEY"],"award-info":[{"award-number":["IN-THE-KIDNEY"]}],"id":[{"id":"10.13039\/501100000781","id-type":"DOI","asserted-by":"publisher"}]},{"name":"the Netherlands Organization for Scientific Research","award":["VIDI 391 09150172110040"],"award-info":[{"award-number":["VIDI 391 09150172110040"]}]},{"name":"the Netherlands Organization for Scientific Research","award":["IMAGE-THE-KIDNEY"],"award-info":[{"award-number":["IMAGE-THE-KIDNEY"]}]},{"DOI":"10.13039\/501100000781","name":"EC | European Research Council","doi-asserted-by":"publisher","award":["H2020-ERC-2017- ADV-788982-COLMIN"],"award-info":[{"award-number":["H2020-ERC-2017- ADV-788982-COLMIN"]}],"id":[{"id":"10.13039\/501100000781","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2026,3,1]]},"abstract":"<jats:p>We show for the first time that CPPs can be directly modulated by incorporating citrate during their formation. Citrate\u2010modified CPPs maintain their hydroxyapatite core but display altered crystall lattice structure, reduced size, and changes in protein composition with fewer apolipoproteins. Importantly, they induce 88% less calcification in VSMCs. These findings provide proof-of-principle that CPP remodeling may represent a novel therapeutic strategy to limit vascular calcification in CKD, warranting further investigation in vivo.<\/jats:p>","DOI":"10.1152\/ajprenal.00391.2025","type":"journal-article","created":{"date-parts":[[2026,1,19]],"date-time":"2026-01-19T16:21:42Z","timestamp":1768839702000},"page":"F313-F325","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Citrate modulates calciprotein particle formation and composition"],"prefix":"10.1152","volume":"330","author":[{"given":"Guido","family":"de La Roij","sequence":"first","affiliation":[{"name":"Radboud University Medical Center","place":["The Netherlands"]}]},{"given":"Robin H. M.","family":"van der Meijden","sequence":"additional","affiliation":[{"name":"Radboud University Medical Center","place":["The Netherlands"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9787-1635","authenticated-orcid":false,"given":"Luco","family":"Rutten","sequence":"additional","affiliation":[{"name":"Radboud University Medical Center","place":["The Netherlands"]},{"name":"Radboud University Medical Center","place":["The Netherlands"]}]},{"given":"Charlotte A.","family":"Hoogstraten","sequence":"additional","affiliation":[{"name":"Radboud University Medical Center","place":["The Netherlands"]}]},{"ORCID":"https:\/\/orcid.org\/0009-0009-4411-0379","authenticated-orcid":false,"given":"Maureen","family":"Hinnen","sequence":"additional","affiliation":[{"name":"Radboud University Medical Center","place":["The Netherlands"]}]},{"given":"Stan","family":"Martens","sequence":"additional","affiliation":[{"name":"Radboud University Medical Center","place":["The Netherlands"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1816-8544","authenticated-orcid":false,"given":"Joost G. J.","family":"Hoenderop","sequence":"additional","affiliation":[{"name":"Radboud University Medical Center","place":["The Netherlands"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2372-8486","authenticated-orcid":false,"given":"Jeroen H. F.","family":"de Baaij","sequence":"additional","affiliation":[{"name":"Radboud University Medical Center","place":["The Netherlands"]}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.18632\/aging.102046"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.120.050686"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/j.jacc.2021.06.049"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.3389\/fcvm.2023.1093355"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.3109\/07853890.2012.660498"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1172\/JCI17202"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1159\/000526609"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-022-11065-3"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1097\/mnh.0000000000000890"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.3390\/jcdd11010005"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1161\/ATVBAHA.117.310578"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.3390\/toxins14090637"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2019.01.024"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1097\/01.tp.0001065316.69557.a1"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.3389\/fcvm.2022.771096"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/j.atherosclerosis.2016.05.044"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1161\/ATVBAHA.122.318420"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1161\/ATVBAHA.120.315697"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.3390\/ijms232314941"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1007\/s00018-025-05702-z"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/j.bone.2018.02.023"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1007\/s00223-022-01036-1"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfac271"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfz190"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1038\/s41467-019-14091-4"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0000000000000509"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1002\/14651858.CD010057.pub2"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1002\/jbmr.5650020308"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.4111\/kju.2014.55.12.775"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/j.atherosclerosis.2016.09.071"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-019-47934-7"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1111\/apm.12667"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1097\/FJC.0000000000000590"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2012030240"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1093\/jbmrpl\/ziaf082"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0230493"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.2478\/jtim-2018-0026"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.3389\/fimmu.2018.01991"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-025-03083-7"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M210868200"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-023-42273-0"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfz234"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-019-47040-8"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0225824"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1007\/s40620-022-01470-2"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00205.2023"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1016\/j.jcis.2022.04.025"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1021\/acsbiomaterials.1c00196"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1021\/acsbiomaterials.4c01283"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.2147\/IJN.S145386"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1134\/S1061933X24600027"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1039\/b710974a"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M114.596445"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1016\/j.jbc.2021.100616"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00239.2023"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.3389\/fcell.2021.633925"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1146\/annurev-physiol-021317-121550"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1097\/MOL.0000000000000411"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1007\/s00428-013-1468-3"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1126\/scisignal.aar2566"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1919702117"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.180216"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.2174\/092986710791233706"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.3324\/haematol.13547"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.3265\/nefrologia.pre2013.dec.12385"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1161\/01.res.87.11.1055"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1038\/386078a0"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00391.2025","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,3,26]],"date-time":"2026-03-26T14:00:03Z","timestamp":1774533603000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00391.2025"}},"issued":{"date-parts":[[2026,3,1]]},"references-count":67,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2026,3,1]]}},"alternative-id":["10.1152\/ajprenal.00391.2025"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00391.2025","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2026,3,1]]},"assertion":[{"value":"2025-10-21","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2025-11-18","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2026-01-10","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2026-02-23","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,3,25]],"date-time":"2026-03-25T19:48:22Z","timestamp":1774468102554,"version":"3.50.1"},"reference-count":46,"publisher":"American Physiological Society","issue":"4","funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"crossref","award":["055831"],"award-info":[{"award-number":["055831"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"crossref","award":["087843"],"award-info":[{"award-number":["087843"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000738","name":"U.S. Department of Veterans Affairs","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000738","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2020,10,1]]},"abstract":"<jats:p>Tubular changes contribute to the development of renal pathologies in diabetic kidney disease (DKD), including interstitial fibrosis. It is unclear how tubular cells relay signals to interstitial fibroblasts. Recently, exosomes have been recognized as crucial mediators of intercellular communication. We hypothesized that exosomes secreted from tubular cells may stimulate fibroblasts for interstitial fibrosis in DKD. In this study, we isolated and purified exosomes from the renal cortex of DKD mice and high glucose-treated mouse proximal tubular cells. Compared with nondiabetic mice, exosome secretion in kidney tissues decreased in DKD mice. Likewise, high glucose incubation reduced exosome secretion in mouse kidney proximal tubular BUMPT cells. To study the effect of tubular cell exosomes on fibroblasts, exosomes from BUMPT cells were added to renal fibroblast NRK-49F cell cultures. Notably, exosomes from high glucose conditioned BUMPT cells induced higher proliferation, significant morphological change, and substantial production of fibronectin, \u03b1-smooth muscle actin, and collagen type \u0399 in NRK-49F fibroblasts. Proteomics analysis was further performed to profile the proteins within tubular cell exosomes. Interestingly, 22 proteins were found to be differentially expressed between tubular exosomes derived from high glucose conditioned cells and those from normal glucose conditioned cells. Cytoscape analysis suggested the existence of two protein-protein interaction networks in these exosomal differentially expressed proteins. While one of the protein-protein interaction networks comprised enolase 1 (Eno1), heat shock protein family A member 8 (Hspa8), thioredoxin 1 (Txn1), peptidylprolyl isomerase A (Ppia), phosphoglycerate kinase 1 (Pgk1), DNA topoisomerase II-\u03b2 (Top2b), and \u03b2-actin (Actb), the other had the family proteins of human leucocyte antigen F (Ywhag), a component of the ND10 nuclear body (Ywhae), interferon regulatory factor-8 (Ywhaq), and human leucocyte antigen A (Ywhaz). Gene expression analysis via Nephroseq showed a correlation of Eno1 expression with DKD clinical manifestation. In conclusion, DKD is associated with a decrease in exosome secretion in renal tubular cells. Exosomes from high glucose conditioned tubular cells may regulate the proliferation and activation of fibroblasts, contributing to the paracrine signaling mechanism responsible for the pathological onset of renal interstitial fibrosis in DKD.<\/jats:p>","DOI":"10.1152\/ajprenal.00292.2020","type":"journal-article","created":{"date-parts":[[2020,7,27]],"date-time":"2020-07-27T06:14:27Z","timestamp":1595830467000},"page":"F664-F673","source":"Crossref","is-referenced-by-count":44,"title":["Decreased secretion and profibrotic activity of tubular exosomes in diabetic kidney disease"],"prefix":"10.1152","volume":"319","author":[{"given":"Jin","family":"Wen","sequence":"first","affiliation":[{"name":"Department of Nephrology, West China Hospital of Sichuan University, Chengdu, China"},{"name":"Department of Nephrology and Rheumatology, Yongchuan Hospital of Chongqing Medical University, Chongqing, China"},{"name":"Department of Cellular Biology and Anatomy, Medical College of Georgia and Charlie Norwood Veterans Affairs Medical Center, Augusta, Georgia"}]},{"given":"Zhengwei","family":"Ma","sequence":"additional","affiliation":[{"name":"Department of Cellular Biology and Anatomy, Medical College of Georgia and Charlie Norwood Veterans Affairs Medical Center, Augusta, Georgia"}]},{"given":"Man J.","family":"Livingston","sequence":"additional","affiliation":[{"name":"Department of Cellular Biology and Anatomy, Medical College of Georgia and Charlie Norwood Veterans Affairs Medical Center, Augusta, Georgia"}]},{"given":"Wei","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Cellular Biology and Anatomy, Medical College of Georgia and Charlie Norwood Veterans Affairs Medical Center, Augusta, Georgia"}]},{"given":"Yanggang","family":"Yuan","sequence":"additional","affiliation":[{"name":"Department of Cellular Biology and Anatomy, Medical College of Georgia and Charlie Norwood Veterans Affairs Medical Center, Augusta, Georgia"}]},{"given":"Chunyuan","family":"Guo","sequence":"additional","affiliation":[{"name":"Department of Cellular Biology and Anatomy, Medical College of Georgia and Charlie Norwood Veterans Affairs Medical Center, Augusta, Georgia"}]},{"given":"Yutao","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Cellular Biology and Anatomy, Medical College of Georgia and Charlie Norwood Veterans Affairs Medical Center, Augusta, Georgia"}]},{"given":"Ping","family":"Fu","sequence":"additional","affiliation":[{"name":"Department of Nephrology, West China Hospital of Sichuan University, Chengdu, China"}]},{"given":"Zheng","family":"Dong","sequence":"additional","affiliation":[{"name":"Department of Cellular Biology and Anatomy, Medical College of Georgia and Charlie Norwood Veterans Affairs Medical Center, Augusta, Georgia"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00318.2018"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/j.pharmthera.2014.02.009"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009070721"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2018.6"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.3390\/cells8080853"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1038\/srep44186"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2016121278"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa1806891"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2015010074"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/j.biocel.2012.10.001"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.2337\/dc18-2585"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0170628"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1146\/annurev-physiol-022516-034227"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.pathol.4.110807.092150"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2017.98"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-017-01905-y"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1080\/00365521.2018.1516799"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.3389\/fgene.2019.00663"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2019.11.026"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008121226"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1080\/15548627.2016.1166317"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1155\/2016\/8749417"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2017050523"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2015010006"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1038\/s41556-018-0250-9"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1242\/dmm.019117"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.101.3.942"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.15171\/jlms.2017.s4"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2019.09.003"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1165\/rcmb.2017-0268OC"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.3349\/ymj.2015.56.6.1619"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1016\/j.ceb.2009.03.007"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00172.2002"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1007\/s11010-019-03583-y"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1002\/cpbi.5"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1038\/ncomms15287"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2016.01.043"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1038\/s41581-020-0256-y"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1001\/jama.290.16.2159"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-017-09907-6"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1242\/bio.015990"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1186\/1477-5956-11-30"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00178.2017"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00429.2016"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1016\/j.febslet.2011.07.042"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00078.2017"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00292.2020","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2020,10,7]],"date-time":"2020-10-07T13:26:35Z","timestamp":1602077195000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00292.2020"}},"issued":{"date-parts":[[2020,10,1]]},"references-count":46,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2020,10,1]]}},"alternative-id":["10.1152\/ajprenal.00292.2020"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00292.2020","relation":{"has-review":[{"id-type":"doi","id":"10.3410\/f.738395908.793577249","asserted-by":"object"}]},"ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2020,10,1]]}},{"indexed":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T04:39:19Z","timestamp":1773290359692,"version":"3.50.1"},"reference-count":36,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2003,10]]},"abstract":"<jats:p>In the passive Heymann nephritis (PHN) model of rat membranous nephropathy, complement C5b-9 causes sublytic injury of glomerular epithelial cells (GEC). We previously showed that sublytic concentration of C5b-9 triggers a variety of biological events in GEC. In the current study, we demonstrate that complement activates p38 MAPK in GEC and address the role of p38 in complement-mediated cell injury. When cultured rat GEC were stimulated with complement, p38 kinase activity and phosphorylation were increased by \u223c2.4-fold, compared with control. Treatment with p38 inhibitors significantly augmented complement-mediated cytotoxicity. In contrast, when the constitutively active mutant of transforming growth factor-\u03b2-activated kinase 1 (TAK1), a kinase upstream of p38, was expressed in GEC in an inducible manner, cytotoxicity was significantly reduced, compared with uninduced cells. p38 inhibitors abolished the protective effect of TAK1 expression. By analogy to cultured cells, p38 activity was also increased in glomeruli from rats with PHN and treatment with the p38 inhibitor FR-167653 increased proteinuria. Complement induced phosphorylation of MAPK-associated protein kinase-2 (MAPKAPK-2), a kinase downstream of p38 in GEC. Heat shock protein (HSP27) is a cytoskeleton-interacting substrate of MAPKAPK-2. Overexpression of the wild-type HSP27, but not a non-phosphorylatable mutant, markedly reduced complement-mediated GEC injury. In summary, complement activates p38 MAPK in GEC in vitro and in glomeruli from rats with PHN. The activation of p38 MAPK appears to be cytoprotective for GEC against complement-mediated GEC injury. Phosphorylation of HSP27 may mediate this cytoprotection.<\/jats:p>","DOI":"10.1152\/ajprenal.00100.2003","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:39:30Z","timestamp":1425415170000},"page":"F765-F774","source":"Crossref","is-referenced-by-count":32,"title":["p38 Mitogen-activated protein kinase protects glomerular epithelial cells from complement-mediated cell injury"],"prefix":"10.1152","volume":"285","author":[{"given":"Lamine","family":"Aoudjit","sequence":"first","affiliation":[{"name":"Department of Medicine, McGill University Health Centre, Montreal, Quebec, Canada H3A 2B4"}]},{"given":"Monica","family":"Stanciu","sequence":"additional","affiliation":[{"name":"Department of Medicine, McGill University Health Centre, Montreal, Quebec, Canada H3A 2B4"}]},{"given":"Hongping","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Medicine, McGill University Health Centre, Montreal, Quebec, Canada H3A 2B4"}]},{"given":"Serge","family":"Lemay","sequence":"additional","affiliation":[{"name":"Department of Medicine, McGill University Health Centre, Montreal, Quebec, Canada H3A 2B4"}]},{"given":"Tomoko","family":"Takano","sequence":"additional","affiliation":[{"name":"Department of Medicine, McGill University Health Centre, Montreal, Quebec, Canada H3A 2B4"}]}],"member":"24","reference":[{"key":"REF1","doi-asserted-by":"publisher","DOI":"10.1038\/74166"},{"key":"REF2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.5.F739"},{"key":"REF3","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00013.x"},{"key":"REF4","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00932.x"},{"key":"REF5","doi-asserted-by":"crossref","unstructured":"Guay J, Lambert H, Gingras-Breton G, Lavoie JN, Huot J, and Landry J.Regulation of actin filament dynamics by p38 map kinase-mediated phosphorylation of heat shock protein 27.J Cell Sci110: 357\u2013368, 1997.","DOI":"10.1242\/jcs.110.3.357"},{"key":"REF6","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000037402.83851.5F"},{"key":"REF7","doi-asserted-by":"publisher","DOI":"10.1038\/73456"},{"key":"REF8","doi-asserted-by":"publisher","DOI":"10.1172\/JCI200114629"},{"key":"REF9","doi-asserted-by":"publisher","DOI":"10.1016\/S1097-2765(00)80057-X"},{"key":"REF10","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.14.9378"},{"key":"REF11","doi-asserted-by":"crossref","unstructured":"Lavoie JN, Gingras-Breton G, Tanguay RM, and Landry J.Induction of Chinese hamster HSP27 gene expression in mouse cells confers resistance to heat shock. HSP27 stabilization of the microfilament organization.J Biol Chem268: 3420\u20133429, 1993.","DOI":"10.1016\/S0021-9258(18)53711-X"},{"key":"REF12","doi-asserted-by":"crossref","unstructured":"Lavoie JN, Hickey E, Weber LA, and Landry J.Modulation of actin microfilament dynamics and fluid phase pinocytosis by phosphorylation of heat shock protein 27.J Biol Chem268: 24210\u201324214, 1993.","DOI":"10.1016\/S0021-9258(20)80512-2"},{"key":"REF13","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1097-4652(199812)177:4<606::AID-JCP11>3.0.CO;2-Z"},{"key":"REF14","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(95)90401-8"},{"key":"REF15","doi-asserted-by":"publisher","DOI":"10.1097\/00003246-200004001-00008"},{"key":"REF16","doi-asserted-by":"crossref","unstructured":"Panesar M, Papillon J, McTavish AJ, and Cybulsky AV.Activation of phospholipase A2by complement C5b-9 in glomerular epithelial cells.J Immunol159: 3584\u20133594, 1997.","DOI":"10.4049\/jimmunol.159.7.3584"},{"key":"REF17","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.169.5.2594"},{"key":"REF18","doi-asserted-by":"publisher","DOI":"10.1172\/JCI200315645"},{"key":"REF19","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1988.143"},{"key":"REF20","unstructured":"Salant DJand Cybulsky AV.Experimental glomerulonephritis. In:Methods in Enzymology, edited by DiSabato G. New York: Academic, 1988, p. 421\u2013461."},{"key":"REF21","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1989.81"},{"key":"REF22","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1097-4652(199812)177:4<575::AID-JCP8>3.0.CO;2-1"},{"key":"REF23","doi-asserted-by":"publisher","DOI":"10.1096\/fasebj.9.9.7601337"},{"key":"REF24","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118723"},{"key":"REF25","doi-asserted-by":"publisher","DOI":"10.1096\/fj.01-0681com"},{"key":"REF26","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000048715.12315.FD"},{"key":"REF27","doi-asserted-by":"crossref","unstructured":"Takahashi S, Keto Y, Fujita T, Uchiyama T, and Yamamoto A.FR167653, a p38 mitogen-activated protein kinase inhibitor, prevents helicobacter pylori-induced gastritis in mongolian gerbils.J Pharmacol Exp Ther296: 48\u201356, 2001.","DOI":"10.1016\/S0022-3565(24)29661-0"},{"key":"REF28","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-5793(99)01328-9"},{"key":"REF29","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)65080-8"},{"key":"REF30","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.102.043604"},{"key":"REF31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.0048.2001"},{"key":"REF32","unstructured":"Tischer DGand Couser WG.Milestones in nephrology.J Am Soc Nephrol11: 183\u2013188, 2000."},{"key":"REF33","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00407.x"},{"key":"REF34","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000038687.24289.83"},{"key":"REF35","doi-asserted-by":"crossref","unstructured":"Wada T, Furuichi K, Sakai N, Iwata Y, Yoshimoto K, Shimizu M, Kobayashi K, Mukaida N, Matsushima K, and Yokoyama H.A new anti-inflammatory compound, FR167653, ameliorates crescentic glomerulonephritis in Wistar-Kyoto rats.J Am Soc Nephrol11: 1534\u20131541, 2000.","DOI":"10.1681\/ASN.V1181534"},{"key":"REF36","doi-asserted-by":"publisher","DOI":"10.1126\/science.270.5244.2008"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00100.2003","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,5,20]],"date-time":"2025-05-20T17:52:17Z","timestamp":1747763537000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00100.2003"}},"issued":{"date-parts":[[2003,10]]},"references-count":36,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2003,10]]}},"alternative-id":["10.1152\/ajprenal.00100.2003"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00100.2003","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2003,10]]}},{"indexed":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T06:24:34Z","timestamp":1773296674285,"version":"3.50.1"},"reference-count":42,"publisher":"American Physiological Society","issue":"1","funder":[{"name":"The Danish Council for Independent Research, Medical Sciences","award":["FSS 11-104255"],"award-info":[{"award-number":["FSS 11-104255"]}]},{"name":"Maskinfabrikant Jochum Jensen og hustru Mette Marie Jensen F Poulsens Mindelegat"},{"name":"S\u00f8ster og Verner Lipperts Fond"},{"name":"Bagenkop Nielsens Myopi-Fond"},{"DOI":"10.13039\/100009584","name":"The Toyota Foundation","doi-asserted-by":"crossref","id":[{"id":"10.13039\/100009584","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2017,1,1]]},"abstract":"<jats:p> The aim was to quantify the glomerular capillary surface area, the segmental tubular radius, length, and area of single nephrons in mouse and rat kidneys. Multiple 2.5-\u00b5m-thick serial Epon sections were obtained from three mouse and three rat kidneys for three-dimensional reconstruction of the nephron tubules. Micrographs were aligned for each kidney, and 359 nephrons were traced and their segments localized. Thirty mouse and thirty rat nephrons were selected for further investigation. The luminal radius of each segment was determined by two methods. The luminal surface area was estimated from the radius and length of each segment. High-resolution micrographs were recorded for five rat glomeruli, and the capillary surface area determined. The capillary volume and surface area were corrected for glomerular shrinkage. A positive correlation was found between glomerular capillary area and proximal tubule area. The thickest part of the nephron, i.e., the proximal tubule, was followed by the thinnest part of the nephron, i.e., the descending thin limb, and the diameters of the seven identified nephron segments share the same rank in the two species. The radius and length measurements from mouse and rat nephrons generally share the same pattern; rat tubular radius-to-mouse tubular radius ratio \u2248 1.47, and rat tubular length-to-mouse tubular length ratio \u2248 2.29, suggesting relatively longer tubules in the rat. The detailed tables of mouse and rat glomerular capillary area and segmental radius, length, and area values may be used to enhance understanding of the associated physiology, including existing steady-state models of the urine-concentrating mechanism. <\/jats:p>","DOI":"10.1152\/ajprenal.00207.2016","type":"journal-article","created":{"date-parts":[[2016,10,5]],"date-time":"2016-10-05T22:38:43Z","timestamp":1475707123000},"page":"F210-F229","source":"Crossref","is-referenced-by-count":12,"title":["Nephron morphometry in mice and rats using tomographic microscopy"],"prefix":"10.1152","volume":"312","author":[{"given":"Robyn F. R.","family":"Letts","sequence":"first","affiliation":[{"name":"Biomedical Engineering Research Group in the School of Electrical and Information Engineering, University of the Witwatersrand, Johannesburg, South Africa;"}]},{"given":"Xiao-Yue","family":"Zhai","sequence":"additional","affiliation":[{"name":"Department of Histology and Embryology, China Medical University, Shenyang, People\u2019s Republic of China; and"}]},{"given":"Charita","family":"Bhikha","sequence":"additional","affiliation":[{"name":"Biomedical Engineering Research Group in the School of Electrical and Information Engineering, University of the Witwatersrand, Johannesburg, South Africa;"}]},{"given":"Birgitte L.","family":"Grann","sequence":"additional","affiliation":[{"name":"Department of Biomedicine\u2013Anatomy, Aarhus University, Aarhus, Denmark"}]},{"given":"Nicklas B.","family":"Blom","sequence":"additional","affiliation":[{"name":"Department of Biomedicine\u2013Anatomy, Aarhus University, Aarhus, Denmark"}]},{"given":"Jesper Skovhus","family":"Thomsen","sequence":"additional","affiliation":[{"name":"Department of Biomedicine\u2013Anatomy, Aarhus University, Aarhus, Denmark"}]},{"given":"David M.","family":"Rubin","sequence":"additional","affiliation":[{"name":"Biomedical Engineering Research Group in the School of Electrical and Information Engineering, University of the Witwatersrand, Johannesburg, South Africa;"}]},{"given":"Erik I.","family":"Christensen","sequence":"additional","affiliation":[{"name":"Department of Biomedicine\u2013Anatomy, Aarhus University, Aarhus, Denmark"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2160-591X","authenticated-orcid":false,"given":"Arne","family":"Andreasen","sequence":"additional","affiliation":[{"name":"Department of Histology and Embryology, China Medical University, Shenyang, People\u2019s Republic of China; and"},{"name":"Department of Biomedicine\u2013Anatomy, Aarhus University, Aarhus, Denmark"}]}],"member":"24","reference":[{"key":"B1","first-page":"S25","volume":"20","author":"Bankir L","year":"1987","journal-title":"Kidney Int Suppl"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.2"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1007\/BF02486566"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1155\/2015\/545809"},{"key":"B5","volume-title":"A Textbook of Histology","author":"Bloom W","year":"1975","edition":"10"},{"key":"B6","first-page":"957","volume":"23","author":"Burg MB","year":"1981","journal-title":"Nihon Jinzo Gakkai Shi"},{"key":"B7","volume-title":"Geometria Indivisibilibus Continuorum Nova Quadam Ratione Promota","author":"Cavalieri B","year":"1653"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00522.2013"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1980.90"},{"key":"B10","volume-title":"Documenta Geigy Scientific Tables","author":"Diem K","year":"1970","edition":"7"},{"key":"B11","first-page":"305","volume":"5","author":"D\u00f8rup J","year":"1997","journal-title":"Exp Nephrol"},{"key":"B12","volume-title":"Basic Transport Phenomena in Biomedical Engineering","author":"Fournier RL","year":"1999"},{"key":"B13","volume-title":"Textbook of Histology","author":"Geneser F","year":"1986"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2818.1987.tb02837.x"},{"key":"B15","volume-title":"Elementary Trigonometry","author":"Hall HS","year":"1906","edition":"4"},{"key":"B16","volume-title":"Basic Histology","author":"Junqueira LC","year":"1980","edition":"3"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1002\/ar.1090820310"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1007\/BF00337120"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.5402\/2012\/170594"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00249.2009"},{"key":"B21","first-page":"862","volume":"63","author":"Miller PL","year":"1990","journal-title":"Lab Invest"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2818.1993.tb03356.x"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.5.3.363"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00285.2003"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00456.2012"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00231.2007"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00276.2014"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1007\/978-3-642-68287-2_1"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00429.2013"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0070898"},{"key":"B31","volume-title":"Physics for Scientists and Engineers","author":"Serway RA","year":"2014","edition":"9"},{"key":"B32","first-page":"9","volume":"93","author":"Seyer-Hansen K","year":"1985","journal-title":"Acta Pathol Microbiol Immunol Scand A"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0032771"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.4103\/2153-3539.109864"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1016\/0378-4754(95)00046-1"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1987.34"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1007\/s002239900373"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1002\/aja.1000410109"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.ph.44.030182.001223"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000051725.00406.0C"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005080796"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1016\/j.micron.2014.10.002"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00207.2016","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T02:06:51Z","timestamp":1567994811000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00207.2016"}},"issued":{"date-parts":[[2017,1,1]]},"references-count":42,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2017,1,1]]}},"alternative-id":["10.1152\/ajprenal.00207.2016"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00207.2016","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2017,1,1]]}},{"indexed":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T01:43:20Z","timestamp":1773279800482,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1993,9,1]]},"abstract":"<jats:p> The pathogenesis of glomerular injury in the remnant kidney (RK) model remains controversial. Increased glomerular transmission of systemic hypertension has been postulated to be an important pathogenic mechanism, but the precise relationship between systemic pressures and glomerular injury has not been defined because of the limitations of the tail-cuff method. Systolic blood pressure (BP) was continuously recorded radiotelemetrically at 10-min intervals for 6 wk in rats after approximately 5\/6 renal ablation (n = 16) or sham ablation (n = 7). Overall mean systolic BP in RK rats was significantly higher than sham (138 +\/- 3.3 vs. 117 +\/- 1.3 mmHg, P &lt; 0.01). Additionally, marked lability of systolic BP was observed in RK rats as compared with sham rats. Glomerular injury was essentially confined to RK rats, but the percentage of injured glomeruli ranged between 1 and 55%. Glomerular injury in individual animals was strongly correlated (r = 0.88) with the mean systolic BP during the last approximately 4 wk and with the frequency of systolic BP readings of &gt; 140 mmHg. These data strongly suggest that transmission of systemic hypertension to the renal microvasculature plays a predominant role in the pathogenesis of glomerular injury in the RK model and also support the potential usefulness of the radiotelemetric technique to investigate hypertensive target organ injury. <\/jats:p>","DOI":"10.1152\/ajprenal.1993.265.3.f391","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T05:17:13Z","timestamp":1514006233000},"page":"F391-F398","source":"Crossref","is-referenced-by-count":26,"title":["Continuous telemetric blood pressure monitoring and glomerular injury in the rat remnant kidney model"],"prefix":"10.1152","volume":"265","author":[{"given":"A. K.","family":"Bidani","sequence":"first","affiliation":[{"name":"Department of Medicine, Loyola University Medical Center, Maywood60153."}]},{"given":"K. A.","family":"Griffin","sequence":"additional","affiliation":[{"name":"Department of Medicine, Loyola University Medical Center, Maywood60153."}]},{"given":"M.","family":"Picken","sequence":"additional","affiliation":[{"name":"Department of Medicine, Loyola University Medical Center, Maywood60153."}]},{"given":"D. M.","family":"Lansky","sequence":"additional","affiliation":[{"name":"Department of Medicine, Loyola University Medical Center, Maywood60153."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1993.265.3.F391","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:27:21Z","timestamp":1567960041000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1993.265.3.F391"}},"issued":{"date-parts":[[1993,9,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1993,9,1]]}},"alternative-id":["10.1152\/ajprenal.1993.265.3.F391"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1993.265.3.f391","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1993,9,1]]}},{"indexed":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T05:06:38Z","timestamp":1773291998000,"version":"3.50.1"},"reference-count":81,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2011,5]]},"abstract":"<jats:p>Urinary flow is not constant but in fact highly variable, altering the mechanical forces (shear stress, stretch, and pressure) exerted on the epithelial cells of the nephron as well as solute delivery. Nitric oxide (NO) and superoxide (O<jats:sub>2<\/jats:sub><jats:sup>\u2212<\/jats:sup>) play important roles in various processes within the kidney. Reductions in NO and increases in O<jats:sub>2<\/jats:sub><jats:sup>\u2212<\/jats:sup>lead to abnormal NaCl and water absorption and hypertension. In the last few years, luminal flow has been shown to be a regulator of NO and O<jats:sub>2<\/jats:sub><jats:sup>\u2212<\/jats:sup>production along the nephron. Increases in luminal flow enhance fluid, Na, and bicarbonate transport in the proximal tubule. However, we know of no reports directly addressing flow regulation of NO and O<jats:sub>2<\/jats:sub><jats:sup>\u2212<\/jats:sup>in this segment. In the thick ascending limb, flow-stimulated NO and O<jats:sub>2<\/jats:sub><jats:sup>\u2212<\/jats:sup>formation has been extensively studied. Luminal flow stimulates NO production by nitric oxide synthase type 3 and its translocation to the apical membrane in medullary thick ascending limbs. These effects are mediated by flow-induced shear stress. In contrast, flow-induced stretch and NaCl delivery stimulate O<jats:sub>2<\/jats:sub><jats:sup>\u2212<\/jats:sup>production by NADPH oxidase in this segment. The interaction between flow-induced NO and O<jats:sub>2<\/jats:sub><jats:sup>\u2212<\/jats:sup>is complex and involves more than one simply scavenging the other. Flow-induced NO prevents flow from increasing O<jats:sub>2<\/jats:sub><jats:sup>\u2212<\/jats:sup>production via cGMP-dependent protein kinase in thick ascending limbs. In macula densa cells, shear stress increases NO production and this requires that the primary cilia be intact. The role of luminal flow in NO and O<jats:sub>2<\/jats:sub><jats:sup>\u2212<\/jats:sup>production in the distal tubule is not known. In cultured inner medullary collecting duct cells, shear stress enhances nitrite accumulation, a measure of NO production. Although much progress has been made on this subject in the last few years, there are still many unanswered questions.<\/jats:p>","DOI":"10.1152\/ajprenal.00724.2010","type":"journal-article","created":{"date-parts":[[2011,2,24]],"date-time":"2011-02-24T03:57:56Z","timestamp":1298519876000},"page":"F1047-F1053","source":"Crossref","is-referenced-by-count":29,"title":["Luminal flow regulates NO and O<sub>2<\/sub><sup>\u2212<\/sup>along the nephron"],"prefix":"10.1152","volume":"300","author":[{"given":"Pablo D.","family":"Cabral","sequence":"first","affiliation":[{"name":"Hypertension and Vascular Research Division, Department of Internal Medicine, Henry Ford Hospital, and"}]},{"given":"Jeffrey L.","family":"Garvin","sequence":"additional","affiliation":[{"name":"Hypertension and Vascular Research Division, Department of Internal Medicine, Henry Ford Hospital, and"},{"name":"Department of Physiology, Wayne State University, Detroit, Michigan"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00407.2005"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1042\/bj3570593"},{"key":"B3","doi-asserted-by":"crossref","first-page":"1464","DOI":"10.1182\/blood.V93.5.1464","volume":"93","author":"Babior BM","year":"1999","journal-title":"Blood"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1978.68"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.bi.63.070194.001135"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00238.2007"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00112.2010"},{"key":"B8","first-page":"812","volume":"24","author":"Cabral PD","year":"2010","journal-title":"FASEB J"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.2.F270"},{"key":"B10","first-page":"409","volume":"235","author":"DiBona GF","year":"1978","journal-title":"Am J Physiol"},{"key":"B11","first-page":"1","volume":"18","author":"Dwyer TM","year":"2003","journal-title":"News Physiol Sci"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1998.9790"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-201x.2000.00627.x"},{"key":"B14","doi-asserted-by":"crossref","first-page":"702","DOI":"10.1016\/S0022-3565(24)36447-X","volume":"280","author":"Fulton D","year":"1997","journal-title":"J Pharmacol Exp Ther"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.42.30101"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.107.102228"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.130135897"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1046\/j.1471-4159.2003.01995.x"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.6.2788"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1042\/bj3310801"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.2.F193"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000077044.60138.7C"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1993.265.3.H828"},{"key":"B24","first-page":"e50","volume":"56","author":"Herrera M","year":"2010","journal-title":"Hypertension"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000196274.78603.85"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.96.10.3610"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.256.6.F1007"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.258.5.F1448"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00383.2006"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90707.2008"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00543.2009"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.3109\/10715769309145868"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1172\/JCI116615"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006070700"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.57.1.142"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1081\/CEH-200044249"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1994.266.5.R1544"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1095\/biolreprod.102.013474"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M302836200"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00282.x"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90204.2008"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00515.2006"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00622.2009"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00727.x"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00530.2010"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1161\/hy0202.104137"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.260.6.F890"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00578.2007"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.37.2.467"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1161\/hy0202.103287"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00102.2002"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.0075.2001"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00382.2003"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00383.2003"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000085561.00001.81"},{"key":"B56","first-page":"87","volume":"548","author":"Parks DA","year":"1986","journal-title":"Acta Physiol Scand Suppl"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.35.1.319"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.1.F159"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.260.6.F946"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.14.9573"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.42.27383"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.108.124107"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1161\/hy0202.103299"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002190"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-008-0852-8"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2000.00377.x"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.275.1.F46"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-3495(86)83521-4"},{"key":"B69","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1995.268.5.R1087"},{"key":"B70","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.252.1.F83"},{"key":"B71","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00795.x"},{"key":"B72","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000197954.93874.ef"},{"key":"B73","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000236646.83354.51"},{"key":"B74","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008101099"},{"key":"B75","doi-asserted-by":"crossref","first-page":"89","DOI":"10.1681\/ASN.V6189","volume":"6","author":"Stoos BA","year":"1995","journal-title":"J Am Soc Nephrol"},{"key":"B76","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.62"},{"key":"B77","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00403.2010"},{"key":"B78","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.5.F769"},{"key":"B79","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.264.3.F427"},{"key":"B80","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.270.6.F1004"},{"key":"B81","first-page":"e50","volume":"56","author":"Zhu X","year":"2010","journal-title":"Hypertension"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00724.2010","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,3,2]],"date-time":"2025-03-02T23:15:18Z","timestamp":1740957318000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00724.2010"}},"issued":{"date-parts":[[2011,5]]},"references-count":81,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2011,5]]}},"alternative-id":["10.1152\/ajprenal.00724.2010"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00724.2010","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2011,5]]}},{"indexed":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T04:54:02Z","timestamp":1773291242638,"version":"3.50.1"},"reference-count":51,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2004,5]]},"abstract":"<jats:p>The distal nephron plays a capital role in the fine regulation of sodium reabsorption. Compared with the cortical collecting duct, much less information is available on the hormonal regulation of sodium transporter genes in the distal convoluted tubule (DCT), where the thiazide-sensitive Na<jats:sup>+<\/jats:sup>-Cl<jats:sup>-<\/jats:sup>cotransporter (NCC) is the major entry pathway for Na<jats:sup>+<\/jats:sup>. The purpose of this study was to characterize the in vitro effects of aldosterone (Aldo; 1 \u03bcM) and cAMP (8-BrcAMP; 0.5 mM) on mouse DCT (mDCT) by using an immortalized mDCT cell line. Western blot analysis and semiquantitative RT-PCR were performed to analyze the expression of genes involved in sodium transport. The mDCTcell line expressed the 11\u03b2-hydroxysteroid dehydrogenase type 2 gene and both the mineralocorticoid and glucocorticoid receptor genes, suggesting Aldo responsiveness. In this sense, we found that mDCT cells expressed the amiloride-sensitive Na<jats:sup>+<\/jats:sup>channel (ENaC) and responded to Aldo by upregulating the \u03b1-subunit protein. Similarly, \u03b1<jats:sub>1<\/jats:sub>Na<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-ATPase protein was upregulated by Aldo and 8-BrcAMP. In addition, the Aldo intermediate gene sgk1 mRNA was increased in response to both Aldo and 8-BrcAMP, and the transcription factor HNF\u20133\u03b1 mRNA was induced by 8-BrcAMP. With respect to NCC regulation, although Aldo induced NCC protein levels in mice in vivo, neither Aldo nor 8-BrcAMP significantly induced the NCC mRNA or protein levels in mDCT cells. These results suggest that in mDCT, Aldo and cAMP modulate some downstream mediators and effectors in vitro but do not influence the expression of NCC in this cell model.<\/jats:p>","DOI":"10.1152\/ajprenal.00070.2003","type":"journal-article","created":{"date-parts":[[2004,3,9]],"date-time":"2004-03-09T01:14:04Z","timestamp":1078794844000},"page":"F936-F944","source":"Crossref","is-referenced-by-count":23,"title":["In vitro characterization of aldosterone and cAMP effects in mouse distal convoluted tubule cells"],"prefix":"10.1152","volume":"286","author":[{"given":"Daniel","family":"Gonz\u00e1lez-N\u00fa\u00f1ez","sequence":"first","affiliation":[]},{"given":"Manuel","family":"Morales-Ruiz","sequence":"additional","affiliation":[]},{"given":"Alberto","family":"Leivas","sequence":"additional","affiliation":[]},{"given":"Steven C.","family":"Hebert","sequence":"additional","affiliation":[]},{"given":"Esteban","family":"Poch","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"REF1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M006591200"},{"key":"REF2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118311"},{"key":"REF3","doi-asserted-by":"crossref","unstructured":"Bens M, Vallet V, Cluzeaud F, Pascual-Letallec L, Kahn A, Rafestin-Oblin ME, Rossier BC, and Vandewalle A.Corticosteroid-dependent sodium transport in a novel immortalized mouse collecting duct principal cell line.J Am Soc Nephrol10: 923-934, 1999.","DOI":"10.1681\/ASN.V105923"},{"key":"REF4","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.16.9424"},{"key":"REF5","doi-asserted-by":"publisher","DOI":"10.1210\/endo.142.4.8095"},{"key":"REF6","doi-asserted-by":"crossref","unstructured":"Bostanjoglo M, Reeves WB, Reilly RF, Velazquez H, Robertson N, Litwack G, Morsing P, Dorup J, Bachmann S, Ellison DH, and Bostonjoglo M.11\u03b2-Hydroxysteroid dehydrogenase, mineralocorticoid receptor, and thiazide-sensitive Na-Cl cotransporter expression by distal tubules.J Am Soc Nephrol9: 1347-1358, 1998.","DOI":"10.1681\/ASN.V981347"},{"key":"REF7","doi-asserted-by":"publisher","DOI":"10.1016\/0003-2697(76)90527-3"},{"key":"REF8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.0148.2001"},{"key":"REF9","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.5.2514"},{"key":"REF10","doi-asserted-by":"crossref","unstructured":"Chen Z, Vaughn DA, Blakely P, and Fanestil DD.Adrenocortical steroids increase renal thiazide diuretic receptor density and response.J Am Soc Nephrol5: 1361-1368, 1994.","DOI":"10.1681\/ASN.V561361"},{"key":"REF11","doi-asserted-by":"crossref","unstructured":"Chen ZF, Vaughn DA, Beaumont K, and Fanestil DD.Effects of diuretic treatment and of dietary sodium on renal binding of 3H-metolazone.J Am Soc Nephrol1: 91-98, 1990.","DOI":"10.1681\/ASN.V1191"},{"key":"REF12","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.8.4545"},{"key":"REF13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.2.F328"},{"key":"REF14","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.52.32919"},{"key":"REF15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1981.241.6.F605"},{"key":"REF16","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00408.2001"},{"key":"REF17","unstructured":"Farman N.Steroid receptors: distribution along the nephron.Semin Nephrol12: 12-17, 1992."},{"key":"REF18","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.2001.81.1.345"},{"key":"REF19","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1997.77.2.359"},{"key":"REF20","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115878"},{"key":"REF21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.268.1.F89"},{"key":"REF22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.265.3.F449"},{"key":"REF23","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000043903.93452.D0"},{"key":"REF24","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000013702.73570.3B"},{"key":"REF25","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.011513098"},{"key":"REF26","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1992.260"},{"key":"REF27","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.24.14552"},{"key":"REF28","doi-asserted-by":"publisher","DOI":"10.1038\/227680a0"},{"key":"REF29","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.2001.4673"},{"key":"REF30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00016.2002"},{"key":"REF31","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.24.16973"},{"key":"REF32","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M007052200"},{"key":"REF33","doi-asserted-by":"publisher","DOI":"10.1007\/BF02630961"},{"key":"REF34","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.300"},{"key":"REF35","doi-asserted-by":"publisher","DOI":"10.1172\/JCI112433"},{"key":"REF36","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.2000.80.1.277"},{"key":"REF37","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.051603198"},{"key":"REF38","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.262.4.F679"},{"key":"REF39","doi-asserted-by":"publisher","DOI":"10.1038\/ng0196-24"},{"key":"REF40","doi-asserted-by":"publisher","DOI":"10.1007\/s004240050403"},{"key":"REF41","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M101614200"},{"key":"REF42","doi-asserted-by":"publisher","DOI":"10.1210\/endo.138.3.5004"},{"key":"REF43","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.264.5.F781"},{"key":"REF44","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.253.5.F874"},{"key":"REF45","doi-asserted-by":"publisher","DOI":"10.2337\/diab.46.8.1364"},{"key":"REF46","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/16.2.238"},{"key":"REF47","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.270.1.F211"},{"key":"REF48","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00962.x"},{"key":"REF49","doi-asserted-by":"crossref","unstructured":"Wang J, Barbry P, Maiyar AC, Rozansky DJ, Bhargava A, Leong M, Firestone GL, and Pearce D.SGK integrates insulin and mineralocorticoid regulation of epithelial sodium transport.Am J Physiol Renal Physiol280: F303-F313, 2001.","DOI":"10.1152\/ajprenal.2001.280.2.F303"},{"key":"REF50","doi-asserted-by":"publisher","DOI":"10.1172\/JCI10366"},{"key":"REF51","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.0028.2001"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00070.2003","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,6,15]],"date-time":"2021-06-15T01:56:35Z","timestamp":1623722195000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00070.2003"}},"issued":{"date-parts":[[2004,5]]},"references-count":51,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2004,5]]}},"alternative-id":["10.1152\/ajprenal.00070.2003"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00070.2003","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2004,5]]}},{"indexed":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T07:43:12Z","timestamp":1773301392740,"version":"3.50.1"},"reference-count":57,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2006,10]]},"abstract":"<jats:p>The maintenance of apical and basolateral membrane domains with distinct protein and lipid compositions is necessary for the proper function of polarized epithelial cells. Delivery of cargo to the basolateral surface is thought to be mediated by the interaction of cytoplasmically disposed sorting signals with sorting receptors, whereas apically destined cargoes are sorted via mechanisms dependent on cytoplasmic, glycan-mediated, or lipid-interacting sorting signals. Apical and basolateral cargo are delivered to the surface in discrete tubular and vesicular carriers that bud from the trans-Golgi network (TGN). While it has long been thought that the TGN is the primary compartment in which apical and basolateral cargoes are segregated, recent studies suggest that sorting may begin earlier along the biosynthetic pathway. Moreover, rather than being delivered directly from the TGN to the cell surface, at least a subset of biosynthetic cargo appears to transit recycling endosomes en route to the plasma membrane. The implications and limitations of these challenges to the conventional model for how proteins are sorted and trafficked along the biosynthetic pathway are discussed.<\/jats:p>","DOI":"10.1152\/ajprenal.00161.2006","type":"journal-article","created":{"date-parts":[[2006,6,21]],"date-time":"2006-06-21T04:13:21Z","timestamp":1150863201000},"page":"F707-F713","source":"Crossref","is-referenced-by-count":36,"title":["Polarized biosynthetic traffic in renal epithelial cells: sorting, sorting, everywhere"],"prefix":"10.1152","volume":"291","author":[{"given":"Mark A.","family":"Ellis","sequence":"first","affiliation":[]},{"given":"Beth A.","family":"Potter","sequence":"additional","affiliation":[]},{"given":"Kerry O.","family":"Cresawn","sequence":"additional","affiliation":[]},{"given":"Ora A.","family":"Weisz","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M505924200"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200307046"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200408165"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1038\/ncb1260"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1034\/j.1600-0854.2000.010205.x"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1007\/s10254-004-0037-1"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.142.5.1245"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1016\/j.cub.2005.12.046"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1016\/S0962-8924(03)00174-0"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)81650-5"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200309020"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.152.3.595"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.18.10999"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1038\/ncb827"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M601239200"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M502265200"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.143.6.1485"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-0854.2006.00398.x"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200512012"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1016\/S0960-9822(03)00188-X"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1016\/S0960-9822(01)00446-8"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1038\/35055042"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1038\/35000081"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1006\/excr.2000.5006"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.22.10109"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.87.19.7419"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.E04-10-0867"},{"key":"R28","unstructured":"Madin SH, Andriese PC, and Darby NB.The in vitro cultivation of tissues of domestic and laboratory animals.Am J Vet Res18: 932\u2013941, 1957."},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(83)90154-X"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(01)00215-X"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.133.3.543"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.092150699"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-5793(99)00432-9"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.275.20.15207"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.4.2201"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200507116"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200407094"},{"key":"R38","doi-asserted-by":"crossref","unstructured":"Paladino S, Sarnataro D, and Zurzolo C.Detergent-resistant membrane microdomains and apical sorting of GPI-anchored proteins in polarized epithelial cells.Int J Med Microbiol291: 439\u2013445, 2002.","DOI":"10.1078\/1438-4221-00151"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1038\/ncb1109"},{"key":"R40","doi-asserted-by":"crossref","unstructured":"Potter BA, Hughey RP, and Weisz OA.Role of N- and O-glycans in polarized biosynthetic sorting.Am J Physiol Cell Physiol290: C1\u2013C10, 2006.","DOI":"10.1152\/ajpcell.00333.2005"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.E02-10-0692"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1016\/S0962-8924(99)01595-0"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1038\/nrm1593"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbamcr.2005.04.007"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1016\/S0960-9822(00)00384-5"},{"key":"R46","doi-asserted-by":"publisher","DOI":"10.1016\/S0968-0004(02)00004-X"},{"key":"R47","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0631579100"},{"key":"R48","doi-asserted-by":"publisher","DOI":"10.1038\/ncb745"},{"key":"R49","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00514.2002"},{"key":"R50","doi-asserted-by":"publisher","DOI":"10.1046\/j.1398-9219.2003.0138.x"},{"key":"R51","doi-asserted-by":"crossref","unstructured":"Toomre D, Keller P, White J, Olivo JC, and Simons K.Dual-color visualization oftrans-Golgi network to plasma membrane traffic along microtubules in living cells.J Cell Sci112: 21\u201333, 1999.","DOI":"10.1242\/jcs.112.1.21"},{"key":"R52","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbamcr.2005.04.005"},{"key":"R53","doi-asserted-by":"publisher","DOI":"10.1038\/ncb1203-1045"},{"key":"R54","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M503691200"},{"key":"R55","doi-asserted-by":"publisher","DOI":"10.1093\/glycob\/cwj075"},{"key":"R56","doi-asserted-by":"publisher","DOI":"10.1038\/ncb1090"},{"key":"R57","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.133.2.247"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00161.2006","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,7,28]],"date-time":"2021-07-28T16:38:21Z","timestamp":1627490301000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00161.2006"}},"issued":{"date-parts":[[2006,10]]},"references-count":57,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2006,10]]}},"alternative-id":["10.1152\/ajprenal.00161.2006"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00161.2006","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2006,10]]}},{"indexed":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T07:23:28Z","timestamp":1773300208841,"version":"3.50.1"},"reference-count":34,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,3,15]]},"abstract":"<jats:p> Bardoxolone methyl is an antioxidant inflammation modulator acting through induction of Keap1-Nrf2 pathway. Results from a recent phase IIb clinical trial reported that bardoxolone methyl was associated with improvement in the estimated glomerular filtration rate in patients with advanced chronic kidney disease and Type 2 diabetes. However, increases in albuminuria, serum transaminase, and frequency of adverse events were noted. We studied the effect of 3-mo treatment with RTA 405, a synthetic triterpenoid analog of bardoxolone methyl in Zucker diabetic fatty rats with overt Type 2 diabetes. Rats were treated from 3 mo of age with vehicle, RTA 405, ramipril, or RTA 405 plus ramipril. RTA 405 caused severe changes in food intake and diuresis with decline in body weight, worsening of dyslipidemia, and increase in blood pressure. Early elevation in serum transaminase was followed by liver injury. RTA 405 worsened proteinuria, glomerulosclerosis, and tubular damage. Ramipril was renoprotective, but when given with RTA 405 it was not able to limit its worsening effects. These data could be due to degradation products in the drug substance used, as disclosed by the company once the study was concluded. To overcome such a drawback, the company offered to test dh404, a variant of RTA 405, in Zucker diabetic fatty rats. The dh404 did not display beneficial effects on proteinuria, glomerulosclerosis, and interstitial inflammation. Rather, kidneys from three rats receiving dh404 showed the presence of a granulomatous and inflammatory process reminiscent of a pseudotumor. Altogether these data raise serious concerns on the use of bardoxolone analogs in Type 2 diabetic nephropathy. <\/jats:p>","DOI":"10.1152\/ajprenal.00376.2012","type":"journal-article","created":{"date-parts":[[2012,11,8]],"date-time":"2012-11-08T07:08:10Z","timestamp":1352358490000},"page":"F808-F819","source":"Crossref","is-referenced-by-count":83,"title":["Analogs of bardoxolone methyl worsen diabetic nephropathy in rats with additional adverse effects"],"prefix":"10.1152","volume":"304","author":[{"given":"Carla","family":"Zoja","sequence":"first","affiliation":[{"name":"Mario Negri Institute for Pharmacological Research, Centro Anna Maria Astori, Science and Technology Park Kilometro Rosso, Bergamo, Italy;"}]},{"given":"Daniela","family":"Corna","sequence":"additional","affiliation":[{"name":"Mario Negri Institute for Pharmacological Research, Centro Anna Maria Astori, Science and Technology Park Kilometro Rosso, Bergamo, Italy;"}]},{"given":"Valeria","family":"Nava","sequence":"additional","affiliation":[{"name":"Mario Negri Institute for Pharmacological Research, Centro Anna Maria Astori, Science and Technology Park Kilometro Rosso, Bergamo, Italy;"}]},{"given":"Monica","family":"Locatelli","sequence":"additional","affiliation":[{"name":"Mario Negri Institute for Pharmacological Research, Centro Anna Maria Astori, Science and Technology Park Kilometro Rosso, Bergamo, Italy;"}]},{"given":"Mauro","family":"Abbate","sequence":"additional","affiliation":[{"name":"Mario Negri Institute for Pharmacological Research, Centro Anna Maria Astori, Science and Technology Park Kilometro Rosso, Bergamo, Italy;"}]},{"given":"Flavio","family":"Gaspari","sequence":"additional","affiliation":[{"name":"Mario Negri Institute for Pharmacological Research, Centro Aldo e Cele Dacc\u00f2, Ranica, Bergamo, Italy; and"}]},{"given":"Fabiola","family":"Carrara","sequence":"additional","affiliation":[{"name":"Mario Negri Institute for Pharmacological Research, Centro Aldo e Cele Dacc\u00f2, Ranica, Bergamo, Italy; and"}]},{"given":"Fabio","family":"Sangalli","sequence":"additional","affiliation":[{"name":"Mario Negri Institute for Pharmacological Research, Centro Anna Maria Astori, Science and Technology Park Kilometro Rosso, Bergamo, Italy;"}]},{"given":"Giuseppe","family":"Remuzzi","sequence":"additional","affiliation":[{"name":"Mario Negri Institute for Pharmacological Research, Centro Anna Maria Astori, Science and Technology Park Kilometro Rosso, Bergamo, Italy;"},{"name":"Unit of Nephrology and Dialysis, Azienda Ospedaliera Ospedali Riuniti di Bergamo, Bergamo, Italy"}]},{"given":"Ariela","family":"Benigni","sequence":"additional","affiliation":[{"name":"Mario Negri Institute for Pharmacological Research, Centro Anna Maria Astori, Science and Technology Park Kilometro Rosso, Bergamo, Italy;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M607160200"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.110.170084"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.103.055616"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa011161"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1159\/000108359"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0500815102"},{"key":"B7","first-page":"280A","volume":"21","author":"Dulubova I","year":"2010","journal-title":"J Am Soc Nephrol"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1016\/S1054-8807(03)00109-1"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00340.2009"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1292\/jvms.71.275"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0008391"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00421.2009"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1042\/bj20031049"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa011303"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1038\/nrc2129"},{"key":"B16","first-page":"1746","volume":"365","author":"McMahon GM","year":"2011","journal-title":"N Engl J Med"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1093\/toxsci\/kfn079"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00020.x"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa1105351"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2012050457"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMcp011773"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMc1110239"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.055003984.x"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M110.176545"},{"key":"B25","first-page":"375A","volume":"21","author":"Shelkovnikov S","year":"2010","journal-title":"J Am Soc Nephrol"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejphar.2009.08.022"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1021\/np100826q"},{"key":"B28","first-page":"451","volume":"125","author":"Srinivasan K","year":"2007","journal-title":"Indian J Med Res"},{"key":"B29","first-page":"1746","volume":"365","author":"Upadhyay A","year":"2011","journal-title":"N Engl J Med"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.2337\/diacare.27.5.1047"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00353.2010"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1158\/1535-7163.MCT-06-0516"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00122.2011"},{"key":"B34","first-page":"275A","volume":"21","author":"Zoja C","year":"2010","journal-title":"J Am Soc Nephrol"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00376.2012","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T23:40:40Z","timestamp":1567986040000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00376.2012"}},"issued":{"date-parts":[[2013,3,15]]},"references-count":34,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2013,3,15]]}},"alternative-id":["10.1152\/ajprenal.00376.2012"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00376.2012","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2013,3,15]]}},{"indexed":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T17:56:33Z","timestamp":1773424593883,"version":"3.50.1"},"reference-count":38,"publisher":"American Physiological Society","issue":"2","funder":[{"DOI":"10.13039\/100000050","name":"HHS | NIH | National Heart, Lung, and Blood Institute (NHBLI)","doi-asserted-by":"publisher","award":["T32-HL-083810"],"award-info":[{"award-number":["T32-HL-083810"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"HHS | NIH | National Heart, Lung, and Blood Institute (NHBLI)","doi-asserted-by":"publisher","award":["T32-HL-083810"],"award-info":[{"award-number":["T32-HL-083810"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000071","name":"HHS | NIH | National Institute of Child Health and Human Development (NICHD)","doi-asserted-by":"publisher","award":["R01-HD-041571"],"award-info":[{"award-number":["R01-HD-041571"]}],"id":[{"id":"10.13039\/100000071","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)","doi-asserted-by":"publisher","award":["R01-DK-56843"],"award-info":[{"award-number":["R01-DK-56843"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)","doi-asserted-by":"publisher","award":["R01-DK-63049"],"award-info":[{"award-number":["R01-DK-63049"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)","doi-asserted-by":"publisher","award":["R01-DK-093501"],"award-info":[{"award-number":["R01-DK-093501"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)","doi-asserted-by":"publisher","award":["DK-085193"],"award-info":[{"award-number":["DK-085193"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)","doi-asserted-by":"publisher","award":["R01-DK-54231"],"award-info":[{"award-number":["R01-DK-54231"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)","doi-asserted-by":"publisher","award":["R01-DK-093501"],"award-info":[{"award-number":["R01-DK-093501"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)","doi-asserted-by":"publisher","award":["DK-085193"],"award-info":[{"award-number":["DK-085193"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100001463","name":"American Society of Nephrology (ASN)","doi-asserted-by":"publisher","award":["Foundation for Kidney Research Grant"],"award-info":[{"award-number":["Foundation for Kidney Research Grant"]}],"id":[{"id":"10.13039\/100001463","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100001463","name":"American Society of Nephrology (ASN)","doi-asserted-by":"publisher","award":["Career Development Award"],"award-info":[{"award-number":["Career Development Award"]}],"id":[{"id":"10.13039\/100001463","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2018,2,1]]},"abstract":"<jats:p> Gestational potassium retention, most of which occurs during late pregnancy, is essential for fetal development. The purpose of this study was to examine mechanisms underlying changes in potassium handling by the kidney and colon in pregnancy. We found that potassium intake and renal excretion increased in late pregnancy while fecal potassium excretion remained unchanged and that pregnant rats exhibited net potassium retention. By quantitative PCR we found markedly increased H<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-ATPase type 2 (HKA2) mRNA expression in the cortex and outer medullary of late pregnant vs. virgin. Renal outer medullary potassium channel (ROMK) mRNA was unchanged in the cortex, but apical ROMK abundance (by immunofluorescence) was decreased in pregnant vs. virgin in the distal convoluted tubule (DCT) and connecting tubule (CNT). Big potassium-\u03b1 (BK\u03b1) channel-\u03b1 protein abundance in intercalated cells in the cortex and outer medullary collecting ducts (by immunohistochemistry) fell in late pregnancy. In the distal colon we found increased HKA2 mRNA and protein abundance (Western blot) and decreased BK\u03b1 protein with no observed changes in mRNA. Therefore, the potassium retention of pregnancy is likely to be due to increased collecting duct potassium reabsorption (via increased HKA2), decreased potassium secretion (via decreased ROMK and BK), as well as increased colonic reabsorption via HKA2. <\/jats:p>","DOI":"10.1152\/ajprenal.00288.2017","type":"journal-article","created":{"date-parts":[[2017,10,18]],"date-time":"2017-10-18T08:50:18Z","timestamp":1508316618000},"page":"F251-F259","source":"Crossref","is-referenced-by-count":26,"title":["Renal and colonic potassium transporters in the pregnant rat"],"prefix":"10.1152","volume":"314","author":[{"given":"Crystal A.","family":"West","sequence":"first","affiliation":[{"name":"Department of Medicine, Georgetown University, Washington, District of Columiba"}]},{"given":"Paul A.","family":"Welling","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland"}]},{"suffix":"Jr.","given":"David A.","family":"West","sequence":"additional","affiliation":[{"name":"Department of Medicine, Georgetown University, Washington, District of Columiba"}]},{"given":"Richard A.","family":"Coleman","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland"}]},{"given":"Kit-Yan","family":"Cheng","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Florida, Gainesville, Florida"}]},{"given":"Chao","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Florida, Gainesville, Florida"}]},{"suffix":"Jr.","given":"Thomas D.","family":"DuBose","sequence":"additional","affiliation":[{"name":"Department of Medicine, Wake Forest School of Medicine, Winston-Salem, North Carolina"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4096-4897","authenticated-orcid":false,"given":"Jill W.","family":"Verlander","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Florida, Gainesville, Florida"}]},{"given":"Chris","family":"Baylis","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Florida, Gainesville, Florida"},{"name":"Department of Physiology and Functional Genomics, University of Florida, Gainesville, Florida"}]},{"given":"Michelle L.","family":"Gumz","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Florida, Gainesville, Florida"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1080\/10641950701825887"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/0006-291X(79)90945-8"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.3109\/10641959309031053"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1210\/endo.138.6.5198"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1980.239.1.R143"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.14.7894"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0115515"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2011.15"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2015070751"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1172\/JCI106926"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1677\/joe.0.1130435"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/j.intimp.2014.06.040"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010030311"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1172\/JCI78558"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra1313341"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00051.2003"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1210\/jcem-18-11-1237"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1006\/meth.2001.1262"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.3181\/00379727-216-44156"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00220.2015"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.1996.270.4.E601"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-013-1252-x"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-009-0781-9"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2008.156968"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.1991.260.5.E743"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-012-1145-4"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013111156"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00030.2013"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.281.2.F357"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00592.2010"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1113\/expphysiol.2013.076273"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00147.2015"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00129.2016"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1113\/EP085396"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00082.2010"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1990.302"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1016\/j.steroids.2007.10.010"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.010908.163241"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00288.2017","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,10,1]],"date-time":"2019-10-01T18:34:04Z","timestamp":1569954844000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00288.2017"}},"issued":{"date-parts":[[2018,2,1]]},"references-count":38,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2018,2,1]]}},"alternative-id":["10.1152\/ajprenal.00288.2017"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00288.2017","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2018,2,1]]}},{"indexed":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T18:52:20Z","timestamp":1773427940691,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1989,10,1]]},"abstract":"<jats:p> Renal blood flow, renal sympathetic nerve activity, and renin release responses to mental stress (Stroop's color-word conflict test; CWT) and intravenously infused epinephrine (Epi) were evaluated in 12 healthy volunteers. The overflows of norepinephrine (NE) and dopamine (DA) to renal venous plasma were measured as indexes of nerve activity; the fractional extraction of Epi was used to assess renal catecholamine extraction from arterial plasma. At rest, NE and DA levels were higher in renal venous plasma than in arterial plasma. Arterial Epi levels were 0.26 +\/- 0.04 nmol\/l, and the fractional extraction of Epi by the kidney was 46 +\/- 4%. CWT increased renal vascular resistance (RVR) by 48%, renal venous NE overflow by 214% (to 708 +\/- 79 pmol\/min), and DA overflow by 42% (to 34 +\/- 4 pmol\/min). Arterial Epi increased by 197%. The vasoconstrictor response was correlated with the NE overflow response. The increased renin release (from 75 to 247 U\/min, median values; P less than 0.001) was correlated to increases in mean arterial pressure and NE and DA overflows. Epi infusion increased arterial plasma Epi and renin release dose dependently to 6.43 +\/- 0.27 nmol\/l and by 664%, respectively. RVR and NE and DA overflows were unchanged. Renal venous DA data support the existence of a subset of renal dopaminergic nerves. Mental stress causes renal vasoconstriction, apparently due to increased renal sympathetic nerve activity. Physiological increments of circulating Epi do not affect renal blood flow but enhance renin release markedly without apparent activation of the renal nerves in humans. <\/jats:p>","DOI":"10.1152\/ajprenal.1989.257.4.f682","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T21:53:58Z","timestamp":1513979638000},"page":"F682-F689","source":"Crossref","is-referenced-by-count":21,"title":["Renal responses to mental stress and epinephrine in humans"],"prefix":"10.1152","volume":"257","author":[{"given":"B.","family":"Tidgren","sequence":"first","affiliation":[{"name":"Department of Clinical Physiology, Karolinska Hospital, Stockholm, Sweden."}]},{"given":"P.","family":"Hjemdahl","sequence":"additional","affiliation":[{"name":"Department of Clinical Physiology, Karolinska Hospital, Stockholm, Sweden."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1989.257.4.F682","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:14:50Z","timestamp":1567970090000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1989.257.4.F682"}},"issued":{"date-parts":[[1989,10,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1989,10,1]]}},"alternative-id":["10.1152\/ajprenal.1989.257.4.F682"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1989.257.4.f682","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1989,10,1]]}},{"indexed":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T18:56:42Z","timestamp":1773428202213,"version":"3.50.1"},"reference-count":37,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1998,3,1]]},"abstract":"<jats:p> It is generally accepted that Na(HCO<jats:sub>3<\/jats:sub>)<jats:sub> n <\/jats:sub>cotransport is the most important mechanism mediating basolateral bicarbonate efflux in the early proximal tubule. The presence of basolateral Na(HCO<jats:sub>3<\/jats:sub>)<jats:sub> n <\/jats:sub>cotransport in the late proximal tubule (S<jats:sub>3<\/jats:sub> segment) and in the juxtamedullary S<jats:sub>1<\/jats:sub> and S<jats:sub>2<\/jats:sub> segments has been controversial. The renal sodium-bicarbonate cotransporter (NBC) has been recently cloned from rat (M. F. Romero, M. A. Hediger, E. L. Boulpaep, and W. F. Boron. J. Am. Soc. Nephrol. 7: 1259, 1996), salamander (M. F. Romero, M. A. Hediger, E. L. Boulpaep, and W. F. Boron. Nature 387: 409\u2013413, 1997), and human (C. E. Burnham, H. Amlal, Z. Wang, G. E. Shull, and M. Soleimani. J. Biol. Chem. 272: 19111\u201319114, 1997). The localization of NBC in the kidney is unknown. The present study was designed to localize NBC mRNA expression in the rabbit proximal tubule. In situ hybridization studies were combined with functional studies of basolateral Na(HCO<jats:sub>3<\/jats:sub>)<jats:sub> n <\/jats:sub>cotransport in superficial and juxtamedullary S<jats:sub>1<\/jats:sub>, S<jats:sub>2<\/jats:sub>, and S<jats:sub>3<\/jats:sub> segments of the rabbit proximal tubule. The results demonstrate that NBC mRNA is localized predominantly to the cortex, with less expression in the outer medulla. NBC expression was not detected in the inner medulla. The highest level of NBC mRNA is in the S<jats:sub>1<\/jats:sub> proximal tubule. NBC is expressed at a low levels in the S<jats:sub>3<\/jats:sub> segment, with intermediate expression in the S<jats:sub>2<\/jats:sub> segment. In bicarbonate-buffered solutions, the rate of base efflux mediated by Na(HCO<jats:sub>3<\/jats:sub>)<jats:sub> n <\/jats:sub>cotransport followed a similar pattern in superficial and juxtamedullary proximal tubule segments, i.e., S<jats:sub>1<\/jats:sub> &gt; S<jats:sub>2<\/jats:sub> &gt; S<jats:sub>3<\/jats:sub>. The juxtamedullary S<jats:sub>1<\/jats:sub> segment had the greatest rate of basolateral Na(HCO<jats:sub>3<\/jats:sub>)<jats:sub> n <\/jats:sub>cotransport and the highest level of NBC expression in the proximal tubule. <\/jats:p>","DOI":"10.1152\/ajprenal.1998.274.3.f628","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T11:00:40Z","timestamp":1514026840000},"page":"F628-F633","source":"Crossref","is-referenced-by-count":25,"title":["Axial heterogeneity of sodium-bicarbonate cotransporter  expression in the rabbit proximal tubule"],"prefix":"10.1152","volume":"274","author":[{"given":"N.","family":"Abuladze","sequence":"first","affiliation":[{"name":"Division of Nephrology, Center for Health Sciences, University of California Los Angeles School of Medicine, Los Angeles, California 90095-1698"}]},{"given":"I.","family":"Lee","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Center for Health Sciences, University of California Los Angeles School of Medicine, Los Angeles, California 90095-1698"}]},{"given":"D.","family":"Newman","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Center for Health Sciences, University of California Los Angeles School of Medicine, Los Angeles, California 90095-1698"}]},{"given":"J.","family":"Hwang","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Center for Health Sciences, University of California Los Angeles School of Medicine, Los Angeles, California 90095-1698"}]},{"given":"A.","family":"Pushkin","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Center for Health Sciences, University of California Los Angeles School of Medicine, Los Angeles, California 90095-1698"}]},{"given":"I.","family":"Kurtz","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Center for Health Sciences, University of California Los Angeles School of Medicine, Los Angeles, California 90095-1698"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.86.5.613"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.89.4.581"},{"issue":"25","key":"B3","first-page":"F335","volume":"256","author":"Baum M.","year":"1989","journal-title":"Am. J. Physiol."},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1172\/JCI114465"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.81.1.53"},{"issue":"2","key":"B6","first-page":"F307","volume":"233","author":"Burg M. B.","year":"1977","journal-title":"Am. J. Physiol."},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.31.19111"},{"issue":"9","key":"B8","first-page":"F222","volume":"240","author":"Chan Y. L.","year":"1981","journal-title":"Am. J. Physiol."},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1992.sp019169"},{"issue":"19","key":"B10","first-page":"G491","volume":"256","author":"Fitz J. G.","year":"1989","journal-title":"Am. J. Physiol."},{"key":"B11","first-page":"106","volume":"139","author":"Fr\u00f6mter E.","year":"1988","journal-title":"Ciba Found. Symp."},{"issue":"26","key":"B12","first-page":"F790","volume":"257","author":"Geibel J.","year":"1989","journal-title":"Am. J. Physiol."},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1007\/BF01875464"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1996.sp021582"},{"issue":"9","key":"B15","first-page":"F54","volume":"240","author":"Jacobson H. R.","year":"1981","journal-title":"Am. J. Physiol."},{"issue":"6","key":"B16","first-page":"F114","volume":"237","author":"Katz A. I.","year":"1979","journal-title":"Am. J. Physiol."},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1007\/BF00586529"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1172\/JCI113184"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1172\/JCI113925"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117304"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1977.72"},{"issue":"7","key":"B22","first-page":"F166","volume":"238","author":"McKinney T. D.","year":"1980","journal-title":"Am. J. Physiol."},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1994.sp020001"},{"issue":"27","key":"B24","first-page":"F371","volume":"258","author":"Nakhoul N. L.","year":"1990","journal-title":"Am. J. Physiol."},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115444"},{"key":"B26","first-page":"1259","volume":"7","author":"Romero M. F.","year":"1996","journal-title":"J. Am. Soc. Nephrol."},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1038\/387409a0"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1981.61.2.296"},{"issue":"21","key":"B29","first-page":"F11","volume":"252","author":"Sasaki S.","year":"1987","journal-title":"Am. J. Physiol."},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1172\/JCI113410"},{"issue":"14","key":"B31","first-page":"F382","volume":"245","author":"Schwartz G. J.","year":"1983","journal-title":"Am. J. Physiol."},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1007\/BF00374866"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1007\/BF00370766"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1007\/BF00374954"},{"key":"B35","first-page":"1276","volume":"79","author":"Soleimani M.","year":"1987","journal-title":"J. Biol. Chem."},{"issue":"1","key":"B36","first-page":"F20","volume":"232","author":"Warnock D. G.","year":"1977","journal-title":"Am. J. Physiol."},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1007\/BF00595689"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1998.274.3.F628","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T17:16:08Z","timestamp":1567962968000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1998.274.3.F628"}},"issued":{"date-parts":[[1998,3,1]]},"references-count":37,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1998,3,1]]}},"alternative-id":["10.1152\/ajprenal.1998.274.3.F628"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1998.274.3.f628","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1998,3,1]]}},{"indexed":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T16:12:22Z","timestamp":1773418342952,"version":"3.50.1"},"reference-count":48,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1999,3,1]]},"abstract":"<jats:p>The discovery of the aquaporin family of water channels has greatly improved our understanding of how water crosses epithelial cells, particularly in the kidney. The study of the mechanisms involved in the regulation of collecting duct water permeability, in particular, has advanced very rapidly since the identification and characterization of aquaporin-2 (AQP2) in 1993. One of the more surprising findings has been the dramatic long-term changes that are seen in the abundance of this protein, as well as the recognition that these changes represent a way of modulating the acute antidiuretic effects of vasopressin. Furthermore, such changes seem to be of etiological and pathological significance in a number of clinical disorders of water balance. This review focuses on the various conditions in which AQP2 expression is altered (either increased or decreased) and on what this can tell us about the signals and mechanisms controlling these changes. Ultimately, this may be of great value in the clinical management of water balance disorders. Evidence is also now beginning to emerge that there are similar changes in the expression of other renal aquaporins, which had previously been thought to provide an essentially constitutive water permeability pathway, suggesting that they too should be considered as regulatory factors in the control of body water balance.<\/jats:p>","DOI":"10.1152\/ajprenal.1999.276.3.f331","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T18:10:12Z","timestamp":1514052612000},"page":"F331-F339","source":"Crossref","is-referenced-by-count":30,"title":["Long-term regulation of aquaporins in the kidney"],"prefix":"10.1152","volume":"276","author":[{"given":"David","family":"Marples","sequence":"first","affiliation":[{"name":"Department of Physiology, University of Leeds, Leeds LS2 9NQ, United Kingdom; and"}]},{"given":"J\u00f8rgen","family":"Fr\u00f8kiaer","sequence":"additional","affiliation":[{"name":"Institute of Experimental Clinical Research and"}]},{"given":"S\u00f8ren","family":"Nielsen","sequence":"additional","affiliation":[{"name":"Department of Cell Biology, Institute of Anatomy, University of Aarhus, DK-8000 Aarhus, Denmark"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.24.14659"},{"key":"B2","doi-asserted-by":"crossref","first-page":"15","DOI":"10.1681\/ASN.V8115","volume":"8","author":"Apostol E.","year":"1997","journal-title":"J. Am. Soc. Nephrol."},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1002\/hep.1840210128"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(87)80098-7"},{"issue":"44","key":"B5","first-page":"F328","volume":"275","author":"Brown D.","year":"1998","journal-title":"Am. J. Physiol."},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1998.274.2.C549"},{"issue":"44","key":"B7","first-page":"F285","volume":"275","author":"Christensen B. M.","year":"1998","journal-title":"Am. J. Physiol."},{"key":"B8","first-page":"20","volume":"2","author":"Christensen S.","year":"1988","journal-title":"Lithium Therapy Monographs"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.91.19.8984"},{"issue":"43","key":"B11","first-page":"F1161","volume":"274","author":"Ecelbarger C. A.","year":"1998","journal-title":"Am. J. Physiol."},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119352"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1172\/JCI103462"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00984.x"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00878.x"},{"key":"B16","first-page":"576","volume":"9","author":"Fernandez-Llama P.","year":"1998","journal-title":"J. Am. Soc. Nephrol."},{"key":"B17","first-page":"18","volume":"9","author":"Fernandez-Llama P.","year":"1998","journal-title":"J. Am. Soc. Nephrol."},{"issue":"42","key":"B18","first-page":"F213","volume":"273","author":"Fr\u00f8kiaer J.","year":"1997","journal-title":"Am. J. Physiol."},{"key":"B19","first-page":"18","volume":"9","author":"Fr\u00f8kiaer J.","year":"1998","journal-title":"J. Am. Soc. Nephrol."},{"issue":"39","key":"B20","first-page":"F657","volume":"270","author":"Fr\u00f8kiaer J.","year":"1996","journal-title":"Am. J. Physiol."},{"issue":"45","key":"B21","first-page":"F179","volume":"276","author":"Fr\u00f8kiaer J.","year":"1999","journal-title":"Am. J. Physiol."},{"issue":"38","key":"B22","first-page":"F926","volume":"269","author":"Fujita N.","year":"1995","journal-title":"Am. J. Physiol."},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117525"},{"key":"B24","first-page":"18","volume":"8","author":"Ishibashi K.","year":"1997","journal-title":"J. Am. Soc. Nephrol."},{"issue":"44","key":"B25","first-page":"F216","volume":"275","author":"Jonassen T.","year":"1998","journal-title":"Am. J. Physiol."},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199506083322303"},{"issue":"42","key":"B27","first-page":"F949","volume":"273","author":"Klein J. D.","year":"1997","journal-title":"Am. J. Physiol."},{"issue":"41","key":"B28","first-page":"F3","volume":"272","author":"Knepper M. A.","year":"1997","journal-title":"Am. J. Physiol."},{"issue":"44","key":"B29","first-page":"F724","volume":"275","author":"Kwon T.","year":"1998","journal-title":"Am. J. Physiol."},{"issue":"30","key":"B30","first-page":"F554","volume":"261","author":"Lankford S. P.","year":"1991","journal-title":"Am. J. Physiol."},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1172\/JCI231"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.8.4296"},{"issue":"44","key":"B33","first-page":"F400","volume":"275","author":"Marples D.","year":"1998","journal-title":"Am. J. Physiol."},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117863"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118628"},{"key":"B36","first-page":"P91","volume":"497","author":"Marples D.","year":"1996","journal-title":"J. Physiol. (Lond.)"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.90.24.11663"},{"issue":"37","key":"B38","first-page":"F1023","volume":"268","author":"Nielsen S.","year":"1995","journal-title":"Am. J. Physiol."},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.120.2.371"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.94.10.5450"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1172\/JCI649"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.2165\/00003495-199346010-00002"},{"key":"B43","doi-asserted-by":"crossref","first-page":"24","DOI":"10.1681\/ASN.V981359","volume":"9","author":"Promeneur D.","year":"1998","journal-title":"J. Am. Soc. Nephrol."},{"key":"B44","first-page":"1823","volume":"82","author":"Saito T.","year":"1997","journal-title":"J. Clin. Endocrinol. Metab."},{"issue":"43","key":"B45","first-page":"F978","volume":"274","author":"Sands J. M.","year":"1998","journal-title":"Am. J. Physiol."},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118736"},{"issue":"40","key":"B47","first-page":"F414","volume":"271","author":"Terris J.","year":"1996","journal-title":"Am. J. Physiol."},{"key":"B48","doi-asserted-by":"crossref","first-page":"23451","DOI":"10.1016\/S0021-9258(17)31537-5","volume":"269","author":"Uchida S.","year":"1994","journal-title":"J. Biol. Chem."},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119312"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1999.276.3.F331","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:55:08Z","timestamp":1660190108000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1999.276.3.F331"}},"issued":{"date-parts":[[1999,3,1]]},"references-count":48,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1999,3,1]]}},"alternative-id":["10.1152\/ajprenal.1999.276.3.F331"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1999.276.3.f331","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1999,3,1]]}},{"indexed":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T17:15:07Z","timestamp":1773422107123,"version":"3.50.1"},"reference-count":29,"publisher":"American Physiological Society","issue":"11","funder":[{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)","doi-asserted-by":"publisher","award":["54983"],"award-info":[{"award-number":["54983"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2015,6,1]]},"abstract":"<jats:p> The aim of the present study is to examine the role of Kcnj10 (Kir.4.1) in contributing to the basolateral K conductance in the cortical thick ascending limb (cTAL) using Kcnj10<jats:sup>+\/+<\/jats:sup> wild-type (WT) and Kcnj10<jats:sup>\u2212\/\u2212<\/jats:sup> knockout (KO) mice. The patch-clamp experiments detected a 40- and an 80-pS K channel in the basolateral membrane of the cTAL. Moreover, the probability of finding the 40-pS K was significantly higher in the late part of the cTAL close to the distal convoluted tubule than those in the initial part. Immunostaining showed that Kcnj10 staining was detected in the basolateral membrane of the cTAL but the expression was not uniformly distributed. The disruption of Kcnj10 completely eliminated the 40-pS K channel but not the 80-pS K channel, suggesting the role of Kcnj10 in forming the 40-pS K channel of the cTAL. Also, the disruption of Kcnj10 increased the probability of finding the 80-pS K channel in the cTAL, especially in the late part of the cTAL. Because the channel open probability of the 80-pS K channel in KO was similar to those of WT mice, the increase in the 80-pS K channel may be achieved by increasing K channel number. The whole cell recording further showed that K reversal potential measured with 5 mM K in the bath and 140 mM K in the pipette was the same in the WT and KO mice. Moreover, Western blot and immunostaining showed that the disruption of Kcnj10 did not affect the expression of Na-K-Cl cotransporter 2 (NKCC2). We conclude that Kir.4.1 is expressed in the basolateral membrane of cTAL and that the disruption of Kir.4.1 has no significant effect on the membrane potential of the cTAL and NKCC2 expression. <\/jats:p>","DOI":"10.1152\/ajprenal.00687.2014","type":"journal-article","created":{"date-parts":[[2015,4,2]],"date-time":"2015-04-02T11:24:15Z","timestamp":1427973855000},"page":"F1288-F1296","source":"Crossref","is-referenced-by-count":50,"title":["KCNJ10 (Kir4.1) is expressed in the basolateral membrane of the cortical thick ascending limb"],"prefix":"10.1152","volume":"308","author":[{"given":"Chengbiao","family":"Zhang","sequence":"first","affiliation":[{"name":"Jiangsu Province Key Laboratory of Anesthesiology, Xuzhou Medical College, Xuzhou, Jiangsu, China; and"},{"name":"Department of Pharmacology, New York Medical College, Valhalla, New York"}]},{"given":"Lijun","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, New York Medical College, Valhalla, New York"}]},{"given":"Xiao-Tong","family":"Su","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, New York Medical College, Valhalla, New York"}]},{"given":"Dao-Hong","family":"Lin","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, New York Medical College, Valhalla, New York"}]},{"given":"Wen-Hui","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, New York Medical College, Valhalla, New York"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-010-0915-0"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa0810276"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.258.3.F562"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1985.65.3.760"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.198"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00008.2007"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1984.246.6.F745"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00051.2003"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1007\/BF00212991"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.20-15-05733.2000"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00288.2007"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2001.012961"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.21-15-05429.2001"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00238.2001"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1101400108"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.200509360"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1002\/j.1460-2075.1996.tb00661.x"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1126\/scisignal.2005050"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0802966105"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1003072107"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0813238106"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1007\/BF00587521"},{"key":"B23","first-page":"65","volume":"12","author":"Schlatter E","year":"1989","journal-title":"Renal Physiol Biochem"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0901749106"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1007\/BF01868594"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2736(87)90016-2"},{"key":"B27","author":"Wang L","journal-title":"J Am Soc Nephrol"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M113.478453"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1411705111"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00687.2014","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T21:09:49Z","timestamp":1567976989000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00687.2014"}},"issued":{"date-parts":[[2015,6,1]]},"references-count":29,"journal-issue":{"issue":"11","published-print":{"date-parts":[[2015,6,1]]}},"alternative-id":["10.1152\/ajprenal.00687.2014"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00687.2014","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2015,6,1]]}},{"indexed":{"date-parts":[[2026,3,14]],"date-time":"2026-03-14T03:24:19Z","timestamp":1773458659895,"version":"3.50.1"},"reference-count":17,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2006,7]]},"abstract":"<jats:p> The Gamble phenomenon (initially described over 70 years ago as \u201can economy of water in renal function referable to urea\u201d) suggested that urea plays a special role in the urinary concentrating mechanism and that the concentrating mechanism depends in some complex way on an interaction between NaCl and urea. In this study, the role of collecting duct urea transporters in the Gamble phenomenon was investigated in wild-type mice and mice in which the inner medulla collecting duct (IMCD) facilitative urea transporters, UT-A1 and UT-A3, had been deleted ( UT-A1\/3<jats:sup>\u2212\/\u2212<\/jats:sup> mice). The general features of the Gamble phenomenon were confirmed in wild-type mice, namely 1) the water requirement for the excretion of urea is less than for the excretion of an osmotically equivalent amount of NaCl; and 2) when fed various mixtures of urea and salt in the diet, less water is required for the excretion of the two substances together than the amount of water needed for the excretion of the two substances separately. In UT-A1\/3<jats:sup>\u2212\/\u2212<\/jats:sup> mice both of these elements of the phenomenon were absent, indicating that IMCD urea transporters play a central role in the Gamble phenomenon. A titration study in which wild-type mice were given progressively increasing amounts of urea showed that the ability of the kidney to reabsorb urea was saturable, resulting in osmotic diuresis above excretion rates of \u223c6,000 \u03bcosmol\/day. In the same titration experiments, when increasing amounts of NaCl were added to the diet, mice were unable to increase urinary NaCl concentrations to &gt;420 mM, resulting in osmotic diuresis at NaCl excretion rates of \u223c3,500 \u03bcosmol\/day. Thus both urea and NaCl can induce osmotic diuresis when large amounts are given, supporting the conclusion that the decrease in water excretion with mixtures of urea and NaCl added to the diet (compared with pure NaCl or urea) is due to the separate abilities of urea and NaCl to induce osmotic diuresis, rather than to any specific interaction of urea transport and NaCl transport at an epithelial level. <\/jats:p>","DOI":"10.1152\/ajprenal.00348.2005","type":"journal-article","created":{"date-parts":[[2006,2,15]],"date-time":"2006-02-15T03:03:36Z","timestamp":1139972616000},"page":"F148-F154","source":"Crossref","is-referenced-by-count":37,"title":["Gamble's \u201ceconomy of water\u201d revisited: studies in urea transporter knockout mice"],"prefix":"10.1152","volume":"291","author":[{"given":"Robert A.","family":"Fenton","sequence":"first","affiliation":[]},{"given":"Chung-Lin","family":"Chou","sequence":"additional","affiliation":[]},{"given":"Holly","family":"Sowersby","sequence":"additional","affiliation":[]},{"given":"Craig P.","family":"Smith","sequence":"additional","affiliation":[]},{"given":"Mark A.","family":"Knepper","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1016\/0002-9343(58)90377-2"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.258.3.F486"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.258.5.F1173"},{"key":"R4","doi-asserted-by":"crossref","unstructured":"Crawford JD, Doyle AP, and Probst JH. Service of urea in renal water conservation. Am J Physiol 196: 545\u2013548, 1959.","DOI":"10.1152\/ajplegacy.1959.196.3.545"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1172\/JCI103463"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0401704101"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005010031"},{"key":"R8","doi-asserted-by":"crossref","unstructured":"Gamble JL, McKhann CF, Butler AM, and Tuthill E. An economy of water in renal function referable to urea. Am J Physiol 109: 139\u2013154, 1934.","DOI":"10.1152\/ajplegacy.1934.109.1.139"},{"key":"R9","doi-asserted-by":"crossref","unstructured":"Gamble JL, Putnam MC, and McKhann CF. The optimal water requirement in renal function. the optimal water requirement in renal function. I. Measurements of water drinking by rats according to increments of urea and of several salts in the food. Am J Physiol 88: 571\u2013580, 1929.","DOI":"10.1152\/ajplegacy.1929.88.4.571"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1159\/000421921"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00067.2002"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1972.97"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.270.1.F9"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.65.092101.142638"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200409000-00008"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1972.75"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1098\/rspb.1947.0037"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00348.2005","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T23:10:33Z","timestamp":1567984233000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00348.2005"}},"issued":{"date-parts":[[2006,7]]},"references-count":17,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2006,7]]}},"alternative-id":["10.1152\/ajprenal.00348.2005"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00348.2005","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2006,7]]}},{"indexed":{"date-parts":[[2026,3,14]],"date-time":"2026-03-14T03:14:08Z","timestamp":1773458048345,"version":"3.50.1"},"reference-count":20,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2000,10,1]]},"abstract":"<jats:p>p-Aminohippurate (PAH) is widely used as a model substrate to characterize organic anion transport in kidney proximal tubules. The carrier responsible for uptake of PAH across the basolateral membrane has been cloned and well characterized, whereas transporters mediating PAH excretion across the brush-border (apical) membrane are yet unknown. In this study we investigated whether PAH is a substrate for the apical multidrug resistance protein 2 (Mrp2). Overexpression of recombinant rabbit Mrp2 in Sf9 cells significantly increased ATP-dependent [<jats:sup>14<\/jats:sup>C]PAH uptake into isolated membrane vesicles compared with endogenous ATP-dependent uptake. The Michaelis-Menten constant and maximal velocity for Mrp2-mediated ATP-dependent [<jats:sup>14<\/jats:sup>C]PAH transport were 1.9 \u00b1 0.8 mM and 187 \u00b1 29 pmol \u00b7 mg<jats:sup>\u22121<\/jats:sup>\u00b7 min<jats:sup>\u22121<\/jats:sup>, respectively. On the basis of the inhibitory profile, the endogenous ATP-dependent PAH transporter does not appear to be an ortholog of Mrp2. Together, our results show that Mrp2 is a low-affinity ATP-dependent PAH transporter, indicating that Mrp2 might contribute to urinary PAH excretion.<\/jats:p>","DOI":"10.1152\/ajprenal.2000.279.4.f713","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T12:27:09Z","timestamp":1514032029000},"page":"F713-F717","source":"Crossref","is-referenced-by-count":34,"title":["Multidrug resistance protein Mrp2 mediates ATP-dependent transport of classic renal organic anion<i>p<\/i>-aminohippurate"],"prefix":"10.1152","volume":"279","author":[{"given":"R\u00e9mon A. M. H.","family":"Van Aubel","sequence":"first","affiliation":[{"name":"Departments of Pharmacology and Toxicology and"}]},{"given":"Janny G. P.","family":"Peters","sequence":"additional","affiliation":[{"name":"Departments of Pharmacology and Toxicology and"}]},{"given":"Rosalinde","family":"Masereeuw","sequence":"additional","affiliation":[{"name":"Departments of Pharmacology and Toxicology and"}]},{"given":"Carel H.","family":"Van Os","sequence":"additional","affiliation":[{"name":"Cell Physiology, Faculty of Medical Sciences, University Medical Centre Nijmegen, 6500 HB Nijmegen, The Netherlands"}]},{"given":"Frans G. M.","family":"Russel","sequence":"additional","affiliation":[{"name":"Departments of Pharmacology and Toxicology and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1124\/mol.57.4.760"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.1996.271.2.G231"},{"key":"B3","first-page":"3243","volume":"19","author":"Ding GY","year":"1999","journal-title":"Anticancer Res"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1042\/bj1720057"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.21.15181"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.270.2.F319"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/S0005-2736(99)00169-8"},{"key":"B8","doi-asserted-by":"crossref","first-page":"1104","DOI":"10.1016\/S0022-3565(24)38241-2","volume":"289","author":"Masereeuw R","year":"1999","journal-title":"J Pharmacol Exp Ther"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.6.F1173"},{"key":"B10","doi-asserted-by":"crossref","first-page":"59","DOI":"10.1016\/S0026-895X(24)26442-7","volume":"57","author":"Masereeuw R","year":"2000","journal-title":"Mol Pharmacol"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-5793(97)00314-1"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1248\/bpb.16.395"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/0006-2952(88)90258-4"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.34.20719"},{"key":"B16","doi-asserted-by":"crossref","first-page":"1159","DOI":"10.1681\/ASN.V1061159","volume":"10","author":"Schaub TP","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B17","doi-asserted-by":"crossref","first-page":"1213","DOI":"10.1681\/ASN.V881213","volume":"8","author":"Schaub TP","year":"1997","journal-title":"J Am Soc Nephrol"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1055\/s-2007-1007170"},{"key":"B19","doi-asserted-by":"crossref","first-page":"714","DOI":"10.1016\/S0026-895X(24)12532-1","volume":"56","author":"Van Aubel RAMH","year":"1999","journal-title":"Mol Pharmacol"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.2.F216"},{"key":"B21","doi-asserted-by":"crossref","first-page":"1062","DOI":"10.1016\/S0026-895X(24)13277-4","volume":"53","author":"Van Aubel RAMH","year":"1998","journal-title":"Mol Pharmacol"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.2000.279.4.F713","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,6,29]],"date-time":"2025-06-29T04:36:31Z","timestamp":1751171791000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.2000.279.4.F713"}},"issued":{"date-parts":[[2000,10,1]]},"references-count":20,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2000,10,1]]}},"alternative-id":["10.1152\/ajprenal.2000.279.4.F713"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.2000.279.4.f713","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2000,10,1]]}},{"indexed":{"date-parts":[[2026,3,14]],"date-time":"2026-03-14T03:25:53Z","timestamp":1773458753511,"version":"3.50.1"},"reference-count":28,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2001,2,1]]},"abstract":"<jats:p>UT-A3 has recently been identified as a splicing variant transcript of the UT-A gene present in the kidney. To study the cellular and subcellular localization of UT-A3, we raised a new polyclonal antibody to its COOH-terminal end. Immunoblots identified bands at 44 and 67 kDa predominately in the inner medulla and showed that the antibody does not recognize UT-A1. Deglycosylation with PNGase decreased the molecular mass of both forms to 40 kDa. UT-A3 is most abundant in the inner third of the inner medulla and is present in membrane fractions. Cell fractionation studies showed that UT-A3 is only detectable in inner medullary collecting duct (IMCD) cells. These observations were confirmed with immunolocalization studies demonstrating an exclusive labeling of IMCD cells. Double-labeling studies with anti-Na-K-ATPase demonstrated UT-A3 in intracellular membranes and in the apical region but were incompatible with a basolateral site for UT-A3. Although the function of this isoform in the inner medulla is unknown, the large abundance suggests that it may be important in the renal handling of urea.<\/jats:p>","DOI":"10.1152\/ajprenal.2001.280.2.f325","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T13:20:15Z","timestamp":1514035215000},"page":"F325-F332","source":"Crossref","is-referenced-by-count":77,"title":["UT-A3: localization and characterization of an additional urea transporter isoform in the IMCD"],"prefix":"10.1152","volume":"280","author":[{"given":"James M.","family":"Terris","sequence":"first","affiliation":[{"name":"Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda;"},{"name":"Department of Physiology, Uniformed Services University of the Health Sciences, Bethesda; and"}]},{"given":"Mark A.","family":"Knepper","sequence":"additional","affiliation":[{"name":"Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda;"}]},{"given":"James B.","family":"Wade","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland 21201"}]}],"member":"24","reference":[{"key":"B1","first-page":"A24","volume":"11","author":"Bradford AD","year":"1997","journal-title":"FASEB J"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.1.F78"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.257.3.F359"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.3.F564"},{"key":"B5","doi-asserted-by":"crossref","first-page":"13A","DOI":"10.1681\/ASN.V10113","volume":"10","author":"Cottingham CA","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.4.F559"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.91.14.6269"},{"key":"B8","doi-asserted-by":"crossref","first-page":"230","DOI":"10.1681\/ASN.V102230","volume":"10","author":"Karakashian A","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.273.6.F949"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.259.3.F393"},{"key":"B12","doi-asserted-by":"crossref","first-page":"517","DOI":"10.1681\/ASN.V84517","volume":"8","author":"Naruse M","year":"1997","journal-title":"J Am Soc Nephrol"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.93.11.5495"},{"key":"B14","doi-asserted-by":"crossref","first-page":"31649","DOI":"10.1016\/S0021-9258(18)31744-7","volume":"269","author":"Olives B","year":"1994","journal-title":"J Biol Chem"},{"key":"B15","doi-asserted-by":"crossref","first-page":"1359","DOI":"10.1681\/ASN.V981359","volume":"9","author":"Promeneur D","year":"1998","journal-title":"J Am Soc Nephrol"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.5.F978"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.253.5.F823"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.273.3.F321"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.272.5.F654"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.4.F620"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119077"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118194"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1172\/JCI114823"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.2.F414"},{"key":"B25","doi-asserted-by":"crossref","first-page":"729","DOI":"10.1681\/ASN.V95729","volume":"9","author":"Terris J","year":"1998","journal-title":"J Am Soc Nephrol"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119313"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.1.F52"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.17"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1038\/365844a0"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.2001.280.2.F325","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:42:51Z","timestamp":1660189371000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.2001.280.2.F325"}},"issued":{"date-parts":[[2001,2,1]]},"references-count":28,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2001,2,1]]}},"alternative-id":["10.1152\/ajprenal.2001.280.2.F325"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.2001.280.2.f325","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2001,2,1]]}},{"indexed":{"date-parts":[[2026,3,14]],"date-time":"2026-03-14T03:28:03Z","timestamp":1773458883017,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1978,6,1]]},"abstract":"<jats:p> The formation of glomerular ultrafiltrate is dependent on the interplay of glomerular pressures and flows as well as the intrinsic permselectivity properties of the glomerular capillary wall. These intrinsic permeability properties serve to exclude macromolecules from the urinary space, based on size as well as net molecular charge discrimination. Neutral dextrans with molecular radii less than 20 A cross the glomerular wall without measurable restriction, whereas dextrans with radii greater than 42 A are almost completely barred. For any given size, negatively charged macromolecules are restricted to a greater extent than neutral molecules. Additionally, positively charged molecules are enhanced in their ability to cross the glomerular wall compared to similarly sized neutral polymers. The concept of a charge barrier, due to fixed negative charges within the glomerular wall, is also supported by morphological studies. Glomerular injury, leading to proteinuria, has been associated with loss of the charge-selective properties of these capillaries. Loss of glomerular fixed negative charges may also result in the foot process fusion and mesangial cell dysfunction often observed in proteinuric states. <\/jats:p>","DOI":"10.1152\/ajprenal.1978.234.6.f455","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T20:45:29Z","timestamp":1513975529000},"page":"F455-F460","source":"Crossref","is-referenced-by-count":33,"title":["Glomerular permselectivity: barrier function based on discrimination of molecular size and charge"],"prefix":"10.1152","volume":"234","author":[{"given":"B. M.","family":"Brenner","sequence":"first","affiliation":[]},{"given":"T. H.","family":"Hostetter","sequence":"additional","affiliation":[]},{"given":"H. D.","family":"Humes","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1978.234.6.F455","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:01:39Z","timestamp":1567969299000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1978.234.6.F455"}},"issued":{"date-parts":[[1978,6,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1978,6,1]]}},"alternative-id":["10.1152\/ajprenal.1978.234.6.F455"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1978.234.6.f455","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1978,6,1]]}},{"indexed":{"date-parts":[[2026,3,14]],"date-time":"2026-03-14T03:48:54Z","timestamp":1773460134084,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1990,5,1]]},"abstract":"<jats:p> Oxygen consumption (QO2) and net K+ transport were studied in rabbit proximal tubule suspensions to define the early effects of cisplatin on proximal tubule function. Cisplatin caused dose-dependent inhibition of QO2, which was delayed in onset. The concentration of cisplatin required for inhibition decreased as the duration of exposure was increased [40-min exposure, threshold concentration of 10(-4) M, inhibitor constant (Ki) of 10(-3) M; 4-h exposure, threshold concentration of 3 X 10(-5) M, Ki of 10(-4) M]. Both ouabain-sensitive and ouabain-insensitive QO2 were reduced, indicating inhibition of all adenosinetriphosphatases, including Na(+)- K(+)-ATPase activity. There was a parallel fall in ouabain-sensitive net K+ transport and cytosolic K+ content, confirming the latter observation. Na(+)-K(+)-ATPase activity was unchanged in cell membranes prepared by hypotonic lysis from cisplatin-treated tubules, indicating an indirect cytosol-dependent mechanism of enzyme inhibition. Nystatin-stimulated QO2 was reduced in cisplatin-treated tubules, excluding inhibition of Na+ entry as the mechanism of injury and suggesting mitochondrial injury. The latter was confirmed by measurement of carbonylcyanide-m-chlorophenylhydrazone (CCCP)-uncoupled QO2 in intact cells and ADP-stimulated (state 3) QO2 in digitonin-permeabilized tubules. Furthermore, by maximally stimulating mitochondrial respiration with CCCP and nystatin, it was possible to demonstrate mitochondrial injury at a time when basal QO2 and K+ transport were apparently normal. These data suggest that mitochondrial injury is a central event in cisplatin toxicity to the proximal tubule. <\/jats:p>","DOI":"10.1152\/ajprenal.1990.258.5.f1181","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T23:21:57Z","timestamp":1513984917000},"page":"F1181-F1187","source":"Crossref","is-referenced-by-count":20,"title":["Mitochondrial injury: an early event in cisplatin toxicity to renal proximal tubules"],"prefix":"10.1152","volume":"258","author":[{"given":"H. R.","family":"Brady","sequence":"first","affiliation":[{"name":"Department of Medicine, Brigham and Women's Hospital, Boston,Massachusetts 02115."}]},{"given":"B. C.","family":"Kone","sequence":"additional","affiliation":[{"name":"Department of Medicine, Brigham and Women's Hospital, Boston,Massachusetts 02115."}]},{"given":"M. E.","family":"Stromski","sequence":"additional","affiliation":[{"name":"Department of Medicine, Brigham and Women's Hospital, Boston,Massachusetts 02115."}]},{"given":"M. L.","family":"Zeidel","sequence":"additional","affiliation":[{"name":"Department of Medicine, Brigham and Women's Hospital, Boston,Massachusetts 02115."}]},{"given":"G.","family":"Giebisch","sequence":"additional","affiliation":[{"name":"Department of Medicine, Brigham and Women's Hospital, Boston,Massachusetts 02115."}]},{"given":"S. R.","family":"Gullans","sequence":"additional","affiliation":[{"name":"Department of Medicine, Brigham and Women's Hospital, Boston,Massachusetts 02115."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1990.258.5.F1181","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:23:49Z","timestamp":1567970629000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1990.258.5.F1181"}},"issued":{"date-parts":[[1990,5,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1990,5,1]]}},"alternative-id":["10.1152\/ajprenal.1990.258.5.F1181"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1990.258.5.f1181","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1990,5,1]]}},{"indexed":{"date-parts":[[2026,3,14]],"date-time":"2026-03-14T03:16:12Z","timestamp":1773458172106,"version":"3.50.1"},"reference-count":42,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2000,5,1]]},"abstract":"<jats:p>Transforming growth factor-\u03b2 (TGF-\u03b2) is important in the pathogenesis of diabetic nephropathy, but little is known about the regulation of the ligand-binding TGF-\u03b2 type II signaling receptor (T\u03b2IIR). There were significant increases in T\u03b2IIR protein and mRNA levels in kidney cortex after 1\u20136 wk of streptozotocin-induced diabetes. Mouse mesangial cells cultured in high glucose demonstrated significantly increased T\u03b2IIR protein and mRNA levels compared with normal glucose. This effect was independent of stimulation of TGF-\u03b2 bioactivity by high glucose. Consistent with transcriptional activation by high glucose, the half-life (\u223c4 h) of T\u03b2IIR mRNA was not affected by glucose concentration. Moreover, mouse mesangial cells transiently transfected with reporter constructs containing the first 47- or 274-bp promoter fragments of T\u03b2IIR demonstrated significantly increased reporter activity in high glucose. Cells grown in high glucose demonstrated increased responsiveness to a relatively small dose of exogenous TGF-\u03b2<jats:sub>1<\/jats:sub>(0.5 ng\/ml): [<jats:sup>3<\/jats:sup>H]proline incorporation and \u03b1<jats:sub>1<\/jats:sub>(IV) collagen mRNA were significantly greater in cells cultured in high than in normal glucose. Hence, the expression of T\u03b2IIR is increased in the diabetic kidney and in mesangial cells cultured in high glucose, primarily because of stimulation of gene transcription. T\u03b2IIR upregulation by high ambient glucose may contribute to the increased sensitivity of mesangial cells to the profibrogenic action of TGF-\u03b2<jats:sub>1<\/jats:sub>.<\/jats:p>","DOI":"10.1152\/ajprenal.2000.278.5.f830","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T12:47:32Z","timestamp":1514033252000},"page":"F830-F838","source":"Crossref","is-referenced-by-count":45,"title":["Stimulation of TGF-\u03b2 type II receptor by high glucose in mouse mesangial cells and in diabetic kidney"],"prefix":"10.1152","volume":"278","author":[{"given":"Motohide","family":"Isono","sequence":"first","affiliation":[{"name":"Renal-Electrolyte and Hypertension Division, Department of Medicine, and Penn Center for the Molecular Studies of Kidney Diseases, University of Pennsylvania, Philadelphia, Pennsylvania 19104-6144"}]},{"given":"Andr\u00e1s","family":"Mogyor\u00f3si","sequence":"additional","affiliation":[{"name":"Renal-Electrolyte and Hypertension Division, Department of Medicine, and Penn Center for the Molecular Studies of Kidney Diseases, University of Pennsylvania, Philadelphia, Pennsylvania 19104-6144"}]},{"given":"Dong Cheol","family":"Han","sequence":"additional","affiliation":[{"name":"Renal-Electrolyte and Hypertension Division, Department of Medicine, and Penn Center for the Molecular Studies of Kidney Diseases, University of Pennsylvania, Philadelphia, Pennsylvania 19104-6144"}]},{"given":"Brenda B.","family":"Hoffman","sequence":"additional","affiliation":[{"name":"Renal-Electrolyte and Hypertension Division, Department of Medicine, and Penn Center for the Molecular Studies of Kidney Diseases, University of Pennsylvania, Philadelphia, Pennsylvania 19104-6144"}]},{"given":"Fuad N.","family":"Ziyadeh","sequence":"additional","affiliation":[{"name":"Renal-Electrolyte and Hypertension Division, Department of Medicine, and Penn Center for the Molecular Studies of Kidney Diseases, University of Pennsylvania, Philadelphia, Pennsylvania 19104-6144"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.49.29460"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1990.35"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1993.336"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.3.1385"},{"key":"B5","first-page":"2095","volume":"149","author":"Di Paolo S","year":"1996","journal-title":"Am J Pathol"},{"key":"B6","doi-asserted-by":"crossref","first-page":"1207","DOI":"10.1681\/ASN.V781207","volume":"7","author":"Guh JY","year":"1996","journal-title":"J Am Soc Nephrol"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00119.x"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1994.2284"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.162"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.91.13.6002"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.249"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1210\/endo-123-4-2124"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1172\/JCI113996"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.biochem.67.1.753"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118333"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/0378-1119(80)90129-8"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.275.5.F827"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-199605000-00010"},{"key":"B19","doi-asserted-by":"crossref","first-page":"271","DOI":"10.1681\/ASN.V102271","volume":"10","author":"Mozes MM","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1097-4652(199809)176:3<612::AID-JCP18>3.0.CO;2-0"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00600.x"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1992.14"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1002\/ijc.2910540523"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.294"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.291"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1995.1156"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.2337\/diab.45.4.522"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.2337\/diab.44.10.1139"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.2337\/diab.46.5.854"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.68"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.29.17366"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00888.x"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1992.330"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1007\/s001099900028"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1038\/370341a0"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.65"},{"key":"B37","doi-asserted-by":"crossref","first-page":"2253","DOI":"10.1681\/ASN.V9122253","volume":"9","author":"Yamamoto T","year":"1998","journal-title":"J Am Soc Nephrol"},{"key":"B38","doi-asserted-by":"crossref","first-page":"182","DOI":"10.1681\/ASN.V92182","volume":"9","author":"Yang Y","year":"1998","journal-title":"J Am Soc Nephrol"},{"key":"B39","first-page":"154","volume":"68","author":"Yoshioka K","year":"1993","journal-title":"Lab Invest"},{"key":"B40","first-page":"292","volume":"21","author":"Ziyadeh FN.","year":"1995","journal-title":"Miner Electrolyte Metab"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117004"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.259.4.F704"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.2000.278.5.F830","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:40:35Z","timestamp":1660189235000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.2000.278.5.F830"}},"issued":{"date-parts":[[2000,5,1]]},"references-count":42,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2000,5,1]]}},"alternative-id":["10.1152\/ajprenal.2000.278.5.F830"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.2000.278.5.f830","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2000,5,1]]}},{"indexed":{"date-parts":[[2026,3,14]],"date-time":"2026-03-14T03:16:13Z","timestamp":1773458173262,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1991,5,1]]},"abstract":"<jats:p> The effects of insulin on Na(+)-H+ exchange were examined in isolated proximal segments from normotensive Sprague-Dawley (SD) and Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR), with monitoring of rates of intracellular pH change (delta pHi\/min) and ethylisopropyl amiloride (EIPA)-suppressible 22Na+ uptakes. A 12-min insulin preincubation was necessary for steady-state 22Na+ uptake and rate of pHi change. Insulin responses were similar for 4-wk (prehypertensive) SHR and WKY tubules; 8- (rising hypertension) and 16-wk (established hypertension) SHR responses were increased (P less than 0.05) 23 and 36% with 10(-6) M insulin, respectively. Insulin-like growth factors (IGF-I, IGF-II; 10(-10)-10(-7) M) had no effect on Na(+)-H+ exchange activity. Incubation with physiological concentrations of insulin in combination with hormones that stimulate Na(+)-H+ exchange (angiotensin II; alpha-adrenoceptor agonists) demonstrated no synergistic increases in SHR or WKY tubules; incubation with hormones that inhibit Na(+)-H+ exchange [parathyroid hormone (PTH), dopamine (DA)] indicated that insulin stimulation was decreased with PTH or DA in WKY segments, but PTH or DA reduction of insulin stimulation was lacking in SHR tubules. In summary, these data indicate a direct stimulation by insulin of Na(+)-H+ exchange in the proximal nephron, indicate an increased responsiveness in SHR compared with WKY tubules, and suggest a modulatory role of insulin with other hormones in regulating proximal nephron Na(+)-H+ exchange. <\/jats:p>","DOI":"10.1152\/ajprenal.1991.260.5.f695","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T23:33:48Z","timestamp":1513985628000},"page":"F695-F703","source":"Crossref","is-referenced-by-count":18,"title":["Insulin increases Na(+)-H+ exchange activity in proximal tubules from normotensive and hypertensive rats"],"prefix":"10.1152","volume":"260","author":[{"given":"F. A.","family":"Gesek","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, Medical College of Virginia, VirginiaCommonwealth University, Richmond 23298-0160."}]},{"given":"A. C.","family":"Schoolwerth","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Medical College of Virginia, VirginiaCommonwealth University, Richmond 23298-0160."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1991.260.5.F695","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:24:00Z","timestamp":1567970640000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1991.260.5.F695"}},"issued":{"date-parts":[[1991,5,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1991,5,1]]}},"alternative-id":["10.1152\/ajprenal.1991.260.5.F695"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1991.260.5.f695","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1991,5,1]]}},{"indexed":{"date-parts":[[2026,3,14]],"date-time":"2026-03-14T03:19:22Z","timestamp":1773458362896,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1984,5,1]]},"abstract":"<jats:p> Dopamine receptors in glomeruli and renal cortical tubules were characterized using radioligand binding and adenylate cyclase studies. The binding of [3H]haloperidol to glomeruli and tubules was rapid, saturable with time and ligand concentration, reversible, of high affinity, and demonstrated stereoselectivity and antagonist and agonist rank potency for binding to dopamine receptors. Analysis of kinetic data and Rosenthal plots in glomeruli revealed a single class of [3H]haloperidol binding sites with an apparent dissociation constant (Kd) of 6 nM and maximum receptor density (Bmax) of 0.42 pmol\/mg protein. In tubules, at least two binding sites were noted, one with an apparent Kd of 38 nM and Bmax of 1.90 pmol\/mg protein and another with an apparent Kd of 183 nM and Bmax of 3.50 pmol\/mg protein. Dopamine and apomorphine increased adenylate cyclase in tubular membranes while no increases were noted in glomeruli. These studies suggest that glomeruli have D2 dopamine receptors, while renal cortical tubules contain the D1 dopamine receptor. <\/jats:p>","DOI":"10.1152\/ajprenal.1984.246.5.f557","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T16:46:51Z","timestamp":1513961211000},"page":"F557-F568","source":"Crossref","is-referenced-by-count":8,"title":["Cortical tubular and glomerular dopamine receptors in the rat kidney"],"prefix":"10.1152","volume":"246","author":[{"given":"R. A.","family":"Felder","sequence":"first","affiliation":[]},{"given":"M.","family":"Blecher","sequence":"additional","affiliation":[]},{"given":"G. M.","family":"Eisner","sequence":"additional","affiliation":[]},{"given":"P. A.","family":"Jose","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1984.246.5.F557","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:34:45Z","timestamp":1567967685000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1984.246.5.F557"}},"issued":{"date-parts":[[1984,5,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1984,5,1]]}},"alternative-id":["10.1152\/ajprenal.1984.246.5.F557"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1984.246.5.f557","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1984,5,1]]}},{"indexed":{"date-parts":[[2026,3,14]],"date-time":"2026-03-14T03:29:28Z","timestamp":1773458968114,"version":"3.50.1"},"reference-count":29,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1999,12,1]]},"abstract":"<jats:p>Mutations in the PKD2 gene account for \u223c15% of all cases of autosomal-dominant polycystic kidney disease. In the present study the cellular distribution of the Pkd2 protein was investigated by immunohistochemistry in different rat organs. Although the Pkd2 protein showed a widespread expression, a strikingly different distribution of the protein was observed between individual organs. Whereas in renal distal tubules and in striated ducts of salivary glands a basal-to-basolateral distribution of Pkd2 was found, a punctate cytoplasmic location was detected in the adrenal gland, ovary, cornea, and smooth muscle cells of blood vessels. Interestingly, in the adrenal gland and ovary, the rat Pkd2 protein was more heavily N-glycosylated than in the kidney and salivary gland. These results suggest that Pkd2 accomplishes its functions by interacting with proteins located in different cellular compartments. The extrarenal expression pattern of the Pkd2 protein hints at other candidate sites of disease manifestations in patients carrying PKD2 mutations.<\/jats:p>","DOI":"10.1152\/ajprenal.1999.277.6.f914","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T12:08:51Z","timestamp":1514030931000},"page":"F914-F925","source":"Crossref","is-referenced-by-count":7,"title":["The rat Pkd2 protein assumes distinct subcellular distributions in different organs"],"prefix":"10.1152","volume":"277","author":[{"given":"Nicholas","family":"Oberm\u00fcller","sequence":"first","affiliation":[{"name":"Medical Research Center, Klinikum Mannheim, University of Heidelberg, 68167 Mannheim;"}]},{"given":"A. Rachel","family":"Gallagher","sequence":"additional","affiliation":[{"name":"Institute for Anatomy and Cell Biology I, University of Heidelberg, 69120 Heidelberg, Germany;"}]},{"given":"Yiqiang","family":"Cai","sequence":"additional","affiliation":[{"name":"Section of Nephrology, Yale University School of Medicine, New Haven, Connecticut 06520-8029; and"}]},{"given":"Nikolaus","family":"Gassler","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Heidelberg, 69120 Heidelberg, Germany"}]},{"given":"Norbert","family":"Gretz","sequence":"additional","affiliation":[{"name":"Medical Research Center, Klinikum Mannheim, University of Heidelberg, 68167 Mannheim;"}]},{"given":"Stefan","family":"Somlo","sequence":"additional","affiliation":[{"name":"Section of Nephrology, Yale University School of Medicine, New Haven, Connecticut 06520-8029; and"}]},{"given":"Ralph","family":"Witzgall","sequence":"additional","affiliation":[{"name":"Institute for Anatomy and Cell Biology I, University of Heidelberg, 69120 Heidelberg, Germany;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1007\/BF00216564"},{"key":"B2","first-page":"43","volume":"42","author":"Bergeron M.","year":"1981","journal-title":"Biol. Cell"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/0003-2697(76)90527-3"},{"key":"B3a","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.40.28557"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/0888-7543(95)80020-M"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/12.1Part1.387"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2559.1987.tb01901.x"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.354"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.35.22664"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199307293290508"},{"key":"B10","first-page":"168","volume":"41","author":"Hoyer J. R.","year":"1979","journal-title":"Lab. Invest."},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/8.3.509"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.426"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1126\/science.272.5266.1339"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.40.25967"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)65428-4"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1007\/s003359900857"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1159\/000421651"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1210\/endo.137.11.8895352"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/4.4.575"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(94)90137-6"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(95)90339-9"},{"key":"B23","doi-asserted-by":"crossref","first-page":"382","DOI":"10.1681\/ASN.V881283","volume":"8","author":"Torres V. E.","year":"1997","journal-title":"J. Am. Soc. Nephrol."},{"key":"B24","doi-asserted-by":"crossref","first-page":"1670","DOI":"10.1681\/ASN.V661670","volume":"6","author":"van Dijk M. A.","year":"1995","journal-title":"J. Am. Soc. Nephrol."},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1096-8628(19970120)68:2<222::AID-AJMG20>3.0.CO;2-V"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)81570-6"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1006\/geno.1998.5618"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1006\/geno.1997.4920"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1007\/BF01871211"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1999.277.6.F914","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:38:36Z","timestamp":1660189116000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1999.277.6.F914"}},"issued":{"date-parts":[[1999,12,1]]},"references-count":29,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1999,12,1]]}},"alternative-id":["10.1152\/ajprenal.1999.277.6.F914"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1999.277.6.f914","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1999,12,1]]}},{"indexed":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T16:24:46Z","timestamp":1773419086333,"version":"3.50.1"},"reference-count":29,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2002,1,1]]},"abstract":"<jats:p>The role of endothelium-derived nitric oxide (NO) in renal baroreceptor stimulation of renin was tested comparing endothelial nitric oxide synthase (eNOS)-deficient mice with C57BL\/6J (C57) controls. We measured blood pressure, renal blood flow (RBF), and plasma renin concentration (PRC) in Inactin-anesthetized mice. Blood pressure in eNOS knockout mice was higher than in controls (100 \u00b1 3 vs. 86 \u00b1 1 mmHg, respectively; P &lt; 0.001), but RBF was similar (1.71 \u00b1 0.06 vs. 1.66 \u00b1 0.09 ml \u00b7 min<jats:sup>\u22121<\/jats:sup>\u00b7 100 mg kidney wt<jats:sup>\u22121<\/jats:sup>, respectively), so that renal vascular resistance was also higher in the knockouts (59.81 \u00b1 2.07 vs. 51.81 \u00b1 2.66 resistance units, respectively; P &lt; 0.025). PRC was similar (8.24 \u00b1 1.57 in eNOS knockouts vs. 7.10 \u00b1 1.19 ng ANG I \u00b7 ml<jats:sup>\u22121<\/jats:sup>\u00b7 h<jats:sup>\u22121<\/jats:sup>in C57). NOS inhibition with nitro-l-arginine methyl ester (l-NAME) in C57 controls increased blood pressure (from 85 \u00b1 2 to 106 \u00b1 1 mmHg, P &lt; 0.001) and decreased RBF (from 1.66 \u00b1 0.09 to 1.08 \u00b1 0.02; P&lt; 0.005), but l-NAME had no effect in eNOS knockout mice. When renal perfusion pressure was reduced in C57 controls to 55 mmHg, PRC increased from 6.6 \u00b1 0.9 to 14.5 \u00b1 1.9 \u03bcg \u00b7 ml<jats:sup>\u22121<\/jats:sup>\u00b7 h<jats:sup>\u22121<\/jats:sup>( P&lt; 0.025), but this response was blocked by l-NAME. However, in eNOS knockouts, reduced renal perfusion pressure increased PRC from 7.6 \u00b1 1.4 to 15.0 \u00b1 2.8 \u03bcg \u00b7 ml<jats:sup>\u22121<\/jats:sup>\u00b7 h<jats:sup>\u22121<\/jats:sup>( P&lt; 0.001). Thus in the chronic absence of eNOS, blood pressure was elevated, but RBF was normal. Additionally, the absence of eNOS did not modify baroreceptor-stimulated renin, suggesting that eNOS-derived NO does not directly mediate this renin-regulating pathway.<\/jats:p>","DOI":"10.1152\/ajprenal.0144.2001","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:33:25Z","timestamp":1425414805000},"page":"F59-F64","source":"Crossref","is-referenced-by-count":15,"title":["Renal baroreceptor-stimulated renin in the eNOS knockout mouse"],"prefix":"10.1152","volume":"282","author":[{"given":"William H.","family":"Beierwaltes","sequence":"first","affiliation":[{"name":"Hypertension and Vascular Research Division, Henry Ford Hospital, Detroit Medical Campus of Case Western Reserve School of Medicine, Detroit, Michigan 48202"}]},{"given":"D'Anna L.","family":"Potter","sequence":"additional","affiliation":[{"name":"Hypertension and Vascular Research Division, Henry Ford Hospital, Detroit Medical Campus of Case Western Reserve School of Medicine, Detroit, Michigan 48202"}]},{"given":"Edward G.","family":"Shesely","sequence":"additional","affiliation":[{"name":"Hypertension and Vascular Research Division, Henry Ford Hospital, Detroit Medical Campus of Case Western Reserve School of Medicine, Detroit, Michigan 48202"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118181"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.06720.x"},{"key":"B3","doi-asserted-by":"crossref","first-page":"875","DOI":"10.1681\/ASN.V16875","volume":"1","author":"Baylis C.","year":"1990","journal-title":"J Am Soc Nephrol"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.1.F134"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1997.272.5.R1359"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.262.6.F943"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.29.18185"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.2.F193"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/0014-2999(92)90051-5"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1038\/377239a0"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.28.5.738"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(97)90275-4"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.272.5.F561"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.32.5.856"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-120-3-199402010-00009"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.262.1.F40"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.32.2.266"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.264.6.F943"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1997.272.3.R879"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1172\/JCI116266"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.402"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.93.23.13176"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.263.2.F256"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1172\/JCI103838"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.13.6.658"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/0014-2999(88)90679-6"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1007\/s004240050979"},{"key":"B29","doi-asserted-by":"crossref","first-page":"1666","DOI":"10.1152\/ajplegacy.1971.221.6.1666","volume":"221","author":"Witty RT","year":"1971","journal-title":"Am J Physiol"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.32.6.958"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.0144.2001","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,5,1]],"date-time":"2022-05-01T09:33:23Z","timestamp":1651397603000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.0144.2001"}},"issued":{"date-parts":[[2002,1,1]]},"references-count":29,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2002,1,1]]}},"alternative-id":["10.1152\/ajprenal.0144.2001"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.0144.2001","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2002,1,1]]}},{"indexed":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T17:00:21Z","timestamp":1773421221080,"version":"3.50.1"},"reference-count":32,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2008,7]]},"abstract":"<jats:p>Collecting duct cells swell when exposed to arginine vasopressin (AVP) in the presence of a transepithelial osmolality gradient. We investigated the mechanisms of AVP-induced cell swelling in isolated, perfused rat inner medullary collecting ducts (IMCDs) using quantitative video microscopy and fluorescence-based measurements of transepithelial water transport. We tested the roles of transepithelial water flow, basolateral solute entry, and the cytoskeleton (actomyosin). When a transepithelial osmolality gradient was imposed by addition of NaCl to the bath, AVP significantly increased both water flux and cell height. When the osmolality gradient was imposed by addition of mannitol, AVP increased water flux but not cell height, suggesting that AVP-induced cell swelling requires a NaCl gradient and is not merely dependent on the associated water flux. Bumetanide (Na-K-2Cl cotransporter inhibitor) added to the bath markedly diminished the AVP-induced cell height increase. AVP-induced cell swelling was absent in IMCDs from NKCC1-knockout mice. In rat IMCDs, replacement of Na, K, or Cl in the peritubular bath caused significant cell shrinkage, consistent with a basolateral solute transport pathway dependent on all three ions. Immunocytochemistry using an antibody to NKCC1 confirmed basolateral expression in IMCD cells. The conventional nonmuscle myosin II inhibitor blebbistatin also diminished the AVP-induced cell height increase and cell shape change, consistent with a role for the actin cytoskeleton and myosin II. We conclude that the AVP-induced cell height increase is dependent on basolateral solute uptake via NKCC1 and changes in actin organization via myosin II, but is not dependent specifically on increased apical water entry.<\/jats:p>","DOI":"10.1152\/ajprenal.00011.2008","type":"journal-article","created":{"date-parts":[[2008,4,17]],"date-time":"2008-04-17T00:55:04Z","timestamp":1208393704000},"page":"F192-F201","source":"Crossref","is-referenced-by-count":32,"title":["Roles of basolateral solute uptake via NKCC1 and of myosin II in vasopressin-induced cell swelling in inner medullary collecting duct"],"prefix":"10.1152","volume":"295","author":[{"given":"Chung-Lin","family":"Chou","sequence":"first","affiliation":[]},{"given":"Ming-Jiun","family":"Yu","sequence":"additional","affiliation":[]},{"given":"Eliza M.","family":"Kassai","sequence":"additional","affiliation":[]},{"given":"Ryan G.","family":"Morris","sequence":"additional","affiliation":[]},{"given":"Jason D.","family":"Hoffert","sequence":"additional","affiliation":[]},{"given":"Susan M.","family":"Wall","sequence":"additional","affiliation":[]},{"given":"Mark A.","family":"Knepper","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1007\/BF01869401"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.2170\/jjphysiol.49.201"},{"key":"R3","unstructured":"Burg MB.Perfusion of isolated renal tubules.Yale J Biol Med45: 321\u2013326, 1972."},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1998.275.5.C1349"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M408565200"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1998.274.2.H564"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00018.2002"},{"key":"R8","doi-asserted-by":"crossref","unstructured":"Evans RL, Park K, Turner RJ, Watson GE, Nguyen HV, Dennett MR, Hand AR, Flagella M, Shull GE, Melvin JE.Severe impairment of salivation in Na+\/K+\/2Cl\u2212cotransporter (NKCC1)-deficient mice.J Biol Chem275: 26720\u201326726, 2000.","DOI":"10.1016\/S0021-9258(19)61435-3"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.38.26946"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.36.2.355"},{"key":"R11","doi-asserted-by":"crossref","unstructured":"Ginns SM, Knepper MA, Ecelbarger CA, Terris J, He X, Coleman RA, Wade JB.Immunolocalization of the secretory isoform of Na-K-Cl contransporter in rat renal intercalated cells.J Am Soc Nephrol7: 2533\u20132542, 1996.","DOI":"10.1681\/ASN.V7122533"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1007\/BF00580961"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1989.180"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M500040200"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1016\/j.cbpa.2006.11.023"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1989.69.2.315"},{"key":"R17","doi-asserted-by":"crossref","unstructured":"Ikebe M, Nonoguchi H, Nakayama Y, Tashima Y, Tomita K.Upregulation of the secretory-type Na+\/K+\/2Cl\u2212-cotransporter in the kidney by metabolic acidosis and dehydration in rats.J Am Soc Nephrol12: 423\u2013430, 2001.","DOI":"10.1681\/ASN.V123423"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118844"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1999.277.6.C1184"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.265.2.F225"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1529\/biophysj.107.104893"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1986.251.3.F475"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1126\/science.1081412"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1007\/BF01869332"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1126\/science.3823867"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1989.269"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.5.F913"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.262.6.F989"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.4.F536"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.5.F841"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1172\/JCI107509"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1074\/mcp.M600177-MCP200"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00011.2008","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,9,8]],"date-time":"2021-09-08T08:45:38Z","timestamp":1631090738000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00011.2008"}},"issued":{"date-parts":[[2008,7]]},"references-count":32,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2008,7]]}},"alternative-id":["10.1152\/ajprenal.00011.2008"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00011.2008","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2008,7]]}},{"indexed":{"date-parts":[[2026,3,14]],"date-time":"2026-03-14T07:23:11Z","timestamp":1773472991956,"version":"3.50.1"},"reference-count":39,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2003,5,1]]},"abstract":"<jats:p>The expression of aquaporin-2 (AQP2) is decreased in rats with bilateral ureteral obstruction (BUO) and unilateral ureteral obstruction (UUO). Therefore, the expression of additional renal aquaporins (AQP1\u20134) and phosphorylated AQP2 (p-AQP2), known to play a role in urinary concentration, was examined in a Wistar rat model with 24 h of UUO. In obstructed kidneys, immunoblotting revealed a significant decrease in the expression of inner medullary AQP2 to 42 \u00b1 4, p-AQP2 to 23 \u00b1 5, AQP3 to 19 \u00b1 6, AQP4 to 11 \u00b1 5, and AQP1 to 64 \u00b1 8% of sham levels. AQP1 expression located in the proximal tubule decreased to 74 \u00b1 4% of sham levels ( P &lt; 0.05). Immunocytochemistry confirmed the downregulation of AQP3, AQP4, and p-AQP2. In contralateral nonobstructed kidneys, immunoblotting also revealed significant reductions of AQP1 in the inner medulla, outer medulla, and cortex, whereas expression of AQP2, AQP3, AQP4, and p-AQP2 was unchanged. Furthermore, we collected the urine from both obstructed and nonobstructed kidneys for 2 h, respectively, after 24 h of UUO. Urine collection from obstructed kidneys during 2 h after release of UUO revealed a significant reduction in urine osmolality and solute-free water reabsorption (T<jats:sup>c<\/jats:sup>H<jats:sub>2<\/jats:sub>O). Moreover, an increase in urine production and T<jats:sup>c<\/jats:sup>H<jats:sub>2<\/jats:sub>O was observed in contralateral kidneys. To examine whether vasopressin-independent mechanisms are involved in AQP2 regulation, vasopressin-deficient Brattleboro (BB) rats with 24 h of UUO were examined. Immunoblotting revealed downregulation of AQP2, p-AQP2, AQP3, and AQP1 in obstructed kidneys and downregulation of p-AQP2 and AQP1 in nonobstructed kidneys. In conclusion, 1) UUO is associated with severe downregulation of AQP2, AQP3, AQP4, and AQP1; thus all of these AQPs may play important roles in the impaired urinary concentrating capacity in the obstructed kidney; 2) the reduced levels of AQP1 in the nonobstructed kidney may contribute to the compensatory increase in urine production; and 3) downregulation of AQPs in BB rats supports the view that vasopressin-independent pathways may be involved in AQP2 and AQP3 regulation in the obstructed kidney.<\/jats:p>","DOI":"10.1152\/ajprenal.00090.2002","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:38:06Z","timestamp":1425415086000},"page":"F1066-F1079","source":"Crossref","is-referenced-by-count":69,"title":["Downregulation of renal aquaporins in response to unilateral ureteral obstruction"],"prefix":"10.1152","volume":"284","author":[{"given":"Chunling","family":"Li","sequence":"first","affiliation":[{"name":"The Water and Salt Research Center and"},{"name":"Institute of Experimental Clinical Research and"}]},{"given":"Weidong","family":"Wang","sequence":"additional","affiliation":[{"name":"The Water and Salt Research Center and"},{"name":"Institute of Anatomy, University of Aarhus, DK-8000 Aarhus C;"}]},{"given":"Mark A.","family":"Knepper","sequence":"additional","affiliation":[{"name":"Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892"}]},{"given":"S\u00f8ren","family":"Nielsen","sequence":"additional","affiliation":[{"name":"The Water and Salt Research Center and"},{"name":"Institute of Anatomy, University of Aarhus, DK-8000 Aarhus C;"}]},{"given":"J\u00f8rgen","family":"Fr\u00f8ki\u00e6r","sequence":"additional","affiliation":[{"name":"The Water and Salt Research Center and"},{"name":"Institute of Experimental Clinical Research and"},{"name":"Department of Clinical Physiology, Aarhus University Hospital-Skejby, DK-8200 Aarhus N, Denmark; and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI5704"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1998.274.2.C549"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.1.F29"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1980.57"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1997.77.1.75"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.91.19.8984"},{"key":"B7","doi-asserted-by":"crossref","first-page":"2181","DOI":"10.1681\/ASN.V9122181","volume":"9","author":"Earm JH","year":"1998","journal-title":"J Am Soc Nephrol"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.6.F1161"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119352"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.5.F663"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.273.2.F213"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.270.4.F657"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117525"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1081\/JDI-100100883"},{"key":"B15","doi-asserted-by":"crossref","first-page":"2019","DOI":"10.1681\/ASN.V12102019","volume":"12","author":"Kim SW","year":"2001","journal-title":"J Am Soc Nephrol"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00008.x"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.1.F62"},{"key":"B18","first-page":"156","volume":"11","author":"Klahr S.","year":"1991","journal-title":"Semin Nephrol"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1007\/BF00870378"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.3.F413"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.281.1.F163"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.080499597"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.8.4296"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.275.3.F400"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117863"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118628"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.2.F384"},{"key":"B28","first-page":"246","volume":"13","author":"Moody TE","year":"1975","journal-title":"Invest Urol"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00024.2001"},{"key":"B30","doi-asserted-by":"crossref","first-page":"647","DOI":"10.1681\/ASN.V103647","volume":"10","author":"Nielsen S","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.2.F370"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.3181\/00379727-197-43223"},{"key":"B33","doi-asserted-by":"crossref","first-page":"2614","DOI":"10.1681\/ASN.V10122614","volume":"10","author":"Schnermann J.","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.16.9660"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1172\/JCI110986"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.6.F775"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.2.F414"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-4615-4871-3_51"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-445X.2000.tb00028.x"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00090.2002","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,5,1]],"date-time":"2022-05-01T09:37:53Z","timestamp":1651397873000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00090.2002"}},"issued":{"date-parts":[[2003,5,1]]},"references-count":39,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2003,5,1]]}},"alternative-id":["10.1152\/ajprenal.00090.2002"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00090.2002","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2003,5,1]]}},{"indexed":{"date-parts":[[2026,3,16]],"date-time":"2026-03-16T10:48:31Z","timestamp":1773658111220,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1983,2,1]]},"abstract":"<jats:p> The effect of cold exposure (CE) on renal water excretion has not been clearly delineated. Conscious rats were exposed to decreased ambient temperature (15 degrees C). Forty-five minutes of CE resulted in reversible increases in urine flow and decreases in urine osmolality. The diuresis was not due to a diminished response to vasopressin (VP), as the antidiuresis associated with 500 microU of Pitressin given to water-diuresing rats was comparable at 15 and 30 degrees C. To determine whether the diuresis was due to intrarenal factors, glomerular filtration rate, renal blood flow, sodium excretion, and osmolar clearances were measured and found to be equivalent during control and cold conditions. To determine whether the observed diuresis was due to suppression of endogenous VP, VP-free Brattleboro rats undergoing a constant VP infusion were cold exposed. In these rats, CE was not associated with a change in either urine flow or urinary osmolality. This antidiuretic hormone-mediated mechanism was corroborated by a decrease in immunoassayable VP levels. To determine the mechanism whereby CE suppresses endogenous VP, plasma osmolality and hemodynamic parameters were measured. Although CE was not associated with a change in plasma osmolality, it did result in a significant increase in both mean arterial pressure and cardiac index. Pretreatment of rats with 6-hydroxydopamine prevented both the increase in mean arterial pressure and cold diuresis. We conclude that the diuresis observed upon exposure to 15 degrees C results from nonosmotic suppression of endogenous VP, as a consequence of the increase in mean arterial pressure. <\/jats:p>","DOI":"10.1152\/ajprenal.1983.244.2.f210","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T15:21:01Z","timestamp":1513956061000},"page":"F210-F216","source":"Crossref","is-referenced-by-count":5,"title":["Mechanism of cold diuresis in the rat"],"prefix":"10.1152","volume":"244","author":[{"given":"M. L.","family":"Morgan","sequence":"first","affiliation":[]},{"given":"R. J.","family":"Anderson","sequence":"additional","affiliation":[]},{"given":"M. A.","family":"Ellis","sequence":"additional","affiliation":[]},{"given":"T.","family":"Berl","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1983.244.2.F210","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:28:02Z","timestamp":1567967282000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1983.244.2.F210"}},"issued":{"date-parts":[[1983,2,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1983,2,1]]}},"alternative-id":["10.1152\/ajprenal.1983.244.2.F210"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1983.244.2.f210","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1983,2,1]]}},{"indexed":{"date-parts":[[2026,3,11]],"date-time":"2026-03-11T18:16:39Z","timestamp":1773252999903,"version":"3.50.1"},"reference-count":27,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2004,6]]},"abstract":"<jats:p>Aldosterone participates in the pathophysiology of several models of progressive chronic renal disease. Because of the causal connection between transforming growth factor-\u03b2<jats:sub>1<\/jats:sub>(TGF-\u03b2) and scarring in many such models, we hypothesized that aldosterone could evoke TGF-\u03b2 in the kidney. Aldosterone infusion for 3 days in otherwise normal rats caused a more than twofold increase in TGF-\u03b2 excretion without changes in systolic pressure or evidence of kidney damage. Concurrent treatment with amiloride did not alter this effect, indicating that aldosterone's stimulation of TGF-\u03b2 was independent of its regulation of sodium or potassium transport. However, concurrent treatment with spironolactone did block the increase in TGF-\u03b2, indicating that the effect depends on the mineralocorticoid receptor. Renal mRNA for serum glucocorticoid kinase rose, but no change in TGF-\u03b2 message occurred, suggesting posttranscriptional enhancement of renal TGF-\u03b2. In summary, aldosterone provokes renal TGF-\u03b2, and this action may contribute to aldosterone's fibrotic propensity.<\/jats:p>","DOI":"10.1152\/ajprenal.00202.2003","type":"journal-article","created":{"date-parts":[[2004,5,6]],"date-time":"2004-05-06T22:02:37Z","timestamp":1083880957000},"page":"F1059-F1062","source":"Crossref","is-referenced-by-count":71,"title":["Effect of aldosterone on renal transforming growth factor-\u03b2"],"prefix":"10.1152","volume":"286","author":[{"given":"Irmantas","family":"Juknevicius","sequence":"first","affiliation":[]},{"given":"Yoav","family":"Segal","sequence":"additional","affiliation":[]},{"given":"Stefan","family":"Kren","sequence":"additional","affiliation":[]},{"given":"Rutha","family":"Lee","sequence":"additional","affiliation":[]},{"given":"Thomas H.","family":"Hostetter","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1053\/snep.2001.26795"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.31.1.181"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000033611.79556.AE"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00277.x"},{"key":"R5","unstructured":"Hostetter T, Rosenberg ME, Kren S, and Greene E.Aldosterone induces glomerular lesions in the remnant kidney (Abstract).J Am Soc Nephrol10: 1016, 1996."},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200303000-00006"},{"key":"R7","doi-asserted-by":"crossref","unstructured":"Junaid A, Rosenberg ME, and Hostetter TH.Interaction of angiotensin II and TGF-\u03b2 1 in the rat remnant kidney.J Am Soc Nephrol8: 1732\u20131738, 1997.","DOI":"10.1681\/ASN.V8111732"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117251"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.24.2.195"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.1996.tb16241.x"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1016\/S0065-230X(08)60872-6"},{"key":"R12","unstructured":"Kopp JB, Factor VM, Mozes M, Nagy P, Sanderson N, Bottinger EP, Klotman PE, and Thorgeirsson SS.Transgenic mice with increased plasma levels of TGF-\u03b2 1 develop progressive renal disease.Lab Invest74: 991\u20131003, 1996."},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1038\/labinvest.3780196"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1172\/JCI108624"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1990.318"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.cb.06.110190.003121"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1016\/S1043-2760(01)00439-8"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00305.2002"},{"key":"R19","unstructured":"Sporn MBand Roberts AD.The transforming gowth factors-\u03b2. In:Handbook of Experimental Pharmacology. Peptide Growth Factors and Their Receptors, edited by Sporn AB and Roberts AD. New York: Springer, 1990, p. 419."},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00421.2002"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00969.x"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)64454-9"},{"key":"R23","unstructured":"Suthanthiran M, Li B, Song JO, Ding R, Sharma VK, Schwartz JE, and August P.Transforming growth factor-\u03b2 1 hyperexpression in African-American hypertensives: a novel mediator of hypertension and\/or target organ damage.Proc Natl Acad Sci USA97: 3479\u20133484, 2000."},{"key":"R24","unstructured":"Suzuki S, Ebihara I, Tomino Y, and Koide H.Transcriptional activation of matrix genes by transforming growth factor \u03b2 1 in mesangial cells.Exp Nephrol1: 229\u2013237, 1993."},{"key":"R25","doi-asserted-by":"crossref","unstructured":"Wakefield L, Kim SJ, Glick A, Winokur T, Colletta A, and Sporn M.Regulation of transforming growth factor-\u03b2 subtypes by members of the steroid hormone superfamily.J Cell Sci Suppl13: 139\u2013148, 1990.","DOI":"10.1242\/jcs.1990.Supplement_13.13"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra000050"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1172\/JCI116710"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00202.2003","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,6,17]],"date-time":"2021-06-17T10:08:46Z","timestamp":1623924526000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00202.2003"}},"issued":{"date-parts":[[2004,6]]},"references-count":27,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2004,6]]}},"alternative-id":["10.1152\/ajprenal.00202.2003"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00202.2003","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2004,6]]}},{"indexed":{"date-parts":[[2026,3,11]],"date-time":"2026-03-11T21:31:51Z","timestamp":1773264711286,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1990,8,1]]},"abstract":"<jats:p> To determine a renal tubular mechanism for the natriuretic effect of dopamine (DA) and DA-1 agonists, we measured Na(+)-H+ exchange activity (amiloride sensitive) in rat renal cortical brush-border membrane vesicles (BBMV). Renal cortical tissues were preincubated with ligands before BBMV preparation to study Na(+)-H+ exchange activity in the absence of the added ligands that may compete for ion binding sites of the exchanger. DA and DA-1 agonist-inhibited Na(+)-H+ exchange activity was concentration and time dependent. The inhibitory effect was not due to increased permeability, collapse of the proton gradient, or change in vesicle size and did not extend to Na(+)-glucose symport. DA-2 agonists had no effect, whereas alpha-adrenergic agonists increased Na(+)-H+ exchange activity. Kinetic analysis revealed that the DA-1 agonist inhibited Na(+)-H+ exchange activity by a noncompetitive process. 2',5'-Dideoxyadenosine inhibited adenylate cyclase activity and reversed the inhibitory effect of DA-1 agonist on the exchanger. H4, an isoquinoline sulfonamide, which inhibits protein kinase A, also reversed the inhibitory effect of DA-1 agonist on the exchanger. Thus the DA-1 agonist-mediated inhibition of Na(+)-H+ exchange activity in BBMV is a receptor-mediated adenylate cyclase-linked process. <\/jats:p>","DOI":"10.1152\/ajprenal.1990.259.2.f297","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T17:26:51Z","timestamp":1513963611000},"page":"F297-F303","source":"Crossref","is-referenced-by-count":31,"title":["Dopamine inhibits Na(+)-H+ exchanger activity in renal BBMV by stimulation of adenylate cyclase"],"prefix":"10.1152","volume":"259","author":[{"given":"C. C.","family":"Felder","sequence":"first","affiliation":[{"name":"Section of Pharmacology, National Institute of Mental Health,Bethesda, Maryland 20892."}]},{"given":"T.","family":"Campbell","sequence":"additional","affiliation":[{"name":"Section of Pharmacology, National Institute of Mental Health,Bethesda, Maryland 20892."}]},{"given":"F.","family":"Albrecht","sequence":"additional","affiliation":[{"name":"Section of Pharmacology, National Institute of Mental Health,Bethesda, Maryland 20892."}]},{"given":"P. A.","family":"Jose","sequence":"additional","affiliation":[{"name":"Section of Pharmacology, National Institute of Mental Health,Bethesda, Maryland 20892."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1990.259.2.F297","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:19:00Z","timestamp":1567955940000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1990.259.2.F297"}},"issued":{"date-parts":[[1990,8,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1990,8,1]]}},"alternative-id":["10.1152\/ajprenal.1990.259.2.F297"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1990.259.2.f297","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1990,8,1]]}},{"indexed":{"date-parts":[[2026,3,11]],"date-time":"2026-03-11T21:31:52Z","timestamp":1773264712754,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1980,6,1]]},"DOI":"10.1152\/ajprenal.1980.238.6.f461","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T13:15:49Z","timestamp":1513948549000},"page":"F461-F469","source":"Crossref","is-referenced-by-count":16,"title":["Properties of the Na+-H+ exchanger in renal microvillus membrane vesicles"],"prefix":"10.1152","volume":"238","author":[{"given":"J. L.","family":"Kinsella","sequence":"first","affiliation":[]},{"given":"P. S.","family":"Aronson","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1980.238.6.F461","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:13:26Z","timestamp":1567966406000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1980.238.6.F461"}},"issued":{"date-parts":[[1980,6,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1980,6,1]]}},"alternative-id":["10.1152\/ajprenal.1980.238.6.F461"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1980.238.6.f461","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1980,6,1]]}},{"indexed":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T16:17:09Z","timestamp":1773332229696,"version":"3.50.1"},"reference-count":43,"publisher":"American Physiological Society","issue":"4","funder":[{"name":"Application and basic research project of wuhan city","award":["2018060401011321"],"award-info":[{"award-number":["2018060401011321"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2019,10,1]]},"abstract":"<jats:p> Diabetes could aggravate ischemia-reperfusion (I\/R) injury, but the underlying mechanism is unclear. In the present study, we aimed to investigate whether diabetes exacerbates renal I\/R injury and its possible mechanism. In vitro, HK-2 cells under normal or high glucose conditions were subjected to hypoxia (12 h) followed by reoxygenation (3 h) (H\/R). Cell viability, intracellular ATP content, mitochondrial membrane potential, reactive oxygen species production, and apoptosis were measured. In vivo, streptozotocin-induced diabetic and nondiabetic rats were subjected to I\/R. Renal pathology, function, and apoptosis were evaluated by hematoxylin and eosin staining, transmission electron microscopy, and Western blot analysis. Compared with the normal glucose + H\/R group, mitochondrial function (ATP, mitochondrial membrane potential, and reactive oxygen species) and mitophagy were reduced in the high glucose + H\/R group, as was expression of phosphatase and tensin homolog-induced putative kinase 1 (PINK1) and Parkin. Also, cells in the high glucose + H\/R group exhibited more apoptosis compared with the normal glucose + H\/R group, as assessed by flow cytometry, TUNEL staining, and Western blot analysis. Compared with normal rats that underwent I\/R, diabetic rats that underwent I\/R exhibited more severe tubular damage and renal dysfunction as well as expression of the apoptotic protein caspase-3. Meanwhile, diabetes alleviated mitophagy-associated protein expression in rats subjected to I\/R, including expression of PINK1 and Parkin. Transmission electron microscopy indicated that the mitophagosome could be hardly observed and that mitochondrial morphology and structure were obviously damaged in the diabetes + I\/R group. In conclusion, our results, for the first time, indicate that diabetes could aggravate I\/R injury by repressing mitochondrial function and PINK1\/Parkin-mediated mitophagy in vivo and in vitro. <\/jats:p>","DOI":"10.1152\/ajprenal.00181.2019","type":"journal-article","created":{"date-parts":[[2019,8,7]],"date-time":"2019-08-07T13:34:55Z","timestamp":1565184895000},"page":"F852-F864","source":"Crossref","is-referenced-by-count":38,"title":["Diabetes aggravates renal ischemia-reperfusion injury by repressing mitochondrial function and PINK1\/Parkin-mediated mitophagy"],"prefix":"10.1152","volume":"317","author":[{"given":"Yuan-Yuan","family":"Yang","sequence":"first","affiliation":[{"name":"Department of Urology, Renmin Hospital of Wuhan University, Wuhan, Hubei, China"}]},{"given":"Dao-Jing","family":"Gong","sequence":"additional","affiliation":[{"name":"Department of Urology, Renmin Hospital of Wuhan University, Wuhan, Hubei, China"}]},{"given":"Jian-Jian","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Urology, Renmin Hospital of Wuhan University, Wuhan, Hubei, China"}]},{"given":"Xiu-Heng","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Urology, Renmin Hospital of Wuhan University, Wuhan, Hubei, China"}]},{"given":"Lei","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Urology, Renmin Hospital of Wuhan University, Wuhan, Hubei, China"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2015.13"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2017.107"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/j.jtcvs.2006.12.059"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/j.ebiom.2015.04.002"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/j.redox.2016.09.007"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbabio.2017.01.003"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1186\/s13054-019-2314-z"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/nchembio.2287"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1159\/000452598"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00272.2006"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1016\/j.brainresbull.2018.06.018"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1155\/2018\/9494052"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.18632\/aging.101511"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/j.lfs.2004.03.039"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.3892\/mmr.2014.2234"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gft313"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00184.2018"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/j.tcb.2016.05.008"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1038\/s41556-018-0176-2"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/j.cub.2018.01.004"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.00314.2018"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002568"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1007\/s12020-007-0012-0"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1016\/j.freeradbiomed.2019.02.018"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00415.2004"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1172\/JCI122035"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.3389\/fphys.2018.01670"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1089\/ars.2008.2331"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1124\/pr.115.011502"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1002\/jcb.27711"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1080\/15548627.2017.1405880"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2016.11.088"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1016\/j.urology.2018.10.015"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.3892\/mmr.2015.3344"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2015.240"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1016\/j.brainres.2018.06.028"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1155\/2016\/2386068"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.27754"},{"key":"B39","first-page":"18","volume":"41","author":"Yoo SM","year":"2018","journal-title":"Mol Cells"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1053\/j.ackd.2017.12.005"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1007\/s12576-018-0627-3"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1111\/jpi.12542"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1038\/srep16910"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00181.2019","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,18]],"date-time":"2019-09-18T10:00:34Z","timestamp":1568800834000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00181.2019"}},"issued":{"date-parts":[[2019,10,1]]},"references-count":43,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2019,10,1]]}},"alternative-id":["10.1152\/ajprenal.00181.2019"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00181.2019","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2019,10,1]]}},{"indexed":{"date-parts":[[2026,3,16]],"date-time":"2026-03-16T00:14:15Z","timestamp":1773620055130,"version":"3.50.1"},"reference-count":32,"publisher":"American Physiological Society","issue":"3","funder":[{"DOI":"10.13039\/501100001862","name":"Swedish Research Council Formas (Svenska Forskningsr\u00e5det Formas)","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100001862","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100003793","name":"Hj\u00e4rt-Lungfonden (Swedish Heart-Lung Foundation)","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100003793","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Swedish Diabetes Foundation"},{"DOI":"10.13039\/501100006415","name":"Family Ernfors Foundation","doi-asserted-by":"crossref","id":[{"id":"10.13039\/501100006415","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2018,3,1]]},"abstract":"<jats:p> About one-third of patients with type 1 diabetes develops kidney disease. The mechanism is largely unknown, but intrarenal hypoxia has been proposed as a unifying mechanism for chronic kidney disease, including diabetic nephropathy. The endothelin system has recently been demonstrated to regulate oxygen availability in the diabetic kidney via a pathway involving endothelin type A receptors (ETA-R). These receptors mainly mediate vasoconstriction and tubular sodium retention, and inhibition of ETA-R improves intrarenal oxygenation in the diabetic kidney. Endothelin type B receptors (ETB-R) can induce vasodilation of the renal vasculature and also regulate tubular sodium handling. However, the role of ETB-R in kidney oxygen homeostasis is unknown. The effects of acute intrarenal ETB-R activation (sarafotoxin 6c for 30\u201340 min; 0.78 pmol\/h directly into the renal artery) on kidney function and oxygen metabolism were investigated in normoglycemic controls and insulinopenic male Sprague-Dawley rats administered streptozotocin (55 mg\/kg) 2 wk before the acute experiments. Intrarenal activation of ETB-R improved oxygenation in the hypoxic diabetic kidney. However, the effects on diabetes-induced increased kidney oxygen consumption could not explain the improved oxygenation. Rather, the improved kidney oxygenation was due to hemodynamic effects increasing oxygen delivery without increasing glomerular filtration or tubular sodium load. In conclusion, increased ETB-R signaling in the diabetic kidney improves intrarenal tissue oxygenation due to increased oxygen delivery secondary to increased renal blood flow. <\/jats:p>","DOI":"10.1152\/ajprenal.00498.2017","type":"journal-article","created":{"date-parts":[[2017,12,6]],"date-time":"2017-12-06T12:05:11Z","timestamp":1512561911000},"page":"F439-F444","source":"Crossref","is-referenced-by-count":6,"title":["Intrarenal activation of endothelin type B receptors improves kidney oxygenation in type 1 diabetic rats"],"prefix":"10.1152","volume":"314","author":[{"given":"Stephanie","family":"Franz\u00e9n","sequence":"first","affiliation":[{"name":"Department of Surgical Sciences, Anesthesiology and Intensive Care, Uppsala University, Uppsala, Sweden"}]},{"given":"Liselotte","family":"Pihl","sequence":"additional","affiliation":[{"name":"Department of Medical Cell Biology, Division of Integrative Physiology, Uppsala University, Uppsala, Sweden"}]},{"given":"Angelica","family":"Fasching","sequence":"additional","affiliation":[{"name":"Department of Medical Cell Biology, Division of Integrative Physiology, Uppsala University, Uppsala, Sweden"}]},{"given":"Fredrik","family":"Palm","sequence":"additional","affiliation":[{"name":"Department of Medical Cell Biology, Division of Integrative Physiology, Uppsala University, Uppsala, Sweden"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/0006-291X(92)90826-7"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00595.2013"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1007\/s00125-015-3690-9"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00049.2016"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.113.01425"},{"key":"B6","first-page":"149","volume":"122","author":"Fukui M","year":"1993","journal-title":"J Lab Clin Med"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117268"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1111\/1440-1681.12034"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.92.3.357"},{"key":"B10","first-page":"463","volume":"33","author":"Hocher B","year":"1995","journal-title":"Eur J Clin Chem Clin Biochem"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00060.2009"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/j.cellsig.2013.10.002"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.105.091728"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0701349"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1096\/fj.03-0013fje"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00578.2007"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00228.2009"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013090990"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00275.2005"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1007\/s00125-003-1155-z"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1007\/s00125-012-2469-5"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00502.2011"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1096\/fasebj.9.12.7672512"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0b013e3282f34b02"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.4103\/1319-2442.118098"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00280.2006"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.89.3.1203"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1097\/01.mnh.0000441049.98664.6c"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/0041-0101(88)90234-6"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/j.lfs.2012.03.026"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1016\/0014-2999(93)90032-D"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.3109\/0886022X.2011.647301"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00498.2017","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2020,5,18]],"date-time":"2020-05-18T17:21:02Z","timestamp":1589822462000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00498.2017"}},"issued":{"date-parts":[[2018,3,1]]},"references-count":32,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2018,3,1]]}},"alternative-id":["10.1152\/ajprenal.00498.2017"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00498.2017","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2018,3,1]]}},{"indexed":{"date-parts":[[2026,2,28]],"date-time":"2026-02-28T13:50:03Z","timestamp":1772286603109,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1980,4,1]]},"abstract":"<jats:p> Studies were performed on anesthetized dogs to determine the relationship of interstitial pressure to sodium excretion during renal vein constriction in the presence and absence of volume expansion. Renal interstitial pressure was measured from implanted capsules during basal renal venous pressure and increased pressures of 10, 20, 30, and 40 mmHg. A positive relationship between renal venous pressure and interstitial pressure was demonstrated in hydropenia and in volume expansion, with markedly higher interstitial pressures obtained in volume expansion. A positive correlation was demonstrated between fractional sodium excretion and renal interstitial pressure in hydropenia as compared to a significant negative correlation in volume expansion. Negative correlations were demonstrated in volume expansion between renal interstitial pressure and glomerular filtration rate and renal blood flow as compared to no significant change in these parameters in hydropenia. Accordingly, a positive correlation was demonstrated between renal interstitial pressure and sodium excretion in hydropenia but not in volume expansion. Volume expansion was characterized by higher interstitial pressure and decreased sodium excretion in association with decreased renal blood flow and glomerular filtration rate. <\/jats:p>","DOI":"10.1152\/ajprenal.1980.238.4.f279","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T08:22:56Z","timestamp":1513930976000},"page":"F279-F282","source":"Crossref","is-referenced-by-count":27,"title":["Renal interstitial pressure and sodium excretion during renal vein constriction"],"prefix":"10.1152","volume":"238","author":[{"suffix":"Jr","given":"J. C.","family":"Burnett","sequence":"first","affiliation":[]},{"given":"F. G.","family":"Knox","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1980.238.4.F279","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T14:17:38Z","timestamp":1567952258000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1980.238.4.F279"}},"issued":{"date-parts":[[1980,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1980,4,1]]}},"alternative-id":["10.1152\/ajprenal.1980.238.4.F279"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1980.238.4.f279","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1980,4,1]]}},{"indexed":{"date-parts":[[2026,3,4]],"date-time":"2026-03-04T16:09:24Z","timestamp":1772640564773,"version":"3.50.1"},"reference-count":49,"publisher":"American Physiological Society","issue":"4","funder":[{"name":"NIH\/NIDDK","award":["DK082509"],"award-info":[{"award-number":["DK082509"]}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)","doi-asserted-by":"publisher","award":["R01DK096030"],"award-info":[{"award-number":["R01DK096030"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"name":"HHS\/NIH\/NHLBI","award":["R01HL117062"],"award-info":[{"award-number":["R01HL117062"]}]},{"name":"HHS\/NIH\/NHLBI","award":["R01HL133545"],"award-info":[{"award-number":["R01HL133545"]}]},{"DOI":"10.13039\/100000050","name":"HHS | NIH | National Heart, Lung, and Blood Institute (NHBLI)","doi-asserted-by":"publisher","award":["R01 HL132318"],"award-info":[{"award-number":["R01 HL132318"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2018,10,1]]},"abstract":"<jats:p>Osteopontin (OPN) is a pro-and anti-inflammatory molecule that simultaneously attenuates oxidative stress. Both inflammation and oxidative stress play a role in the pathogenesis of glomerulonephritis and in the progression of kidney injury. Importantly, OPN is highly induced in nephritic kidneys. To characterize further the role of OPN in kidney injury we used OPN<jats:sup>\u2212\/\u2212<\/jats:sup>mice in antiglomerular basement membrane reactive serum-induced immune (NTS) nephritis, an inflammatory and progressive model of kidney disease. Normal wild-type (WT) and OPN<jats:sup>\u2212\/\u2212<\/jats:sup>mice did not show histological differences. However, nephritic kidneys from OPN<jats:sup>\u2212\/\u2212<\/jats:sup>mice showed severe damage compared with WT mice. Glomerular proliferation, necrotizing lesions, crescent formation, and tubulointerstitial injury were significantly higher in OPN<jats:sup>\u2212\/\u2212<\/jats:sup>mice. Macrophage infiltration was increased in the glomeruli and interstitium in OPN<jats:sup>\u2212\/\u2212<\/jats:sup>mice, with higher expression of IL-6, CCL2, and chemokine CXCL1. In addition, collagen (Col) I, Col III, and Col IV deposition were increased in kidneys from OPN<jats:sup>\u2212\/\u2212<\/jats:sup>mice. Elevated expression of the reactive oxygen species-generating enzyme Nox4 and blunted expression of Nrf2, a molecule that inhibits reactive oxygen species and inflammatory pathways, was observed in nephritic kidneys from OPN<jats:sup>\u2212\/\u2212<\/jats:sup>mice. Notably, CD11b diphteria toxin receptor mice with NTS nephritis selectively depleted of macrophages and reconstituted with OPN<jats:sup>\u2212\/\u2212<\/jats:sup>macrophages showed less kidney injury compared with mice receiving WT macrophages. These findings suggest that in global OPN<jats:sup>\u2212\/\u2212<\/jats:sup>mice there is increased inflammation and redox imbalance that mediate kidney damage. However, absence of macrophage OPN is protective, indicating that macrophage OPN plays a role in the induction and progression of kidney injury in NTS nephritis.<\/jats:p>","DOI":"10.1152\/ajprenal.00458.2017","type":"journal-article","created":{"date-parts":[[2018,5,2]],"date-time":"2018-05-02T13:01:37Z","timestamp":1525266097000},"page":"F759-F768","source":"Crossref","is-referenced-by-count":22,"title":["Different effects of global osteopontin and macrophage osteopontin in glomerular injury"],"prefix":"10.1152","volume":"315","author":[{"given":"Jessica","family":"Trostel","sequence":"first","affiliation":[{"name":"Department of Medicine, Division of Renal Diseases and Hypertension"}]},{"given":"Luan D.","family":"Truong","sequence":"additional","affiliation":[{"name":"Department of Pathology, Baylor College of Medicine, and Department of Pathology, The Methodist Hospital, Houston, Texas"}]},{"given":"Carlos","family":"Roncal-Jimenez","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Renal Diseases and Hypertension"}]},{"given":"Makoto","family":"Miyazaki","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Renal Diseases and Hypertension"}]},{"given":"Shinobu","family":"Miyazaki-Anzai","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Renal Diseases and Hypertension"}]},{"given":"Masanari","family":"Kuwabara","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Renal Diseases and Hypertension"}]},{"given":"Rachel","family":"McMahan","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology University of Colorado Denver, Aurora, Colorado"}]},{"given":"Ana","family":"Andres-Hernando","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Renal Diseases and Hypertension"}]},{"given":"Yuka","family":"Sato","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Renal Diseases and Hypertension"}]},{"given":"Thomas","family":"Jensen","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Renal Diseases and Hypertension"}]},{"given":"Miguel A.","family":"Lanaspa","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Renal Diseases and Hypertension"}]},{"given":"Richard J.","family":"Johnson","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Renal Diseases and Hypertension"}]},{"given":"Gabriela E.","family":"Garcia","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Renal Diseases and Hypertension"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1126\/science.287.5454.860"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1996.271.5.C1424"},{"key":"B3","doi-asserted-by":"crossref","first-page":"1647","DOI":"10.1681\/ASN.V1191647","volume":"11","author":"Bonvini JM","year":"2000","journal-title":"J Am Soc Nephrol"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2012-01-380121"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.201510086"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1084\/jem.188.1.193"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1172\/JCI12980"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1172\/JCI200522675"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)61209-6"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00604.x"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2011.101"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1002\/jlb.67.4.577"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)63903-X"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1097\/01.hjh.0000467666.07274.ee"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00717.x"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00557.2010"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.110.175828"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00421.2009"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1038\/sj.gt.3301060"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009060615"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.0901473"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0912228107"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1084\/jem.185.7.1371"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfq498"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1136\/ard.2009.117101"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/18.1.178"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1093\/qjmed\/95.1.3"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2009.518"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2005.04.083"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00526.x"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1016\/j.yexcr.2006.12.026"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00580.x"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006111237"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1017\/S1462399411001839"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1359\/jbmr.1998.13.7.1101"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2012.439"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00615.2012"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1016\/j.yjmcc.2009.06.015"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.172.7.4410"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2012010022"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002033"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1096\/fj.14-262493"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1016\/j.ajpath.2016.06.017"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00032.x"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1016\/j.transproceed.2012.02.048"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0119543"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00939.x"},{"key":"B48","first-page":"50","volume":"110","author":"Yu XQ","year":"1998","journal-title":"Proc Assoc Am Physicians"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1159\/000319490"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00458.2017","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,21]],"date-time":"2022-08-21T15:27:41Z","timestamp":1661095661000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00458.2017"}},"issued":{"date-parts":[[2018,10,1]]},"references-count":49,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2018,10,1]]}},"alternative-id":["10.1152\/ajprenal.00458.2017"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00458.2017","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2018,10,1]]}},{"indexed":{"date-parts":[[2026,3,4]],"date-time":"2026-03-04T06:13:12Z","timestamp":1772604792554,"version":"3.50.1"},"reference-count":58,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,3,1]]},"abstract":"<jats:p>Recent experimental and clinical studies suggest a causal role of uric acid in the development of chronic kidney disease. Most studies have focused on uric acid-induced endothelial dysfunction, oxidative stress, and inflammation in the kidney. The direct effects of uric acid on tubular cells have not been studied in detail, and whether uric acid can mediate phenotypic transition of renal tubular cells such as epithelial-to-mesenchymal transition (EMT) is not known. We therefore investigated whether uric acid could alter E-cadherin expression and EMT in the kidney of hyperuricemic rats and in cultured renal tubular cells (NRK cells). Experimental hyperuricemia was associated with evidence of EMT before the development of significant tubulointerstitial fibrosis at 4 wk, as shown by decreased E-cadherin expression and an increased \u03b1-smooth muscle actin (\u03b1-SMA). Allopurinol significantly inhibited uric acid-induced changes in E-cadherin and \u03b1-SMA with an amelioration of renal fibrosis at 6 wk. In cultured NRK cells, uric acid induced EMT, which was blocked by the organic anion transport inhibitor probenecid. Uric acid increased expression of transcriptional factors associated with decreased synthesis of E-cadherin (Snail and Slug). Uric acid also increased the degradation of E-cadherin via ubiquitination, which is of importance since downregulation of E-cadherin is considered to be a triggering mechanism for EMT. In conclusion, uric acid induces EMT of renal tubular cells decreasing E-cadherin synthesis via an activation of Snail and Slug as well as increasing the degradation of E-cadherin.<\/jats:p>","DOI":"10.1152\/ajprenal.00560.2012","type":"journal-article","created":{"date-parts":[[2013,1,3]],"date-time":"2013-01-03T07:22:31Z","timestamp":1357197751000},"page":"F471-F480","source":"Crossref","is-referenced-by-count":215,"title":["Uric acid-induced phenotypic transition of renal tubular cells as a novel mechanism of chronic kidney disease"],"prefix":"10.1152","volume":"304","author":[{"given":"Eun-Sun","family":"Ryu","sequence":"first","affiliation":[{"name":"Division of Nephrology, Department of Internal Medicine, Ewha Womans University School of Medicine, Ewha Medical Research Center, Seoul, Korea;"}]},{"given":"Mi Jin","family":"Kim","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Internal Medicine, Ewha Womans University School of Medicine, Ewha Medical Research Center, Seoul, Korea;"}]},{"given":"Hyun-Soo","family":"Shin","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Internal Medicine, Ewha Womans University School of Medicine, Ewha Medical Research Center, Seoul, Korea;"}]},{"given":"Yang-Hee","family":"Jang","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Internal Medicine, Ewha Womans University School of Medicine, Ewha Medical Research Center, Seoul, Korea;"}]},{"given":"Hack Sun","family":"Choi","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Internal Medicine, Ewha Womans University School of Medicine, Ewha Medical Research Center, Seoul, Korea;"}]},{"given":"Inho","family":"Jo","sequence":"additional","affiliation":[{"name":"Department of Molecular Medicine, Ewha Womans University School of Medicine, Ewha Medical Research Center, Seoul, Korea; and"}]},{"given":"Richard J.","family":"Johnson","sequence":"additional","affiliation":[{"name":"Division of Renal Diseases and Hypertension, University of Colorado-Denver, Aurora, Colorado"}]},{"given":"Duk-Hee","family":"Kang","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Internal Medicine, Ewha Womans University School of Medicine, Ewha Medical Research Center, Seoul, Korea;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.2741\/3433"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2010.01.019"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1038\/sj.embor.7400408"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/35000025"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200308162"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1097\/HJH.0b013e3282f240bf"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M110.168625"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1001\/jama.1897.02440320005001a"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004030208"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)61208-4"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra0800885"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1186\/1755-1536-4-11"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.01580210"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-011-1772-6"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.275.4.2727"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00104.2006"},{"key":"B17","first-page":"3810","volume":"117","author":"Higgins DF","year":"2007","journal-title":"J Clin Invest"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.2337\/db09-0014"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1001\/archinternmed.2008.605"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2010.090517"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(04)00934-5"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1172\/JCI0215518"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1209701"},{"key":"B24","volume":"38","author":"Jinde K","journal-title":"Am J Kidney Dis"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1007\/s11255-007-9253-3"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000034910.58454.FD"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005050572"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00273.x"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000106015.29070.E7"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008121226"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00283.2001"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1038\/labinvest.2011.111"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1159\/000066303"},{"key":"B34","first-page":"4346","volume":"60","author":"Nass Herman JG SJ","year":"2000","journal-title":"Cancer Res"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008010080"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.01004"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1158\/0008-5472.CAN-07-2938"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.25.1.389-402.2005"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1159\/000325209"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00430.x"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1002\/dvdy.20501"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.04271007"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00170.2002"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.137.6.1403"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M703300200"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2005.10.006"},{"key":"B47","first-page":"267","volume":"4","author":"Strutz F","year":"1996","journal-title":"Exp Nephrol"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1038\/nrm1835"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000028589.66335.AA"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007101075"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.E11-04-0306"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)62533-3"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1002\/hep.23221"},{"key":"B54","doi-asserted-by":"crossref","first-page":"1234","DOI":"10.1097\/HJH.0b013e328337da1d","volume":"28","author":"Yu MA","year":"2010","journal-title":"J Hypertens"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010060616"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1038\/nm888"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1007\/s00109-003-0517-9"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2009.080983"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00560.2012","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,2,5]],"date-time":"2022-02-05T03:36:39Z","timestamp":1644032199000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00560.2012"}},"issued":{"date-parts":[[2013,3,1]]},"references-count":58,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2013,3,1]]}},"alternative-id":["10.1152\/ajprenal.00560.2012"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00560.2012","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2013,3,1]]}},{"indexed":{"date-parts":[[2026,3,6]],"date-time":"2026-03-06T20:40:36Z","timestamp":1772829636590,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2026,2,1]]},"DOI":"10.1152\/ajprenal.2026.330.2.au","type":"journal-article","created":{"date-parts":[[2026,2,19]],"date-time":"2026-02-19T13:52:07Z","timestamp":1771509127000},"page":"i-i","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["First Author Highlights"],"prefix":"10.1152","volume":"330","member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.2026.330.2.AU","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,3,6]],"date-time":"2026-03-06T13:52:08Z","timestamp":1772805128000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.2026.330.2.AU"}},"issued":{"date-parts":[[2026,2,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2026,2,1]]}},"alternative-id":["10.1152\/ajprenal.2026.330.2.AU"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.2026.330.2.au","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2026,2,1]]},"assertion":[{"value":"2026-02-19","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,3,21]],"date-time":"2026-03-21T19:00:31Z","timestamp":1774119631833,"version":"3.50.1"},"reference-count":35,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1998,11,1]]},"abstract":"<jats:p>Vesicle targeting proteins (\u201cSNAREs\u201d) have been proposed to direct vasopressin-induced trafficking of aquaporin-2 water channels in kidney collecting ducts. A newly identified SNARE protein, SNAP-23, is proposed to mediate vesicle targeting to the plasma membrane in diverse tissues. The current studies were done to determine whether SNAP-23 is expressed in collecting ducts with an intracellular distribution compatible with a role in aquaporin-2 trafficking. RT-PCR demonstrated SNAP-23 mRNA in microdissected collecting ducts and other tubular segments including the proximal tubule and thick ascending limb. Immunoblotting using a polyclonal antibody raised against a COOH-terminal peptide revealed a solitary band at an apparent molecular mass of 30 kDa in renal medullary membrane fractions and inner medullary collecting duct suspensions. Differential centrifugation revealed that SNAP-23 is present in membrane fractions including the low-density fraction enriched in intracellular vesicles. Immunocytochemistry revealed SNAP-23 labeling at both the apex and the cytoplasm of collecting duct principal cells. Immunoblotting of intracellular vesicles immunoisolated using an aquaporin-2 antibody revealed the presence of both SNAP-23 and synaptobrevin-2 (VAMP-2) in aquaporin-2-bearing vesicles. We conclude that SNAP-23 is strongly expressed in collecting duct principal cells, consistent with a role in vasopressin-regulated trafficking of aquaporin-2. However, localization of SNAP-23 in both intracytoplasmic vesicles and plasma membranes suggests a function different from that originally proposed for SNAP-25 in synaptic vesicle targeting.<\/jats:p>","DOI":"10.1152\/ajprenal.1998.275.5.f752","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T17:12:38Z","timestamp":1514049158000},"page":"F752-F760","source":"Crossref","is-referenced-by-count":35,"title":["SNAP-23 in rat kidney: colocalization with aquaporin-2 in collecting duct vesicles"],"prefix":"10.1152","volume":"275","author":[{"given":"Takeaki","family":"Inoue","sequence":"first","affiliation":[{"name":"Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892-1603;"}]},{"given":"S\u00f8ren","family":"Nielsen","sequence":"additional","affiliation":[{"name":"Department of Cell Biology, Institute of Anatomy, University of Aarhus, DK-8000 Aarhus, Denmark; and"}]},{"given":"Beatrice","family":"Mandon","sequence":"additional","affiliation":[{"name":"Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892-1603;"}]},{"given":"James","family":"Terris","sequence":"additional","affiliation":[{"name":"Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892-1603;"},{"name":"Department of Physiology, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814-4799"}]},{"given":"Bellamkonda K.","family":"Kishore","sequence":"additional","affiliation":[{"name":"Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892-1603;"}]},{"given":"Mark A.","family":"Knepper","sequence":"additional","affiliation":[{"name":"Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892-1603;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1997.6560"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.5.1971"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1021\/bi962331n"},{"issue":"37","key":"B4","first-page":"F78","volume":"268","author":"Chou C.-L.","year":"1995","journal-title":"Am. J. Physiol."},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.91.19.8984"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1002\/cne.903560111"},{"issue":"39","key":"B7","first-page":"F623","volume":"270","author":"Ecelbarger C. A.","year":"1996","journal-title":"Am. J. Physiol."},{"issue":"38","key":"B8","first-page":"F663","volume":"269","author":"Ecelbarger C. A.","year":"1995","journal-title":"Am. J. Physiol."},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1995.269.3.C797"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1994.267.6.C1507"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(96)00931-3"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.ne.17.030194.001251"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.6.1876"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.91.14.6255"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1016\/S0955-0674(97)80034-8"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/S0168-0102(96)01086-3"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(95)00476-P"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118873"},{"issue":"42","key":"B19","first-page":"F718","volume":"273","author":"Mandon B.","year":"1997","journal-title":"Am. J. Physiol."},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1995.269.3.C655"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1997.6196"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/387199a0"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.389"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.4.1013"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.90.24.11663"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118229"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.94.12.6197"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.23.13300"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1038\/372055a0"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1038\/362318a0"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(96)00932-5"},{"issue":"40","key":"B32","first-page":"F414","volume":"271","author":"Terris J.","year":"1996","journal-title":"Am. J. Physiol."},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.128.4.637"},{"key":"B34","doi-asserted-by":"crossref","first-page":"505","DOI":"10.1242\/jcs.110.4.505","volume":"110","author":"Wang G.","year":"1997","journal-title":"J. Cell Sci."},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1996.5884"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1998.275.5.F752","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:51:57Z","timestamp":1660189917000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1998.275.5.F752"}},"issued":{"date-parts":[[1998,11,1]]},"references-count":35,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1998,11,1]]}},"alternative-id":["10.1152\/ajprenal.1998.275.5.F752"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1998.275.5.f752","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1998,11,1]]}},{"indexed":{"date-parts":[[2026,3,18]],"date-time":"2026-03-18T03:23:05Z","timestamp":1773804185400,"version":"3.50.1"},"reference-count":38,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2019,7,1]]},"abstract":"<jats:p>Emerging evidence has shown that bile acids play important roles in renal physiology and diseases by activating two major receptors, the nuclear farnesoid X receptor (FXR) and the membrane G protein-coupled bile acid receptor-1 (Gpbar1; also known as TGR5). Both FXR and TGR5 have been identified in human and rodent kidneys, where they are deeply involved in renal water handling. In mice, FXR- or TGR5-related gene deficiency has been associated with reduced aquaporin-2 expression accompanied with impaired urinary concentration ability. In this mini-review, we briefly discuss the current understanding of FXR\/TGR5 signaling in the kidneys, with a special focus on the regulation of aquaporin-2 expression by bile acids in the collecting ducts and its potential significance in disease conditions.<\/jats:p>","DOI":"10.1152\/ajprenal.00563.2018","type":"journal-article","created":{"date-parts":[[2019,5,15]],"date-time":"2019-05-15T16:33:37Z","timestamp":1557938017000},"page":"F73-F76","source":"Crossref","is-referenced-by-count":23,"title":["Bile acid signaling in renal water regulation"],"prefix":"10.1152","volume":"317","author":[{"given":"Suchun","family":"Li","sequence":"first","affiliation":[{"name":"Institute of Hypertension, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China"}]},{"given":"Chunling","family":"Li","sequence":"additional","affiliation":[{"name":"Institute of Hypertension, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China"}]},{"given":"Weidong","family":"Wang","sequence":"additional","affiliation":[{"name":"Institute of Hypertension, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China"},{"name":"Department of Pathophysiology, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1002\/hep.1840210128"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1002\/hep.30499"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0136873"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1194\/jlr.R900012-JLR200"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2013.03.013"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/j.jhep.2010.07.012"},{"key":"B7","doi-asserted-by":"crossref","first-page":"1950","DOI":"10.1681\/ASN.V1091950","volume":"10","author":"Fern\u00e1ndez-Llama P","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1002\/hep.26599"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.6.F926"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-017-10168-6"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.3390\/ijms19072069"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005121317"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1172\/JCI76738"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.2337\/db06-1642"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00258.2002"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00485.2016"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M209706200"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbadis.2017.08.028"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014111067"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.3748\/wjg.14.7059"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2018030271"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1053\/j.gastro.2014.08.042"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1126\/science.284.5418.1362"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.2741\/3877"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2016101123"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M117.784322"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1111\/j.1939-165x.2012.00488.x"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1194\/jlr.R500013-JLR200"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1172\/JCI116408"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1038\/nrd2619"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1016\/S2213-8587(16)30155-3"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00404.2009"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.C117.794982"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2017020222"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1007\/s12020-016-1032-4"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1803945115"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.3389\/fnut.2016.00046"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1323977111"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00563.2018","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,9,18]],"date-time":"2022-09-18T02:24:11Z","timestamp":1663467851000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00563.2018"}},"issued":{"date-parts":[[2019,7,1]]},"references-count":38,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2019,7,1]]}},"alternative-id":["10.1152\/ajprenal.00563.2018"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00563.2018","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2019,7,1]]}},{"indexed":{"date-parts":[[2026,3,18]],"date-time":"2026-03-18T08:34:33Z","timestamp":1773822873536,"version":"3.50.1"},"reference-count":68,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2001,2,1]]},"abstract":"<jats:p>Focal glomerulosclerosis (FGS) is the predominant glomerular lesion in patients with human immunodeficiency virus (HIV)-associated nephropathy. Initial mesangial cell hyperplasia and subsequent hypoplasia are common features of FGS. In the present study we evaluated the effect of HIV-1 glycoprotein (gp) 120 on human mesangial cell (HMC) growth. HIV-1 gp 120 stimulated HMC proliferation at lower concentrations, whereas it suppressed cell proliferation at higher concentrations. In parallel to the modulation of cell growth, gp 120 at low concentrations resulted in an increase in the expression of c-Myc, Max, and 14\u20133-3\u03b5 proteins and phosphorylation of ATP-dependent tyrosine kinases (Akt) at Ser<jats:sup>473<\/jats:sup>. However, the expression of these proteins decreased with increasing concentrations of gp 120. Furthermore, gp 120 also exhibited a dose-dependent inhibition of Akt phosphorylation at Ser-473 without any significant alteration of Akt expression. Little or no effects of gp 120 were observed on the expression of extracellular signal-regulated kinase (ERK), phospho-ERK, Bcl-2, and Bax proteins. At a higher concentration, gp 120 not only promoted HMC apoptosis but also enhanced expression of Fas and FasL. These results suggest that HIV-1 gp 120 induces alterations in conflicting survival signaling pathways that contribute to the potential dual effects of gp 120 in promoting or inhibiting HMC proliferation.<\/jats:p>","DOI":"10.1152\/ajprenal.2001.280.2.f333","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T13:20:15Z","timestamp":1514035215000},"page":"F333-F342","source":"Crossref","is-referenced-by-count":16,"title":["Role of 14\u20133-3\u03b5, c-Myc\/Max, and Akt phosphorylation in HIV-1 gp 120-induced mesangial cell proliferation"],"prefix":"10.1152","volume":"280","author":[{"given":"Aditi A.","family":"Kapasi","sequence":"first","affiliation":[{"name":"Departments of Medicine and"}]},{"given":"Saijun","family":"Fan","sequence":"additional","affiliation":[{"name":"Radiation Oncology, Long Island Jewish Medical Center, The Long Island Campus for Albert Einstein College of Medicine, New Hyde Park, New York 11040"}]},{"given":"Pravin C.","family":"Singhal","sequence":"additional","affiliation":[{"name":"Departments of Medicine and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/S0968-0004(00)88971-9"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.46.27489"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(93)90663-B"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/359423a0"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/0959-437X(94)90098-1"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(89)90922-7"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1093\/molehr\/4.12.1099"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.90.7.2739"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1126\/science.2006410"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1021\/bi990935w"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1021\/bi00215a038"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(91)90098-J"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1990.151"},{"key":"B15","first-page":"3211","volume":"8","author":"Bousset K","year":"1993","journal-title":"Oncogene"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1038\/376599a0"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1126\/science.7903479"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.iy.09.040191.003245"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1126\/science.7510905"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.33.19364"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1994.2210"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1172\/JCI3480"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(94)90133-3"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1016\/S0065-230X(08)60994-X"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1016\/0042-6822(91)90759-5"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/S0959-437X(05)80339-9"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(95)90534-0"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)81883-8"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1992.146"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.90.8.3216"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1016\/0167-5699(90)90162-3"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.89.6.2365"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(95)90403-4"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1038\/373123a0"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(95)90405-0"},{"key":"B36","first-page":"495A","volume":"10","author":"Kapasi AA","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1006\/mcbr.1999.0122"},{"key":"B38","first-page":"592A","volume":"10","author":"Kapasi AA","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B39","first-page":"459A","volume":"9","author":"Kapasi AA","year":"1998","journal-title":"J Am Soc Nephrol"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM198903163201118"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1101\/gad.11.6.701"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1993.189"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.89.5.1577"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1038\/359426a0"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1038\/323725a0"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.24.14591"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1097-4644(19990401)73:1<31::AID-JCB4>3.0.CO;2-X"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(86)90590-8"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1126\/science.8052857"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.bi.61.070192.004113"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(95)90401-8"},{"key":"B52","first-page":"814","volume":"143","author":"Mattana J","year":"1993","journal-title":"Am J Pathol"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1126\/science.7939645"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.6.F1193"},{"key":"B55","first-page":"461","volume":"13","author":"Packham G","year":"1996","journal-title":"Oncogene"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1002\/j.1460-2075.1991.tb08021.x"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1016\/0167-5699(90)90100-N"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117260"},{"key":"B59","first-page":"7","volume":"6","author":"Posner MR","year":"1993","journal-title":"J Acquired Immune Defic Syndr"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(91)90457-A"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM198403153101101"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1002\/j.1460-2075.1995.tb07046.x"},{"key":"B63","first-page":"25","volume":"147","author":"Singhal PC","year":"1995","journal-title":"Am J Pathol"},{"key":"B64","first-page":"243","volume":"46","author":"Singhal PC","year":"1998","journal-title":"J Invest Med"},{"key":"B65","doi-asserted-by":"crossref","first-page":"1886","DOI":"10.4049\/jimmunol.160.4.1886","volume":"160","author":"Singhal PC","year":"1998","journal-title":"J Immunol"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1159\/000190193"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1038\/322470a0"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.1038\/373117a0"},{"key":"B69","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.28.17416"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.2001.280.2.F333","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,8,30]],"date-time":"2023-08-30T05:38:10Z","timestamp":1693373890000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.2001.280.2.F333"}},"issued":{"date-parts":[[2001,2,1]]},"references-count":68,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2001,2,1]]}},"alternative-id":["10.1152\/ajprenal.2001.280.2.F333"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.2001.280.2.f333","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2001,2,1]]}},{"indexed":{"date-parts":[[2026,3,17]],"date-time":"2026-03-17T02:13:58Z","timestamp":1773713638193,"version":"3.50.1"},"reference-count":56,"publisher":"American Physiological Society","issue":"6","funder":[{"DOI":"10.13039\/100000968","name":"American Heart Association (AHA)","doi-asserted-by":"publisher","award":["Grant-In-Aid"],"award-info":[{"award-number":["Grant-In-Aid"]}],"id":[{"id":"10.13039\/100000968","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"HHS | NIH | National Heart, Lung, and Blood Institute (NHBLI)","doi-asserted-by":"publisher","award":["HL-071834"],"award-info":[{"award-number":["HL-071834"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"HHS | NIH | National Heart, Lung, and Blood Institute (NHBLI)","doi-asserted-by":"publisher","award":["HL-011835"],"award-info":[{"award-number":["HL-011835"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2018,12,1]]},"abstract":"<jats:p> Myogenic contraction of renal arterioles is an important regulatory mechanism for renal blood flow autoregulation. We have previously demonstrated that integrin-mediated mechanical force increases the occurrence of Ca<jats:sup>2+<\/jats:sup> sparks in freshly isolated renal vascular smooth muscle cells (VSMCs). To further test whether the generation of Ca<jats:sup>2+<\/jats:sup> sparks is a downstream signal of mechanotransduction in pressure-induced myogenic constriction, the relationship between Ca<jats:sup>2+<\/jats:sup> sparks and transmural perfusion pressure was investigated in intact VSMCs of pressurized rat afferent arterioles. Spontaneous Ca<jats:sup>2+<\/jats:sup> sparks were found in VSMCs when afferent arterioles were perfused at 80 mmHg. The spark frequency was significantly increased when perfusion pressure was increased to 120 mmHg. A similar increase of spark frequency was also observed in arterioles stimulated with \u03b2<jats:sub>1<\/jats:sub>-integrin-activating antibody. Moreover, spark frequency was significantly higher in arterioles of spontaneous hypertensive rats at 80 and 120 mmHg. Spontaneous membrane current recorded using whole cell perforated patch in renal VSMCs showed predominant activity of spontaneous transient inward currents instead of spontaneous transient outward currents when holding potential was set close to physiological resting membrane potential. Real-time PCR and immunohistochemistry confirmed the expression of Ca<jats:sup>2+<\/jats:sup>-activated Cl<jats:sup>\u2212<\/jats:sup> channel (Cl<jats:sub>Ca<\/jats:sub>) TMEM16A in renal VSMCs. Inhibition of TMEM16A with T16Ainh-A01 impaired the pressure-induced myogenic contraction in perfused afferent arterioles. Our study, for the first time to our knowledge, detected Ca<jats:sup>2+<\/jats:sup> sparks in VSMCs of intact afferent arterioles, and their frequencies were positively modulated by the perfusion pressure. Our results suggest that Ca<jats:sup>2+<\/jats:sup> sparks may couple to Cl<jats:sub>Ca<\/jats:sub> channels and trigger pressure-induced myogenic constriction via membrane depolarization. <\/jats:p>","DOI":"10.1152\/ajprenal.00239.2018","type":"journal-article","created":{"date-parts":[[2018,8,8]],"date-time":"2018-08-08T13:29:42Z","timestamp":1533734982000},"page":"F1592-F1600","source":"Crossref","is-referenced-by-count":15,"title":["Intraluminal pressure triggers myogenic response via activation of calcium spark and calcium-activated chloride channel in rat renal afferent arteriole"],"prefix":"10.1152","volume":"315","author":[{"given":"Kay-Pong","family":"Yip","sequence":"first","affiliation":[{"name":"Department of Molecular Pharmacology and Physiology, University of South Florida, Tampa, Florida"}]},{"given":"Lavanya","family":"Balasubramanian","sequence":"additional","affiliation":[{"name":"Department of Molecular Pharmacology and Physiology, University of South Florida, Tampa, Florida"}]},{"given":"Chen","family":"Kan","sequence":"additional","affiliation":[{"name":"Department of Industrial, Manufacturing, and System Engineering, University of Texas at Arlington, Arlington, Texas"}]},{"given":"Lei","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Molecular Pharmacology and Physiology, University of South Florida, Tampa, Florida"}]},{"given":"Ruisheng","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Molecular Pharmacology and Physiology, University of South Florida, Tampa, Florida"}]},{"given":"Luisa","family":"Ribeiro-Silva","sequence":"additional","affiliation":[{"name":"Department of Molecular Pharmacology and Physiology, University of South Florida, Tampa, Florida"}]},{"given":"James S. K.","family":"Sham","sequence":"additional","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00025.2007"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00234.2012"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00032.2011"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.ph.49.030187.001343"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1126\/science.1163518"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.258.1.F94"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.2001.280.3.C593"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00030.2007"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/j.bcp.2015.08.088"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1999.79.2.387"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/physiol.00034.2007"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000147311.54833.03"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.4.F583"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.270.1.F69"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.71.4.745"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.266.2.F325"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M600433200"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.253.4.F778"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.19.2.153"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1172\/JCI70025"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1097\/HJH.0000000000000856"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1994.74.3.637"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.2001.281.2.C439"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.272.3.F389"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.270.5.F718"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00177.2006"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M112.423053"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1109\/JBHI.2014.2312293"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.201511380"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1139\/y05-040"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00337.2006"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00035.2007"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00540.2004"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.79.2.295"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00923.2003"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1991.261.3.H950"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.79.4.821"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1007\/BF00374818"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00586.2006"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1152\/ajplung.00468.2001"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1109\/10.216413"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2012.232520"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M606765200"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1016\/j.yjmcc.2015.02.020"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.94.26.14918"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1161\/hh0302.105662"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00553.2006"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M102436200"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1152\/ajplung.00515.2005"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1038\/nature07313"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.261.3.F400"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.264.3.F427"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.273.5.F768"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.5.F1004"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1111\/j.1582-4934.2006.tb00408.x"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1152\/ajplung.00067.2003"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00239.2018","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,23]],"date-time":"2019-09-23T06:41:45Z","timestamp":1569220905000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00239.2018"}},"issued":{"date-parts":[[2018,12,1]]},"references-count":56,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2018,12,1]]}},"alternative-id":["10.1152\/ajprenal.00239.2018"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00239.2018","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2018,12,1]]}},{"indexed":{"date-parts":[[2026,3,17]],"date-time":"2026-03-17T14:27:33Z","timestamp":1773757653930,"version":"3.50.1"},"reference-count":38,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2000,1,1]]},"abstract":"<jats:p>In this study, we have shown that intravenously administered antisense oligodeoxynucleotide (ODN) was demonstrated to be taken up by tubular epithelium, after which it blocked mRNA expression of target genes in normal and nephritic rats. Therefore, we injected osteopontin (OPN) antisense ODN to Goodpasture syndrome (GPS) rats every second day between days 27 and 35, the time when renal OPN expression increased and interstitial monocyte infiltration was aggravated. In parallel to blockade of tubular OPN expression, this treatment significantly attenuated monocyte infiltration and preserved renal plasma flow in GPS rats at day 37, compared with sense ODN-treated and untreated GPS rats. No significant changes were observed in OPN mRNA level by RT-PCR and histopathology of the glomeruli after ODN treatment, which was compatible with an absence of differences in the urinary protein excretion rate. In conclusion, OPN expressed by tubular epithelium played a pivotal role in mediating peritubular monocyte infiltration consequent to glomerular disease.<\/jats:p>","DOI":"10.1152\/ajprenal.2000.278.1.f110","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T12:05:07Z","timestamp":1514030707000},"page":"F110-F121","source":"Crossref","is-referenced-by-count":31,"title":["Osteopontin expressed by renal tubular epithelium mediates interstitial monocyte infiltration in rats"],"prefix":"10.1152","volume":"278","author":[{"given":"Hirokazu","family":"Okada","sequence":"first","affiliation":[{"name":"Departments of Nephrology and"}]},{"given":"Kenshi","family":"Moriwaki","sequence":"additional","affiliation":[{"name":"Departments of Nephrology and"}]},{"given":"Raghuram","family":"Kalluri","sequence":"additional","affiliation":[{"name":"Nephrology Division, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215"}]},{"given":"Tsuneo","family":"Takenaka","sequence":"additional","affiliation":[{"name":"Departments of Nephrology and"}]},{"given":"Hiroe","family":"Imai","sequence":"additional","affiliation":[{"name":"Departments of Nephrology and"}]},{"given":"Shinichi","family":"Ban","sequence":"additional","affiliation":[{"name":"Pathology, Saitama Medical College, Saitama 350-04, Japan; and"}]},{"given":"Motohide","family":"Takahama","sequence":"additional","affiliation":[{"name":"Pathology, Saitama Medical College, Saitama 350-04, Japan; and"}]},{"given":"Hiromichi","family":"Suzuki","sequence":"additional","affiliation":[{"name":"Departments of Nephrology and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1159\/000167514"},{"key":"B2","doi-asserted-by":"crossref","first-page":"1257","DOI":"10.1681\/ASN.V461257","volume":"4","author":"Braam B.","year":"1993","journal-title":"J. Am. Soc. Nephrol."},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.3.10.1169"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.1995.tb44615.x"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1096\/fasebj.7.15.8262332"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00137.x"},{"key":"B7","first-page":"205","volume":"23","author":"Eddy A.","year":"1994","journal-title":"J. Am. Soc. Nephrol."},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.421"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.218"},{"key":"B10","doi-asserted-by":"crossref","first-page":"1881","DOI":"10.1681\/ASN.V9101881","volume":"9","author":"Escudero E.","year":"1998","journal-title":"J. Am. Soc. Nephrol."},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.67"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119764"},{"key":"B13","doi-asserted-by":"crossref","first-page":"15180","DOI":"10.1016\/S0021-9258(18)82453-X","volume":"268","author":"Kohri K.","year":"1993","journal-title":"J. Biol. Chem."},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00748.x"},{"key":"B15","first-page":"355","volume":"69","author":"Lopez C.","year":"1993","journal-title":"Lab. Invest."},{"key":"B16","doi-asserted-by":"crossref","first-page":"1043","DOI":"10.1681\/ASN.V871043","volume":"8","author":"Madsen K.","year":"1997","journal-title":"J. Am. Soc. Nephrol."},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.243"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1997.6399"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118681"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1159\/000425088"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.83.23.8819"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(12)80973-5"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1210\/endo.137.5.8612558"},{"key":"B24","first-page":"915","volume":"144","author":"Pichler R.","year":"1994","journal-title":"Am. J. Pathol."},{"key":"B25","first-page":"317","volume":"21","author":"Pichler R.","year":"1995","journal-title":"Miner. Electrolyte Metab."},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.205"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(68)90589-8"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1053\/ajkd.1998.v31.pm9631856"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1084\/jem.171.6.1931"},{"key":"B30","doi-asserted-by":"crossref","first-page":"4738","DOI":"10.1182\/blood.V91.12.4738","volume":"91","author":"Spiller D.","year":"1998","journal-title":"Blood"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1016\/S0046-8177(70)80060-0"},{"key":"B32","first-page":"S-106","volume":"45","author":"Strutz F.","year":"1994","journal-title":"Kidney Int."},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.130.2.393"},{"key":"B34","doi-asserted-by":"crossref","first-page":"1046","DOI":"10.1681\/ASN.V441046","volume":"4","author":"Takenaka T.","year":"1993","journal-title":"J. Am. Soc. Nephrol."},{"key":"B35","first-page":"456","volume":"71","author":"Van Goor H.","year":"1994","journal-title":"Lab. Invest."},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.312"},{"key":"B37","first-page":"50","volume":"110","author":"Yu X.","year":"1998","journal-title":"Proc. Assoc. Am. Physicians"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1097-4652(199701)170:1<88::AID-JCP10>3.0.CO;2-K"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.2000.278.1.F110","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:38:23Z","timestamp":1660189103000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.2000.278.1.F110"}},"issued":{"date-parts":[[2000,1,1]]},"references-count":38,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2000,1,1]]}},"alternative-id":["10.1152\/ajprenal.2000.278.1.F110"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.2000.278.1.f110","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2000,1,1]]}},{"indexed":{"date-parts":[[2026,3,19]],"date-time":"2026-03-19T12:26:23Z","timestamp":1773923183553,"version":"3.50.1"},"reference-count":43,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2012,8,15]]},"abstract":"<jats:p> Human SLC2A9 (GLUT9) is a novel high-capacity urate transporter belonging to the facilitated glucose transporter family. In the present study, heterologous expression in Xenopus oocytes has allowed us to undertake an in-depth radiotracer flux and electrophysiological study of urate transport mediated by both isoforms of SLC2A9 (a and b). Addition of urate to SLC2A9-producing oocytes generated outward currents, indicating electrogenic transport. Urate transport by SLC2A9 was voltage dependent and independent of the Na<jats:sup>+<\/jats:sup> transmembrane gradient. Urate-induced outward currents were affected by the extracellular concentration of Cl<jats:sup>\u2212<\/jats:sup>, but there was no evidence for exchange of the two anions. [<jats:sup>14<\/jats:sup>C]urate flux studies under non-voltage-clamped conditions demonstrated symmetry of influx and efflux, suggesting that SLC2A9 functions in urate efflux driven primarily by the electrochemical gradient of the cell. Urate uptake in the presence of intracellular hexoses showed marked differences between the two isoforms, suggesting functional differences between the two splice variants. Finally, the permeant selectivity of SLC2A9 was examined by testing the ability to transport a panel of radiolabeled purine and pyrimidine nucleobases. SLC2A9 mediated the uptake of adenine in addition to urate, but did not function as a generalized nucleobase transporter. The differential expression pattern of the two isoforms of SLC2A9 in the human kidney's proximal convoluted tubule and its electrogenic transport of urate suggest that these transporters play key roles in the regulation of plasma urate levels and are therefore potentially important participants in hyperuricemia and hypouricemia. <\/jats:p>","DOI":"10.1152\/ajprenal.00134.2012","type":"journal-article","created":{"date-parts":[[2012,5,31]],"date-time":"2012-05-31T04:47:21Z","timestamp":1338439641000},"page":"F527-F539","source":"Crossref","is-referenced-by-count":62,"title":["Human SLC2A9a and SLC2A9b isoforms mediate electrogenic transport of urate with different characteristics in the presence of hexoses"],"prefix":"10.1152","volume":"303","author":[{"given":"Kate","family":"Witkowska","sequence":"first","affiliation":[{"name":"Membrane Protein Disease Research Group, Department of Physiology, University of Alberta, Edmonton, Alberta, Canada"}]},{"given":"Kyla M.","family":"Smith","sequence":"additional","affiliation":[{"name":"Membrane Protein Disease Research Group, Department of Physiology, University of Alberta, Edmonton, Alberta, Canada"}]},{"given":"Sylvia Y. M.","family":"Yao","sequence":"additional","affiliation":[{"name":"Membrane Protein Disease Research Group, Department of Physiology, University of Alberta, Edmonton, Alberta, Canada"}]},{"given":"Amy M. L.","family":"Ng","sequence":"additional","affiliation":[{"name":"Membrane Protein Disease Research Group, Department of Physiology, University of Alberta, Edmonton, Alberta, Canada"}]},{"given":"Debbie","family":"O'Neill","sequence":"additional","affiliation":[{"name":"Membrane Protein Disease Research Group, Department of Physiology, University of Alberta, Edmonton, Alberta, Canada"}]},{"given":"Edward","family":"Karpinski","sequence":"additional","affiliation":[{"name":"Membrane Protein Disease Research Group, Department of Physiology, University of Alberta, Edmonton, Alberta, Canada"}]},{"given":"James D.","family":"Young","sequence":"additional","affiliation":[{"name":"Membrane Protein Disease Research Group, Department of Physiology, University of Alberta, Edmonton, Alberta, Canada"}]},{"given":"Christopher I.","family":"Cheeseman","sequence":"additional","affiliation":[{"name":"Membrane Protein Disease Research Group, Department of Physiology, University of Alberta, Edmonton, Alberta, Canada"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1097\/BOR.0b013e328032781a"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.C800156200"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M312226200"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pgen.1000246"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00139.2009"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1006\/jmbi.1999.3310"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2362.2001.00812.x"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.2337\/dc08-0349"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pmed.0050197"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(08)61343-4"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.00296.2009"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1038\/ng.107"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1080\/15257770802136024"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1038\/nature742"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1007\/s11906-006-0005-z"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/physiol.00039.2004"},{"key":"B17","first-page":"1882","volume":"34","author":"Hjortnaes J","year":"2007","journal-title":"J Rheumatol"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1007\/s00360-008-0291-7"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1254\/jphs.10228SC"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M303210200"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pgen.1000504"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.2133\/dmpk.24.37"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfn349"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.1.617"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1016\/0896-6273(92)90239-A"},{"key":"B26","first-page":"132","volume":"147","author":"Marangella M","year":"2005","journal-title":"Contrib Nephrol"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/j.ajhg.2008.11.001"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1097\/MOG.0b013e3282f3f4c4"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/j.amjhyper.2006.02.014"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1093\/rheumatology\/kem159"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0904411106"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1007\/s10654-007-9132-3"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1080\/15257770802138558"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1016\/S0005-2736(98)00213-2"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0001948"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00133.2004"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1038\/ng.106"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1016\/j.ajhg.2007.11.001"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1007\/BF01869212"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2736(91)90355-C"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0901249106"},{"key":"B42","first-page":"47","volume-title":"Membrane Transport: A Practical Approach","author":"Yao SYM","year":"2000"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.2174\/138920007782798171"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00134.2012","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T00:29:33Z","timestamp":1567988973000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00134.2012"}},"issued":{"date-parts":[[2012,8,15]]},"references-count":43,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2012,8,15]]}},"alternative-id":["10.1152\/ajprenal.00134.2012"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00134.2012","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2012,8,15]]}},{"indexed":{"date-parts":[[2026,3,18]],"date-time":"2026-03-18T23:28:27Z","timestamp":1773876507976,"version":"3.50.1"},"reference-count":58,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,3,1]]},"abstract":"<jats:p>Increased angiotensin II (ANG II) or adenosine can potentiate each other in the regulation of renal hemodynamics and tubular function. Diabetes is characterized by hyperfiltration, yet the roles of ANG II and adenosine receptors for controlling baseline renal blood flow (RBF) or tubular Na<jats:sup>+<\/jats:sup>handling in diabetes is presently unknown. Accordingly, the changes in their functions were investigated in control and 2-wk streptozotocin-diabetic rats after intrarenal infusion of the ANG II AT<jats:sub>1<\/jats:sub>receptor antagonist candesartan, the adenosine A<jats:sub>1<\/jats:sub>receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), or their combination. Compared with controls, the baseline blood pressure, RBF, and renal vascular resistance (RVR) were similar in diabetics, whereas the glomerular filtration rate (GFR) and filtration fraction (FF) were increased. Candesartan, DPCPX, or the combination increased RBF and decreased RVR similarly in all groups. In controls, the GFR was increased by DPCPX, but in diabetics, it was decreased by candesartan. The FF was decreased by candesartan and DPCPX, independently. DPCPX caused the most pronounced increase in fractional Na<jats:sup>+<\/jats:sup>excretion in both controls and diabetics, whereas candesartan or the combination only affected fractional Li<jats:sup>+<\/jats:sup>excretion in diabetics. These results suggest that RBF, via a unifying mechanism, and tubular function are under strict tonic control of both ANG II and adenosine in both control and diabetic kidneys. Furthermore, increased vascular AT<jats:sub>1<\/jats:sub>receptor activity is a contribution to diabetes-induced hyperfiltration independent of any effect of adenosine A<jats:sub>1<\/jats:sub>receptors.<\/jats:p>","DOI":"10.1152\/ajprenal.00285.2012","type":"journal-article","created":{"date-parts":[[2013,1,3]],"date-time":"2013-01-03T07:22:31Z","timestamp":1357197751000},"page":"F614-F622","source":"Crossref","is-referenced-by-count":27,"title":["Angiotensin II contributes to glomerular hyperfiltration in diabetic rats independently of adenosine type I receptors"],"prefix":"10.1152","volume":"304","author":[{"given":"Daniela","family":"Patinha","sequence":"first","affiliation":[{"name":"Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden;"},{"name":"Departamento de Farmacologia e Terap\u00eautica, Faculdade de Medicina; Neurofarmacologia, Instituto de Biologia Molecular e Celular, Universidade do Porto, Porto, Portugal;"}]},{"given":"Angelica","family":"Fasching","sequence":"additional","affiliation":[{"name":"Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden;"}]},{"given":"Dora","family":"Pinho","sequence":"additional","affiliation":[{"name":"Departamento de Farmacologia e Terap\u00eautica, Faculdade de Medicina; Neurofarmacologia, Instituto de Biologia Molecular e Celular, Universidade do Porto, Porto, Portugal;"},{"name":"Faculdade de Ci\u00eancias da Nutri\u00e7\u00e3o e Alimenta\u00e7\u00e3o, Universidade do Porto, Porto, Portugal;"}]},{"given":"Ant\u00f3nio","family":"Albino-Teixeira","sequence":"additional","affiliation":[{"name":"Departamento de Farmacologia e Terap\u00eautica, Faculdade de Medicina; Neurofarmacologia, Instituto de Biologia Molecular e Celular, Universidade do Porto, Porto, Portugal;"}]},{"given":"Manuela","family":"Morato","sequence":"additional","affiliation":[{"name":"Departamento de Farmacologia e Terap\u00eautica, Faculdade de Medicina; Neurofarmacologia, Instituto de Biologia Molecular e Celular, Universidade do Porto, Porto, Portugal;"},{"name":"Laborat\u00f3rio de Farmacologia, Departamento de Ci\u00eancias do Medicamento, Faculdade de Farm\u00e1cia, REQUIMTE, Universidade do Porto, Porto, Portugal; and"}]},{"given":"Fredrik","family":"Palm","sequence":"additional","affiliation":[{"name":"Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden;"},{"name":"Department of Medical and Health Sciences, Link\u00f6ping University, Link\u00f6ping, Sweden"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1159\/000139528"},{"key":"B2","first-page":"S196","volume":"9","author":"Albino-Teixeira A","year":"1991","journal-title":"J Hypertens Suppl"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.2337\/diacare.26.2007.S33"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1097\/01.hjh.0000133718.86451.6a"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.265.5.F651"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.06822.x"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0b013e32833240fc"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1986.251.4.F610"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1993.264.1.R129"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00511.2006"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00218.2005"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1985.248.3.F340"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1990.95"},{"key":"B14","doi-asserted-by":"crossref","first-page":"1578","DOI":"10.1681\/ASN.V2111578","volume":"2","author":"Hayashi K","year":"1992","journal-title":"J Am Soc Nephrol"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.pa.31.040191.000245"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.253.1.F188"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.1991.tb12550.x"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1124\/pr.59.3.3"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.2337\/diab.43.5.629"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000249530.85542.d4"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.2009.01956.x"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5001650"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.90731.2008"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1007\/s00125-009-1268-0"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-2999(02)02587-6"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.267.5.F783"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.3.F406"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00228.2009"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1096\/fasebj.2.8.3282959"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00123.x"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.2337\/db06-1772"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1007\/BF00501815"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.43.3.465"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.54.11.3282"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00229.2009"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00357.2007"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)62977-X"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.252.4.F678"},{"key":"B39","doi-asserted-by":"crossref","first-page":"3","DOI":"10.1111\/j.1748-1716.2010.02147.x","volume":"200","author":"Persson P","year":"2010","journal-title":"Acta Physiol (Oxf)"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.3.F340"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.4.F529"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00582.2011"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118745"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1983.245.2.F181"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.2007.01705.x"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00072.2002"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.263.6.F1128"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-2999(02)01488-7"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1979.237.6.F463"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1007\/BF00587025"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-008-0581-7"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00809.2010"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00031.2005"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1007\/978-3-540-89615-9_15"},{"key":"B55","doi-asserted-by":"crossref","first-page":"2569","DOI":"10.1681\/ASN.V10122569","volume":"10","author":"Vallon V","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.266.2.F227"},{"key":"B57","doi-asserted-by":"crossref","first-page":"714","DOI":"10.1681\/ASN.V104714","volume":"10","author":"Wilcox CS","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1999.276.3.R790"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00285.2012","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,5,4]],"date-time":"2024-05-04T06:39:32Z","timestamp":1714804772000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00285.2012"}},"issued":{"date-parts":[[2013,3,1]]},"references-count":58,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2013,3,1]]}},"alternative-id":["10.1152\/ajprenal.00285.2012"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00285.2012","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2013,3,1]]}},{"indexed":{"date-parts":[[2026,3,21]],"date-time":"2026-03-21T20:45:02Z","timestamp":1774125902562,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1979,4,1]]},"abstract":"<jats:p> While the existence of an osmotic control for vasopressin (AVP) release has been long recognized, development of a sensitive immunoassay has allowed for better understanding of factors affecting the threshold and sensitivity of AVP release. Individual variation, genetic, environmental, and species differences, and the nature of the solute providing the osmotic stimuli can significantly affect the release of the hormone by altering the threshold and\/or the sensitivity of the osmoreceptor. In addition to the hypothalamic osmoreceptor, AVP secretion is also controlled by an anatomically separate pathway which is responsive to nonosmotic stimuli. It appears that both low-pressure (left atrial) and high-pressure (carotid and aortic) receptors via the parasympathetic pathways provide the major nonosmotic pathway for vasopressin release. Such pathways are activated in response to acute systemic hemodynamic changes, stress, and hypoxia. The precise interaction between osmotic and nonosmotic AVP release remains to be clarified. A model of osmotic and nonosmotic interactions, based on available electrophysiologic studies, is presented and its clinical implications are discussed. <\/jats:p>","DOI":"10.1152\/ajprenal.1979.236.4.f321","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T20:33:38Z","timestamp":1513974818000},"page":"F321-F332","source":"Crossref","is-referenced-by-count":47,"title":["Osmotic and nonosmotic control of vasopressin release"],"prefix":"10.1152","volume":"236","author":[{"given":"R. W.","family":"Schrier","sequence":"first","affiliation":[]},{"given":"T.","family":"Berl","sequence":"additional","affiliation":[]},{"given":"R. J.","family":"Anderson","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1979.236.4.F321","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:00:37Z","timestamp":1567969237000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1979.236.4.F321"}},"issued":{"date-parts":[[1979,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1979,4,1]]}},"alternative-id":["10.1152\/ajprenal.1979.236.4.F321"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1979.236.4.f321","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1979,4,1]]}},{"indexed":{"date-parts":[[2026,3,10]],"date-time":"2026-03-10T15:00:32Z","timestamp":1773154832822,"version":"3.50.1"},"reference-count":48,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2011,1]]},"abstract":"<jats:p>Aging is associated with an increase in oxidative stress and blood pressure (BP). Renal dopamine D1 (D1R) and angiotensin II AT1 (AT1R) receptors maintain sodium homeostasis and BP. We hypothesized that age-associated increase in oxidative stress causes altered D1R and AT1R functions and high BP in aging. To test this, adult (3 mo) and old (21 mo) Fischer 344 \u00d7 Brown Norway F1 rats were supplemented without\/with antioxidant tempol followed by determining oxidative stress markers (urinary antioxidant capacity, proximal tubular NADPH- gp<jats:sup>91phox<\/jats:sup>, and plasma 8-isoprostane), D1R and AT1R functions, and BP. The D1R and AT1R functions were determined by measuring diuretic and natriuretic responses to D1R agonist (SKF-38393; 1 \u03bcg\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7min<jats:sup>\u22121<\/jats:sup>iv) and AT1R antagonist (candesartan; 10 \u03bcg\/kg iv), respectively. We found that the total urinary antioxidant capacity was lower in old rats, which increased with tempol treatment. In addition, tempol decreased the elevated NADPH- gp<jats:sup>91phox<\/jats:sup>and 8-isoprostane levels in old rats. Systolic, diastolic, and mean arterial BPs were higher in old rats and were reduced by tempol. Although SKF-38393 produced diuresis in both adult and old rats, urinary sodium excretion (UNaV) increased only in adult rats. While candesartan increased diuresis and UNaV in adult and old rats, the magnitude of response was greater in old rats. Tempol treatment in old rats reduced candesartan-induced increase in diuresis and UNaV. Our results demonstrate that diminished renal D1R and exaggerated AT1R functions are associated with high BP in old rats. Furthermore, oxidative stress may cause altered renal D1R and AT1R functions and high BP in old rats.<\/jats:p>","DOI":"10.1152\/ajprenal.00465.2010","type":"journal-article","created":{"date-parts":[[2010,10,14]],"date-time":"2010-10-14T07:04:11Z","timestamp":1287039851000},"page":"F133-F138","source":"Crossref","is-referenced-by-count":34,"title":["Oxidative stress alters renal D1 and AT1 receptor functions and increases blood pressure in old rats"],"prefix":"10.1152","volume":"300","author":[{"given":"Gaurav","family":"Chugh","sequence":"first","affiliation":[{"name":"Heart and Kidney Institute, College of Pharmacy, University of Houston, Houston, Texas"}]},{"given":"Mustafa F.","family":"Lokhandwala","sequence":"additional","affiliation":[{"name":"Heart and Kidney Institute, College of Pharmacy, University of Houston, Houston, Texas"}]},{"given":"Mohammad","family":"Asghar","sequence":"additional","affiliation":[{"name":"Heart and Kidney Institute, College of Pharmacy, University of Houston, Houston, Texas"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118670"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.90.17.7915"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1179\/135100007X200254"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/j.freeradbiomed.2005.08.018"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00367.2008"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00272.2007"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00361.2001"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1177\/153537020422900308"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90308.2008"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00217.x"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1161\/hy0901.096422"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/0002-9343(84)90952-5"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.21.3.364"},{"key":"B14","first-page":"615","volume":"14","author":"Chen CJ","year":"1992","journal-title":"Clin Exp Hypertens A"},{"key":"B15","doi-asserted-by":"crossref","first-page":"1016.8","DOI":"10.1096\/fasebj.23.1_supplement.1016.8","volume":"23","author":"Chugh G","year":"2009","journal-title":"FASEB J"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00088.2005"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-199917121-00033"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1081\/CEH-200031904"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1136\/bmj.312.7041.1249"},{"key":"B20","doi-asserted-by":"crossref","first-page":"1106","DOI":"10.1681\/ASN.V781106","volume":"7","author":"Epstein M","year":"1996","journal-title":"J Am Soc Nephrol"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00111.2006"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.15.6.560"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0b013e32831a9e0b"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1016\/S0895-7061(97)00075-7"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1253\/circj.CJ-10-0153"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/0002-9343(86)90291-3"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1177\/153537020322800202"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1007\/s11906-000-0079-y"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/S0163-7258(98)00027-8"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1080\/08037050310001057"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1124\/pr.59.3.3"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1016\/S0895-7061(97)00071-X"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1291\/hypres.21.67"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1016\/0140-6736(90)90878-9"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00287.2006"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000177474.06749.98"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1797.2008.00924.x"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1023\/A:1019552602793"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1254\/jphs.08R02CP"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1080\/10641960500386650"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1093\/ije\/18.3_Supplement_1.S20"},{"key":"B42","first-page":"155","volume":"41","author":"Uemura K","year":"1988","journal-title":"World Health Stat Q"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1001\/jama.287.8.1003"},{"key":"B44","first-page":"1","volume":"2","author":"Vaziri ND","year":"2008","journal-title":"Iran J Kidney Dis"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(94)91285-8"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1124\/pr.108.000240"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1016\/0002-9149(88)91098-3"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.2174\/1568016052773289"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00465.2010","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,11,11]],"date-time":"2021-11-11T20:50:03Z","timestamp":1636663803000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00465.2010"}},"issued":{"date-parts":[[2011,1]]},"references-count":48,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2011,1]]}},"alternative-id":["10.1152\/ajprenal.00465.2010"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00465.2010","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2011,1]]}},{"indexed":{"date-parts":[[2026,3,10]],"date-time":"2026-03-10T14:18:13Z","timestamp":1773152293174,"version":"3.50.1"},"reference-count":31,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2003,4,1]]},"abstract":"<jats:p>The purpose of the present study was to examine whether there is axial heterogeneity in the basolateral plasma membrane (BLM) localization of AQP2 and whether altered vasopressin action or medullary tonicity affects the BLM localization of AQP2. Immunocytochemistry and immunoelectron microscopy revealed AQP2 labeling of the BLM in connecting tubule (CNT) cells and inner medullary collecting duct (IMCD) principal cells in normal rats and vasopressin-deficient Brattleboro rats. In contrast there was little basolateral AQP2 labeling in cortical (CCD) and outer medullary collecting duct principal cells. Short-term desamino-Cys<jats:sup>1<\/jats:sup>,<jats:sub>D<\/jats:sub>-Arg<jats:sup>8<\/jats:sup>vasopressin (dDAVP) treatment (2 h) of Brattleboro rats caused no increase in AQP2 labeling of the BLM. In contrast, long-term dDAVP treatment (6 days) of Brattleboro rats caused an increased BLM labeling in CNT, CCD, and IMCD. Treatment of normal rats with V<jats:sub>2<\/jats:sub>-receptor antagonist for 60 min caused retrieval of AQP2 from the apical plasma membrane. Moreover, AQP2 labeling of the BLM was unchanged in CNT and IMCD but increased in CCD. In conclusion, there is an axial heterogeneity in the subcellular localization of AQP2 with prominent AQP2 labeling of the BLM in CNT and IMCD. There was no increase in AQP2 labeling of the BLM in response to short-term dDAVP. Moreover, acute V<jats:sub>2<\/jats:sub>-receptor antagonist treatment did not cause retrieval of AQP2 from the BLM. In contrast, long-term dDAVP treatment caused a major increase in AQP2 expression in the BLM in CCD.<\/jats:p>","DOI":"10.1152\/ajprenal.00234.2002","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:37:40Z","timestamp":1425415060000},"page":"F701-F717","source":"Crossref","is-referenced-by-count":59,"title":["Axial heterogeneity in basolateral AQP2 localization in rat kidney: effect of vasopressin"],"prefix":"10.1152","volume":"284","author":[{"given":"Birgitte M\u00f8nster","family":"Christensen","sequence":"first","affiliation":[{"name":"The Water and Salt Research Center,"},{"name":"Institute of Anatomy, and"}]},{"given":"Weidong","family":"Wang","sequence":"additional","affiliation":[{"name":"The Water and Salt Research Center,"},{"name":"Institute of Anatomy, and"}]},{"given":"J\u00f8rgen","family":"Fr\u00f8ki\u00e6r","sequence":"additional","affiliation":[{"name":"The Water and Salt Research Center,"},{"name":"Institute of Experimental Clinical Research, University of DK-8000 Aarhus, Denmark"}]},{"given":"S\u00f8ren","family":"Nielsen","sequence":"additional","affiliation":[{"name":"The Water and Salt Research Center,"},{"name":"Institute of Anatomy, and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1159\/000420150"},{"key":"B2","first-page":"14A","volume":"11","author":"Bouley R","year":"2000","journal-title":"J Am Soc Nephrol"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.1.F70"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.275.2.F285"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.5.F874"},{"key":"B6","doi-asserted-by":"crossref","first-page":"1493","DOI":"10.1681\/ASN.V8101493","volume":"8","author":"Deen PM","year":"1997","journal-title":"J Am Soc Nephrol"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.91.19.8984"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.5.F663"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.6.F1093"},{"key":"B10","first-page":"E36","volume":"93","author":"Jeon US","year":"2003","journal-title":"Nephron"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.16.7212"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.2.F252"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.080499597"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1986.250.1.F1"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1002\/jemt.1060090206"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.275.5.F796"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1995.269.3.C655"},{"key":"B18","first-page":"326","volume":"6","author":"Matsumura Y","year":"1995","journal-title":"J Am Soc Nephrol"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.2001.281.1.C55"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.4.1013"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.90.24.11663"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00024.2001"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.268.6.F1023"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.2.F370"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1007\/BF00233445"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000035084.94743.7C"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1982.95"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.2.F414"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.2002.6709"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.40.24365"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1995.268.6.C1546"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00234.2002","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,5,1]],"date-time":"2022-05-01T09:37:23Z","timestamp":1651397843000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00234.2002"}},"issued":{"date-parts":[[2003,4,1]]},"references-count":31,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2003,4,1]]}},"alternative-id":["10.1152\/ajprenal.00234.2002"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00234.2002","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2003,4,1]]}},{"indexed":{"date-parts":[[2026,3,10]],"date-time":"2026-03-10T14:43:22Z","timestamp":1773153802400,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1996,9,1]]},"abstract":"<jats:p> The human ATP1AL1 gene encodes a protein expressed in brain, kidney, and skin and that is highly homologous to the recently cloned nongastric isoforms of H-K-adenosinetriphosphatase H-K-ATPase). We have generated polyclonal antibodies against the protein encoded by ATP1AL1 and used them to monitor the protein's expression and distribution in transfection studies. The protein was retained in the endplasmic reticulum when it was transiently expressed alone in COS cells. In COS cells cotransfected with ATP1AL1 plus gastric H-K-ATPase beta-subunit cDNAs (ATP1AL1-gH-K beta), both proteins reached the surface. Stably transfected lines of HEK 293 cells expressing both of these proteins demonstrate a 86Rb+ uptake activity sensitive to both 2-methyl,8-(phenylmeoxy)imidazo(1,2-a)pyridine 3-acetonitrile (SCH-28080) and ouabain (inhibitory constants of approximately 131 and 42 microM, respectively). Outward proton fluxes were measured in the same cells as the spontaneous intracellular pH (pHi) recovery in Cells loaded with a pH-sensitive dye [2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein] and subjected to acid loading through an NH4Cl pulse. The cells expressing both the ATP1AL1-encoded protein and the gastric H-K-ATPase beta-subunit possess a net acid extrusion activity that can be inhibited by 1 mM ouabain. Comparison of the 86Rb+ influx and proton efflux, however, does not support equal H+\/Rb+ exchange mediated by this pump under the conditions of pHi-monitoring experiments. Moreover, whereas the acid extrusion activity mediated by the pump shows a marked pH dependence, the 86Rb+ uptake activity present in the cells expressing the ATP1AL1-gH-K beta complex cannot be stimulated by acute lowering of pHi. These data suggest that the ATP1AL1-encoded protein is the catalytic alpha-subunit of a human K(+)-dependent ATPase. The possible implications of the discrepancy between 86Rb+ uptake and pHi monitoring data are discussed. <\/jats:p>","DOI":"10.1152\/ajprenal.1996.271.3.f539","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T01:31:13Z","timestamp":1513992673000},"page":"F539-F551","source":"Crossref","is-referenced-by-count":17,"title":["Functional expression of the cDNA encoded by the human ATP1AL1 gene"],"prefix":"10.1152","volume":"271","author":[{"given":"A. V.","family":"Grishin","sequence":"first","affiliation":[{"name":"Department of Cellular and Molecular Physiology, Yale UniversitySchool of Medicine, New Haven, Connecticut 06520, USA."}]},{"given":"M. O.","family":"Bevensee","sequence":"additional","affiliation":[{"name":"Department of Cellular and Molecular Physiology, Yale UniversitySchool of Medicine, New Haven, Connecticut 06520, USA."}]},{"given":"N. N.","family":"Modyanov","sequence":"additional","affiliation":[{"name":"Department of Cellular and Molecular Physiology, Yale UniversitySchool of Medicine, New Haven, Connecticut 06520, USA."}]},{"given":"V.","family":"Rajendran","sequence":"additional","affiliation":[{"name":"Department of Cellular and Molecular Physiology, Yale UniversitySchool of Medicine, New Haven, Connecticut 06520, USA."}]},{"given":"W. F.","family":"Boron","sequence":"additional","affiliation":[{"name":"Department of Cellular and Molecular Physiology, Yale UniversitySchool of Medicine, New Haven, Connecticut 06520, USA."}]},{"given":"M. J.","family":"Caplan","sequence":"additional","affiliation":[{"name":"Department of Cellular and Molecular Physiology, Yale UniversitySchool of Medicine, New Haven, Connecticut 06520, USA."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1996.271.3.F539","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:05:50Z","timestamp":1567958750000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1996.271.3.F539"}},"issued":{"date-parts":[[1996,9,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1996,9,1]]}},"alternative-id":["10.1152\/ajprenal.1996.271.3.F539"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1996.271.3.f539","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1996,9,1]]}},{"indexed":{"date-parts":[[2026,3,7]],"date-time":"2026-03-07T15:20:18Z","timestamp":1772896818911,"version":"3.50.1"},"reference-count":32,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2000,11,1]]},"abstract":"<jats:p>We examined the peptide transport activity in renal basolateral membranes. [<jats:sup>14<\/jats:sup>C]glycylsarcosine (Gly-Sar) uptake in rat renal cortical slices was saturable and inhibited by excess dipeptide and aminocephalosporin cefadroxil. When several renal cell lines were screened for the basolateral peptide transport activity, Madin-Darby canine kidney (MDCK) cells were demonstrated to have the greatest transport activity. [<jats:sup>14<\/jats:sup>C]Gly-Sar uptake across the basolateral membranes of MDCK cells was inhibited by di- and tripeptide and decreased with decreases in extracellular pH from 7.4 to 5.0. The Michaelis-Menten constant value of [<jats:sup>14<\/jats:sup>C]Gly-Sar uptake across the basolateral membranes of MDCK cells was 71 \u03bcM. The basolateral peptide transporter in MDCK cells showed several different [<jats:sup>14<\/jats:sup>C]Gly-Sar transport characteristics in growth dependence, pH profile, substrate affinity, and sensitivities to chemical modifiers from those of the apical H<jats:sup>+<\/jats:sup>-peptide cotransporter of MDCK cells. The findings of the present investigation indicated that the peptide transporter was expressed in the renal basolateral membranes. In addition, from the functional characteristics, the renal basolateral peptide transporter was suggested to be distinguishable from known peptide transporters, i.e., H<jats:sup>+<\/jats:sup>-peptide cotransporters (PEPT1 and PEPT2) and the intestinal basolateral peptide transporter.<\/jats:p>","DOI":"10.1152\/ajprenal.2000.279.5.f851","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T13:38:15Z","timestamp":1514036295000},"page":"F851-F857","source":"Crossref","is-referenced-by-count":30,"title":["Functional expression of novel peptide transporter in renal basolateral membranes"],"prefix":"10.1152","volume":"279","author":[{"given":"Tomohiro","family":"Terada","sequence":"first","affiliation":[{"name":"Department of Pharmacy, Kyoto University Hospital, Faculty of Medicine, Kyoto University, Kyoto 606 \u2013 8507, Japan"}]},{"given":"Kyoko","family":"Sawada","sequence":"additional","affiliation":[{"name":"Department of Pharmacy, Kyoto University Hospital, Faculty of Medicine, Kyoto University, Kyoto 606 \u2013 8507, Japan"}]},{"given":"Tatsuya","family":"Ito","sequence":"additional","affiliation":[{"name":"Department of Pharmacy, Kyoto University Hospital, Faculty of Medicine, Kyoto University, Kyoto 606 \u2013 8507, Japan"}]},{"given":"Hideyuki","family":"Saito","sequence":"additional","affiliation":[{"name":"Department of Pharmacy, Kyoto University Hospital, Faculty of Medicine, Kyoto University, Kyoto 606 \u2013 8507, Japan"}]},{"given":"Yukiya","family":"Hashimoto","sequence":"additional","affiliation":[{"name":"Department of Pharmacy, Kyoto University Hospital, Faculty of Medicine, Kyoto University, Kyoto 606 \u2013 8507, Japan"}]},{"given":"Ken-Ichi","family":"Inui","sequence":"additional","affiliation":[{"name":"Department of Pharmacy, Kyoto University Hospital, Faculty of Medicine, Kyoto University, Kyoto 606 \u2013 8507, Japan"}]}],"member":"24","reference":[{"key":"B1","first-page":"F723","volume":"272","author":"Adibi SA.","year":"1997","journal-title":"Am J Physiol Renal Physiol"},{"key":"B2","first-page":"193","volume":"52","author":"Adibi SA","year":"1977","journal-title":"Clin Sci Mol Med"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2736(82)90386-8"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1988.255.1.F177"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.268.3.F391"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.273.1.F1"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/0024-3205(83)90791-9"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1986.251.6.F945"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1042\/bj2950329"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1986.173"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1994.74.4.993"},{"key":"B12","first-page":"674","volume":"73","author":"Heilig C","year":"1995","journal-title":"Lab Invest"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1016\/0006-2952(82)90113-7"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.264.6.F975"},{"key":"B16","doi-asserted-by":"crossref","first-page":"195","DOI":"10.1016\/S0022-3565(25)10961-0","volume":"261","author":"Inui K","year":"1992","journal-title":"J Pharmacol Exp Ther"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1023\/A:1018871029244"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.nu.16.070196.000531"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1042\/bj2290545"},{"key":"B20","doi-asserted-by":"crossref","first-page":"498","DOI":"10.1016\/S0022-3565(25)22409-0","volume":"270","author":"Matsumoto S","year":"1994","journal-title":"J Pharmacol Exp Ther"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.263.1.F109"},{"key":"B22","doi-asserted-by":"crossref","first-page":"643","DOI":"10.1152\/ajplegacy.1976.230.3.643","volume":"230","author":"Nutzenadel W","year":"1976","journal-title":"Am J Physiol"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.1993.265.2.G289"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1992.262.1.C59"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.5.F658"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.10.5582"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.273.5.F706"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.1999.276.6.G1435"},{"key":"B29","first-page":"A82","volume":"10","author":"Thamotharan M","year":"1996","journal-title":"FASEB J"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1990.259.2.C286"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-5793(99)01491-X"},{"key":"B32","doi-asserted-by":"crossref","first-page":"800","DOI":"10.1016\/S0022-3565(24)37859-0","volume":"287","author":"Urakami Y","year":"1998","journal-title":"J Pharmacol Exp Ther"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1998.275.6.C1573"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.2000.279.5.F851","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,6,29]],"date-time":"2025-06-29T04:37:48Z","timestamp":1751171868000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.2000.279.5.F851"}},"issued":{"date-parts":[[2000,11,1]]},"references-count":32,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2000,11,1]]}},"alternative-id":["10.1152\/ajprenal.2000.279.5.F851"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.2000.279.5.f851","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2000,11,1]]}},{"indexed":{"date-parts":[[2026,3,7]],"date-time":"2026-03-07T19:35:42Z","timestamp":1772912142562,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1989,1,1]]},"abstract":"<jats:p> Unlike the case in rat, rabbit, and other species in which nephron formation continues into the newborn period, nephrogenesis in the guinea pig is completed well before the time of birth. Therefore, the marked increase in proximal tubule reabsorption that occurs during the postnatal period in that species can be attributed entirely to an increase in the absorptive capacity of existing nephron units. The purpose of the present morphometric studies was to correlate that change in proximal tubule function with changes in the apical and basolateral cell membrane surface areas. The apical and basolateral membrane surface densities were found to be approximately equal to each other and to remain constant throughout development. Because of increasing tubule volume, however, both membranes doubled in size between 1 and 3 wk of age and eventually increased by a factor of 3.5 in the adult. At the same time, there was little change in the length of tight function complexes measured in the plane of the luminal surface. Using previously published functional data and tubule length data, a good correlation was found between absolute absorption and total basolateral membrane surface area throughout the entire period of development in proximal tubules. Absorption per unit area of basolateral membrane was approximately 0.55, 0.41, 0.56, and 0.42 X 10(-6) nl.min-1.micron-2 in the 1st, 2nd, and 3rd wk, and in adult animals, respectively, and thus was similar to that reported for proximal tubule segments of adult rabbit and juvenile to adult rat. <\/jats:p>","DOI":"10.1152\/ajprenal.1989.256.1.f13","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T16:05:54Z","timestamp":1513958754000},"page":"F13-F17","source":"Crossref","is-referenced-by-count":4,"title":["Correlation of structure and function in developing proximal tubule of guinea pig"],"prefix":"10.1152","volume":"256","author":[{"given":"L. W.","family":"Welling","sequence":"first","affiliation":[{"name":"Laboratory and Research Services, Veterans Administration MedicalCenter, Kansas City, Missouri 64128."}]},{"given":"A. P.","family":"Evan","sequence":"additional","affiliation":[{"name":"Laboratory and Research Services, Veterans Administration MedicalCenter, Kansas City, Missouri 64128."}]},{"suffix":"2nd","given":"V. H.","family":"Gattone","sequence":"additional","affiliation":[{"name":"Laboratory and Research Services, Veterans Administration MedicalCenter, Kansas City, Missouri 64128."}]},{"given":"S.","family":"Rollins","sequence":"additional","affiliation":[{"name":"Laboratory and Research Services, Veterans Administration MedicalCenter, Kansas City, Missouri 64128."}]},{"given":"R.","family":"Saunders","sequence":"additional","affiliation":[{"name":"Laboratory and Research Services, Veterans Administration MedicalCenter, Kansas City, Missouri 64128."}]},{"given":"F. J.","family":"Kaskel","sequence":"additional","affiliation":[{"name":"Laboratory and Research Services, Veterans Administration MedicalCenter, Kansas City, Missouri 64128."}]},{"given":"A.","family":"Spitzer","sequence":"additional","affiliation":[{"name":"Laboratory and Research Services, Veterans Administration MedicalCenter, Kansas City, Missouri 64128."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1989.256.1.F13","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:07:51Z","timestamp":1567955271000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1989.256.1.F13"}},"issued":{"date-parts":[[1989,1,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1989,1,1]]}},"alternative-id":["10.1152\/ajprenal.1989.256.1.F13"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1989.256.1.f13","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1989,1,1]]}},{"indexed":{"date-parts":[[2026,3,7]],"date-time":"2026-03-07T06:13:17Z","timestamp":1772863997965,"version":"3.50.1"},"reference-count":27,"publisher":"American Physiological Society","issue":"2","funder":[{"DOI":"10.13039\/100004339","name":"Sanofi","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100004339","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2019,2,1]]},"abstract":"<jats:p> Glucagon-like peptide-1 (GLP-1) receptor agonists (RAs) are well-established glucose-lowering drugs for type 2 diabetes mellitus (T2DM) management. Acute GLP-1RA administration increases urinary excretion of sodium and other electrolytes. However, the renal tubular effects of prolonged GLP-1RA treatment are largely unknown. In this secondary analysis of a randomized trial, we determined the renal tubular effects of 8-wk treatment with 20 \u03bcg lixisenatide, a short-acting (prandial) GLP-1RA, versus titrated once-daily insulin glulisine in 35 overweight T2DM-patients on stable insulin glargine background therapy (age: 62\u2009\u00b1\u20097 yr, glycated hemoglobin: 8.0 \u00b1 0.9%, estimated glomerular filtration rate: &gt;60 ml\u00b7min<jats:sup>\u22121<\/jats:sup>\u00b71.73 m<jats:sup>\u22122<\/jats:sup>). After a standardized breakfast, lixisenatide increased absolute and fractional excretions of sodium, chloride, and potassium and increased urinary pH. In contrast, lixisenatide reduced absolute and fractional excretions of magnesium, calcium, and phosphate. At week 8, patients treated with lixisenatide had significantly more phosphorylated sodium-hydrogen exchanger isoform 3 (NHE3) in urinary extracellular vesicles than those on insulin glulisine treatment, which suggested decreased NHE3 activity in the proximal tubule. A rise in postprandial blood pressure with lixisenatide partly explained the changes in the urinary excretion of sodium, potassium, magnesium, and phosphate and the changes in urinary pH. In conclusion, lixisenatide affects postprandial urinary excretion of several electrolytes and increases urinary pH compared with insulin glulisine in T2DM patients after 8 wk of treatment. This is most likely explained by a drug-induced rise in blood pressure or direct inhibitory effects on NHE3 in the proximal tubule. <\/jats:p>","DOI":"10.1152\/ajprenal.00432.2018","type":"journal-article","created":{"date-parts":[[2018,10,24]],"date-time":"2018-10-24T08:08:34Z","timestamp":1540368514000},"page":"F231-F240","source":"Crossref","is-referenced-by-count":46,"title":["Renal tubular effects of prolonged therapy with the GLP-1 receptor agonist lixisenatide in patients with type 2 diabetes mellitus"],"prefix":"10.1152","volume":"316","author":[{"given":"Lennart","family":"Tonneijck","sequence":"first","affiliation":[{"name":"Diabetes Center, Department of Internal Medicine, VU University Medical Center, Amsterdam, The Netherlands"}]},{"given":"Marcel H. A.","family":"Muskiet","sequence":"additional","affiliation":[{"name":"Diabetes Center, Department of Internal Medicine, VU University Medical Center, Amsterdam, The Netherlands"}]},{"given":"Charles J.","family":"Blijdorp","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Division of Nephrology and Transplantation, Erasmus University Medical Center, Rotterdam, The Netherlands"}]},{"given":"Mark M.","family":"Smits","sequence":"additional","affiliation":[{"name":"Diabetes Center, Department of Internal Medicine, VU University Medical Center, Amsterdam, The Netherlands"}]},{"given":"Jos W.","family":"Twisk","sequence":"additional","affiliation":[{"name":"Department of Health Sciences and the EMGO Institute for Health and Care Research, VU University Amsterdam, Amsterdam, The Netherlands; Department of Epidemiology and Biostatistics, VU University Medical Center, Amsterdam, The Netherlands"}]},{"given":"Mark H. H.","family":"Kramer","sequence":"additional","affiliation":[{"name":"Diabetes Center, Department of Internal Medicine, VU University Medical Center, Amsterdam, The Netherlands"}]},{"given":"A. H. J.","family":"Danser","sequence":"additional","affiliation":[{"name":"Division of Pharmacology and Vascular Medicine, Department of Internal Medicine, Erasmus University Medical Center, Rotterdam, The Netherlands"}]},{"given":"Michaela","family":"Diamant","sequence":"additional","affiliation":[{"name":"Diabetes Center, Department of Internal Medicine, VU University Medical Center, Amsterdam, The Netherlands"}]},{"given":"Jaap A.","family":"Joles","sequence":"additional","affiliation":[{"name":"Department of Nephrology and Hypertension, University Medical Center Utrecht, Utrecht, The Netherlands"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8738-3571","authenticated-orcid":false,"given":"Ewout J.","family":"Hoorn","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Division of Nephrology and Transplantation, Erasmus University Medical Center, Rotterdam, The Netherlands"}]},{"given":"Dani\u00ebl H.","family":"van Raalte","sequence":"additional","affiliation":[{"name":"Diabetes Center, Department of Internal Medicine, VU University Medical Center, Amsterdam, The Netherlands"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1159\/000049895"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00560.2015"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.09750913"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-008-0595-1"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00729.2010"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00394.2015"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2009.550"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1080\/14740338.2017.1361400"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1210\/jc.2003-031403"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00365.2001"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.2003.tb07281.x"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2013.272"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1111\/dom.12601"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/S2213-8587(15)00030-3"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2017.123"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.08580813"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1210\/en.2013-1934"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00463.2015"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1210\/jc.2012-3855"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1111\/dom.12651"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1111\/dom.12593"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1517\/14656566.2014.879118"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1517\/14656566.2014.879117"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.47.4.530"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1111\/dom.12985"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1007\/s00125-016-3938-z"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.2337\/dc16-1371"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00432.2018","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,10,1]],"date-time":"2019-10-01T20:39:27Z","timestamp":1569962367000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00432.2018"}},"issued":{"date-parts":[[2019,2,1]]},"references-count":27,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2019,2,1]]}},"alternative-id":["10.1152\/ajprenal.00432.2018"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00432.2018","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2019,2,1]]}},{"indexed":{"date-parts":[[2026,3,11]],"date-time":"2026-03-11T16:32:59Z","timestamp":1773246779855,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1987,12,1]]},"abstract":"<jats:p> To characterize the effect of insulin on ammoniagenesis in renal proximal tubule, ammonia productions were measured in suspensions of canine renal proximal tubular segments incubated with 10 mM L-glutamine and varying concentrations of insulin. Productions of ammonia were linear functions of time for 120 min. Insulin (10(-6) M) increased ammonia production at 2 h by 34 +\/- 5%. At the same time, gluconeogenesis, as measured by glucose production, was decreased by 16 +\/- 2%. Significant enhancement of ammoniagenesis occurred in suspensions of segments incubated with as little as 10(-9) M insulin. Half-maximal stimulation occurred at between 10(-9) and 10(-8) M insulin. Oxidation of L-glutamine in cells within segments was also increased by insulin in a concentration-dependent manner. Insulin increased ammonia productions in segments incubated at pH 7.5 but not at 7.0. Under the former conditions, insulin enhanced ammoniagenesis in proximal tubular segments under conditions such that extracellular [Na+] was greater than intracellular [Na+], but not when extracellular [Na+] equaled intracellular [Na+]. We conclude that insulin stimulates ammonia production in suspensions of canine renal proximal tubular segments. Stimulation of ammonia production in vitro could reflect an action of insulin to enhance proximal tubular ammoniagenesis in vivo. <\/jats:p>","DOI":"10.1152\/ajprenal.1987.253.6.f1171","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T03:25:22Z","timestamp":1513999522000},"page":"F1171-F1177","source":"Crossref","is-referenced-by-count":14,"title":["Insulin stimulates ammoniagenesis in canine renal proximal tubular segments"],"prefix":"10.1152","volume":"253","author":[{"given":"M. C.","family":"Chobanian","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, Washington University School ofMedicine, St. Louis, Missouri 63110."}]},{"given":"M. R.","family":"Hammerman","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Washington University School ofMedicine, St. Louis, Missouri 63110."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1987.253.6.F1171","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:51:16Z","timestamp":1567972276000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1987.253.6.F1171"}},"issued":{"date-parts":[[1987,12,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1987,12,1]]}},"alternative-id":["10.1152\/ajprenal.1987.253.6.F1171"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1987.253.6.f1171","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1987,12,1]]}},{"indexed":{"date-parts":[[2026,3,7]],"date-time":"2026-03-07T12:35:42Z","timestamp":1772886942079,"version":"3.50.1"},"reference-count":26,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2009,3]]},"abstract":"<jats:p> Calcineurin is an important intracellular signaling molecule which can be inhibited by cyclosporin resulting in immune suppression and nephrotoxicity. Previously, we reported that homozygous loss of the \u03b1 isoform of calcineurin impairs kidney development and function and mimics many features of cyclosporin nephrotoxicity. However, early lethality of null mice prevented further study of renal changes. Alternatively, we examined aged heterozygous (CnA\u03b1<jats:sup>+\/\u2212<\/jats:sup>) mice. In addition to renal dysfunction and inflammation, we find that CnA\u03b1<jats:sup>+\/\u2212<\/jats:sup> mice spontaneously develop tertiary lymphoid aggregates in the kidney, small intestine, liver, and lung. Lymphoid aggregates contain both T cells and B cells and exhibited organization suggestive of tertiary lymphoid organs (TLOs). Kidney function and TLO formation were highly correlated suggesting that this process may contribute to nephrotoxicity. Consistent with previous findings, transforming growth factor (TGF)-\u03b2 is significantly increased in CnA\u03b1<jats:sup>+\/\u2212<\/jats:sup> mice. Neutralization of TGF-\u03b2 attenuated TLO formation and improved kidney function. In conclusion, we report that haploinsufficiency of CnA\u03b1 causes uregulation of TGF-\u03b2 which contributes to chronic inflammation and formation of TLOs. While the process that leads to TLOs formation in transplant allografts is unknown, TLOs are associated with poor clinical prognosis. This study suggests that calcineurin inhibition itself may lead to TLO formation and that TGF-\u03b2 may be a novel therapeutic target. <\/jats:p>","DOI":"10.1152\/ajprenal.90629.2008","type":"journal-article","created":{"date-parts":[[2009,1,8]],"date-time":"2009-01-08T01:34:25Z","timestamp":1231378465000},"page":"F512-F520","source":"Crossref","is-referenced-by-count":18,"title":["TGF-\u03b2 upregulation drives tertiary lymphoid organ formation and kidney dysfunction in calcineurin A-\u03b1 heterozygous mice"],"prefix":"10.1152","volume":"296","author":[{"given":"Fiona M.","family":"Kelly","sequence":"first","affiliation":[]},{"given":"Ramesh N.","family":"Reddy","sequence":"additional","affiliation":[]},{"given":"Brian R.","family":"Roberts","sequence":"additional","affiliation":[]},{"given":"Shivaprakash","family":"Gangappa","sequence":"additional","affiliation":[]},{"given":"Ifor R.","family":"Williams","sequence":"additional","affiliation":[]},{"given":"Jennifer L.","family":"Gooch","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"crossref","unstructured":"Baddoura FK, Nasr IW, Wrobel B, Li Q, Ruddle NH, Lakkis FG. Lymphoid neogenesis in murine cardiac allografts undergoing chronic rejection. Am J Transplant 5: 510\u2013516, 2005.","DOI":"10.1111\/j.1600-6143.2004.00714.x"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.152665399"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.072647999"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1016\/j.transproceed.2004.03.014"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2007.07.186"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1385\/MN:22:1-3:115"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1097\/00007890-199909270-00010"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00281.2005"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00158.2002"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000128076.91545.BB"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1097\/01.tp.0000251423.78124.51"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)63430-X"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2007.060554"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000113316.52371.2E"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1016\/j.neures.2004.12.018"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.178.9.5899"},{"key":"R17","doi-asserted-by":"crossref","unstructured":"Liersch R, Nay F, Lu L, Detmar M. Induction of lymphatic endothelial cell differentiation in embryoid bodies. Blood 107: 1214\u20131216, 2006.","DOI":"10.1182\/blood-2005-08-3400"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)81573-1"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000328"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.2000.80.4.1483"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002734"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.380"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.180.5.3190"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/17.9.1568"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1097\/00007890-199508000-00005"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1084\/jem.183.2.413"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.90629.2008","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T22:57:39Z","timestamp":1567983459000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.90629.2008"}},"issued":{"date-parts":[[2009,3]]},"references-count":26,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2009,3]]}},"alternative-id":["10.1152\/ajprenal.90629.2008"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.90629.2008","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2009,3]]}},{"indexed":{"date-parts":[[2026,3,11]],"date-time":"2026-03-11T13:32:12Z","timestamp":1773235932058,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1989,9,1]]},"abstract":"<jats:p> A one-nephron model has been extended to include both short-looped and long-looped nephrons. Variables are volume flow, Na+, K+, Cl-, urea, hydrostatic pressure, and electric potential. The ratio of short-to-long-looped nephrons, one of the parameters of the model, is 5 to 1. With either rabbit or hamster permeability data from perfusion experiments, the model develops an osmolality of approximately 600 mosmol\/l at the junction of inner and outer medulla but no osmolality gradient in the inner medulla. With the rabbit data, osmolalities in excess of 1,000 mosmol\/l can be generated in the papilla with no active transport if urea permeabilities are less than 10(-5) cm\/s; with the hamster data, electrolyte permeabilities must also be reduced. With these modified parameters, urea concentrations are less in the long loops than has been found on micropuncture. These can be increased to experimental levels by increasing the urea permeability and decreasing the hydraulic permeability of thin descending limbs in the inner half of the inner medulla, but to maintain loop osmolality at 1,000 mosmol\/l it is necessary to postulate active NaCl transport in thin ascending limbs in the outer half of the inner medulla. This gives an alternative mode of concentration without active transport in the inner half of the inner medulla, in which electrolytes diffuse out of and urea diffuses into both limbs of Henle's loop and mix in the core with urea and water entering from the collecting duct. Concentration in either mode requires significant modification of perfusion data. <\/jats:p>","DOI":"10.1152\/ajprenal.1989.257.3.f399","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T17:10:00Z","timestamp":1513962600000},"page":"F399-F413","source":"Crossref","is-referenced-by-count":19,"title":["Electrolyte, urea, and water transport in a two-nephron central core model of the renal medulla"],"prefix":"10.1152","volume":"257","author":[{"given":"J. L.","family":"Stephenson","sequence":"first","affiliation":[{"name":"Department of Physiology, Cornell University Medical College, New York10021."}]},{"given":"Y.","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Physiology, Cornell University Medical College, New York10021."}]},{"given":"R.","family":"Tewarson","sequence":"additional","affiliation":[{"name":"Department of Physiology, Cornell University Medical College, New York10021."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1989.257.3.F399","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:16:02Z","timestamp":1567955762000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1989.257.3.F399"}},"issued":{"date-parts":[[1989,9,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1989,9,1]]}},"alternative-id":["10.1152\/ajprenal.1989.257.3.F399"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1989.257.3.f399","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1989,9,1]]}},{"indexed":{"date-parts":[[2026,3,30]],"date-time":"2026-03-30T14:29:30Z","timestamp":1774880970711,"version":"3.50.1"},"reference-count":49,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2005,3]]},"abstract":"<jats:p> The Tamm-Horsfall protein (THP; uromodulin), the dominant protein in normal urine, is produced exclusively in the thick ascending limb of Henle's loop. THP mutations are associated with disease; however, the physiological role of THP remains obscure. We generated THP gene-deficient mice (THP \u2212\/\u2212) and compared them with wild-type (WT) mice. THP \u2212\/\u2212 mice displayed anatomically normal kidneys. Steady-state electrolyte handling was not different between strains. Creatinine clearance was 63% lower in THP \u2212\/\u2212 than in WT mice ( P &lt; 0.05). Sucrose loading induced no changes between strains. However, water deprivation for 24 h decreased urine volume from 58 \u00b1 9 to 28 \u00b1 4 \u03bcl\u00b7g body wt<jats:sup>\u22121<\/jats:sup>\u00b724 h<jats:sup>\u22121<\/jats:sup> in WT mice ( P &lt; 0.05), whereas in THP \u2212\/\u2212 mice this decrease was less pronounced (57 \u00b1 4 to 41 \u00b1 5 \u03bcl\u00b7g body wt<jats:sup>\u22121<\/jats:sup>\u00b724 h<jats:sup>\u22121<\/jats:sup>; P &lt; 0.05), revealing significant interstrain difference ( P &lt; 0.05). We further used RT-PCR, Northern and Western blotting, and histochemistry to study renal transporters, channels, and regulatory systems under steady-state conditions. We found that major distal transporters were upregulated in THP \u2212\/\u2212 mice, whereas juxtaglomerular immunoreactive cyclooxygenase-2 (COX-2) and renin mRNA expression were both decreased in THP \u2212\/\u2212 compared with WT mice. These observations suggest that THP influences transporters in Henle's loop. The decreased COX-2 and renin levels may be related to an altered tubular salt load at the macula densa, whereas the increased expression of distal transporters may reflect compensatory mechanisms. Our data raise the hypothesis that THP plays an important regulatory role in the kidney. <\/jats:p>","DOI":"10.1152\/ajprenal.00143.2004","type":"journal-article","created":{"date-parts":[[2004,11,3]],"date-time":"2004-11-03T03:09:00Z","timestamp":1099451340000},"page":"F559-F567","source":"Crossref","is-referenced-by-count":128,"title":["Renal effects of Tamm-Horsfall protein (uromodulin) deficiency in mice"],"prefix":"10.1152","volume":"288","author":[{"given":"Sebastian","family":"Bachmann","sequence":"first","affiliation":[]},{"given":"Kerim","family":"Mutig","sequence":"additional","affiliation":[]},{"given":"James","family":"Bates","sequence":"additional","affiliation":[]},{"given":"Pia","family":"Welker","sequence":"additional","affiliation":[]},{"given":"Beate","family":"Geist","sequence":"additional","affiliation":[]},{"given":"Volkmar","family":"Gross","sequence":"additional","affiliation":[]},{"given":"Friedrich C.","family":"Luft","sequence":"additional","affiliation":[]},{"given":"Natalia","family":"Alenina","sequence":"additional","affiliation":[]},{"given":"Michael","family":"Bader","sequence":"additional","affiliation":[]},{"given":"Bernd J.","family":"Thiele","sequence":"additional","affiliation":[]},{"given":"Krishna","family":"Prasadan","sequence":"additional","affiliation":[]},{"given":"Hajamohideen S.","family":"Raffi","sequence":"additional","affiliation":[]},{"given":"Satish","family":"Kumar","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1007\/s004290050294"},{"key":"R2","doi-asserted-by":"crossref","unstructured":"Bachmann S, Dawnay AB, Bouby N, and Bankir L. Tamm-Horsfall protein excretion during chronic alterations in urinary concentration and protein intake in the rat. Renal Physiol Biochem 14: 236\u2013245, 1991.","DOI":"10.1159\/000173411"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1007\/BF00492456"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1007\/BF00272616"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00452.x"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.6.F793"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.0148.2001"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00338.2002"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000092147.83480.B5"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.4.F616"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1172\/JCI113847"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1038\/35107099"},{"key":"R13","unstructured":"Fr\u00fchauf JH, Welker P, Mutig K, Jentsch TJ, Kinne-Safran E, and Bachmann S. Lipid raft association of essential proteins of the thick ascending limb. J Am Soc Nephrol 14: 561A, 2003."},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9149(02)02404-9"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1136\/jmg.39.12.882"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200309000-00008"},{"key":"R17","unstructured":"Kelly SJ, Delnomdedieu M, Oliverio MI, Williams LD, Saifer MGP, Sherman MR, Coffman TM, Johnson GA, and Hershfield MS. Diabetes insipidus in uricase-deficient mice: a model for evaluating therapy with poly(ethylene glycol)-modified uricase. J Am Soc Nephrol 12: 1001\u20131009, 2001."},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.1.F96"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-201X.2001.00880.x"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000023434.47132.3D"},{"key":"R21","unstructured":"Lynn KL and Marshall RD. Excretion of Tamm-Horsfall glycoprotein in renal disease. Clin Nephrol 22: 253\u2013257, 1984."},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.459"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1172\/JCI7840"},{"key":"R24","doi-asserted-by":"crossref","unstructured":"Mo L, Zhu XH, Huang HY, Shapiro E, Hasty DL, and Wu XR. Ablation of the Tamm Horsfall protein gene increases susceptibility of mice to bladder colonization by type 1-fimbriated Escherichia coli. Am J Physiol Renal Physiol 286: F786\u2013F795, 2004.","DOI":"10.1152\/ajprenal.00357.2003"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00015.2002"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.275.6.F885"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118834"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.6.F900"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M008610200"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00153.x"},{"key":"R31","doi-asserted-by":"crossref","unstructured":"Rampoldi L, Caridi G, Santon D, Boaretto F, Bernascone I, Lamorte G, Tardanico R, Dagnino M, Colussi G, Scolari F, Ghiggeri GM, Amoroso A, and Casari G. Allelism of MCKD, FJHN and GCKD caused by impairment of uromodulin export dynamics. Hum Mol Genet 15: 3369\u20133384, 2003.","DOI":"10.1093\/hmg\/ddg353"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1007\/BF00400720"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.281.3.F391"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1172\/JCI114474"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.6.F1010"},{"key":"R36","doi-asserted-by":"crossref","unstructured":"Sato K, Oguchi H, Yoshie T, and Toshihiko K. Tubulointerstitial nephritis induced by Tamm-Horsfall protein sensitization in guinea pigs. Virchows Arch 58: 357\u2013363, 1990.","DOI":"10.1007\/BF02890092"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00368.2002"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1007\/s00418-004-0638-4"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000069221.69551.30"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1993.258"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(03)00829-1"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.090091297"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.5.F706"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1159\/000045663"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00269.x"},{"key":"R46","doi-asserted-by":"crossref","unstructured":"Yang T, Singh I, Pham H, Sun D, Smart A, Schnermann JB, and Briggs JP. Regulation of cyclooxygenase expression in the kidney by dietary salt intake. Am J Physiol Renal Physiol 274: F481\u2013F489, 1998.","DOI":"10.1152\/ajprenal.1998.274.3.F481"},{"key":"R47","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00117.x"},{"key":"R48","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)64142-9"},{"key":"R49","doi-asserted-by":"publisher","DOI":"10.1007\/BF01428391"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00143.2004","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T21:49:40Z","timestamp":1567979380000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00143.2004"}},"issued":{"date-parts":[[2005,3]]},"references-count":49,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2005,3]]}},"alternative-id":["10.1152\/ajprenal.00143.2004"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00143.2004","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2005,3]]}},{"indexed":{"date-parts":[[2026,3,30]],"date-time":"2026-03-30T14:13:10Z","timestamp":1774879990751,"version":"3.50.1"},"reference-count":29,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2002,6,1]]},"abstract":"<jats:p> Although mammalian urothelia are generally considered impermeable to constituents of urine, in vivo studies in several species indicate urothelial transport of water and solutes under certain conditions. This study investigates the expression, localization, and regulation of aquaporin (AQP)-1, -2, and -3 in ureteral and bladder tissues in 48-h dehydrated and water-loaded female Wistar rats. Immunoblots of homogenates of whole ureter and bladder identified characteristic \u223c28- and 35- to 44-kDa bands for AQP-1, -2, and -3. AQP-1 was localized to capillary and arteriole endothelial cells, whereas AQP-2 and -3 circumferentially lined the epithelial cell membranes except for the apical membrane of the epithelial cells adjacent to the lumens of both ureter and bladder. AQP-2 was also present in epithelial cell cytoplasm. Dehydration resulted in 160\u2013200% increases of AQP-3 signal and 24\u201349% increases of AQP-2 signal but no change in AQP-1 signal on immunoblots of homogenates of ureters and bladders. AQPs in genitourinary tract urothelia likely play a role in the regulation of epithelial cell volume and osmolality and may play a role in bulk water movement across urothelia. <\/jats:p>","DOI":"10.1152\/ajprenal.00136.2001","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:32:23Z","timestamp":1425414743000},"page":"F1034-F1042","source":"Crossref","is-referenced-by-count":77,"title":["Expression, localization, and regulation of  aquaporin-1 to -3 in rat urothelia"],"prefix":"10.1152","volume":"282","author":[{"given":"David A.","family":"Spector","sequence":"first","affiliation":[{"name":"Division of Renal Medicine, The Johns Hopkins Bayview Medical Center, Baltimore 21224; and Departments of"}]},{"given":"James B.","family":"Wade","sequence":"additional","affiliation":[{"name":"Physiology and"}]},{"given":"Russell","family":"Dillow","sequence":"additional","affiliation":[{"name":"Division of Renal Medicine, The Johns Hopkins Bayview Medical Center, Baltimore 21224; and Departments of"}]},{"given":"Deborah A.","family":"Steplock","sequence":"additional","affiliation":[{"name":"Medicine, University of Maryland School of Medicine, and"}]},{"given":"Edward J.","family":"Weinman","sequence":"additional","affiliation":[{"name":"Medicine, University of Maryland School of Medicine, and"},{"name":"Department of Veterans Affairs, Baltimore, Maryland 21201"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.91.19.8984"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1981.sp013804"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.5.F663"},{"key":"B4","first-page":"303","volume":"16","author":"Fellows GJ","year":"1971","journal-title":"Rev Eur Etudes Clin Biol,"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.10.4328"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1997.77.2.359"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-185X.1975.tb01057.x"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1159\/000472742"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1159\/000281082"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1991.261.4.R865"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.91.14.6269"},{"key":"B12","first-page":"87","volume":"165","author":"Johnson JA","year":"1951","journal-title":"J Physiol"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.1.F230"},{"key":"B14","doi-asserted-by":"crossref","first-page":"549","DOI":"10.1152\/ajplegacy.1959.196.3.549","volume":"196","author":"Levinsky NG","year":"1959","journal-title":"Am J Physiol"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.6.F867"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1007\/BF01869690"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.2.F342"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1038\/icb.1969.157"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.4.F886"},{"key":"B20","first-page":"141","volume":"50","author":"Nelson RA","year":"1975","journal-title":"Mayo Clin Proc"},{"key":"B21","doi-asserted-by":"crossref","first-page":"191","DOI":"10.1152\/ajplegacy.1960.198.1.191","volume":"198","author":"Rapoport A","year":"1960","journal-title":"Am J Physiol"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.1.F91"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.2000.278.4.C791"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.2.F414"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1986.251.1.H115"},{"key":"B26","first-page":"745","volume":"17","author":"Turnbull GJ","year":"1972","journal-title":"Rev Eur Etudes Clin Biol"},{"key":"B27","doi-asserted-by":"crossref","first-page":"607","DOI":"10.1152\/ajplegacy.1924.70.3.607","volume":"70","author":"Vickers JL","year":"1924","journal-title":"Am J Physiol"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.1.F52"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1988.255.2.F244"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00136.2001","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T22:08:12Z","timestamp":1567980492000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00136.2001"}},"issued":{"date-parts":[[2002,6,1]]},"references-count":29,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2002,6,1]]}},"alternative-id":["10.1152\/ajprenal.00136.2001"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00136.2001","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2002,6,1]]}},{"indexed":{"date-parts":[[2026,3,27]],"date-time":"2026-03-27T04:35:56Z","timestamp":1774586156546,"version":"3.50.1"},"reference-count":53,"publisher":"American Physiological Society","issue":"5","funder":[{"DOI":"10.13039\/100000738","name":"U.S. Department of Veterans Affairs","doi-asserted-by":"publisher","award":["IBX004968A"],"award-info":[{"award-number":["IBX004968A"]}],"id":[{"id":"10.13039\/100000738","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000968","name":"American Heart Association","doi-asserted-by":"publisher","award":["24CDA1271666"],"award-info":[{"award-number":["24CDA1271666"]}],"id":[{"id":"10.13039\/100000968","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100009708","name":"Novo Nordisk Fonden","doi-asserted-by":"publisher","award":["NNF21OC0067647"],"award-info":[{"award-number":["NNF21OC0067647"]}],"id":[{"id":"10.13039\/501100009708","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100009708","name":"Novo Nordisk Fonden","doi-asserted-by":"publisher","award":["NNF17OC0029724"],"award-info":[{"award-number":["NNF17OC0029724"]}],"id":[{"id":"10.13039\/501100009708","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100009708","name":"Novo Nordisk Fonden","doi-asserted-by":"publisher","award":["NNF19OC0058439"],"award-info":[{"award-number":["NNF19OC0058439"]}],"id":[{"id":"10.13039\/501100009708","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001674","name":"Fondation Leducq","doi-asserted-by":"publisher","award":["17CVD05"],"award-info":[{"award-number":["17CVD05"]}],"id":[{"id":"10.13039\/501100001674","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Independent Research Fund Denmark","award":["0134-00018B"],"award-info":[{"award-number":["0134-00018B"]}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2025,11,1]]},"abstract":"<jats:p> Disturbances in acid-base regulation are common and can have detrimental effects. Here, we provide evidence that acid-base disturbances in males and females are consistent with female mice being able to defend acid and base challenges more effectively. Our data have potential clinical importance in humans regarding the treatment of acidosis and alkalosis in males versus females. <\/jats:p>","DOI":"10.1152\/ajprenal.00174.2024","type":"journal-article","created":{"date-parts":[[2025,9,28]],"date-time":"2025-09-28T00:30:55Z","timestamp":1759019455000},"page":"F615-F626","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":2,"title":["Sex differences in renal acid-base regulation"],"prefix":"10.1152","volume":"329","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6190-7464","authenticated-orcid":false,"given":"Jessica A.","family":"Dominguez Rieg","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/032db5x82","id-type":"ROR","asserted-by":"publisher"}],"name":"University of South Florida","place":["United States"]},{"name":"James A. Haley Veterans\u2019 Hospital","place":["United States"]}]},{"ORCID":"https:\/\/orcid.org\/0009-0006-3071-7098","authenticated-orcid":false,"given":"Louise Nyrup","family":"Odgaard","sequence":"additional","affiliation":[{"name":"Aarhus University","place":["Denmark"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8847-0581","authenticated-orcid":false,"given":"Jianxiang","family":"Xue","sequence":"additional","affiliation":[{"name":"University of New Mexico","place":["United States"]}]},{"ORCID":"https:\/\/orcid.org\/0009-0007-1643-6772","authenticated-orcid":false,"given":"Jennifer","family":"Nogueira Coelho","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/032db5x82","id-type":"ROR","asserted-by":"publisher"}],"name":"University of South Florida","place":["United States"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2329-3905","authenticated-orcid":false,"given":"Autumn N.","family":"Harris","sequence":"additional","affiliation":[{"name":"North Carolina State University","place":["United States"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3344-1307","authenticated-orcid":false,"given":"Linto","family":"Thomas","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/032db5x82","id-type":"ROR","asserted-by":"publisher"}],"name":"University of South Florida","place":["United States"]},{"name":"James A. Haley Veterans\u2019 Hospital","place":["United States"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1623-199X","authenticated-orcid":false,"given":"Robert A.","family":"Fenton","sequence":"additional","affiliation":[{"name":"University of New Mexico","place":["United States"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6082-662X","authenticated-orcid":false,"given":"Timo","family":"Rieg","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/032db5x82","id-type":"ROR","asserted-by":"publisher"}],"name":"University of South Florida","place":["United States"]},{"name":"James A. Haley Veterans\u2019 Hospital","place":["United States"]},{"id":[{"id":"https:\/\/ror.org\/032db5x82","id-type":"ROR","asserted-by":"publisher"}],"name":"University of South Florida","place":["United States"]}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.63.s83.8.x"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.4161\/org.6.3.12125"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1038\/s41581-023-00757-2"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/j.isci.2021.102667"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00531.2020"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2017030295"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00084.2018"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00282.2021"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00260.2021"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00244.2019"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00671.x"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1042\/CS20180060"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2017111163"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.V105935"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2017.02.001"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1111\/apha.70029"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013101102"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.3.F619"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2010.130"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/j.jbc.2021.100915"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00037.2002"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.V11122179"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00409.2003"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00013.2022"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00347.2023"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.404"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00188.2001"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.51.32749"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.1.F18"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119128"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1172\/JCI36581"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00044.2025"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-024-02940-1"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00266.2011"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00300.2012"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1042\/BST20211005"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2018121250"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1159\/000543068"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.50.33681"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000088321.67254.B7"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00033.2010"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00254.2002"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00205.2002"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00211.2004"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00474.2005"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00419.2008"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1172\/JCI111894"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1016\/j.lfs.2004.10.013"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1021\/bi901438z"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1096\/fasebj.4.6.2156741"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1993.143"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2017.08.018"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.08580813"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00174.2024","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,10,21]],"date-time":"2025-10-21T12:45:57Z","timestamp":1761050757000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00174.2024"}},"issued":{"date-parts":[[2025,11,1]]},"references-count":53,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2025,11,1]]}},"alternative-id":["10.1152\/ajprenal.00174.2024"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00174.2024","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2025,11,1]]},"assertion":[{"value":"2024-06-11","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2024-07-18","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2025-09-23","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2025-10-21","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,3,28]],"date-time":"2026-03-28T08:18:12Z","timestamp":1774685892036,"version":"3.50.1"},"reference-count":67,"publisher":"American Physiological Society","issue":"6","funder":[{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["5UC2DK126006"],"award-info":[{"award-number":["5UC2DK126006"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["R01DK117914"],"award-info":[{"award-number":["R01DK117914"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["U01DK127553"],"award-info":[{"award-number":["U01DK127553"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"HHS | NIH | National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["U01HL152401"],"award-info":[{"award-number":["U01HL152401"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100006108","name":"HHS | NIH | National Center for Advancing Translational Sciences","doi-asserted-by":"publisher","award":["UG3TR002158"],"award-info":[{"award-number":["UG3TR002158"]}],"id":[{"id":"10.13039\/100006108","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100006108","name":"HHS | NIH | National Center for Advancing Translational Sciences","doi-asserted-by":"publisher","award":["UG3TR003288"],"award-info":[{"award-number":["UG3TR003288"]}],"id":[{"id":"10.13039\/100006108","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000005","name":"U.S. Department of Defense","doi-asserted-by":"publisher","award":["W81XWH-21-1-0006"],"award-info":[{"award-number":["W81XWH-21-1-0006"]}],"id":[{"id":"10.13039\/100000005","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000005","name":"U.S. Department of Defense","doi-asserted-by":"publisher","award":["W81XWH-21-1-0007"],"award-info":[{"award-number":["W81XWH-21-1-0007"]}],"id":[{"id":"10.13039\/100000005","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100005674","name":"Cystinosis Research Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100005674","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Allen Institute for Cell Science"},{"DOI":"10.13039\/100007812","name":"Lara Nowak Macklin Research Fund, University of Washington","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100007812","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100004191","name":"Novo Nordisk","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100004191","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Eloxx Pharmaceuticals"},{"name":"Aeovian Pharmaceuticals"},{"DOI":"10.13039\/100006221","name":"United States-Israel Binational Science Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100006221","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100007812","name":"University of Washington","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100007812","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100011751","name":"Northwest Kidney Centers","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100011751","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2022,6,1]]},"abstract":"<jats:p> Kidney organoids derived from human pluripotent stem cells constitute a novel model of disease, development, and regenerative therapy. Organoids are human, experimentally accessible, high throughput, and enable reconstitution of tissue-scale biology in a petri dish. Although gene expression patterns in organoid cells have been analyzed extensively, less is known about the functionality of these structures. Here, we review assays of physiological function in human kidney organoids, including best practices for quality control, and future applications. Tubular structures in organoids accumulate specific molecules through active transport, including dextran and organic anions, and swell with fluid in response to cAMP stimulation. When engrafted into animal models in vivo, organoids form vascularized glomerulus-like structures capable of size-selective filtration. Organoids exhibit metabolic, endocrine, injury, and infection phenotypes, although their specificity is not yet fully clear. To properly interpret organoid physiology assays, it is important to incorporate appropriate negative and positive controls, statistical methods, data presentation, molecular mechanisms, and clinical data sets. Improvements in organoid perfusion, patterning, and maturation are needed to enable branching morphogenesis, urine production, and renal replacement. Reconstituting renal physiology with kidney organoids is a new field with potential to provide fresh insights into classical phenomena. <\/jats:p>","DOI":"10.1152\/ajprenal.00400.2021","type":"journal-article","created":{"date-parts":[[2022,4,5]],"date-time":"2022-04-05T01:28:41Z","timestamp":1649122121000},"page":"F625-F638","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":33,"title":["Physiology assays in human kidney organoids"],"prefix":"10.1152","volume":"322","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2228-7383","authenticated-orcid":true,"given":"Benjamin S.","family":"Freedman","sequence":"first","affiliation":[{"name":"Division of Nephrology, Kidney Research Institute, and Institute for Stem Cell and Regenerative Medicine, Department of Medicine, Department of Laboratory Medicine and Physiology (adjunct), and Department of Bioengineering (adjunct), University of Washington School of Medicine, Seattle, Washington"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/j.stem.2013.11.010"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/ncomms9715"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1038\/nbt.3392"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/nature15695"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/j.stemcr.2018.06.018"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1038\/nmat4994"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/j.stem.2018.04.022"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/s41563-020-00853-9"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/j.ydbio.2008.09.010"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0710428105"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1016\/j.stem.2008.05.020"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1038\/sj.emboj.7601381"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1016\/j.celrep.2014.02.033"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/j.stem.2018.10.010"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1016\/j.stem.2017.10.011"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/j.stem.2020.12.001"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1038\/ncb2872"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2017.11.105"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/j.celrep.2020.108514"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1038\/s41467-021-23911-5"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1038\/s41592-018-0253-2"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/bs.mcb.2019.05.003"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1038\/nprot.2016.098"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1002\/stem.2707"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1038\/s41467-018-07594-z"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/j.stem.2019.06.009"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2020.08.008"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1186\/s13287-022-02752-z"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2020.06.141"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2020030378"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2015010096"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1016\/j.stemcr.2018.01.041"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1038\/s12276-019-0336-x"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1038\/s42003-020-0948-7"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2019060573"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfab264"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00597.2019"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1126\/scitranslmed.abj4772"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1016\/j.isci.2022.103884"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1172\/jci.insight.154882"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1016\/j.stem.2021.12.010"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1172\/JCI111871"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1124\/mol.59.6.1433"},{"key":"B45","first-page":"1104","volume":"289","author":"Masereeuw R","year":"1999","journal-title":"J Pharmacol Exp Ther"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1992.184"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006030295"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1038\/nm.3201"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1096\/fj.202100843R"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.3791\/53035"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00472.2020"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1038\/s41563-019-0287-6"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00552.2020"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1039\/c5lc01050k"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1038\/s41592-019-0325-y"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.3389\/fgene.2021.632810"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00134.2021"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2020.04.004"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1038\/nm812"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1016\/j.ydbio.2021.04.009"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1089\/ten.TEA.2010.0595"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1038\/s41587-019-0048-8"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1681\/asn.2020101537"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1038\/s41467-022-28226-7"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1038\/nbt703"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1507803112"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.4161\/org.1.1.1009"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.5966\/sctm.2014-0219"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00400.2021","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,5,4]],"date-time":"2022-05-04T17:28:39Z","timestamp":1651685319000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00400.2021"}},"issued":{"date-parts":[[2022,6,1]]},"references-count":67,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2022,6,1]]}},"alternative-id":["10.1152\/ajprenal.00400.2021"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00400.2021","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2022,6,1]]},"assertion":[{"value":"2021-10-29","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2022-03-28","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2022-03-29","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2022-05-04","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,3,29]],"date-time":"2026-03-29T17:13:50Z","timestamp":1774804430878,"version":"3.50.1"},"reference-count":33,"publisher":"American Physiological Society","issue":"7","funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China (NSFC)","doi-asserted-by":"publisher","award":["30871174"],"award-info":[{"award-number":["30871174"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China (NSFC)","doi-asserted-by":"publisher","award":["81170662"],"award-info":[{"award-number":["81170662"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"crossref","award":["81170600"],"award-info":[{"award-number":["81170600"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China (NSFC)","doi-asserted-by":"publisher","award":["31200872"],"award-info":[{"award-number":["31200872"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China (NSFC)","doi-asserted-by":"publisher","award":["81300604"],"award-info":[{"award-number":["81300604"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China (NSFC)","doi-asserted-by":"publisher","award":["81400720"],"award-info":[{"award-number":["81400720"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China (NSFC)","doi-asserted-by":"publisher","award":["81471490"],"award-info":[{"award-number":["81471490"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"crossref","award":["81470964"],"award-info":[{"award-number":["81470964"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2015,4,1]]},"abstract":"<jats:p> It is well documented that mitotic arrest deficiency (MAD)2B can inhibit the anaphase-promoting complex\/cyclosome (APC\/C) via cadherin (Cdh)1 and, consequently, can destroy the effective mitotic spindle checkpoint control. Podocytes have been observed to rapidly detach and die when being forced to bypass cell cycle checkpoints. However, the role of MAD2B, a cell cycle regulator, in podocyte impairment of diabetic nephropathy (DN) is unclear. In the present study, we investigated the significance of MAD2B in the pathogenesis of DN in patients, an animal model, and in vitro podocyte cultures. By Western blot and immunohistochemistry analyses, we found that MAD2B was evidently upregulated under high glucose milieu in vivo and in vitro, whereas Cdh1 was inhibited with high glucose exposure. Overexpression of MAD2B in podocytes by plasmid DNA transfection suppressed expression of Cdh1 and triggered the accumulation of cyclin B1 and S phase kinase-associated protein (Skp)2, two key molecules involving in cell cycle regulation, and the subsequent podocyte insult. In contrast, MAD2B deletion alleviated the high glucose-induced reduction of Cdh1 as well as the elevation of cyclin B1 and Skp2, which rescued the podocyte from damage. Taken together, our data demonstrate that MAD2B may play an important role in high glucose-mediated podocyte injury of DN via modulation of Cdh1, cyclin B1, and Skp2 expression. <\/jats:p>","DOI":"10.1152\/ajprenal.00409.2014","type":"journal-article","created":{"date-parts":[[2015,1,29]],"date-time":"2015-01-29T00:31:17Z","timestamp":1422491477000},"page":"F728-F736","source":"Crossref","is-referenced-by-count":21,"title":["MAD2B contributes to podocyte injury of diabetic nephropathy via inducing cyclin B1 and Skp2 accumulation"],"prefix":"10.1152","volume":"308","author":[{"given":"Hua","family":"Su","sequence":"first","affiliation":[{"name":"Department of Nephrology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China;"}]},{"given":"Qiang","family":"Wan","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, China; and"}]},{"given":"Xiu-Juan","family":"Tian","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China;"}]},{"given":"Fang-Fang","family":"He","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China;"}]},{"given":"Pan","family":"Gao","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China;"}]},{"given":"Hui","family":"Tang","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China;"}]},{"given":"Chen","family":"Ye","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China;"}]},{"given":"Di","family":"Fan","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China;"}]},{"given":"Shan","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China;"}]},{"given":"Yu-Mei","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China;"}]},{"given":"Xian-Fang","family":"Meng","sequence":"additional","affiliation":[{"name":"Department of Neurobiology, School of Basic Medical Sciences, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China"}]},{"given":"Chun","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1186\/scrt330"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1007\/s12035-012-8309-2"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.1143-05.2005"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(94)90443-X"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1006\/geno.1999.5831"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1101\/gad.898701"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/j.semcdb.2011.03.010"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1016\/S1097-2765(00)80126-4"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.2174\/1573399052952622"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.081474898"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M112.418103"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/S1097-2765(02)00524-5"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.11.5.1555"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1007\/s00428-004-1121-2"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.2174\/156652413804486250"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.201302060"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1007\/s00251-012-0660-y"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1038\/nrm1988"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1101\/gad.897901"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pgen.1003712"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0b013e3282f2904d"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/labinvest.2011.138"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000410"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.55.01.06.db05-0894"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2443.2011.01553.x"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.2131\/jts.31.449"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1101\/gad.1478306"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1038\/ncb1066"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.54.6.1626"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/S1097-2765(00)80444-X"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1016\/j.freeradbiomed.2010.01.029"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1089\/ars.2010.3091"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.35.1.342"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00409.2014","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T21:06:14Z","timestamp":1567976774000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00409.2014"}},"issued":{"date-parts":[[2015,4,1]]},"references-count":33,"journal-issue":{"issue":"7","published-print":{"date-parts":[[2015,4,1]]}},"alternative-id":["10.1152\/ajprenal.00409.2014"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00409.2014","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2015,4,1]]}},{"indexed":{"date-parts":[[2026,3,27]],"date-time":"2026-03-27T13:51:35Z","timestamp":1774619495759,"version":"3.50.1"},"reference-count":57,"publisher":"American Physiological Society","issue":"5","funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["31330037"],"award-info":[{"award-number":["31330037"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["91439205"],"award-info":[{"award-number":["91439205"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["and 81630013"],"award-info":[{"award-number":["and 81630013"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health","doi-asserted-by":"publisher","award":["DK104072"],"award-info":[{"award-number":["DK104072"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health","doi-asserted-by":"publisher","award":["HL135851"],"award-info":[{"award-number":["HL135851"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health","doi-asserted-by":"publisher","award":["and HL139689"],"award-info":[{"award-number":["and HL139689"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000968","name":"American Heart Association","doi-asserted-by":"publisher","award":["19POST34410068"],"award-info":[{"award-number":["19POST34410068"]}],"id":[{"id":"10.13039\/100000968","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2020,5,1]]},"abstract":"<jats:p> Emerging evidence has demonstrated that (pro)renin receptor (PRR)-mediated activation of intrarenal renin-angiotensin system (RAS) plays an essential role in renal handling of Na<jats:sup>+<\/jats:sup> and water balance and blood pressure. The present study tested the possibility that the intrarenal RAS served as a molecular target for the protective action of ELABELA (ELA), a novel endogenous ligand of apelin receptor, in the distal nephron. By RNAscope and immunofluorescence, mRNA and protein expression of endogenous ELA was consistently localized to the collecting duct (CD). Apelin was also found in the medullary CDs as assessed by immunofluorescence. In cultured CD-derived M1 cells, exogenous ELA induced parallel decreases of full-length PRR (fPRR), soluble PRR (sPRR), and prorenin\/renin protein expression as assessed by immunoblotting and medium sPRR and prorenin\/renin levels by ELISA, all of which were reversed by 8-bromoadenosine 3\u2032,5\u2032-cyclic monophosphate. Conversely, deletion of PRR in the CD or nephron in mice elevated Apela and Apln mRNA levels as well as urinary ELA and apelin excretion, supporting the antagonistic relationship between the two systems. Administration of exogenous ELA-32 infusion (1.5 mg\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7day<jats:sup>\u22121<\/jats:sup>, minipump) to high salt (HS)-loaded Dahl salt-sensitive (SS) rats significantly lowered mean arterial pressure, systolic blood pressure, diastolic blood pressure, and albuminuria, accompanied with a reduction of urinary sPRR, angiotensin II, and prorenin\/renin excretion. HS upregulated renal medullary protein expression of fPRR, sPRR, prorenin, and renin in Dahl SS rats, all of which were significantly blunted by exogenous ELA-32 infusion. Additionally, HS-induced upregulation of inflammatory cytokines ( IL-1\u03b2, IL-2, IL-6, IL-17A, IFN-\u03b3, VCAM-1, ICAM-1, and MCP-1), fibrosis markers ( TGF-\u03b2<jats:sub>1<\/jats:sub>, FN, Col1A1, PAI-1, and TIMP-1), and kidney injury markers ( NGAL, Kim-1, albuminuria, and urinary NGAL excretion) were markedly blocked by exogenous ELA infusion. Together, these results support the antagonistic interaction between ELA and intrarenal RAS in the distal nephron that appears to exert a major impact on blood pressure regulation. <\/jats:p>","DOI":"10.1152\/ajprenal.00606.2019","type":"journal-article","created":{"date-parts":[[2020,3,16]],"date-time":"2020-03-16T11:23:37Z","timestamp":1584357817000},"page":"F1122-F1135","source":"Crossref","is-referenced-by-count":48,"title":["ELABELA antagonizes intrarenal renin-angiotensin system to lower blood pressure and protects against renal injury"],"prefix":"10.1152","volume":"318","author":[{"given":"Chuanming","family":"Xu","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, University of Utah and Veterans Affairs Medical Center, Salt Lake City, Utah"}]},{"given":"Fei","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Utah and Veterans Affairs Medical Center, Salt Lake City, Utah"}]},{"given":"Yanting","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Utah and Veterans Affairs Medical Center, Salt Lake City, Utah"},{"name":"Institute of Hypertension, Sun Yat-sen University School of Medicine, Guangzhou, China"}]},{"given":"Shiying","family":"Xie","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Utah and Veterans Affairs Medical Center, Salt Lake City, Utah"},{"name":"Institute of Hypertension, Sun Yat-sen University School of Medicine, Guangzhou, China"}]},{"given":"Danielle","family":"Sng","sequence":"additional","affiliation":[{"name":"Institute of Medical Biology, A*STAR, 8A Biomedical Grove, Immunos, Singapore"}]},{"given":"Bruno","family":"Reversade","sequence":"additional","affiliation":[{"name":"Institute of Medical Biology, A*STAR, 8A Biomedical Grove, Immunos, Singapore"}]},{"given":"Tianxin","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Utah and Veterans Affairs Medical Center, Salt Lake City, Utah"},{"name":"Institute of Hypertension, Sun Yat-sen University School of Medicine, Guangzhou, China"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.36.5.890"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1161\/CIR.0000000000000659"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.27.5.1121"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1159\/000110021"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2016111210"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90253.2008"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/j.devcel.2013.11.002"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1172\/JCI34871"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1097\/CCM.0000000000002639"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M115.648238"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.5049\/EBP.2014.12.1.7"},{"key":"B12","first-page":"130","volume":"125","author":"Harrison DG","year":"2014","journal-title":"Trans Am Clin Climatol Assoc"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1016\/j.stem.2015.08.010"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1038\/srep21960"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.199"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.23.1.68"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.449"},{"key":"B18","first-page":"14433","volume":"8","author":"Jiang L","year":"2015","journal-title":"Int J Clin Exp Pathol"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000056768.03657.B4"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/j.peptides.2018.04.011"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/j.stem.2015.04.002"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/j.phrs.2017.06.005"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1016\/j.jash.2009.08.002"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1602397113"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.110.163840"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1172\/JCI0214276"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1530\/JOE-13-0227"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0183094"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/S0167-4781(00)00072-5"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/0378-1119(93)90495-O"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1126\/science.1248636"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1177\/1470320316653858"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00178.2016"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1016\/j.peptides.2011.12.005"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00152.2017"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00126.2015"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00088.2016"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1038\/gt.2011.39"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.3390\/ijms20020239"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1093\/cvr\/cvx061"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1172\/JCI69608"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.2174\/1566523217666161121111906"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.2012.02192.x"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1016\/S0024-3205(97)00734-0"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1998.9489"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00981.2007"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2015050592"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1038\/srep08170"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1161\/JAHA.116.005204"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.116.08240"},{"key":"B51","doi-asserted-by":"crossref","first-page":"A13911","DOI":"10.1161\/CIRCULATIONAHA.115.015842","volume":"132","author":"Yang P","year":"2015","journal-title":"Circulation"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.116.023218"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.3.F481"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2016070734"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.117.10156"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(16)31919-5"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1097\/HJH.0b013e328325d861"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00606.2019","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2020,4,13]],"date-time":"2020-04-13T13:08:25Z","timestamp":1586783305000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00606.2019"}},"issued":{"date-parts":[[2020,5,1]]},"references-count":57,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2020,5,1]]}},"alternative-id":["10.1152\/ajprenal.00606.2019"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00606.2019","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2020,5,1]]}},{"indexed":{"date-parts":[[2026,4,3]],"date-time":"2026-04-03T08:18:44Z","timestamp":1775204324555,"version":"3.50.1"},"reference-count":22,"publisher":"American Physiological Society","issue":"5","funder":[{"DOI":"10.13039\/100000062","name":"NIDDK","doi-asserted-by":"crossref","award":["P01DK056788"],"award-info":[{"award-number":["P01DK056788"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2018,11,1]]},"abstract":"<jats:p>Randall\u2019s plaque, an attachment site over which calcium oxalate stones form, begins in the basement membranes of thin limbs of the loop of Henle. The mechanism of its formation is unknown. Possibly, enhanced delivery of calcium out of the proximal tubule, found in many stone formers, increases reabsorption of calcium from the thick ascending limb into the interstitium around descending vasa recta, which convey that calcium into the deep medulla, and raises supersaturations near thin limbs (\u201cvas washdown\u201d). According to this hypothesis, plaque should form preferentially on ascending thin limbs, which do not reabsorb water. We stained serial sections of papillary biopsies from stone-forming patients for aquaporin 1 (which is found in the descending thin limb) and the kidney-specific chloride channel ClC-Ka (which is found in the ascending thin limb). Plaque (which is detected using Yasue stain) colocalized with ClC-Ka, but not with aquaporin 1 (\u03c7<jats:sup>2<\/jats:sup>\u2009=\u2009464, P &lt; 0.001). We conclude that plaque forms preferentially in the basement membranes of ascending thin limbs, fulfilling a critical prediction of the vas washdown theory of plaque pathogenesis. The clinical implication is that treatments such as a low-sodium diet or thiazide diuretics that raise proximal tubule calcium reabsorption may reduce formation of plaque as well as calcium kidney stones.<\/jats:p>","DOI":"10.1152\/ajprenal.00035.2018","type":"journal-article","created":{"date-parts":[[2018,8,1]],"date-time":"2018-08-01T11:35:04Z","timestamp":1533123304000},"page":"F1236-F1242","source":"Crossref","is-referenced-by-count":41,"title":["Randall\u2019s plaque in stone formers originates in ascending thin limbs"],"prefix":"10.1152","volume":"315","author":[{"given":"Andrew P.","family":"Evan","sequence":"first","affiliation":[{"name":"Department of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, Indiana"}]},{"given":"Fredric L.","family":"Coe","sequence":"additional","affiliation":[{"name":"Nephrology Section, Department of Medicine, University of Chicago, Chicago, Illinois"}]},{"given":"James","family":"Lingeman","sequence":"additional","affiliation":[{"name":"Department of Urology, Indiana University School of Medicine, Indianapolis, Indiana"}]},{"given":"Sharon","family":"Bledsoe","sequence":"additional","affiliation":[{"name":"Department of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, Indiana"}]},{"given":"Elaine M.","family":"Worcester","sequence":"additional","affiliation":[{"name":"Nephrology Section, Department of Medicine, University of Chicago, Chicago, Illinois"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1980.239.1.F24"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1007\/s00240-010-0296-z"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2016.101"},{"key":"B4","first-page":"472","volume":"37","author":"Deganello S","year":"1990","journal-title":"Kidney Int"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1002\/ar.20580"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1172\/JCI17038"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1002\/ar.22881"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1002\/ar.23105"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1136\/jclinpath-2017-204387"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1007\/s00240-014-0705-9"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00071.2015"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00316.x"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.257.5.F738"},{"key":"B14","doi-asserted-by":"crossref","first-page":"1","DOI":"10.1681\/ASN.V811","volume":"8","author":"Maunsbach AB","year":"1997","journal-title":"J Am Soc Nephrol"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1111\/jcmm.12514"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1007\/s00240-014-0718-4"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117626"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00236.2015"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(17)47703-2"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90404.2008"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1369\/0022155411398488"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1267\/ahc.2.83"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00035.2018","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,28]],"date-time":"2022-08-28T15:35:17Z","timestamp":1661700917000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00035.2018"}},"issued":{"date-parts":[[2018,11,1]]},"references-count":22,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2018,11,1]]}},"alternative-id":["10.1152\/ajprenal.00035.2018"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00035.2018","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2018,11,1]]}},{"indexed":{"date-parts":[[2026,4,3]],"date-time":"2026-04-03T23:02:11Z","timestamp":1775257331296,"version":"3.50.1"},"reference-count":42,"publisher":"American Physiological Society","issue":"1","funder":[{"DOI":"10.13039\/501100002661","name":"Fonds De La Recherche Scientifique - FNRS","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100002661","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100003134","name":"FNRS | Fonds pour la Formation \u00e0 la Recherche dans l'Industrie et dans l'Agriculture","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100003134","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100006673","name":"Fonds L\u00e9on Fredericq","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100006673","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100005627","name":"Universit\u00e9 de Li\u00e8ge","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100005627","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Soci\u00e9t\u00e9 Francophone de N\u00e9phrologie Dialyse et Transplantation"}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2025,7,1]]},"abstract":"<jats:p> Kidney transplantation outcomes are influenced by donor type. Brain death has been associated with significant kidney injury, with long-term sequelae. We established two rat models mimicking human conditions of kidney donation after brain death or circulatory arrest. We identified TNF\u03b1 as the main driver of BD-induced kidney injury, as validated in human pretransplant biopsies. Notably, kidney denervation before BD failed to prevent TNF\u03b1-mediated damage. Targeting TNF\u03b1 signaling in DBD donors may improve transplant outcomes. <\/jats:p>","DOI":"10.1152\/ajprenal.00109.2025","type":"journal-article","created":{"date-parts":[[2025,6,3]],"date-time":"2025-06-03T16:20:16Z","timestamp":1748967616000},"page":"F128-F142","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":3,"title":["Kidney transplant injury associated with brain death is mediated by TNF\u03b1, independently of renal innervation"],"prefix":"10.1152","volume":"329","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4544-2788","authenticated-orcid":false,"given":"Tiago","family":"Pinto Coelho","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/00afp2z80","id-type":"ROR","asserted-by":"publisher"}],"name":"Liege University","place":["Belgium"]}]},{"given":"Pauline","family":"Erpicum","sequence":"additional","affiliation":[{"name":"University Hospital of Liege","place":["Belgium"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1029-6269","authenticated-orcid":false,"given":"Margaux","family":"Navez","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/00afp2z80","id-type":"ROR","asserted-by":"publisher"}],"name":"Liege University","place":["Belgium"]}]},{"given":"Morgan","family":"Vandermeulen","sequence":"additional","affiliation":[{"name":"University Hospital of Liege","place":["Belgium"]},{"name":"Liege University","place":["Belgium"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9436-6673","authenticated-orcid":false,"given":"Olivier","family":"Detry","sequence":"additional","affiliation":[{"name":"University Hospital of Liege","place":["Belgium"]},{"name":"Liege University","place":["Belgium"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2547-6593","authenticated-orcid":false,"given":"Francois","family":"Jouret","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/00afp2z80","id-type":"ROR","asserted-by":"publisher"}],"name":"Liege University","place":["Belgium"]},{"name":"University Hospital of Liege","place":["Belgium"]}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.05021107"},{"key":"B2","volume-title":"NEWSLETTER TRANSPLANT: International Figures on Donation and Transplantation, 2023","author":"European Directorate for the Quality of Medicines &amp; HealthCare","year":"2024"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1093\/bja\/aer357"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1055\/s-0044-1786020"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(04)17406-0"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-6143.2011.03754.x"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1097\/TP.0b013e3182a19348"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1097\/TXD.0000000000001433"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-4939-3353-2_5"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1186\/S13059-014-0550-8"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1038\/NPROT.2009.97"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1002\/IMT2.177"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1097\/MOT.0B013E328344A5DC"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1007\/S00134-019-05551-Y"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/J.BEEM.2020.101449"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMRA1404726"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1046\/J.1523-1755.2002.00433.X"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1177\/0963689718785629"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007070744"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/J.INTIMP.2022.108746"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1111\/CPR.12829"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.25011\/CIM.V43I2.34189"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1016\/J.TRANSPROCEED.2012.08.004"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1073\/PNAS.1014557107"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/j.smim.2014.05.004"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-017-08785-2"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1097\/MOT.0000000000000599"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1038\/KI.2014.285"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.34067\/KID.0000000000000314"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1155\/2015\/602597"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gft538"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1016\/J.NEPHRO.2013.10.006"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-017-08726-z"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.3390\/IJMS24076053"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.3390\/ANTIOX12071440"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1111\/FEBS.16336"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.3390\/IJMS21082951"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1016\/J.TAAP.2018.09.030"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1124\/JPET.110.170084"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1097\/CCM.0000000000000958"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.4266\/ACC.2019.00430"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1152\/AJPRENAL.00290.2007"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00109.2025","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,6,24]],"date-time":"2025-06-24T12:59:58Z","timestamp":1750769998000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00109.2025"}},"issued":{"date-parts":[[2025,7,1]]},"references-count":42,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2025,7,1]]}},"alternative-id":["10.1152\/ajprenal.00109.2025"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00109.2025","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2025,7,1]]},"assertion":[{"value":"2025-03-20","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2025-04-18","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2025-05-29","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2025-06-24","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,4,4]],"date-time":"2026-04-04T00:40:36Z","timestamp":1775263236070,"version":"3.50.1"},"reference-count":43,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2009,2]]},"abstract":"<jats:p>Mutations of the human CLCN5 gene, which encodes the CLC-5 Cl<jats:sup>\u2212<\/jats:sup>\/H<jats:sup>+<\/jats:sup>exchanger, lead to Dent's disease. Mutations result in functional defects that range from moderate reductions to complete loss of whole cell currents, although the severity of the functional defect rarely correlates with the severity of the disease. To further elucidate the basis of CLC-5 mutations causing Dent's disease, we examined the functional and cell biological consequences of seven previously reported missense mutants, utilizing electrophysiological and cell biological techniques. This revealed three classes of Dent's disease-causing CLC-5 mutations. Class 1 mutations lead to endoplasmic reticulum retention and degradation of CLC-5. Class 2 mutations appear to have little effect on subcellular distribution of CLC-5 but cause defective function resulting in severe defects in endosomal acidification. Class 3 mutations lead to alterations in the endosomal distribution of CLC-5 but are otherwise able to support endosomal acidification. Molecular modeling demonstrates a structural basis that may underlie the nature of the defect resulting from each mutation with each class occupying discrete regions of the protein quaternary structure. Thus these results demonstrate that the cell biological consequences of CLC-5 mutations are heterogeneous and can be classified into three major groups and that a correlation between the nature of the defect and the location of the mutation in the structure may be drawn. This model may prove to be useful as a tool to aid in the diagnosis and future therapeutic intervention of the disease.<\/jats:p>","DOI":"10.1152\/ajprenal.90526.2008","type":"journal-article","created":{"date-parts":[[2008,11,20]],"date-time":"2008-11-20T01:25:33Z","timestamp":1227144333000},"page":"F390-F397","source":"Crossref","is-referenced-by-count":51,"title":["Characterization of Dent's disease mutations of CLC-5 reveals a correlation between functional and cell biological consequences and protein structure"],"prefix":"10.1152","volume":"296","author":[{"given":"Andrew J.","family":"Smith","sequence":"first","affiliation":[]},{"given":"Anita A. C.","family":"Reed","sequence":"additional","affiliation":[]},{"given":"Nellie Y.","family":"Loh","sequence":"additional","affiliation":[]},{"given":"Rajesh V.","family":"Thakker","sequence":"additional","affiliation":[]},{"given":"Jonathan D.","family":"Lippiat","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.200509417"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.412"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.051499698"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(90)90148-8"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/8.2.247"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1126\/science.1722350"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1126\/science.1082708"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1006\/geno.1995.9960"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.2.896"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.14.8075"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-002-0950-6"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2005.02.060"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1086\/427887"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1016\/j.biocel.2005.09.009"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00203.x"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005020207"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/6.8.1233"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1038\/379445a0"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119262"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.110.2.165"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1007\/s00439-005-1303-2"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfl346"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1038\/sj.emboj.7601275"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1038\/28190"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00851.x"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M104762200"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1038\/nature03720"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.cellbio.23.090506.123319"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1038\/35042597"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1038\/nature03860"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00718.x"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M010642200"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/gkg520"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(01)80067-6"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M200363200"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1159\/000020689"},{"key":"R37","doi-asserted-by":"crossref","unstructured":"Wang Y, Bartlett MC, Loo TW, Clarke DM.Specific rescue of cystic fibrosis transmembrane conductance regulator processing mutants using pharmacological chaperones.Mol Pharmacol70: 297\u2013302, 2006.","DOI":"10.1124\/mol.106.023994"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00011.2005"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00859.x"},{"key":"R40","doi-asserted-by":"crossref","unstructured":"Yamamoto K, Cox JP, Friedrich T, Christie PT, Bald M, Houtman PN, Lapsley MJ, Patzer L, Tsimaratos M, Van THWG, Yamaoka K, Jentsch TJ, Thakker RV.Characterization of renal chloride channel (CLCN5) mutations in Dent's disease.J Am Soc Nephrol11: 1460\u20131468, 2000.","DOI":"10.1681\/ASN.V1181460"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M312810200"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.5414\/CNP62306"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.44.31123"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.90526.2008","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,9,21]],"date-time":"2021-09-21T20:25:52Z","timestamp":1632255952000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.90526.2008"}},"issued":{"date-parts":[[2009,2]]},"references-count":43,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2009,2]]}},"alternative-id":["10.1152\/ajprenal.90526.2008"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.90526.2008","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2009,2]]}},{"indexed":{"date-parts":[[2026,4,4]],"date-time":"2026-04-04T12:06:07Z","timestamp":1775304367222,"version":"3.50.1"},"reference-count":44,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2004,9]]},"abstract":"<jats:p>Identifying genes underlying common forms of kidney disease in humans has proven difficult, expensive, and time consuming. Quantitative trait loci (QTL) for several complex traits are concordant among mice, rats, and humans, suggesting that genetic findings from these animal models are relevant to human disease. Therefore, we reviewed the literature on genetic studies of kidney disease in rat and mouse and examined the concordance between kidney disease QTL across species. Fifteen genomic regions contribute to kidney disease in the rat, with 12 replicated either in a separate rat cross or in another species. Five loci found in humans were concordant to QTL found in the rat. Two of these were found by homology to a previously identified rat QTL on chromosome 1, demonstrating that kidney disease loci in animal models can predict the location of kidney disease loci in humans. In contrast to the rat, the mouse has been underutilized in the genetic analysis of polygenic kidney disease, although mutagenesis and QTL analysis in the mouse are likely to contribute new findings in the near future. Knowledge of kidney disease loci conserved between the mouse and rat will identify prime candidate loci to test for association with chronic kidney disease in humans.<\/jats:p>","DOI":"10.1152\/ajprenal.00159.2004","type":"journal-article","created":{"date-parts":[[2004,8,5]],"date-time":"2004-08-05T17:12:50Z","timestamp":1091725970000},"page":"F347-F352","source":"Crossref","is-referenced-by-count":42,"title":["Unraveling the genetics of chronic kidney disease using animal models"],"prefix":"10.1152","volume":"287","author":[{"given":"Ron","family":"Korstanje","sequence":"first","affiliation":[]},{"given":"Keith","family":"DiPetrillo","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)64892-4"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.genom.2.1.463"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.63.s83.3.x"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1038\/ng0196-44"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.37.2.456"},{"key":"R6","unstructured":"Culleton BF, Larson MG, Parfrey PS, Kannel WB, and Levy D.Proteinuria as a risk factor for cardiovascular disease and mortality in older people: a prospective study.Am J Med109: 1\u20138, 2000."},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1086\/316927"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1016\/S0735-1097(02)02165-4"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1152\/physiolgenomics.00212.2003"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.21.14.4829-4836.2001"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00534.x"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000060572.13794.58"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1034\/j.1600-065x.2001.1840116.x"},{"key":"R14","unstructured":"Grimm RH Jr, Svendsen KH, Kasiske B, Keane WF, and Wahi MM.Proteinuria is a risk factor for mortality over 10 years of follow-up. MRFIT Research Group Multiple Risk Factor Intervention Trial.Kidney Int Suppl63: S10\u2013S14, 1997."},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118539"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000031732.78052.81"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2002.kid557.x"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.47.5.821"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1161\/01.ATV.19.3.617"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1016\/0002-8703(84)90763-4"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(99)70442-7"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1038\/9642"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1016\/0895-7061(96)00102-1"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00828.x"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1161\/01.STR.27.11.2033"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1016\/1074-7613(94)90100-7"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1007\/s003359900888"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1053\/ajkd.2002.29865"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1152\/physiolgenomics.00053.2003"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1152\/physiolgenomics.00030.2000"},{"key":"R31","doi-asserted-by":"crossref","unstructured":"Rathkolb B, Fuchs E, Kolb HJ, Renner-Muller I, Krebs O, Balling R, Hrabe de Angelis M, and Wolf E.Large-scaleN-ethyl-N-nitrosourea mutagenesis of mice\u2014from phenotypes to genes.Exp Physiol85: 635\u2013644, 2000.","DOI":"10.1017\/S0958067000020947"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1161\/hc2501.091353"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000095676.90936.80"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000031803.55613.86"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000100126.62370.25"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1007\/s11886-002-0106-5"},{"key":"R37","doi-asserted-by":"crossref","unstructured":"Shiozawa M, Provoost AP, van Dokkum RPE, Majewski RR, and Jacob HJ.Evidence of gene-gene interactions in the genetic susceptibility to renal impairment after unilateral nephrectomy.J Am Soc Nephrol11: 2068\u20132078, 2000.","DOI":"10.1681\/ASN.V11112068"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1101\/gr.10.4.473"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1006\/geno.2000.6401"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.01029.2003"},{"key":"R41","unstructured":"US Renal Data System.USRDS 2003 Annual Data Report. In:Atlas of End-Stage Renal Disease in the United States. Bethesda, MD: National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases, 2003."},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1161\/01.ATV.0000030201.29121.A3"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1006\/geno.1999.5828"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1152\/physiolgenomics.00014.2002"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00159.2004","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,6,24]],"date-time":"2021-06-24T21:11:05Z","timestamp":1624569065000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00159.2004"}},"issued":{"date-parts":[[2004,9]]},"references-count":44,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2004,9]]}},"alternative-id":["10.1152\/ajprenal.00159.2004"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00159.2004","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2004,9]]}},{"indexed":{"date-parts":[[2026,4,5]],"date-time":"2026-04-05T06:46:27Z","timestamp":1775371587009,"version":"3.50.1"},"reference-count":46,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2007,9]]},"abstract":"<jats:p>Clostridium perfringens epsilon toxin (ET) is a potent pore-forming cytotoxin causing fatal enterotoxemia in livestock. ET accumulates in brain and kidney, particularly in the renal distal-collecting ducts. ET binds and oligomerizes in detergent-resistant membranes (DRMs) microdomains and causes cell death. However, the causal linkage between membrane permeabilization and cell death is not clear. Here, we show that ET binds and forms 220-kDa insoluble complexes in plasma membrane DRMs of renal mpkCCD<jats:sub>cl4<\/jats:sub>collecting duct cells. Phosphatidylinositol-specific phospholipase C did not impair binding or the formation of ET complexes, suggesting that the receptor for ET is not GPI anchored. ET induced a dose-dependent fall in the transepithelial resistance and potential in confluent cells grown on filters, transiently stimulated Na<jats:sup>+<\/jats:sup>absorption, and induced an inward ionic current and a sustained rise in [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>. ET also induced rapid depletion of cellular ATP, and stimulated the AMP-activated protein kinase, a metabolic-sensing Ser\/Thr kinase. ET also induced mitochondrial membrane permeabilization and mitochondrial-nuclear translocation of apoptosis-inducing factor, a potent caspase-independent cell death effector. Finally, ET induced cell necrosis characterized by a marked reduction in nucleus size without DNA fragmentation. DRM disruption by methyl-\u03b2-cyclodextrin impaired ET oligomerization, and significantly reduced the influx of Na<jats:sup>+<\/jats:sup>and [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>, but did not impair ATP depletion and cell death caused by the toxin. These findings indicate that ET causes rapid necrosis of renal collecting duct cells and establish that ATP depletion-mediated cell death is not strictly correlated with the plasma membrane permeabilization and ion diffusion caused by the toxin.<\/jats:p>","DOI":"10.1152\/ajprenal.00199.2007","type":"journal-article","created":{"date-parts":[[2007,6,14]],"date-time":"2007-06-14T04:08:35Z","timestamp":1181794115000},"page":"F927-F937","source":"Crossref","is-referenced-by-count":85,"title":["Pore-forming epsilon toxin causes membrane permeabilization and rapid ATP depletion-mediated cell death in renal collecting duct cells"],"prefix":"10.1152","volume":"293","author":[{"given":"C.","family":"Chassin","sequence":"first","affiliation":[]},{"given":"M.","family":"Bens","sequence":"additional","affiliation":[]},{"given":"J.","family":"de Barry","sequence":"additional","affiliation":[]},{"given":"R.","family":"Courjaret","sequence":"additional","affiliation":[]},{"given":"J. L.","family":"Bossu","sequence":"additional","affiliation":[]},{"given":"F.","family":"Cluzeaud","sequence":"additional","affiliation":[]},{"given":"S.","family":"Ben Mkaddem","sequence":"additional","affiliation":[]},{"given":"M.","family":"Gibert","sequence":"additional","affiliation":[]},{"given":"B.","family":"Poulain","sequence":"additional","affiliation":[]},{"given":"M. R.","family":"Popoff","sequence":"additional","affiliation":[]},{"given":"A.","family":"Vandewalle","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.140.3.525"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.147.1.175"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.71.2.739-746.2003"},{"key":"R4","doi-asserted-by":"crossref","unstructured":"Bens M, Vallet V, Cluzeaud F, Pascual-Letallec L, Kahn A, Rafestin-Oblin ME, Rossier BC, Vandewalle A.Corticosteroid-dependent sodium transport in a novel immortalized mouse collecting duct principal cell line.J Am Soc Nephrol10: 923\u2013934, 1999.","DOI":"10.1681\/ASN.V105923"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-006-0123-0"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.cellbio.14.1.111"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.01311"},{"key":"R8","doi-asserted-by":"crossref","unstructured":"Chakrabarti G, McClane BA.The importance of calcium influx, calpain and calmodulin for the activation of CaCo-2 cell death pathways byClostridium perfringensenterotoxin.Cell Microbiol7: 129\u2013146, 2005.","DOI":"10.1111\/j.1462-5822.2004.00442.x"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1038\/nsmb804"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-5793(00)01731-2"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1096\/fasebj.14.5.729"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.4.2355"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1053\/jcpa.1998.0289"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.69.10.6310-6317.2001"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.E05-05-0398"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.38.27274"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1016\/j.micpath.2004.09.001"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.01540"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1152\/physiol.00044.2005"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1101\/gad.1212704"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.29.17250"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.3109\/09687689709068435"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1042\/bj2440001"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.32.22604"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1126\/science.281.5385.2027"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1111\/j.1348-0421.1997.tb01888.x"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1111\/j.1574-6968.2000.tb09215.x"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M011527200"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M206731200"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.2001.6031"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1016\/0041-0101(91)90105-Z"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.25.14681"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1207559"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1128\/jb.179.20.6480-6487.1997"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M010412200"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1046\/j.1462-5822.2003.00262.x"},{"key":"R37","doi-asserted-by":"crossref","unstructured":"Popoff MR.Purification and characterization ofClostridium sordelliilethal toxin and cross-reactivity withClostridium difficilecytotoxin.Infect Immun55: 35\u201343, 1987.","DOI":"10.1128\/IAI.55.1.35-43.1987"},{"key":"R38","doi-asserted-by":"crossref","unstructured":"Richards JF, Mainguy G, Bibert M, Marvaud JC, Stiles B, Popoff MR.Transcytosis of iota toxin across polarized CaCo-2 cell monolayers.Mol Microbiol43: 901\u2013917, 2002.","DOI":"10.1046\/j.1365-2958.2002.02806.x"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00049.2003"},{"key":"R40","unstructured":"Sakurai J.Toxins ofClostridium perfringens.Rev Med Microbiol6: 175\u2013185, 1995."},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.2.1150"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1369\/jhc.4A6254.2004"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1038\/17135"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.71.9.5371-5375.2003"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1053\/jcpa.2001.0514"},{"key":"R46","doi-asserted-by":"crossref","unstructured":"Vuagniaux G, Vallet V, Jaeger NF, Pfister C, Bens M, Farman N, Courtois-Coutry N, Vandewalle A, Rossier BC, Hummler E.Activation of the amiloride-sensitive epithelial sodium channel by the mouse serine protease mCAP1 expressed in a mouse cortical collecting duct cell line.J Am Soc Nephrol11: 828\u2013834, 2000.","DOI":"10.1681\/ASN.V115828"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00199.2007","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,5,12]],"date-time":"2023-05-12T11:04:58Z","timestamp":1683889498000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00199.2007"}},"issued":{"date-parts":[[2007,9]]},"references-count":46,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2007,9]]}},"alternative-id":["10.1152\/ajprenal.00199.2007"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00199.2007","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2007,9]]}},{"indexed":{"date-parts":[[2026,4,2]],"date-time":"2026-04-02T16:21:49Z","timestamp":1775146909084,"version":"3.50.1"},"reference-count":60,"publisher":"American Physiological Society","issue":"1","funder":[{"name":"NIH","award":["R01HL095638"],"award-info":[{"award-number":["R01HL095638"]}]},{"name":"NIH","award":["P20GM104357"],"award-info":[{"award-number":["P20GM104357"]}]},{"name":"NIH","award":["and P01HL51971"],"award-info":[{"award-number":["and P01HL51971"]}]},{"name":"NIH","award":["R01HL095638 and R01HL121527"],"award-info":[{"award-number":["R01HL095638 and R01HL121527"]}]},{"name":"AHA","award":["IPA34170267"],"award-info":[{"award-number":["IPA34170267"]}]},{"name":"AHA","award":["PRE34380274"],"award-info":[{"award-number":["PRE34380274"]}]},{"name":"AHA","award":["PRE34380314"],"award-info":[{"award-number":["PRE34380314"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2020,7,1]]},"abstract":"<jats:p>Inflammation is a major determinant for the progression of chronic kidney disease (CKD). NF-\u03baB is a master transcription factor upregulated in CKD that promotes inflammation and regulates apoptosis and vascular remodeling. We aimed to modulate this pathway for CKD therapy in a swine model of CKD using a peptide inhibitor of the NF-\u03baB p50 subunit (p50i) fused to a protein carrier [elastin-like polypeptide (ELP)] and equipped with a cell-penetrating peptide (SynB1). We hypothesized that intrarenal SynB1-ELP-p50i therapy would inhibit NF-\u03baB-driven inflammation and induce renal recovery. CKD was induced in 14 pigs. After 6 wk, pigs received single intrarenal SynB1-ELP-p50i therapy (10 mg\/kg) or placebo ( n = 7 each). Renal hemodynamics were quantified in vivo using multidetector computed tomography before and 8 wk after treatment. Pigs were then euthanized. Ex vivo experiments were performed to quantify renal activation of NF-\u03baB, expression of downstream mediators of NF-\u03baB signaling, renal microvascular density, inflammation, and fibrosis. Fourteen weeks of CKD stimulated NF-\u03baB signaling and downstream mediators (e.g., TNF-\u03b1, monocyte chemoattractant protein-1, and IL-6) accompanying loss of renal function, inflammation, fibrosis, and microvascular rarefaction versus controls. All of these were improved after SynB1-ELP-p50i therapy, accompanied by reduced circulating inflammatory cytokines as well, which were evident up to 8 wk after treatment. Current treatments for CKD are largely ineffective. Our study shows the feasibility of a new treatment to induce renal recovery by offsetting inflammation at a molecular level. It also supports the therapeutic potential of targeted inhibition of the NF-\u03baB pathway using novel drug delivery technology in a translational model of CKD.<\/jats:p>","DOI":"10.1152\/ajprenal.00155.2020","type":"journal-article","created":{"date-parts":[[2020,6,15]],"date-time":"2020-06-15T09:47:15Z","timestamp":1592214435000},"page":"F139-F148","source":"Crossref","is-referenced-by-count":24,"title":["Molecular targeting of renal inflammation using drug delivery technology to inhibit NF-\u03baB improves renal recovery in chronic kidney disease"],"prefix":"10.1152","volume":"319","author":[{"given":"Alejandro R.","family":"Chade","sequence":"first","affiliation":[{"name":"Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi"},{"name":"Department of Medicine, University of Mississippi Medical Center, Jackson, Mississippi"},{"name":"Department of Radiology, University of Mississippi Medical Center, Jackson, Mississippi"}]},{"given":"Maxx L.","family":"Williams","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi"}]},{"given":"Jason E.","family":"Engel","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi"}]},{"given":"Erika","family":"Williams","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9104-150X","authenticated-orcid":false,"suffix":"III","given":"Gene L.","family":"Bidwell","sequence":"additional","affiliation":[{"name":"Department of Neurology, University of Mississippi Medical Center, Jackson, Mississippi"},{"name":"Department of Cell and Molecular Biology, University of Mississippi Medical Center, Jackson, Mississippi"},{"name":"Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.13121215"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2009-07-232132"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2016030317"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00143.2016"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00179.2018"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00752.x"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00170.x"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004080674"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCINTERVENTIONS.110.951277"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00674.2011"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000027105.02327.48"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000117774.83396.E9"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014040323"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2015040346"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00063.2018"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2017.09.029"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.108.788653"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1096\/fj.05-5680fje"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/j.coi.2012.12.005"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1159\/000059327"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1148\/radiol.2432060655"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.17.11721"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00006.2013"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.18632\/aging.100080"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1159\/000066278"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.119.13368"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.119.13469"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-5793(03)00003-6"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/j.smim.2014.05.004"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1111\/j.1549-8719.2010.00020.x"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfp605"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.281.4.F630"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1101\/cshperspect.a001651"},{"key":"B34","doi-asserted-by":"crossref","first-page":"1455","DOI":"10.1681\/ASN.V1071455","volume":"10","author":"Lerman LO","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.24.14255"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1038\/sigtrans.2017.23"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1186\/1479-5876-9-13"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.3892\/or.2016.4711"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00254.2006"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1016\/j.jim.2007.10.015"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90435.2008"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1053\/j.ackd.2010.03.002"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010020218"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2018.01.002"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00195.2018"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1096\/fj.201701543RR"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.3389\/fimmu.2019.00815"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.2337\/db06-0188"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00422.x"},{"key":"B51","first-page":"375","volume":"33","author":"Sui X","year":"2019","journal-title":"J Biol Regul Homeost Agents"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2002.kid577.x"},{"key":"B53","unstructured":"Thomas EH. Optimizing the Delivery of Therapeutic Peptides Using Elastin-Like Polypeptide (Master\u2019s thesis). Jackson, MS: University of Mississippi Medical Center, 2010."},{"key":"B54","doi-asserted-by":"crossref","first-page":"2659","DOI":"10.1158\/1538-7445.AM10-2659","volume":"70","author":"Thomas EH","year":"2010","journal-title":"Cancer Res"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfu361"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.00490116"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1096\/fasebj.14.3.532"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1042\/bj20020752"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1016\/j.molimm.2015.09.002"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1097\/HJH.0b013e3283300192"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00273.x"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00155.2020","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,10,28]],"date-time":"2022-10-28T16:56:36Z","timestamp":1666976196000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00155.2020"}},"issued":{"date-parts":[[2020,7,1]]},"references-count":60,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2020,7,1]]}},"alternative-id":["10.1152\/ajprenal.00155.2020"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00155.2020","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2020,7,1]]}},{"indexed":{"date-parts":[[2026,4,7]],"date-time":"2026-04-07T18:36:57Z","timestamp":1775587017432,"version":"3.50.1"},"reference-count":56,"publisher":"American Physiological Society","issue":"6","funder":[{"DOI":"10.13039\/100000968","name":"American Heart Association","doi-asserted-by":"publisher","award":["19POST34381041"],"award-info":[{"award-number":["19POST34381041"]}],"id":[{"id":"10.13039\/100000968","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100006108","name":"HHS | NIH | National Center for Advancing Translational Sciences","doi-asserted-by":"publisher","award":["TL1TR001431"],"award-info":[{"award-number":["TL1TR001431"]}],"id":[{"id":"10.13039\/100006108","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["5R01DK116567"],"award-info":[{"award-number":["5R01DK116567"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100004336","name":"Novartis","doi-asserted-by":"publisher","award":["LCZ696BUSNC07T"],"award-info":[{"award-number":["LCZ696BUSNC07T"]}],"id":[{"id":"10.13039\/100004336","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2021,6,1]]},"abstract":"<jats:p> The first-in-class drug sacubitril\/valsartan, a combination of the angiotensin II receptor blocker valsartan and neprilysin inhibitor sacubitril, was tested for its effects in diabetic kidney disease using db\/db mice and KKAy mice. We found that Sac\/Val has sufficient therapeutical potential to counter the pathophysiological effects of diabetic kidney disease. We further revealed a new mechanism to cause inflammation, self-DNA-activated cGAS-STING signaling, which was activated in diabetic kidneys and prevented by sacubitril\/valsartan or valsartan treatment. <\/jats:p>","DOI":"10.1152\/ajprenal.00614.2020","type":"journal-article","created":{"date-parts":[[2021,4,19]],"date-time":"2021-04-19T10:13:48Z","timestamp":1618827228000},"page":"F1133-F1151","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":42,"title":["Sacubitril\/valsartan treatment has differential effects in modulating diabetic kidney disease in <i>db\/db<\/i> mice and KKAy mice compared with valsartan treatment"],"prefix":"10.1152","volume":"320","author":[{"given":"Komuraiah","family":"Myakala","sequence":"first","affiliation":[{"name":"Department of Biochemistry and Molecular & Cellular Biology, Georgetown University, Washington, District of Columbia"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6950-8414","authenticated-orcid":false,"given":"Bryce A.","family":"Jones","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Physiology, Georgetown University, Washington, District of Columbia"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9205-6228","authenticated-orcid":false,"given":"Xiaoxin X.","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular & Cellular Biology, Georgetown University, Washington, District of Columbia"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6403-2261","authenticated-orcid":false,"given":"Moshe","family":"Levi","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular & Cellular Biology, Georgetown University, Washington, District of Columbia"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.03640413"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI72271"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1038\/nrdp.2015.70"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1186\/1478-7954-8-29"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa1310799"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1001\/jama.2011.861"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010040354"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00211.2018"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1159\/000471765"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/0024-3205(81)90370-2"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1038\/332078a0"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1517\/13543784.13.6.643"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1210\/er.2005-0014"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1038\/nrcardio.2014.64"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0043238"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0089201"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa1100171"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000141829.04031.25"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1161\/01.cir.97.23.2323"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115477"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000153269.07762.3B"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/j.amjcard.2012.03.034"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1177\/0091270009343932"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa1409077"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1016\/j.cardfail.2017.12.010"},{"key":"B26","first-page":"5473","volume":"9","author":"Jing W","year":"2017","journal-title":"Am J Transl Res"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00125.2020"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.2174\/1573399810666140508121012"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.5812\/numonthly.1954"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014121271"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.C117.794982"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2017020222"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-62703-739-6_31"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20180139"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejphar.2020.173444"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.15420\/cfr.2016:1:1"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.2337\/db17-0392"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.7717\/peerj.9196"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1097\/HJH.0000000000002326"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1126\/science.aat8657"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.2337\/dbi18-0052"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1038\/nature08476"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1038\/s41576-019-0151-1"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.15252\/embr.201949799"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1126\/science.1232458"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1038\/nri.2017.21"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1016\/j.tcb.2020.05.006"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.50.12.2792"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1016\/j.humimm.2018.03.008"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.2337\/db06-0477"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2019.08.003"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1016\/j.celrep.2019.09.050"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbadis.2016.07.019"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00384.2019"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1002\/cphy.c100049"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009070721"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00614.2020","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,6,23]],"date-time":"2021-06-23T08:45:13Z","timestamp":1624437913000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00614.2020"}},"issued":{"date-parts":[[2021,6,1]]},"references-count":56,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2021,6,1]]}},"alternative-id":["10.1152\/ajprenal.00614.2020"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00614.2020","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2021,6,1]]},"assertion":[{"value":"2020-11-16","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2021-04-12","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2021-06-02","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,4,7]],"date-time":"2026-04-07T06:46:17Z","timestamp":1775544377941,"version":"3.50.1"},"reference-count":78,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2007,6]]},"abstract":"<jats:p>In many forms of experimental kidney diseases, renal VEGF is low, and administering VEGF can be shown to be protective. A paradox occurs in diabetes, in which renal VEGF levels are high and a deleterious effect of VEGF on kidney disease has been shown. We have hypothesized that endothelial dysfunction induced by hyperglycemia or other factors may underlie the pathogenic mechanisms of a high VEGF state. VEGF normally stimulates endothelial nitric oxide (NO) release and acts in concert with elevated NO levels as a trophic factor for vascular endothelium. The increased NO derived from the endothelial cell acts as an inhibitory factor that prevents excess endothelial cell proliferation, vascular smooth muscle cell proliferation, and macrophage infiltration. In the setting where NO bioavailability is reduced in diabetes, high levels of VEGF lead to excessive endothelial cell proliferation, stimulation of macrophage chemotaxis, and vascular smooth muscle cell activation. Consistent with this hypothesis is our recent observation that diabetes induced in endothelial NO-deficient mice results in clinical and histological features identical to human diabetic nephropathy. The discovery of the key role for impaired endothelial NO bioavailability in the stimulation of VEGF and VEGF-dependent disease may provide key insights into not only the pathogenesis of diabetic nephropathy but also the utility and hazard of administering VEGF as a treatment for kidney disease.<\/jats:p>","DOI":"10.1152\/ajprenal.00495.2006","type":"journal-article","created":{"date-parts":[[2007,6,1]],"date-time":"2007-06-01T15:28:27Z","timestamp":1180711707000},"page":"F1665-F1672","source":"Crossref","is-referenced-by-count":110,"title":["Uncoupling of the VEGF-endothelial nitric oxide axis in diabetic nephropathy: an explanation for the paradoxical effects of VEGF in renal disease"],"prefix":"10.1152","volume":"292","author":[{"given":"Takahiko","family":"Nakagawa","sequence":"first","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.4.F791"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.3.F480"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115014"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)61775-0"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1007\/s001250100529"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.48.11.2229"},{"key":"R7","doi-asserted-by":"crossref","unstructured":"De Vriese AS, Tilton RG, Elger M, Stephan CC, Kriz W, Lameire NH.Antibodies against vascular endothelial growth factor improve early renal dysfunction in experimental diabetes.J Am Soc Nephrol12: 993\u20131000, 2001.","DOI":"10.1681\/ASN.V125993"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1172\/JCI11235"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1172\/JCI17423"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1097\/00005344-199601000-00022"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00331.2005"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.51.10.3090"},{"key":"R13","doi-asserted-by":"crossref","unstructured":"Fong GH, Zhang L, Bryce DM, Peng J.Increased hemangioblast commitment, not vascular disorganization, is the primary defect in flt-1 knock-out mice.Development126: 3015\u20133025, 1999.","DOI":"10.1242\/dev.126.13.3015"},{"key":"R14","doi-asserted-by":"crossref","unstructured":"Franco M, Tapia E, Santamaria J, Zafra I, Garcia-Torres R, Gordon KL, Pons H, Rodriguez-Iturbe B, Johnson RJ, Herrera-Acosta J.Renal cortical vasoconstriction contributes to development of salt-sensitive hypertension after angiotensin II exposure.J Am Soc Nephrol12: 2263\u20132271, 2001.","DOI":"10.1681\/ASN.V12112263"},{"key":"R15","doi-asserted-by":"crossref","unstructured":"Fujihara CK, De Nucci G, Zatz R.Chronic nitric oxide synthase inhibition aggravates glomerular injury in rats with subtotal nephrectomy.J Am Soc Nephrol5: 1498\u20131507, 1995.","DOI":"10.1681\/ASN.V571498"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.66035.x"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1097-4652(199706)171:3<252::AID-JCP3>3.0.CO;2-N"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7580.2005.00492.x"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)64957-7"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.94"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000294"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.2337\/db05-1367"},{"key":"R23","unstructured":"Ishida S, Shinoda K, Kawashima S, Oguchi Y, Okada Y, Ikeda E.Coexpression of VEGF receptors VEGF-R2 and neuropilin-1 in proliferative diabetic retinopathy.Invest Ophthalmol Vis Sci41: 1649\u20131656, 2000."},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1089\/hum.1996.7.8-959"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005010063"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2004.09.020"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)64175-2"},{"key":"R28","unstructured":"Kang DH, Hughes J, Mazzali M, Schreiner GF, Johnson RJ.Impaired angiogenesis in the remnant kidney model: II. Vascular endothelial growth factor administration reduces renal fibrosis and stabilizes renal function.J Am Soc Nephrol12: 1448\u20131457, 2001."},{"key":"R29","doi-asserted-by":"crossref","unstructured":"Kang DH, Joly AH, Oh SW, Hugo C, Kerjaschki D, Gordon KL, Mazzali M, Jefferson JA, Hughes J, Madsen KM, Schreiner GF, Johnson RJ.Impaired angiogenesis in the remnant kidney model. I. Potential role of vascular endothelial growth factor and thrombospondin-1.J Am Soc Nephrol12: 1434\u20131447, 2001.","DOI":"10.1016\/S0272-6386(01)80019-6"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.4.F727"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)63155-0"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.93.17.9114"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00273.x"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00422.x"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-200208000-00021"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1999.276.6.H1943"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00428.2002"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.33.4.1013"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00096.2006"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M313897200"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)61731-2"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1172\/JCI17189"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1007\/s00125-002-0956-9"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1007\/BF01614771"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1053\/ajkd.1998.v31.pm9531171"},{"key":"R46","doi-asserted-by":"publisher","DOI":"10.1172\/JCI1560"},{"key":"R47","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006050459"},{"key":"R48","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005070759"},{"key":"R49","doi-asserted-by":"publisher","DOI":"10.1007\/BF00399948"},{"key":"R50","doi-asserted-by":"publisher","DOI":"10.1172\/JCI6740"},{"key":"R51","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/14.2.348"},{"key":"R52","doi-asserted-by":"publisher","DOI":"10.1007\/s004280000311"},{"key":"R53","doi-asserted-by":"publisher","DOI":"10.1007\/s004280100485"},{"key":"R54","doi-asserted-by":"publisher","DOI":"10.1016\/S0891-6632(87)80069-7"},{"key":"R55","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119868"},{"key":"R56","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00112.x"},{"key":"R57","doi-asserted-by":"publisher","DOI":"10.1096\/fj.02-0321fje"},{"key":"R58","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000099374.58607.C9"},{"key":"R59","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1201380"},{"key":"R60","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1988.193"},{"key":"R61","doi-asserted-by":"publisher","DOI":"10.1161\/01.ATV.0000178171.61754.cd"},{"key":"R62","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.78.2.225"},{"key":"R63","unstructured":"Sato W, Zhang L, Johnson RJ, Nakagawa T.Uncoupling of VEGF with nitric oxide as a causal mechanism for macrophage migration (Abstract).J Am Soc Nephrol17: 308A, 2006."},{"key":"R64","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00621.x"},{"key":"R65","doi-asserted-by":"publisher","DOI":"10.1038\/376062a0"},{"key":"R66","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.46.33057"},{"key":"R67","doi-asserted-by":"publisher","DOI":"10.1016\/0046-8177(93)90066-P"},{"key":"R68","doi-asserted-by":"publisher","DOI":"10.1007\/s001250051198"},{"key":"R69","doi-asserted-by":"publisher","DOI":"10.1038\/nm0897-879"},{"key":"R70","doi-asserted-by":"publisher","DOI":"10.1006\/niox.2001.0382"},{"key":"R71","doi-asserted-by":"publisher","DOI":"10.1016\/j.lfs.2004.10.062"},{"key":"R72","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.1998.00830.x"},{"key":"R73","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1991.234"},{"key":"R74","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.139"},{"key":"R75","doi-asserted-by":"publisher","DOI":"10.1161\/01.ATV.0000207319.28254.8c"},{"key":"R76","doi-asserted-by":"publisher","DOI":"10.1161\/hc0902.104718"},{"key":"R77","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000138688.78906.6b"},{"key":"R78","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119451"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00495.2006","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,5,12]],"date-time":"2023-05-12T04:07:47Z","timestamp":1683864467000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00495.2006"}},"issued":{"date-parts":[[2007,6]]},"references-count":78,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2007,6]]}},"alternative-id":["10.1152\/ajprenal.00495.2006"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00495.2006","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2007,6]]}},{"indexed":{"date-parts":[[2026,4,7]],"date-time":"2026-04-07T21:55:17Z","timestamp":1775598917377,"version":"3.50.1"},"reference-count":49,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,8,15]]},"abstract":"<jats:p>\n                    Autophagy is a cellular recycling process induced in response to many types of stress. However, little is known of the signaling pathways that regulate autophagy during acute kidney injury (AKI). Bcl-2\/adenovirus E1B 19 kDa-interacting protein (BNIP)3 and sestrin-2 are the target proteins of hypoxia-inducible factor (HIF)-1\u03b1 and p53, respectively. The aim of this study was to investigate the roles of BNIP3 and sestrin-2 in oxidative stress-induced autophagy during AKI. We used rat ischemia-reperfusion injury and cultured renal tubular (NRK-52E) cells as in vivo and in vitro models of AKI, respectively. Renal ischemia-reperfusion injury upregulated the expression of BNIP3 and sestrin-2 in the proximal tubules, as measured by immunohistochemical staining and Western blot analysis. In vitro, NRK-52E cells exposed to hypoxia showed increased expression of BNIP3 mRNA and protein in a HIF-1\u03b1-dependent manner. In contrast, sestrin-2 mRNA and protein expression were upregulated in a p53-dependent manner after exposure to oxidative stress (exogenous H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    ). NRK-52E cells stably transfected with a fusion protein between green fluorescent protein and light chain 3 were used to investigate autophagy. Overexpression of BNIP3 or sestrin-2 in these cells induced light chain 3 expression and formation of autophagosomes. Interestingly, BNIP3-induced autophagosomes were mainly localized to the mitochondria, suggesting that this protein selectively induces mitophagy. These observations demonstrate that autophagy is induced in renal tubules by at least two independent pathways involving p53-sestrin-2 and HIF-1\u03b1-BNIP3, which may be activated by different types of stress to protect the renal tubules during AKI.\n                  <\/jats:p>","DOI":"10.1152\/ajprenal.00642.2012","type":"journal-article","created":{"date-parts":[[2013,5,22]],"date-time":"2013-05-22T22:06:57Z","timestamp":1369260417000},"page":"F495-F509","source":"Crossref","is-referenced-by-count":181,"title":["Sestrin-2 and BNIP3 regulate autophagy and mitophagy in renal tubular cells in acute kidney injury"],"prefix":"10.1152","volume":"305","author":[{"given":"Masayuki","family":"Ishihara","sequence":"first","affiliation":[{"name":"Department of Endocrinology, Metabolism and Nephrology, Kochi Medical School, Kochi University, Nankoku, Japan;"}]},{"given":"Madoka","family":"Urushido","sequence":"additional","affiliation":[{"name":"Center for Innovative and Translational Medicine, Kochi Medical School, Kochi University, Nankoku, Japan; and"}]},{"given":"Kazu","family":"Hamada","sequence":"additional","affiliation":[{"name":"Department of Endocrinology, Metabolism and Nephrology, Kochi Medical School, Kochi University, Nankoku, Japan;"}]},{"given":"Tatsuki","family":"Matsumoto","sequence":"additional","affiliation":[{"name":"Department of Endocrinology, Metabolism and Nephrology, Kochi Medical School, Kochi University, Nankoku, Japan;"}]},{"given":"Yoshiko","family":"Shimamura","sequence":"additional","affiliation":[{"name":"Department of Endocrinology, Metabolism and Nephrology, Kochi Medical School, Kochi University, Nankoku, Japan;"}]},{"given":"Koji","family":"Ogata","sequence":"additional","affiliation":[{"name":"Department of Endocrinology, Metabolism and Nephrology, Kochi Medical School, Kochi University, Nankoku, Japan;"}]},{"given":"Kosuke","family":"Inoue","sequence":"additional","affiliation":[{"name":"Department of Endocrinology, Metabolism and Nephrology, Kochi Medical School, Kochi University, Nankoku, Japan;"}]},{"given":"Yoshinori","family":"Taniguchi","sequence":"additional","affiliation":[{"name":"Department of Endocrinology, Metabolism and Nephrology, Kochi Medical School, Kochi University, Nankoku, Japan;"}]},{"given":"Taro","family":"Horino","sequence":"additional","affiliation":[{"name":"Department of Endocrinology, Metabolism and Nephrology, Kochi Medical School, Kochi University, Nankoku, Japan;"}]},{"given":"Mikiya","family":"Fujieda","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Kochi Medical School, Kochi University, Nankoku, Japan"}]},{"given":"Shimpei","family":"Fujimoto","sequence":"additional","affiliation":[{"name":"Department of Endocrinology, Metabolism and Nephrology, Kochi Medical School, Kochi University, Nankoku, Japan;"}]},{"given":"Yoshio","family":"Terada","sequence":"additional","affiliation":[{"name":"Department of Endocrinology, Metabolism and Nephrology, Kochi Medical School, Kochi University, Nankoku, Japan;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000067652.51441.21"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2008.06.028"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1205877"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/j.neulet.2009.06.011"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1038\/sj.cdd.4400978"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1084\/jem.186.12.1975"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1097\/01.tp.0000287334.38933.e3"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2006.05.034"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006010017"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0610666104"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1172\/JCI32490"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.111.246108"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1096\/fj.01-0206fje"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/j.febslet.2009.10.017"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0502857102"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/j.tibs.2012.02.004"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00097.2010"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1186\/1756-9966-29-150"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.4161\/auto.19821"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1007\/s10157-009-0254-7"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2010.090594"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010070705"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.74"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00552.2008"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1042\/BJ20111451"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.4161\/cc.8.10.8498"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1038\/ncb0910-823"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2010.01.028"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1038\/embor.2009.256"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.214"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000029232.42227.16"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1038\/nm1320"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1038\/nature07006"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0032035"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009040383"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0708818104"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2008.01.059"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000145459.54236.D3"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.060002553.x"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000060577.94532.06"},{"key":"B41","doi-asserted-by":"crossref","first-page":"31296","DOI":"10.1016\/S0021-9258(18)47422-4","volume":"269","author":"Terada Y","year":"1994","journal-title":"J Biol Chem"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1038\/sj.emboj.7601963"},{"key":"B43","first-page":"474","volume":"66","author":"Wallin A","year":"1992","journal-title":"Lab Invest"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.4161\/auto.7.3.14502"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1186\/1423-0127-16-19"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1007\/s00280-010-1391-0"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00590.2007"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.20.12415"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1016\/j.brainres.2006.12.086"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00642.2012","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,2,22]],"date-time":"2022-02-22T13:07:31Z","timestamp":1645535251000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00642.2012"}},"issued":{"date-parts":[[2013,8,15]]},"references-count":49,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2013,8,15]]}},"alternative-id":["10.1152\/ajprenal.00642.2012"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00642.2012","relation":{"has-review":[{"id-type":"doi","id":"10.3410\/f.718012810.793481005","asserted-by":"object"}]},"ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2013,8,15]]}},{"indexed":{"date-parts":[[2026,4,7]],"date-time":"2026-04-07T09:18:47Z","timestamp":1775553527091,"version":"3.50.1"},"reference-count":70,"publisher":"American Physiological Society","issue":"2","funder":[{"DOI":"10.13039\/501100001711","name":"Swiss National Science Foundation (Schweizerische Nationalfonds)","doi-asserted-by":"publisher","award":["310030_159735"],"award-info":[{"award-number":["310030_159735"]}],"id":[{"id":"10.13039\/501100001711","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001711","name":"Swiss National Science Foundation (Schweizerische Nationalfonds)","doi-asserted-by":"publisher","award":["310030_143929\/1"],"award-info":[{"award-number":["310030_143929\/1"]}],"id":[{"id":"10.13039\/501100001711","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100002339","name":"National Center of Competence in Research Affective Sciences - Emotions in Individual Behaviour and Social Processes (National Centre of Competence in Research Affective Sciences)","doi-asserted-by":"publisher","award":["Kidney.ch"],"award-info":[{"award-number":["Kidney.ch"]}],"id":[{"id":"10.13039\/501100002339","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000921","name":"European Cooperation in Science and Technology (COST)","doi-asserted-by":"publisher","award":["BM1301"],"award-info":[{"award-number":["BM1301"]}],"id":[{"id":"10.13039\/501100000921","id-type":"DOI","asserted-by":"publisher"}]},{"name":"NIH","award":["R01DK098145"],"award-info":[{"award-number":["R01DK098145"]}]},{"name":"Marie-Curie","award":["IKPP"],"award-info":[{"award-number":["IKPP"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2016,8,1]]},"abstract":"<jats:p> The stimulation of postprandial K<jats:sup>+<\/jats:sup> clearance involves aldosterone-independent and -dependent mechanisms. In this context, serum- and glucocorticoid-induced kinase (SGK)1, a ubiquitously expressed kinase, is one of the primary aldosterone-induced proteins in the aldosterone-sensitive distal nephron. Germline inactivation of SGK1 suggests that this kinase is fundamental for K<jats:sup>+<\/jats:sup> excretion under conditions of K<jats:sup>+<\/jats:sup> load, but the specific role of renal SGK1 remains elusive. To avoid compensatory mechanisms that may occur during nephrogenesis, we used inducible, nephron-specific Sgk1<jats:sup> Pax8\/ LC1<\/jats:sup> mice to assess the role of renal tubular SGK1 in K<jats:sup>+<\/jats:sup> regulation. Under a standard diet, these animals exhibited normal K<jats:sup>+<\/jats:sup> handling. When challenged by a high-K<jats:sup>+<\/jats:sup> diet, they developed severe hyperkalemia accompanied by a defect in K<jats:sup>+<\/jats:sup> excretion. Molecular analysis revealed reduced neural precursor cell expressed developmentally downregulated protein (NEDD)4-2 phosphorylation and total expression. \u03b3-Epithelial Na<jats:sup>+<\/jats:sup> channel (ENaC) expression and \u03b1\/\u03b3ENaC proteolytic processing were also decreased in mutant mice. Moreover, with no lysine kinase (WNK)1, which displayed in control mice punctuate staining in the distal convoluted tubule and diffuse distribution in the connecting tubule\/cortical colleting duct, was diffused in the distal convoluted tubule and less expressed in the connecting tubule\/collecting duct of Sgk<jats:sup> Pax8\/ LC1<\/jats:sup> mice. Moreover, Ste20-related proline\/alanine-rich kinase phosphorylation, and Na<jats:sup>+<\/jats:sup>-Cl<jats:sup>\u2212<\/jats:sup> cotransporter phosphorylation\/apical localization were reduced in mutant mice. Consistent with the altered WNK1 expression, increased renal outer medullary K<jats:sup>+<\/jats:sup> channel apical localization was observed. In conclusion, our data suggest that renal tubular SGK1 is important in the regulation of K<jats:sup>+<\/jats:sup> excretion via the control of NEDD4-2, WNK1, and ENaC. <\/jats:p>","DOI":"10.1152\/ajprenal.00002.2016","type":"journal-article","created":{"date-parts":[[2016,3,23]],"date-time":"2016-03-23T22:20:30Z","timestamp":1458771630000},"page":"F330-F342","source":"Crossref","is-referenced-by-count":44,"title":["Renal tubular SGK1 deficiency causes impaired K<sup>+<\/sup> excretion via loss of regulation of NEDD4-2\/WNK1 and ENaC"],"prefix":"10.1152","volume":"311","author":[{"given":"Lama","family":"Al-Qusairi","sequence":"first","affiliation":[{"name":"Department of Pharmacology and Toxicology, University of Lausanne, Lausanne, Switzerland;"},{"name":"National Centre of Competence in Research \u201cKidney.ch,\u201d Lausanne, Switzerland"}]},{"given":"Denis","family":"Basquin","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, University of Lausanne, Lausanne, Switzerland;"},{"name":"National Centre of Competence in Research \u201cKidney.ch,\u201d Lausanne, Switzerland"}]},{"given":"Ankita","family":"Roy","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Pittsburgh School of Medicine and Veterans Affairs Pittsburgh Healthcare System, Pittsburgh, Pennsylvania;"}]},{"given":"Matteo","family":"Stifanelli","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, University of Lausanne, Lausanne, Switzerland;"}]},{"given":"Renuga Devi","family":"Rajaram","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, University of Lausanne, Lausanne, Switzerland;"}]},{"given":"Anne","family":"Debonneville","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, University of Lausanne, Lausanne, Switzerland;"}]},{"given":"Izabela","family":"Nita","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, University of Lausanne, Lausanne, Switzerland;"}]},{"given":"Marc","family":"Maillard","sequence":"additional","affiliation":[{"name":"Service of Nephrology, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland;"}]},{"given":"Johannes","family":"Loffing","sequence":"additional","affiliation":[{"name":"Institute of Anatomy, University of Zurich, Zurich, Switzerland; and"},{"name":"National Centre of Competence in Research \u201cKidney.ch,\u201d Lausanne, Switzerland"}]},{"given":"Arohan R.","family":"Subramanya","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Pittsburgh School of Medicine and Veterans Affairs Pittsburgh Healthcare System, Pittsburgh, Pennsylvania;"}]},{"given":"Olivier","family":"Staub","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, University of Lausanne, Lausanne, Switzerland;"},{"name":"National Centre of Competence in Research \u201cKidney.ch,\u201d Lausanne, Switzerland"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI5713"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1126\/scisignal.2005365"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2011020132"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014050470"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1210\/me.2005-0193"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-008-0559-5"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00255.2013"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M111.293233"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.114.04036"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.5.2514"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.5.2514"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010060681"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009101077"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005111224"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0115515"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00605.2013"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/20.24.7052"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00535.2011"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00579.2007"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004100828"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1172\/JCI73935"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.C000906200"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000120368.59693.A8"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M307003200"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M412884200"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1096\/fj.00-0191com"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0511184103"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.3109\/09687688.2013.874598"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1007\/s10157-011-0488-z"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0510609103"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M601360200"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00676.2011"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005060659"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.68.040104.131654"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.4.F675"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M206644200"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.24.16973"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2003.10.037"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2015020154"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1126\/scisignal.2005050"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00258.2015"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00015.2014"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.025312"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0611728104"},{"key":"B45","first-page":"657","volume":"123","author":"Ronzaud C","year":"2013","journal-title":"J Clin Invest"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.010908.163108"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1172\/JCI75245"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1172\/JCI38323"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007101130"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M110.176156"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90300.2008"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.C100623200"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2013.14"},{"key":"B54","author":"Terker AS","year":"2015","journal-title":"Kidney Int"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2014.12.006"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013111156"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1038\/nm.1865"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00030.2009"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00201.2013"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1304230110"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1042\/BJ20051180"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0603109103"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00613.2007"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2013.04.002"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1172\/JCI0215696"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M212301200"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.010908.163241"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0907855106"},{"key":"B69","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000035085.54451.81"},{"key":"B70","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1411705111"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00002.2016","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:43:53Z","timestamp":1567975433000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00002.2016"}},"issued":{"date-parts":[[2016,8,1]]},"references-count":70,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2016,8,1]]}},"alternative-id":["10.1152\/ajprenal.00002.2016"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00002.2016","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2016,8,1]]}},{"indexed":{"date-parts":[[2026,4,8]],"date-time":"2026-04-08T03:56:09Z","timestamp":1775620569056,"version":"3.50.1"},"reference-count":59,"publisher":"American Physiological Society","issue":"1","funder":[{"DOI":"10.13039\/501100000291","name":"Kidney Research UK","doi-asserted-by":"publisher","award":["RP40\/2013"],"award-info":[{"award-number":["RP40\/2013"]}],"id":[{"id":"10.13039\/501100000291","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000968","name":"American Heart Association","doi-asserted-by":"publisher","award":["14PRE20460061"],"award-info":[{"award-number":["14PRE20460061"]}],"id":[{"id":"10.13039\/100000968","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK044628"],"award-info":[{"award-number":["DK044628"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"HHS | NIH | National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["HL098135"],"award-info":[{"award-number":["HL098135"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2023,7,1]]},"abstract":"<jats:p> Functional data here offer novel insight into the vasoactive activity of the renal GABA\/glutamate system. These data show that activation of endogenous GABA and glutamate receptors in the kidney significantly alters microvessel diameter. Furthermore, the results show that these antiepileptic drugs are as potentially challenging to the kidney as nonsteroidal anti-inflammatory drugs. <\/jats:p>","DOI":"10.1152\/ajprenal.00425.2021","type":"journal-article","created":{"date-parts":[[2023,4,27]],"date-time":"2023-04-27T12:49:31Z","timestamp":1682599771000},"page":"F38-F49","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":11,"title":["A novel functional role for the classic CNS neurotransmitters, GABA, glycine, and glutamate, in the kidney: potent and opposing regulators of the renal vasculature"],"prefix":"10.1152","volume":"325","author":[{"given":"Scott S.","family":"Wildman","sequence":"first","affiliation":[{"name":"Northeastern University London, London, United Kingdom"}]},{"given":"Kadeshia","family":"Dunn","sequence":"additional","affiliation":[{"name":"Division of Natural Sciences, University of Kent, Kent, United Kingdom"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9265-9915","authenticated-orcid":false,"given":"Justin P.","family":"Van Beusecum","sequence":"additional","affiliation":[{"name":"Ralph H. Johnson Veterans Affairs Medical Center, Charleston, South Carolina, United States"},{"name":"Medical University of South Carolina, Charleston, South Carolina, United States"}]},{"given":"Edward W.","family":"Inscho","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, United States"}]},{"given":"Stephen","family":"Kelley","sequence":"additional","affiliation":[{"name":"Division of Natural Sciences, University of Kent, Kent, United Kingdom"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9944-5944","authenticated-orcid":false,"given":"Rebecca J.","family":"Lilley","sequence":"additional","affiliation":[{"name":"Division of Natural Sciences, University of Kent, Kent, United Kingdom"}]},{"given":"Anthony K.","family":"Cook","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4379-1095","authenticated-orcid":false,"given":"Kirsti D.","family":"Taylor","sequence":"additional","affiliation":[{"name":"Division of Natural Sciences, University of Kent, Kent, United Kingdom"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4406-8571","authenticated-orcid":false,"given":"Claire M.","family":"Peppiatt-Wildman","sequence":"additional","affiliation":[{"name":"Division of Natural Sciences, University of Kent, Kent, United Kingdom"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1038\/nature13165"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1101\/cshperspect.a020388"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1038\/nature05193"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/S0008-6363(96)00063-6"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/0040-8166(86)90026-1"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1159\/000339110"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuron.2015.06.001"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1016\/j.tcm.2007.05.001"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.2011.02310.x"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1111\/apha.12026"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200201000-00014"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1159\/000052608"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.266.6.F850"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0b013e32835b4e6e"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0b013e328344c3d4"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90391.2008"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1097\/01.asn.0000013293.11876.4e"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0702524"},{"key":"B19","first-page":"602","volume":"279","author":"Monasterolo LA","year":"1996","journal-title":"J Pharmacol Exp Ther"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.107.129957"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00169.2003"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0105835"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.12970\/2310-984X.2014.02.02.5"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1172\/JCI18499"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1167\/iovs.12-9838"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1093\/jat\/bkv125"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.3389\/fphys.2013.00307"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.23907\/2017.012"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2125.1981.tb01099.x"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1177\/0897190012451910"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1186\/s13054-020-02915-5"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1002\/j.1552-4604.1996.tb04754.x"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1111\/j.1528-1157.1996.tb06032.x"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1067\/mcp.2002.129500"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuropharm.2007.07.013"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1016\/s0304-3835(00)00620-0"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1177\/0148607106030004277"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1159\/000324393"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013101143"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/gks1193"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejphar.2021.174023"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1159\/000505456"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1165\/rcmb.2015-0176OC"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1016\/j.exer.2010.02.012"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.108.114116"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00481.2007"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1985.194"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.107.092858"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejphar.2014.09.020"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1977.233.1.F61"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1991.78"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1988.255.3.F397"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.258.3.F504"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1177\/42.5.7908911"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.112.195214"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1016\/j.amjmed.2009.09.030"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1111\/j.1526-4637.2008.00492.x"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1155\/2015\/260385"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00199.2015"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00425.2021","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,7,4]],"date-time":"2023-07-04T03:09:13Z","timestamp":1688440153000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00425.2021"}},"issued":{"date-parts":[[2023,7,1]]},"references-count":59,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2023,7,1]]}},"alternative-id":["10.1152\/ajprenal.00425.2021"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00425.2021","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2023,7,1]]},"assertion":[{"value":"2021-12-01","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2023-03-29","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2023-04-22","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2023-06-21","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,4,8]],"date-time":"2026-04-08T05:08:46Z","timestamp":1775624926484,"version":"3.50.1"},"reference-count":43,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2009,7]]},"abstract":"<jats:p>Overactive bladder is a highly prevalent clinical condition that is often caused by bladder outlet obstruction (BOO). Increased coupling of bladder smooth muscle cells (BSMC) via gap junctions has been hypothesized as a mechanism for myogenic bladder overactivity in BOO, although little is known about the regulatory system underlying such changes. Here, we report the involvement of basic fibroblast growth factor (bFGF) and connexin 43, a bladder gap junction protein, in bladder overactivity. BOO created by urethral constriction in rats resulted in elevated bFGF and connexin 43 levels in the bladder urothelium and muscle layer, respectively, and muscle strips from these bladders were more sensitive than those from sham-operated controls to a cholinergic agonist. In vitro bFGF treatment increased connexin 43 expression in cultured rat BSMC via the ERK 1\/2 pathway. This finding was supported by another in vivo model, where bFGF released from gelatin hydrogels fixed on rat bladder walls caused connexin 43 upregulation and gap junction formation in the muscle layer. Bladder muscle strips in this model showed increased sensitivity to a cholinergic agonist that was blocked by inhibition of gap junction function with \u03b1-glycyrrhetinic acid. Cystometric analyses of this model showed typical features of detrusor overactivity such as significantly increased micturition frequency and decreased bladder capacity. These findings suggest that bFGF from the urothelium could induce bladder hypersensitivity to acetylcholine via gap junction generation in the smooth muscle, thereby contributing to the myogenic overactivity of obstructed bladders.<\/jats:p>","DOI":"10.1152\/ajprenal.90207.2008","type":"journal-article","created":{"date-parts":[[2009,4,23]],"date-time":"2009-04-23T00:35:13Z","timestamp":1240446913000},"page":"F46-F54","source":"Crossref","is-referenced-by-count":35,"title":["Basic fibroblast growth factor causes urinary bladder overactivity through gap junction generation in the smooth muscle"],"prefix":"10.1152","volume":"297","author":[{"given":"Masaaki","family":"Imamura","sequence":"first","affiliation":[]},{"given":"Hiromitsu","family":"Negoro","sequence":"additional","affiliation":[]},{"given":"Akihiro","family":"Kanematsu","sequence":"additional","affiliation":[]},{"given":"Shingo","family":"Yamamoto","sequence":"additional","affiliation":[]},{"given":"Yu","family":"Kimura","sequence":"additional","affiliation":[]},{"given":"Kentaro","family":"Nagane","sequence":"additional","affiliation":[]},{"given":"Toshinari","family":"Yamasaki","sequence":"additional","affiliation":[]},{"given":"Isao","family":"Kanatani","sequence":"additional","affiliation":[]},{"given":"Noriyuki","family":"Ito","sequence":"additional","affiliation":[]},{"given":"Yasuhiko","family":"Tabata","sequence":"additional","affiliation":[]},{"given":"Osamu","family":"Ogawa","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1016\/j.urology.2003.09.050"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1464-410X.2007.07205.x"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1016\/S0090-4295(97)00591-8"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1124\/mol.63.4.821"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00030.2002"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1016\/S0090-4295(97)00587-6"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.79.4.647"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1007\/BF00925930"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1078\/0171-9335-00080"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1016\/j.urology.2003.11.005"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1006\/excr.2001.5465"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1016\/j.lfs.2007.02.010"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00183.2007"},{"key":"R14","doi-asserted-by":"crossref","unstructured":"Imamura M, Kanematsu A, Yamamoto S, Kimura Y, Kanatani I, Ito N, Tabata Y, Ogawa O.Basic fibroblast growth factor modulates proliferation and collagen expression in urinary bladder smooth muscle cells.Am J Physiol Renal Physiol293: F1007\u2013F1017, 2007.","DOI":"10.1152\/ajprenal.00107.2007"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.104.3.325"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1016\/j.jss.2006.11.007"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbamem.2004.10.001"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(05)64006-2"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)62278-X"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1097\/01.ju.0000084021.51099.8a"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1016\/j.pbiomolbio.2007.03.009"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)81282-9"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00122.2007"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1016\/S0090-4295(97)00605-5"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1016\/j.urology.2005.01.043"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1111\/j.1464-410X.2005.05703.x"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra032662"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1520-6777(1999)18:2<81::AID-NAU3>3.0.CO;2-Z"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbamem.2004.01.007"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1080\/cac.10.4-6.173.180"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbamem.2004.09.013"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1038\/nbt1257"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(17)43675-5"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1046\/j.1464-410X.2003.04342.x"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1016\/S0142-9612(98)00233-6"},{"key":"R36","doi-asserted-by":"crossref","unstructured":"Tambara K, Premaratne GU, Sakaguchi G, Kanemitsu N, Lin X, Nakajima H, Sakakibara Y, Kimura Y, Yamamoto M, Tabata Y, Ikeda T, Komeda M.Administration of control-released hepatocyte growth factor enhances the efficacy of skeletal myoblast transplantation in rat infarcted hearts by greatly increasing both quantity and quality of the graft.Circulation112: 129\u2013134, 2005.","DOI":"10.1161\/CIRCULATIONAHA.104.526293"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1097\/01.ju.0000074713.69589.4a"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1097\/01.ju.0000071479.02427.7d"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002720"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1002\/nau.20482"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1002\/nau.20487"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.3023-06.2006"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(05)64261-9"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.90207.2008","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,10,4]],"date-time":"2021-10-04T11:18:37Z","timestamp":1633346317000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.90207.2008"}},"issued":{"date-parts":[[2009,7]]},"references-count":43,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2009,7]]}},"alternative-id":["10.1152\/ajprenal.90207.2008"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.90207.2008","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2009,7]]}},{"indexed":{"date-parts":[[2026,4,8]],"date-time":"2026-04-08T03:36:45Z","timestamp":1775619405678,"version":"3.50.1"},"reference-count":53,"publisher":"American Physiological Society","issue":"5","funder":[{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["R01DK106102"],"award-info":[{"award-number":["R01DK106102"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["R01DK112042"],"award-info":[{"award-number":["R01DK112042"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["P30DK079337"],"award-info":[{"award-number":["P30DK079337"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"HHS | NIH | National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["R01HL142814"],"award-info":[{"award-number":["R01HL142814"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000049","name":"HHS | NIH | National Institute on Aging","doi-asserted-by":"publisher","award":["RF1AG061296"],"award-info":[{"award-number":["RF1AG061296"]}],"id":[{"id":"10.13039\/100000049","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["P30DK079337"],"award-info":[{"award-number":["P30DK079337"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000738","name":"U.S. Department of Veterans Affairs","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000738","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2020,5,1]]},"abstract":"<jats:p> In the early proximal tubule, Na<jats:sup>+<\/jats:sup>-glucose cotransporter 2 (SGLT2) mediates the bulk of renal glucose reabsorption. Gene deletion in mice ( Sglt2<jats:sup>\u2212\/\u2212<\/jats:sup>) was used to determine the role of SGLT2 in acute kidney injury induced by bilateral ischemia-reperfusion (IR). In Sglt2<jats:sup>\u2212\/\u2212<\/jats:sup> and littermate wild-type mice, plasma creatinine increased similarly on day 1 after IR. This was associated with an equal increase in both genotypes in the urinary kidney injury molecule-1-to-creatinine ratio, a tubular injury marker, and similarly reduced urine osmolality and increased plasma osmolality, indicating impaired urine concentration. In both IR groups, FITC-sinistrin glomerular filtration rate was equally reduced on day 14, and plasma creatinine was similarly and incompletely restored on day 23. In Sglt2<jats:sup>\u2212\/\u2212<\/jats:sup> mice subjected to IR, fractional urinary glucose excretion was increased on day 1 but reduced and associated with normal renal Na<jats:sup>+<\/jats:sup>-glucose cotransporter 1 (Sglt1) mRNA expression on day 23, suggesting temporary SGLT1 suppression. In wild-type mice subjected to IR, renal Sglt1 mRNA was likewise normal on day 23, whereas Sglt2 mRNA was reduced by 57%. In both genotypes, IR equally reduced urine osmolality and renal mRNA expression of the Na<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-2Cl<jats:sup>\u2212<\/jats:sup> cotransporter and renin on day 23, suggesting thick ascending limb dysfunction, and similarly increased renal mRNA expression of markers of injury, inflammation, oxidative stress, and fibrosis (kidney injury molecule-1, neutrophil gelatinase-associated lipocalin, monocyte chemoattractant protein-1, transforming growth factor-\u03b21, NADPH oxidase-2, and collagen type 1). This was associated with equal increases in kidney histological damage scores and similar degree of capillary loss in both genotypes. The data indicate that genetic deletion of SGLT2 did not protect the kidneys in the initial injury phase or the subsequent recovery phase in a mouse model of IR-induced acute kidney injury. <\/jats:p>","DOI":"10.1152\/ajprenal.00607.2019","type":"journal-article","created":{"date-parts":[[2020,3,2]],"date-time":"2020-03-02T12:06:17Z","timestamp":1583150777000},"page":"F1100-F1112","source":"Crossref","is-referenced-by-count":32,"title":["Gene knockout of the Na<sup>+<\/sup>-glucose cotransporter SGLT2 in a murine model of acute kidney injury induced by ischemia-reperfusion"],"prefix":"10.1152","volume":"318","author":[{"given":"Josselin","family":"Nespoux","sequence":"first","affiliation":[{"name":"Department of Medicine, University of California, and Veterans Affairs San Diego Healthcare System , San Diego, California"}]},{"given":"Rohit","family":"Patel","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of California, and Veterans Affairs San Diego Healthcare System , San Diego, California"}]},{"given":"Haiyan","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of California, San Diego, California"}]},{"given":"Winnie","family":"Huang","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of California, and Veterans Affairs San Diego Healthcare System , San Diego, California"}]},{"given":"Brent","family":"Freeman","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of California, and Veterans Affairs San Diego Healthcare System , San Diego, California"}]},{"given":"Paul W.","family":"Sanders","sequence":"additional","affiliation":[{"name":"Departments of Medicine, Cell, and Developmental and Integrative Biology, University of Alabama at Birmingham, and Department of Veterans Affairs Medical Center, Birmingham, Alabama"}]},{"given":"Young Chul","family":"Kim","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of California, and Veterans Affairs San Diego Healthcare System , San Diego, California"}]},{"given":"Volker","family":"Vallon","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of California, and Veterans Affairs San Diego Healthcare System , San Diego, California"},{"name":"Department of Pharmacology, University of California, San Diego, California"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1093\/ckj\/sfx133"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.602"},{"key":"B3","first-page":"385","volume":"60","author":"Ash SR","year":"1970","journal-title":"Am J Pathol"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1007\/s00125-016-4134-x"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200401000-00001"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002312"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1097\/01.mnh.0000441051.36783.f3"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(11)61454-2"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1172\/jci.insight.99123"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1172\/JCI45161"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0158810"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/j.ekir.2017.06.020"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014010060"},{"key":"B14","first-page":"1045","volume":"29","author":"Fattah H","year":"2018","journal-title":"J Am Soc Nephrol"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1159\/000484962"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1111\/dom.13754"},{"key":"B17","first-page":"620.17","volume":"32","author":"Huang W","year":"2018","journal-title":"FASEB J"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1984.246.2.F159"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1111\/ajt.13368"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1146\/annurev-med-042017-094221"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2011.01.085"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2015020177"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0152153"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.7326\/AITC201711070"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00263.2017"},{"key":"B26","first-page":"20","volume":"4","author":"Malek M","year":"2015","journal-title":"J Renal Inj Prev"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1172\/JCI113117"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa1611925"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00111.2019"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1042\/CS20171298"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0000000000000584"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1016\/S2213-8587(19)30256-6"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa1811744"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejmech.2005.03.020"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00324.2003"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00518.2013"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00120.2019"},{"key":"B38","volume-title":"Principles and Procedures of Statistics, A Biometrical Approach","author":"Steel RGD","year":"1997","edition":"3"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1016\/S2213-8587(14)70227-X"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1016\/j.amjcard.2019.10.027"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1007\/s00125-017-4509-7"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1093\/cvr\/cvz004"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00520.2013"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010030246"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00409.2012"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1007\/s00125-016-4157-3"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1980.156"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa1812389"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00055.2009"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.26760"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2018.05.002"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa1504720"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1146\/annurev-med-050214-013407"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00607.2019","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2020,4,13]],"date-time":"2020-04-13T13:08:36Z","timestamp":1586783316000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00607.2019"}},"issued":{"date-parts":[[2020,5,1]]},"references-count":53,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2020,5,1]]}},"alternative-id":["10.1152\/ajprenal.00607.2019"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00607.2019","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2020,5,1]]}},{"indexed":{"date-parts":[[2022,3,30]],"date-time":"2022-03-30T16:00:21Z","timestamp":1648656021508},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1986,2,1]]},"abstract":"<jats:p> The role of the renal nerves in the natriuresis seen after cholinergic stimulation of the hypothalamus was studied in anesthetized rats treated with injection into the lateral hypothalamus (LH) of 1 microgram of carbamylcholine chloride (carbachol) in 1 microliter of 0.15 M NaCl or NaCl alone. Injection of carbachol exhibited diuresis and natriuresis both in acutely denervated kidneys (P less than 0.01) and in contralateral innervated kidneys (P less than 0.01) without changes in glomerular filtration rate (GFR) or renal plasma flow (RPF) (n = 10). Salt and water excretion was unchanged in 10 rats after injection of NaCl. Micropuncture studies in denervated kidneys showed that, after carbachol injection, tubular fluid-to-plasma inulin concentration ratio [(F\/P)In] in the late proximal tubule fell from 1.86 +\/- 0.08 to 1.64 +\/- 0.07 (P less than 0.01) without changes in single-nephron GFR. In nine other carbachol-treated rats in which renal perfusion pressure was maintained low and constant, diuresis and natriuresis, although attenuated, were again observed both in denervated (P less than 0.01) and in contralateral innervated kidneys (P less than 0.05). In another group of 11 animals, efferent renal nerve activity (ERNA) was recorded before and after LH injection of carbachol and isotonic saline. ERNA was significantly depressed for 30 min, only after carbachol injection. Our results suggest that the renal nerves, although involved, are not essential for the natriuretic response after cholinergic stimulation of LH. By exclusion, other factors, presumably hormones, must contribute to the response. <\/jats:p>","DOI":"10.1152\/ajprenal.1986.250.2.f322","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T01:43:52Z","timestamp":1513993432000},"page":"F322-F328","source":"Crossref","is-referenced-by-count":4,"title":["Cholinergic stimulation of the hypothalamus and natriuresis in rats: role of the renal nerves"],"prefix":"10.1152","volume":"250","author":[{"given":"C. R.","family":"Silva-Netto","sequence":"first","affiliation":[]},{"given":"R. H.","family":"Jackson","sequence":"additional","affiliation":[]},{"given":"R. E.","family":"Colindres","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1986.250.2.F322","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:38:17Z","timestamp":1567971497000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1986.250.2.F322"}},"issued":{"date-parts":[[1986,2,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1986,2,1]]}},"alternative-id":["10.1152\/ajprenal.1986.250.2.F322"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1986.250.2.f322","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1986,2,1]]}},{"indexed":{"date-parts":[[2022,3,30]],"date-time":"2022-03-30T16:47:53Z","timestamp":1648658873301},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1988,6,1]]},"abstract":"<jats:p> Tissue culture media from incubations of fragments of rat brain were collected and partially purified. These supernatants were effective in inhibiting the Na+-K<jats:sup>+<\/jats:sup> pump as indicated by a 77% reduction of ouabain-sensitive 86Rb<jats:sup>+<\/jats:sup> uptake into human erythrocytes. Release of the Na<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-ATPase inhibitor depended on the amount of tissue, the temperature, and the length of incubation. Atrial natriuretic peptide (ANP) injected intravenously, or included (10(-8) M) in the in vitro incubation of brain tissue, decreased the release of the Na<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-ATPase inhibitor by 74 and 42%, respectively. Control experiments using the neuropeptide arginine vasopressin showed no effect on release of the inhibitor. These studies indicate that ANP is capable of regulating the release from brain of a Na<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-ATPase inhibitor with similar chromatographic characteristics to the one previously obtained from extraction of bovine hypothalamus and raise the possibility that the two factors are interrelated in the regulation of fluid and electrolyte balance. <\/jats:p>","DOI":"10.1152\/ajprenal.1988.254.6.f912","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T02:54:00Z","timestamp":1513997640000},"page":"F912-F917","source":"Crossref","is-referenced-by-count":1,"title":["Atrial natriuretic peptide regulates release of Na+-K+-ATPase inhibitor from rat brain"],"prefix":"10.1152","volume":"254","author":[{"given":"M.","family":"Crabos","sequence":"first","affiliation":[{"name":"Renal Unit, Massachusetts General Hospital, Harvard University, Boston 02114."}]},{"given":"D. A.","family":"Ausiello","sequence":"additional","affiliation":[{"name":"Renal Unit, Massachusetts General Hospital, Harvard University, Boston 02114."}]},{"suffix":"Jr","given":"G. T.","family":"Haupert","sequence":"additional","affiliation":[{"name":"Renal Unit, Massachusetts General Hospital, Harvard University, Boston 02114."}]},{"given":"H. F.","family":"Cantiello","sequence":"additional","affiliation":[{"name":"Renal Unit, Massachusetts General Hospital, Harvard University, Boston 02114."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1988.254.6.F912","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:47:39Z","timestamp":1567972059000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1988.254.6.F912"}},"issued":{"date-parts":[[1988,6,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1988,6,1]]}},"alternative-id":["10.1152\/ajprenal.1988.254.6.F912"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1988.254.6.f912","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1988,6,1]]}},{"indexed":{"date-parts":[[2022,3,30]],"date-time":"2022-03-30T14:29:39Z","timestamp":1648650579242},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1983,8,1]]},"abstract":"<jats:p> Renal adaptation to changes in phosphate intake was studied by comparing phosphate uptake by proximal tubule brush border membrane vesicles from rabbits on a relatively high or low phosphorus diet. The low phosphorus diet increased Na+ gradient-dependent phosphate uptake. Uptake in the absence of Na+ and in the presence of Na+, but no gradient, was not significantly affected. The phosphorus diet did not alter Na+ gradient-dependent D-glucose and L-proline uptake. The low phosphorus diet increased Vmax; affinity for phosphate was not appreciably changed. At all concentrations of extravesicular Na+, phosphate uptake was higher in membrane vesicles from animals fed the low phosphorus diet; the kinetics of the phosphate uptake system, with respect to Na+, was also altered by the change in dietary phosphate. These findings suggest that adaptation involves an alteration in the rate of translocation of the Na+-phosphate carrier when energized by a Na+ gradient driving force rather than a change in the number of Na+-phosphate carrier sites. With membrane vesicles from rabbits fed a low phosphorus diet, phosphate uptake increased several-fold when the pH of the uptake medium was raised, whereas with membrane vesicles from animals fed a high phosphorus diet the enhancement of uptake with alkalinization was relatively small. Irrespective of the diet, divalent phosphate was the probable preferred species for transport. Dietary adaptation was associated, however, with an alteration in the pH dependency of the transport system per se. These findings provide evidence that the adaptation of the kidney phosphate transport system to dietary phosphate load involves an intrinsic change in the Na+-phosphate carrier. <\/jats:p>","DOI":"10.1152\/ajprenal.1983.245.2.f175","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T09:39:38Z","timestamp":1513935578000},"page":"F175-F180","source":"Crossref","is-referenced-by-count":3,"title":["Phosphate uptake by renal membrane vesicles of rabbits adapted to high and low phosphorus diets"],"prefix":"10.1152","volume":"245","author":[{"given":"L.","family":"Cheng","sequence":"first","affiliation":[]},{"given":"C. T.","family":"Liang","sequence":"additional","affiliation":[]},{"given":"B.","family":"Sacktor","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1983.245.2.F175","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T14:23:21Z","timestamp":1567952601000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1983.245.2.F175"}},"issued":{"date-parts":[[1983,8,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1983,8,1]]}},"alternative-id":["10.1152\/ajprenal.1983.245.2.F175"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1983.245.2.f175","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1983,8,1]]}},{"indexed":{"date-parts":[[2022,4,3]],"date-time":"2022-04-03T06:35:46Z","timestamp":1648967746985},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1991,7,1]]},"abstract":"<jats:p> We examined characteristics of atrial natriuretic peptide (ANP) receptors in glomeruli isolated from subacutely (3-5 days) denervated (DNX) and contralateral nondenervated (non-DNX) kidneys of normal rats (NL) and rats subjected to water deprivation for 48 h (WD). Total ANP receptor density in DNX kidneys of WD rats, measured by competitive inhibition binding between 125I-labeled ANP and ANP, was twofold higher than non-DNX kidneys (726 +\/- 96 vs. 384 +\/- 32 fmol\/mg protein, P less than 0.05). Equilibrium association constant (Ka) was not significantly different (2.33 +\/- 0.43 vs. 3.34 +\/- 0.78 x 10(9) M-1). In NL rats, there was no difference in ANP receptor density between DNX and non-DNX kidneys (244 +\/- 20 and 264 +\/- 16 fmol\/mg protein). Production of guanosine 3',5'-cyclic monophosphate (cGMP), a putative second messenger of ANP, in response to ANP (10(-7) M) in glomeruli isolated from DNX was significantly larger than non-DNX kidneys of WD rats. To determine whether these changes in ANP receptors have functional consequences in vivo, glomerular capillary ultrafiltration coefficient (Kf) was assessed by micropuncture technique in WD Munich-Wistar rats. In DNX kidneys, ANP infusion (4 micrograms.kg-1.h-1) significantly increased whole kidney glomerular filtration rate (GFR) and single-nephron (SN) GFR (0.64 +\/- 0.06 to 0.89 +\/- 0.17 ml\/min and 25 +\/- 2 to 33 +\/- 2 nl\/min, respectively; n = 7) and Kf (1.26 +\/- 0.29 to 2.18 +\/- 0.41 nl.min-1.mmHg-1).(ABSTRACT TRUNCATED AT 250 WORDS) <\/jats:p>","DOI":"10.1152\/ajprenal.1991.261.1.f29","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T18:39:32Z","timestamp":1513967972000},"page":"F29-F35","source":"Crossref","is-referenced-by-count":0,"title":["Renal sympathetic nerves modulate glomerular ANP receptors and filtration"],"prefix":"10.1152","volume":"261","author":[{"given":"M.","family":"Awazu","sequence":"first","affiliation":[{"name":"Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232."}]},{"given":"V.","family":"Kon","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232."}]},{"given":"R. C.","family":"Harris","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232."}]},{"given":"T.","family":"Imada","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232."}]},{"given":"T.","family":"Inagami","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232."}]},{"given":"I.","family":"Ichikawa","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1991.261.1.F29","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:25:25Z","timestamp":1567956325000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1991.261.1.F29"}},"issued":{"date-parts":[[1991,7,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1991,7,1]]}},"alternative-id":["10.1152\/ajprenal.1991.261.1.F29"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1991.261.1.f29","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1991,7,1]]}},{"indexed":{"date-parts":[[2022,3,31]],"date-time":"2022-03-31T21:08:30Z","timestamp":1648760910171},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1993,8,1]]},"abstract":"<jats:p> Angiotensin (ANG) II is now recognized as a powerful direct controller of Na+ reabsorption in the proximal convoluted tubule, a property that predominantly reflects stimulation of the transepithelial NaHCO3 flux. Numerous studies have established that this effect of ANG II represents stimulation of the apical Na+\/H+ exchanger, but a single microperfusion study has also suggested direct stimulation of the basolateral Na(+)-HCO3- cotransporter. We have carried out studies in basolateral membrane vesicles from rabbit renal cortex to examine directly whether ANG II exerts an independent effect on the Na(+)-HCO3- cotransporter. Preincubation of vesicles with ANG II (10(-11) to 10(-9) M) for 15 min enhanced the activity of the cotransporter, the greatest effect occurring at 10(-11) M (41 +\/- 1.1%, P &lt; 0.005). This stimulation reflected an increase in the maximal enzyme reaction velocity of the cotransporter but no change in the Michaelis constant for Na+. ANG II had no effect on Na(+)-dependent succinate transport. ANG I (10(-9) M) and ANG III (10(-10) M) also stimulated the Na(+)-HCO3- cotransporter, and captopril (10(-4) M) attenuated the ANG I stimulation by 68 +\/- 3.5% (P &lt; 0.01) but not that of ANG II and III. Saralasin (10(-11) to 10(-8) M) by itself behaved as an agonist, and its stimulation was additive to that by ANG II. The nonpeptide ANG II receptor antagonist, losartan potassium (10(-6) M), and the disulfide-reducing agent, dithiothreitol (10 mM), each by itself had no effect on the cotransporter but each markedly attenuated the ANG II effect (by 77 +\/- 1.4%, P &lt; 0.01 and 74 +\/- 1.6%, P &lt; 0.005, respectively) in accord with the view that the basolateral receptor belongs to subtype 1. These results identify physiological concentrations of ANG II as a potent, direct, and specific stimulator of the basolateral Na(+)-HCO3- cotransporter. <\/jats:p>","DOI":"10.1152\/ajprenal.1993.265.2.f195","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T10:16:32Z","timestamp":1514024192000},"page":"F195-F203","source":"Crossref","is-referenced-by-count":6,"title":["Stimulation of basolateral Na(+)-HCO3- cotransporter by angiotensin II in rabbit renal cortex"],"prefix":"10.1152","volume":"265","author":[{"given":"S.","family":"Eiam-Ong","sequence":"first","affiliation":[{"name":"Department of Medicine, Tufts University School of Medicine, Boston,Massachusetts."}]},{"given":"S. A.","family":"Hilden","sequence":"additional","affiliation":[{"name":"Department of Medicine, Tufts University School of Medicine, Boston,Massachusetts."}]},{"given":"C. A.","family":"Johns","sequence":"additional","affiliation":[{"name":"Department of Medicine, Tufts University School of Medicine, Boston,Massachusetts."}]},{"given":"N. E.","family":"Madias","sequence":"additional","affiliation":[{"name":"Department of Medicine, Tufts University School of Medicine, Boston,Massachusetts."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1993.265.2.F195","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:27:05Z","timestamp":1567974425000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1993.265.2.F195"}},"issued":{"date-parts":[[1993,8,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1993,8,1]]}},"alternative-id":["10.1152\/ajprenal.1993.265.2.F195"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1993.265.2.f195","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1993,8,1]]}},{"indexed":{"date-parts":[[2022,4,1]],"date-time":"2022-04-01T00:55:48Z","timestamp":1648774548948},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1989,10,1]]},"abstract":"<jats:p> The regulation of plasma renin activity (PRA) by thromboxane (Tx) A2 was studied in anesthetized rats by measuring PRA before and after administration of drugs that block cyclooxygenase (CO) (indomethacin [INDO], 5 mg\/kg), thromboxane synthase (TS) (UK 38485 [UK], 100 mg\/kg), or Tx receptors (SQ 29548 [SQ], 8 mg\/kg or L 641953 [L], 50 mg\/kg) or that activate Tx receptors (U 46619 [U], 10 ng.kg-1.min-1). PRA (ng ANG I.ml-1.h-1) was unaffected by vehicle; it was reduced by INDO (25 +\/- 2 to 13 +\/- 3, n = 13, P less than 0.001) but was increased by UK (24 +\/- 3 to 50 +\/- 6, n = 18, P less than 0.005), SQ (27 +\/- 4 to 44 +\/- 7, n = 6, P less than 0.05), and L (32 +\/- 4 to 51 +\/- 7, n = 10, P less than 0.05). U reduced PRA in each rat (17 +\/- 3 to 10 +\/- 3, n = 6, P less than 0.005). UK caused dose-dependent stimulation of PRA (mean effective dose 50 mg\/kg) and inhibition of TxB2 excretion (mean inhibitory dose 15 mg\/kg). After INDO, SQ no longer changed PRA (-1 +\/- 10, n = 7). Prolonged administration of SQ for 4-6 days (20 mg.kg-1.day-1 ip) did not change Na+ or K+ balances, blood pressure, renal hemodynamics, or urine flow. However, SQ stimulated PRA (P less than 0.007) independent of prior salt intake. In conclusion in anesthetized rats 1) PRA is stimulated by products of CO but inhibited by products of TS and by a Tx mimetic; 2) stimulation of PRA by SQ depends on ongoing PG and Tx synthesis; 3) rise in PRA with Tx antagonists is not closely related to changes in salt balance, blood pressure, or renal hemodynamics. <\/jats:p>","DOI":"10.1152\/ajprenal.1989.257.4.f554","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T21:53:58Z","timestamp":1513979638000},"page":"F554-F560","source":"Crossref","is-referenced-by-count":3,"title":["Modulation of renin by thromboxane: studies with thromboxane synthase inhibitor, receptor antagonists, and mimetic"],"prefix":"10.1152","volume":"257","author":[{"given":"W. J.","family":"Welch","sequence":"first","affiliation":[{"name":"Department of Medicine, University of Florida College of Medicine, Gainesville 32610."}]},{"given":"C. S.","family":"Wilcox","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Florida College of Medicine, Gainesville 32610."}]},{"given":"K. R.","family":"Dunbar","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Florida College of Medicine, Gainesville 32610."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1989.257.4.F554","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:14:40Z","timestamp":1567970080000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1989.257.4.F554"}},"issued":{"date-parts":[[1989,10,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1989,10,1]]}},"alternative-id":["10.1152\/ajprenal.1989.257.4.F554"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1989.257.4.f554","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1989,10,1]]}},{"indexed":{"date-parts":[[2022,4,3]],"date-time":"2022-04-03T09:02:13Z","timestamp":1648976533079},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1992,3,1]]},"abstract":"<jats:p> Activation of phospholipase C (PLC) is considered to be one of the cellular signaling events involved in dopamine (DA)-mediated natriuresis. In the present study we have examined the role of renal cortical PLC in contributing to the increase in urinary sodium excretion during high sodium intake and its relationship with intrarenal DA synthesis. Rats were given either 1% NaCl (high sodium intake) or tap water (normal sodium intake) to drink for 24 h, and urine was collected over this time period. PLC activity in the renal cortex from these rats was measured by prelabeling cortical slices with myo-[2-3H]inositol and was expressed as fractional release (FR) of inositol (mono-, bis-, and tris-) phosphates. Acute increase in sodium intake produced 93 +\/- 8% increase over control in urinary DA excretion. These changes were accompanied by significant increases (30 +\/- 8%) in basal FR of inositol phosphates and 243 +\/- 40 and 76 +\/- 14% increases in urinary sodium and water excretion, respectively. The elevated basal PLC activity in rats with high sodium intake was significantly reduced in the presence of Sch 23390, a selective DA-1 receptor antagonist. Exogenously added DA (3 mM) also produced significant increases in PLC activity, although the magnitudes of increases were different in rats with high (37 +\/- 8%) and normal (66 +\/- 9%) sodium intake. However, Sch 23390 alone or carbidopa pretreatment did not affect the basal PLC activity in rats maintained on normal sodium intake.(ABSTRACT TRUNCATED AT 250 WORDS) <\/jats:p>","DOI":"10.1152\/ajprenal.1992.262.3.f494","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T08:57:12Z","timestamp":1514019432000},"page":"F494-F498","source":"Crossref","is-referenced-by-count":2,"title":["Dopamine receptor-mediated activation of phospholipase C is associated with natriuresis during high salt intake"],"prefix":"10.1152","volume":"262","author":[{"given":"S. J.","family":"Vyas","sequence":"first","affiliation":[{"name":"Department of Pharmacology, University of Houston, Texas77204-5515."}]},{"given":"A. L.","family":"Jadhav","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, University of Houston, Texas77204-5515."}]},{"given":"J.","family":"Eichberg","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, University of Houston, Texas77204-5515."}]},{"given":"M. F.","family":"Lokhandwala","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, University of Houston, Texas77204-5515."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1992.262.3.F494","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:19:43Z","timestamp":1567973983000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1992.262.3.F494"}},"issued":{"date-parts":[[1992,3,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1992,3,1]]}},"alternative-id":["10.1152\/ajprenal.1992.262.3.F494"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1992.262.3.f494","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1992,3,1]]}},{"indexed":{"date-parts":[[2022,4,3]],"date-time":"2022-04-03T08:27:39Z","timestamp":1648974459509},"reference-count":9,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2017,8,1]]},"DOI":"10.1152\/ajprenal.00217.2017","type":"journal-article","created":{"date-parts":[[2017,5,3]],"date-time":"2017-05-03T20:10:42Z","timestamp":1493842242000},"page":"F308-F309","source":"Crossref","is-referenced-by-count":0,"title":["Coping with nephron loss: transport at a price"],"prefix":"10.1152","volume":"313","author":[{"given":"Alan M.","family":"Weinstein","sequence":"first","affiliation":[{"name":"Department of Physiology and Biophysics, Department of Medicine, Weill Medical College of Cornell University, New York, New York"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.07512.x"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00149.2014"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00005.2010"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1979.59.1.137"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.ph.57.030195.001403"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00018.2017"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00293.2016"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM196906262802606"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00276.2014"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00217.2017","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:07:08Z","timestamp":1567969628000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00217.2017"}},"issued":{"date-parts":[[2017,8,1]]},"references-count":9,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2017,8,1]]}},"alternative-id":["10.1152\/ajprenal.00217.2017"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00217.2017","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2017,8,1]]}},{"indexed":{"date-parts":[[2022,3,31]],"date-time":"2022-03-31T19:08:31Z","timestamp":1648753711630},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1995,6,1]]},"abstract":"<jats:p> Protein phosphorylation on tyrosine residues is one of the main cell signaling mechanisms. Cellular phosphotyrosyl levels are regulated by the activities of protein tyrosine kinases (PTK) and protein tyrosine phosphatases (PTPase). We have previously reported cDNA cloning of several types of PTPase from rat kidney, including LRP (leukocyte common antigen-related protein; also known as the transmembrane-type tyrosine phosphatase, i.e., RPTP alpha). LRP mRNA was shown to be abundant in the kidney; however, our understanding of the functional role of LRP in the kidney is very limited. To gain keener insight into the function of LRP in the kidney, our first approach was to reveal its mRNA distribution along rat nephron segments. Large signals were found in inner medulla by Northern blot analysis. By using a reverse transcription and polymerase chain reaction assay of individual microdissected tubule segments along the nephron [proximal convoluted tubule (PCT), medullary thick ascending limb (MTAL), cortical collecting duct (CCD), outer medullary collecting duct (OMCD), and inner medullary collecting duct (IMCD)] and glomeruli, we revealed intrarenal localization of LRP mRNA. LRP mRNA was detected in all nephron segments tested but was relatively rich in the IMCD. Rank order of the signal intensity was IMCD &gt; PCT = OMCD &gt; CCD &gt; MTAL = glomeruli. Immunohistochemistry also revealed that LRP was abundant in IMCD. This pattern of expression gives rise to an interesting possibility that LRP might be involved in the specific renal tubule function, such as urinary concentrating mechanism; however, further study is required to describe the function of LRP in more detail. <\/jats:p>","DOI":"10.1152\/ajprenal.1995.268.6.f1102","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T05:34:24Z","timestamp":1514007264000},"page":"F1102-F1108","source":"Crossref","is-referenced-by-count":1,"title":["Expression of transmembrane-type protein tyrosine phosphatase mRNA along rat nephron segments"],"prefix":"10.1152","volume":"268","author":[{"given":"T.","family":"Kaneko","sequence":"first","affiliation":[{"name":"First Department of Medicine, Osaka University School of Medicine, Japan."}]},{"given":"T.","family":"Moriyama","sequence":"additional","affiliation":[{"name":"First Department of Medicine, Osaka University School of Medicine, Japan."}]},{"given":"E.","family":"Imai","sequence":"additional","affiliation":[{"name":"First Department of Medicine, Osaka University School of Medicine, Japan."}]},{"given":"Y.","family":"Akagi","sequence":"additional","affiliation":[{"name":"First Department of Medicine, Osaka University School of Medicine, Japan."}]},{"given":"M.","family":"Arai","sequence":"additional","affiliation":[{"name":"First Department of Medicine, Osaka University School of Medicine, Japan."}]},{"given":"T.","family":"Inoue","sequence":"additional","affiliation":[{"name":"First Department of Medicine, Osaka University School of Medicine, Japan."}]},{"given":"C.","family":"Xia","sequence":"additional","affiliation":[{"name":"First Department of Medicine, Osaka University School of Medicine, Japan."}]},{"given":"T.","family":"Noguchi","sequence":"additional","affiliation":[{"name":"First Department of Medicine, Osaka University School of Medicine, Japan."}]},{"given":"T.","family":"Kamada","sequence":"additional","affiliation":[{"name":"First Department of Medicine, Osaka University School of Medicine, Japan."}]},{"given":"N.","family":"Ueda","sequence":"additional","affiliation":[{"name":"First Department of Medicine, Osaka University School of Medicine, Japan."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1995.268.6.F1102","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:00:58Z","timestamp":1567972858000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1995.268.6.F1102"}},"issued":{"date-parts":[[1995,6,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1995,6,1]]}},"alternative-id":["10.1152\/ajprenal.1995.268.6.F1102"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1995.268.6.f1102","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1995,6,1]]}},{"indexed":{"date-parts":[[2022,4,5]],"date-time":"2022-04-05T07:15:41Z","timestamp":1649142941900},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1990,1,1]]},"abstract":"<jats:p> The present studies examined the effect of three-fourths nephrectomy on the rate of acidification, i.e., total CO2 (tCO2) absorption (JtCO2) in the superficial distal tubule of the rat. Total glomerular filtration rate following three-fourths nephrectomy was 1.29 +\/- 0.06 vs. 3.29 +\/- 0.08 ml\/min in sham controls, P less than 0.001. Systemic acid-base parameters were the same in both groups, but urine pH was lower in nephrectomized rats. In vivo microperfusion with identical isohydric solutions revealed that the JtCO2, fluid absorption (Jv), lumen-negative transepithelial potential difference (VT) were all significantly greater in the distal tubule of remnant kidneys. As the relative increase in Jv exceeded JtCO2, the perfusate tCO2 concentration increased markedly in remnant kidney distal tubules from 30.3 +\/- 0.59 to 39.9 +\/- 1.73 mM. To determine if the increase in tCO2 concentration accounted for the difference in JtCO2, a second control group was studied using a perfusate tCO2 concentration of 39.6 +\/- 0.79 mM. Distal tubular JtCO2, Jv, and VT were significantly less in this control group than in the remnant kidney group. In separate studies, 10(-4) M amiloride was added to the perfusate used in remnant kidneys and controls studied with the elevated perfusate tCO2 concentration. The addition of 10(-4) M amiloride to the perfusate reduced VT and JtCO2. At identical values for VT, JtCO2 was higher in the distal tubule of remnant kidneys than in controls. We conclude the following. 1) The rate of acidification is increased in the distal tubule of remnant kidneys.(ABSTRACT TRUNCATED AT 250 WORDS) <\/jats:p>","DOI":"10.1152\/ajprenal.1990.258.1.f69","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T16:46:30Z","timestamp":1513961190000},"page":"F69-F74","source":"Crossref","is-referenced-by-count":1,"title":["Distal tubular acidification in the remnant kidney"],"prefix":"10.1152","volume":"258","author":[{"suffix":"Jr","given":"R. T.","family":"Kunau","sequence":"first","affiliation":[{"name":"Department of Medicine, University of Texas Health Science Center, San Antonio 78284."}]},{"given":"K. A.","family":"Walker","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Texas Health Science Center, San Antonio 78284."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1990.258.1.F69","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:12:52Z","timestamp":1567955572000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1990.258.1.F69"}},"issued":{"date-parts":[[1990,1,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1990,1,1]]}},"alternative-id":["10.1152\/ajprenal.1990.258.1.F69"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1990.258.1.f69","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1990,1,1]]}},{"indexed":{"date-parts":[[2022,4,5]],"date-time":"2022-04-05T02:47:07Z","timestamp":1649126827047},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1991,11,1]]},"abstract":"<jats:p> alpha 2-Adrenoceptor subtype expression was investigated in cultured rat inner medullary collecting duct (IMCD) cells using radioligand binding studies, Northern blot analysis, and adenosine 3',5'-cyclic monophosphate (cAMP) assays. [3H]rauwolscine bound to a single class of alpha 2-adrenoceptors with high affinity [Kd = 1.7 +\/- 0.3 nM, maximum binding (Bmax) = 45.2 +\/- 10.8 fmol\/mg protein]. alpha 2-Adrenoceptor ligands inhibited [3H]rauwolscine binding with a rank order of potency characteristic of interaction with the alpha 2B-adrenoceptor [inhibitory constant (Ki) values (in nM) rauwolscine (1.95) greater than ARC-239 (8.52) greater than prazosin (237) greater than oxymetazoline (30,000)]. Northern blot analysis was performed using poly(A)+ RNA isolated from 90% confluent rat IMCD cells and probes derived from alpha 2-adrenoceptor DNA sequences from the rat nonglycosylated alpha 2B-adrenoceptor and the human alpha 2A-adrenoceptor. The alpha 2B probe hybridized to a 4.2-kb band under high stringency conditions, but the alpha 2A-adrenoceptor probe did not hybridize to this band. In functional studies, the full alpha 2-adrenoceptor agonists epinephrine and UK-14,304 potently inhibited vasopressin-stimulated cAMP accumulation by 50 to 70% [half-maximal response (EC50) (in nM) epinephrine = 11.2, UK-14,304 = 6.4]. Guanabenz and clonidine were partial agonists, inhibiting cAMP accumulation by 30 to 40% and were less potent than the full agonists [EC50 (in nM) 56.0 guanabenz and 94.5 clonidine]. Epinephrine-induced inhibition of cAMP accumulation was blocked by rauwolscine, prazosin, and ARC-239 but not by the alpha 1-adrenoceptor antagonist corynanthine. We conclude that rat IMCD cells in primary culture express functional alpha 2-adrenoceptors of the alpha 2B-subtype. <\/jats:p>","DOI":"10.1152\/ajprenal.1991.261.5.f760","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T04:17:21Z","timestamp":1514002641000},"page":"F760-F766","source":"Crossref","is-referenced-by-count":4,"title":["Characterization of prazosin-sensitive alpha 2 B-adrenoceptors expressed by cultured rat IMCD cells"],"prefix":"10.1152","volume":"261","author":[{"given":"G.","family":"Yasuda","sequence":"first","affiliation":[{"name":"Department of Medicine, Creighton University School of Medicine,Omaha, Nebraska 68131."}]},{"given":"L.","family":"Sun","sequence":"additional","affiliation":[{"name":"Department of Medicine, Creighton University School of Medicine,Omaha, Nebraska 68131."}]},{"given":"S.","family":"Umemura","sequence":"additional","affiliation":[{"name":"Department of Medicine, Creighton University School of Medicine,Omaha, Nebraska 68131."}]},{"given":"W. A.","family":"Pettinger","sequence":"additional","affiliation":[{"name":"Department of Medicine, Creighton University School of Medicine,Omaha, Nebraska 68131."}]},{"given":"W. B.","family":"Jeffries","sequence":"additional","affiliation":[{"name":"Department of Medicine, Creighton University School of Medicine,Omaha, Nebraska 68131."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1991.261.5.F760","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:20:06Z","timestamp":1567959606000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1991.261.5.F760"}},"issued":{"date-parts":[[1991,11,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1991,11,1]]}},"alternative-id":["10.1152\/ajprenal.1991.261.5.F760"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1991.261.5.f760","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1991,11,1]]}},{"indexed":{"date-parts":[[2023,5,13]],"date-time":"2023-05-13T17:41:35Z","timestamp":1683999695966},"reference-count":49,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2008,1]]},"abstract":"<jats:p>Individuals with chronic kidney disease (CKD) and\/or diabetes mellitus (DM) are at increased risk of cardiovascular events and have elevated externalization of phosphatidylserine (PS; which propagates thrombus formation) in a small subpopulation of platelets. The purpose of this study was to examine the effect of 1) removing uremic toxins by hemodialysis on PS externalization in patients with either CKD or CKD and DM and 2) ultrafiltrate (UF) from these individuals on PS externalization in healthy platelets. PS externalization was quantified by a fluorescence-activated cell sorter using annexin V in platelet-rich plasma. PS externalization was elevated threefold in CKD patients and returned to basal values during 3-h hemodialysis. In contrast, it was elevated fivefold in individuals with CKD and DM and was still threefold above control after 3-h treatment. UF significantly increased PS externalization in a small subpopulation of platelets from healthy controls. The effect of UF from individuals with CKD and DM was significantly greater than that from patients with CKD alone, and the responses were partially inhibited by the protein kinase C\u03b4 (PKC\u03b4) inhibitor rottlerin and the 5-hydroxytryptamine (5-HT)<jats:sub>2A\/2C<\/jats:sub>receptor antagonist ritanserin. The data suggest that uremic toxins present in UF mediate PS externalization in a small subpopulation of platelets, at least in part, via the 5-HT<jats:sub>2A\/2C<\/jats:sub>receptor and PKC\u03b4 and demonstrate that DM further enhances platelet PS externalization in CKD patients undergoing hemodialysis. This may explain, at least in part, the additional increase in vascular damage observed in CKD patients when DM is present.<\/jats:p>","DOI":"10.1152\/ajprenal.00279.2007","type":"journal-article","created":{"date-parts":[[2007,8,2]],"date-time":"2007-08-02T00:53:22Z","timestamp":1186016002000},"page":"F220-F228","source":"Crossref","is-referenced-by-count":2,"title":["Differential effects of dialysis and ultrafiltrate from individuals with CKD, with or without diabetes, on platelet phosphatidylserine externalization"],"prefix":"10.1152","volume":"294","author":[{"given":"Yingjie","family":"Wang","sequence":"first","affiliation":[]},{"given":"Werner","family":"Beck","sequence":"additional","affiliation":[]},{"given":"Reinhold","family":"Deppisch","sequence":"additional","affiliation":[]},{"given":"Sally M.","family":"Marshall","sequence":"additional","affiliation":[]},{"given":"Nicholas A.","family":"Hoenich","sequence":"additional","affiliation":[]},{"given":"Michael G.","family":"Thompson","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004080635"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1053\/ajkd.2002.34510"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00173.x"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/16.6.1222"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1194\/jlr.R200019-JLR200"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1016\/S1388-1981(00)00052-4"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2141.2006.06045.x"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1177\/039139880202501203"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00399.x"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1021\/bi9912544"},{"key":"R11","doi-asserted-by":"crossref","unstructured":"Fadok VA, Voelker DR, Campbell PA, Cohen JJ, Bratton DL, Henson PM.Exposure of phosphatidylserine on the surface of apoptotic lymphocytes triggers specific recognition and removal by macrophages.J Immunol148: 2207\u20132216, 1992.","DOI":"10.4049\/jimmunol.148.7.2207"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1002\/med.20028"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.4065\/80.10.1270"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1016\/S1471-4914(03)00028-5"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M003116200"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1038\/192531a0"},{"key":"R17","doi-asserted-by":"crossref","unstructured":"Garcia-Calvo M, Petersen EP, Leiting B, Ruel R, Nicholson DW, Thornberry NA.Inhibition of human caspases by peptide-based and macromolecular inhibitors.J Biol Chem273: 22608\u201322613, 1998.","DOI":"10.1074\/jbc.273.49.32608"},{"key":"R18","doi-asserted-by":"crossref","unstructured":"Gawaz M, Bogner C.Changes in platelet membrane glycoproteins and platelet-leucocyte interaction during hemodialysis.Clin Invest72: 424\u2013429, 1994.","DOI":"10.1007\/BF00180515"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa041031"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000100127.54107.57"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1002\/psc.519"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1016\/S1286-4579(01)01458-7"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1021\/bi0107492"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1258\/0004563011900245"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.2337\/diacare.22.9.1543"},{"key":"R26","unstructured":"Leysen JE, Gommeren W, Van Gompel P, Wynants J, Janssen PFM, Laduran PM.Receptor-binding properties in vitro and in vivo of ritanserin: a very potent and long acting serotonin-S2 antagonist.Mol Pharmacol27: 600\u2013611, 1985."},{"key":"R27","doi-asserted-by":"crossref","unstructured":"Matthews JN, Altman DG, Campbell MJ, Royston P.Analysis of serial measurements in medical research.Br Med J330: 230\u2013235, 1990.","DOI":"10.1136\/bmj.300.6719.230"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2004.04.034"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1161\/01.ATV.0000031340.68494.34"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.52.37329"},{"key":"R31","unstructured":"Reverter JC, Escolar G, Sanz C, Cases A, Villamor N, Nieuwenhuis HK, Lopez S, Ordinas A.Platelet activation during hemodialysis measured through exposure of P-selectin: Analysis of flow cytometric and ultrastructural techniques.J Lab Clin Med124: 79\u201385, 1994."},{"key":"R32","doi-asserted-by":"crossref","unstructured":"Rosing J, Bevers EM, Comfurious P, Henker HC, van Dieijen G, Weiss HJ, Zwaal RF.Impaired factor X and prothrombin activation associated with decreased phospholipid exposure in platelets from a patient with a bleeding disorder.Blood65: 1557\u20131561, 1985.","DOI":"10.1182\/blood.V65.6.1557.bloodjournal6561557"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199901143400207"},{"key":"R34","doi-asserted-by":"crossref","unstructured":"Shcherbina A, Remold-O'Donnell E.Role of caspase in a subset of human platelet activation responses.Blood93: 4222\u20134231, 1999.","DOI":"10.1182\/blood.V93.12.4222"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1001\/jama.293.14.1737"},{"key":"R36","doi-asserted-by":"crossref","unstructured":"Sloand JA, Sloand EM.Studies on platelet membrane glycoproteins and platelet function during hemodialysis.J Am Soc Nephrol8: 799\u2013803, 1997.","DOI":"10.1681\/ASN.V85799"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1016\/0272-6386(95)90123-X"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1021\/ja0529135"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.2174\/1389450054021873"},{"key":"R40","doi-asserted-by":"crossref","unstructured":"Toullec D, Pianetti P, Coste H, Bellevergue P, Grand-Perrett T, Ajakane M, Baudet V, Boissin P, Boursier E, Loriolle F, Duhamel L, Charon D, Kirilovsky J.The bisindolylmaleimide GF 109203X is a potent and selective inhibitor of protein kinase C.J Biol Chem266: 15771\u201315781, 1991.","DOI":"10.1016\/S0021-9258(18)98476-0"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M606950200"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00924.x"},{"key":"R43","unstructured":"Vanholder R, De Smet R, Lameire N.Protein-bound uremic solutes: The forgotten toxins.Kidney Int59,Suppl78: S266\u2013S270, 2001."},{"key":"R44","doi-asserted-by":"crossref","unstructured":"Walter R, Mischak H, Haller H.Haemodialysis, atherosclerosis and inflammation\u2013identifying molecular mechanisms of chronic vascular disease in ESRD patients.Nephrol Dial Transplant17: 24\u201329, 2002.","DOI":"10.1093\/ndt\/17.suppl_3.24"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00560.2006"},{"key":"R46","doi-asserted-by":"publisher","DOI":"10.1042\/bj2940335"},{"key":"R47","doi-asserted-by":"crossref","unstructured":"Wolf BB, Goldstein JC, Stenmicke HR, Beere H, Amarante-Mendes GP, Salvesen GS, Green DR.Calpain functions in a caspase-independent manner to promote apoptosis-like events during platelet activation.Blood94: 1683\u20131692, 1999.","DOI":"10.1182\/blood.V94.5.1683.417k37_1683_1692"},{"key":"R48","doi-asserted-by":"publisher","DOI":"10.1007\/s00018-005-5099-y"},{"key":"R49","doi-asserted-by":"crossref","unstructured":"Zwaal RF, Schroit AJ.Pathophysiologic implications of membrane phospholipid asymmetry in blood cells.Blood89: 1121\u20131132, 1997.","DOI":"10.1182\/blood.V89.4.1121"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00279.2007","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,5,13]],"date-time":"2023-05-13T17:01:57Z","timestamp":1683997317000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00279.2007"}},"issued":{"date-parts":[[2008,1]]},"references-count":49,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2008,1]]}},"alternative-id":["10.1152\/ajprenal.00279.2007"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00279.2007","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2008,1]]}},{"indexed":{"date-parts":[[2022,4,3]],"date-time":"2022-04-03T03:24:34Z","timestamp":1648956274807},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1988,5,1]]},"abstract":"<jats:p> The mechanism of renal transport of L-proline by luminal membrane vesicles prepared from proximal straight tubules (pars recta) of rabbit kidney was investigated. The following picture emerges from transport studies: an electrogenic and Na+-requiring system confined to this region of nephron exists for transport of L-proline with a high affinity (Km = 0.16 mM) and low capacity (Vmax = 3.5 nmol.mg protein-1.15 S-1). Lowering the pH from 7.5 to 5.5 increased the affinity (Km lowered from 0.16 mM at pH 7.5 to 0.08 mM at pH 5.5) without changing the maximal capacity of this system. Modification of histidyl residues of the intact luminal membrane vesicles by diethyl-pyrocarbonate (DEP) completely abolished the transient renal accumulation of L-proline. Simultaneous presence of Na+ and L-proline (10 mM) protects against DEP inactivation of renal transport of radioactive L-proline. We propose that a histidyl residue may be at or close to the active site of L-proline transporter in vesicles from the pars recta. <\/jats:p>","DOI":"10.1152\/ajprenal.1988.254.5.f628","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T03:22:43Z","timestamp":1513999363000},"page":"F628-F633","source":"Crossref","is-referenced-by-count":0,"title":["Transport of L-proline by luminal membrane vesicles from pars recta of rabbit proximal tubule"],"prefix":"10.1152","volume":"254","author":[{"given":"H.","family":"Roigaard-Petersen","sequence":"first","affiliation":[{"name":"Institute of Medical Biochemistry, University of Aarhus,Denmark."}]},{"given":"C.","family":"Jacobsen","sequence":"additional","affiliation":[{"name":"Institute of Medical Biochemistry, University of Aarhus,Denmark."}]},{"given":"M. I.","family":"Sheikh","sequence":"additional","affiliation":[{"name":"Institute of Medical Biochemistry, University of Aarhus,Denmark."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1988.254.5.F628","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:51:04Z","timestamp":1567972264000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1988.254.5.F628"}},"issued":{"date-parts":[[1988,5,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1988,5,1]]}},"alternative-id":["10.1152\/ajprenal.1988.254.5.F628"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1988.254.5.f628","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1988,5,1]]}},{"indexed":{"date-parts":[[2022,4,20]],"date-time":"2022-04-20T00:33:34Z","timestamp":1650414814385},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1990,8,1]]},"abstract":"<jats:p> A method is described that allows perfusion of the inner medullary collecting duct (IMCD) of the rat kidney in situ and in vivo. Fine polyethylene catheters connected to a microperfusion pump were inserted into collecting ducts via the openings at the exposed papilla tip. Perfusate contained 22Na as well as [3H]inulin. During perfusion at 30 nl\/min, urine was simultaneously collected. A decrease in the Na-to-inulin concentration ratio in the urinary sample, compared with the perfusate, was taken as indicating unidirectional efflux of Na from the perfused duct system. The effects of luminal amiloride (2 X 10(-4) M) or atrial natriuretic factor (ANF, 10(-8) M) were studied. Compared with control perfusions, both agonists reduced Na efflux from the IMCD to approximately 50%, indicating luminal sites of action. Combination of amiloride and ANF at their respective concentrations had no further effect. The lack of statistically significant additivity suggests, but does not prove, that ANF, administered from the luminal side, is able to block amiloride-sensitive Na channels in the apical membrane of IMCD cells. <\/jats:p>","DOI":"10.1152\/ajprenal.1990.259.2.f222","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T17:26:51Z","timestamp":1513963611000},"page":"F222-F226","source":"Crossref","is-referenced-by-count":4,"title":["In vivo microperfusion of inner medullary collecting duct in rats: effect of amiloride and ANF"],"prefix":"10.1152","volume":"259","author":[{"given":"H.","family":"Sonnenberg","sequence":"first","affiliation":[{"name":"Department of Physiology, University of Toronto, Ontario,Canada."}]},{"given":"U.","family":"Honrath","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Toronto, Ontario,Canada."}]},{"given":"D. R.","family":"Wilson","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Toronto, Ontario,Canada."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1990.259.2.F222","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:18:54Z","timestamp":1567955934000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1990.259.2.F222"}},"issued":{"date-parts":[[1990,8,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1990,8,1]]}},"alternative-id":["10.1152\/ajprenal.1990.259.2.F222"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1990.259.2.f222","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1990,8,1]]}},{"indexed":{"date-parts":[[2022,4,1]],"date-time":"2022-04-01T15:15:20Z","timestamp":1648826120975},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1985,2,1]]},"DOI":"10.1152\/ajprenal.1985.248.2.f161","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T00:43:27Z","timestamp":1513989807000},"page":"F161-F162","source":"Crossref","is-referenced-by-count":0,"title":["The modeling methodology forum: an expanded department"],"prefix":"10.1152","volume":"248","author":[{"suffix":"III","given":"Joseph J.","family":"DiStefano","sequence":"first","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1985.248.2.F161","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:33:19Z","timestamp":1567971199000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1985.248.2.F161"}},"issued":{"date-parts":[[1985,2,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1985,2,1]]}},"alternative-id":["10.1152\/ajprenal.1985.248.2.F161"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1985.248.2.f161","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1985,2,1]]}},{"indexed":{"date-parts":[[2022,4,1]],"date-time":"2022-04-01T13:43:43Z","timestamp":1648820623344},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2003,6,1]]},"DOI":"10.1152\/ajprenal.00098.2003","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T15:38:08Z","timestamp":1425397088000},"page":"F1280-F1280","source":"Crossref","is-referenced-by-count":0,"title":["Corrigenda for vol. 283, p. F1351"],"prefix":"10.1152","volume":"284","member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00098.2003","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:27:23Z","timestamp":1567967243000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00098.2003"}},"issued":{"date-parts":[[2003,6,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2003,6,1]]}},"alternative-id":["10.1152\/ajprenal.00098.2003"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00098.2003","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2003,6,1]]}},{"indexed":{"date-parts":[[2022,4,1]],"date-time":"2022-04-01T16:18:21Z","timestamp":1648829901324},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1977,11,1]]},"abstract":"<jats:p> Biochemical studies of renal tissue have so far not shown the presence of any active pump mechanism other than Na-K-ATPase. In this review of possible transport mechanisms for the ions Na, K, H, Cl, and HCO3, it is suggested that transport of these ions can be coupled to ATPase by conductance (uniport) processes or by ion gradients by co-transport (symport) or countertransport (antiport) systems. These may be neutral or electrogenic. Accordingly, the function of any region of the tubule will be determined by the porter(s) present in the apical or basal-lateral membrane, and by the Na-K-ATPase located almost exclusively in the basal-lateral membrane. Future research in this area will probably define these porters in vesicles isolated from specific cell types of the kidney. <\/jats:p>","DOI":"10.1152\/ajprenal.1977.233.5.f359","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T20:08:13Z","timestamp":1513973293000},"page":"F359-F365","source":"Crossref","is-referenced-by-count":1,"title":["Ion pumps in the renal tubule"],"prefix":"10.1152","volume":"233","author":[{"given":"G.","family":"Sachs","sequence":"first","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1977.233.5.F359","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:56:02Z","timestamp":1567968962000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1977.233.5.F359"}},"issued":{"date-parts":[[1977,11,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1977,11,1]]}},"alternative-id":["10.1152\/ajprenal.1977.233.5.F359"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1977.233.5.f359","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1977,11,1]]}},{"indexed":{"date-parts":[[2022,4,2]],"date-time":"2022-04-02T13:03:45Z","timestamp":1648904625684},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1996,7,1]]},"abstract":"<jats:p> Pages F1004'F1014: Y. Zhang, A. K. Mircheff, C. B. Hensley, C. E. Magyar, D. G. Warnock, R. Chambrey, K.-P. Yip, D. J. Marsh, N.-H. Holstein-Rathlou, and A. A. McDonough. \u201cRapid redistribution and inhibition of renal sodium transporters during acute pressure natriuresis.\u201d The immunoblot panels in Figures 2 and 5\u20137 were inadvertently printed from low-resolution copies of the original artwork; in addition, the panels in Fig. 6 were incorrectly labeled. The correct figures are reproduced on the following pages. <\/jats:p><jats:p> (See PDF) <\/jats:p>","DOI":"10.1152\/ajprenal.1996.271.1.f242-t","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T01:50:32Z","timestamp":1513993832000},"page":"F242-F242","source":"Crossref","is-referenced-by-count":0,"title":["Rapid redistribution and inhibition of renal sodium transporters during acute pressure natriuresis"],"prefix":"10.1152","volume":"271","author":[{"given":"Y.","family":"Zhang","sequence":"first","affiliation":[]},{"given":"A. K.","family":"Mircheff","sequence":"additional","affiliation":[]},{"given":"C. B.","family":"Hensley","sequence":"additional","affiliation":[]},{"given":"C. E.","family":"Magyar","sequence":"additional","affiliation":[]},{"given":"D. G.","family":"Warnock","sequence":"additional","affiliation":[]},{"given":"R.","family":"Chambrey","sequence":"additional","affiliation":[]},{"given":"K. -P.","family":"Yip","sequence":"additional","affiliation":[]},{"given":"D. J.","family":"Marsh","sequence":"additional","affiliation":[]},{"given":"N. -H.","family":"Holstein-Rathlou","sequence":"additional","affiliation":[]},{"given":"A. A.","family":"McDonough","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1996.271.1.F242-t","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:07:06Z","timestamp":1567958826000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1996.271.1.F242-t"}},"issued":{"date-parts":[[1996,7,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1996,7,1]]}},"alternative-id":["10.1152\/ajprenal.1996.271.1.F242-t"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1996.271.1.f242-t","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1996,7,1]]}},{"indexed":{"date-parts":[[2022,4,5]],"date-time":"2022-04-05T18:15:19Z","timestamp":1649182519595},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1995,2,1]]},"abstract":"<jats:p> The influence of guanosine 3',5'-cyclic monophosphate (cGMP)-dependent dilators on autoregulatory responses (AR) of arcuate arteries (ArcA) and afferent arterioles at early sites and at juxtaglomerular sites (JAA) was assessed by videomicroscopy using in vitro blood-perfused juxtamedullary nephron preparations. AR were quantified as fractional changes in luminal diameter induced by doubling blood perfusion pressure (60-120 mmHg). Baseline AR ranged from 17 +\/- 2% to 21 +\/- 2% in ArcA and from 24 +\/- 2% to 34 +\/- 4% in JAA. Direct perivascular applications of increasing concentrations of 8-bromo-cGMP (8-BrcGMP, 10 microM to 1 mM), of the NO donors sodium nitroprusside (10 microM to 1 mM) and 3-morpholino-sydnonimine chlorhydrate (SIN1; 10 microM to 1 mM), and of rat atrial natriuretic factor (ANF, 0.1 nM to 10 nM) dose- and pressure-dependently dilated all vessels at 60 mmHg. Concomitantly, AR values were dose-dependently reduced or reversed to pressure-induced dilations. During application of 8-BrcGMP and NO donors, the segmental gradient of sensitivity of AR was ArcA &gt; JAA; the opposite gradient was found with ANF (i.e., JAA &gt; ArcA). The present results demonstrate that compounds known to utilize the cGMP-signaling pathway act as modulators of AR along the juxtamedullary preglomerular vasculature. <\/jats:p>","DOI":"10.1152\/ajprenal.1995.268.2.f338","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T23:32:24Z","timestamp":1513985544000},"page":"F338-F346","source":"Crossref","is-referenced-by-count":8,"title":["Interaction between cGMP-dependent dilators and autoregulation in rat preglomerular vasculature"],"prefix":"10.1152","volume":"268","author":[{"given":"N.","family":"Bouriquet","sequence":"first","affiliation":[{"name":"Groupe Rein et Hypertension, Hopital St. Charles, Montpellier,France."}]},{"given":"D.","family":"Casellas","sequence":"additional","affiliation":[{"name":"Groupe Rein et Hypertension, Hopital St. Charles, Montpellier,France."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1995.268.2.F338","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:55:30Z","timestamp":1567958130000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1995.268.2.F338"}},"issued":{"date-parts":[[1995,2,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1995,2,1]]}},"alternative-id":["10.1152\/ajprenal.1995.268.2.F338"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1995.268.2.f338","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1995,2,1]]}},{"indexed":{"date-parts":[[2022,4,4]],"date-time":"2022-04-04T17:50:54Z","timestamp":1649094654666},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1992,7,1]]},"abstract":"<jats:p> Pages F449\u2013F453: E. Dafnis, M. Spohn, B. Lonis, N. A. Kurtzman, and S. Sabatini. \u201cVanadate causes hypokalemic distal renal tubular acidosis.\u201d The value for urine anion gap in NH4Cl-treated animals on page F450 (last sentence in first paragraph of results), as well as on page F51 (Table 2, last value in last line), should be -82 \u00b1 7 meq\/l instead of -232 \u00b1 27 meq\/l. <\/jats:p>","DOI":"10.1152\/ajprenal.1992.263.1.f179-r","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T10:12:07Z","timestamp":1514023927000},"page":"F179-F179","source":"Crossref","is-referenced-by-count":0,"title":["Vanadate causes hypokalemic distal renal tubular acidosis"],"prefix":"10.1152","volume":"263","author":[{"given":"E.","family":"Dafnis","sequence":"first","affiliation":[]},{"given":"M.","family":"Spohn","sequence":"additional","affiliation":[]},{"given":"B.","family":"Lonis","sequence":"additional","affiliation":[]},{"given":"N. A.","family":"Kurtzman","sequence":"additional","affiliation":[]},{"given":"S.","family":"Sabatini","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1992.263.1.F179-r","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:26:38Z","timestamp":1567974398000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1992.263.1.F179-r"}},"issued":{"date-parts":[[1992,7,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1992,7,1]]}},"alternative-id":["10.1152\/ajprenal.1992.263.1.F179-r"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1992.263.1.f179-r","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1992,7,1]]}},{"indexed":{"date-parts":[[2022,4,1]],"date-time":"2022-04-01T19:20:19Z","timestamp":1648840819760},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1979,10,1]]},"DOI":"10.1152\/ajprenal.1979.237.4.f307","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T20:26:32Z","timestamp":1513974392000},"page":"F307-F311","source":"Crossref","is-referenced-by-count":0,"title":["Renal handling and utilization of citrate in starvation-induced hypocitricemia"],"prefix":"10.1152","volume":"237","author":[{"given":"A. J.","family":"Gold","sequence":"first","affiliation":[]},{"given":"M.","family":"Onwochei","sequence":"additional","affiliation":[]},{"given":"L. C.","family":"Costello","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1979.237.4.F307","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:59:28Z","timestamp":1567969168000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1979.237.4.F307"}},"issued":{"date-parts":[[1979,10,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1979,10,1]]}},"alternative-id":["10.1152\/ajprenal.1979.237.4.F307"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1979.237.4.f307","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1979,10,1]]}},{"indexed":{"date-parts":[[2023,10,11]],"date-time":"2023-10-11T22:52:54Z","timestamp":1697064774487},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1992,11,1]]},"abstract":"<jats:p> Angiotensin II (ANG II) normally induces cellular hypertrophy in proximal tubular epithelium by engaging receptor systems that use a G-protein-signaling mechanism. The c-mas oncogene also encodes part of a superfamily of vasoactive peptide receptor-like moieties that couple to G proteins. To determine whether the stable expression of the c-mas gene might alter or modify the induction of cellular hypertrophy by ANG II in tubular epithelium, a rat c-mas cDNA was cloned into the pSV2 expression vector for use in cell transfection. Scatchard analysis of ANG II binding revealed no significant differences in ANG II receptor number or in the dissociation constant between pSV2mas-transfected or wild-type MCT cells, but rather an increase in the number of receptors not replaceable by known inhibitors. ANG II also induced proliferation in pSV2mas-transfected MCT cells that was not blocked by conventional inhibitors and increased intracellular levels of inositol trisphosphate. ANG II, furthermore, did not increase de novo protein synthesis in pSV2-transfected MCT cells and failed to lower their intracellular concentration of adenosine 3',5'-cyclic monophosphate, both expected parameters of cellular hypertrophy. Our findings demonstrate that expression of c-mas in tubular epithelium can modulate tubular cell phenotype toward proliferation rather than hypertrophy. This effect is likely mediated by a reshuffling of the heterogeneity of ANG II receptors on the cell surface, or perhaps by the emergence of a new ANG II receptor, followed by alterations in the process of signal transduction. <\/jats:p>","DOI":"10.1152\/ajprenal.1992.263.5.f931","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T10:05:20Z","timestamp":1514023520000},"page":"F931-F938","source":"Crossref","is-referenced-by-count":1,"title":["Effects of angiotensin II on proximal tubular cells stably transfected with the c-mas oncogene"],"prefix":"10.1152","volume":"263","author":[{"given":"G.","family":"Wolf","sequence":"first","affiliation":[{"name":"Department of Medicine, University of Frankfurt, Federal Republic of Germany."}]},{"given":"E. G.","family":"Neilson","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Frankfurt, Federal Republic of Germany."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1992.263.5.F931","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:24:51Z","timestamp":1567974291000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1992.263.5.F931"}},"issued":{"date-parts":[[1992,11,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1992,11,1]]}},"alternative-id":["10.1152\/ajprenal.1992.263.5.F931"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1992.263.5.f931","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1992,11,1]]}},{"indexed":{"date-parts":[[2023,2,7]],"date-time":"2023-02-07T12:28:15Z","timestamp":1675772895724},"reference-count":36,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2007,3]]},"abstract":"<jats:p> Single injection of a small quantity of phenol into the cortex of one kidney in rats results in development of persistent hypertension (HTN) which is thought to be mediated by activation of renal afferent and efferent sympathetic pathways and sodium retention. Nitric oxide (NO) plays a major role in regulation of renal vascular resistance, tubular Na<jats:sup>+<\/jats:sup> reabsorption, pressure natriuresis, and thereby systemic arterial pressure. The present study was performed to test the hypothesis that chronic renal injury-induced HTN may be associated with dysregulation of NO system in the kidney. Accordingly, urinary NO metabolite (NO<jats:sub>x<\/jats:sub>) and cGMP excretions as well as renal cortical tissue (right kidney) expressions of NO synthase (NOS) isoforms [endothelial, neuronal, and inducible NOS, respectively (eNOS, nNOS, and iNOS)], NOS-regulatory factors (Caveolin-1, phospho-AKt, and calmodulin), and second-messenger system (soluble guanylate cyclase [sGC] and phosphodiesterase-5 [PDE-5]) were determined in male Sprague-Dawley rats 4 wk after injection of phenol (50 \u03bcl of 10% phenol) or saline into the lower pole of left kidney. The phenol-injected group exhibited a significant elevation of arterial pressure, marked reductions of urinary NO<jats:sub>x<\/jats:sub> and cGMP excretions, downregulations of renal tissue nNOS, eNOS, Phospho-eNOS, iNOS, and alpha chain of sGC. However, renal tissue AKt, phospho-AKT, Calmodulin, and PDE-5 proteins were unchanged in the phenol-injected animals. In conclusion, renal injury in this model results in significant downregulations of NOS isoforms and sGC and consequent reductions of NO production and cGMP generation by the kidney, events that may contribute to maintenance of HTN in this model. <\/jats:p>","DOI":"10.1152\/ajprenal.00157.2006","type":"journal-article","created":{"date-parts":[[2006,11,23]],"date-time":"2006-11-23T02:18:44Z","timestamp":1164248324000},"page":"F974-F980","source":"Crossref","is-referenced-by-count":3,"title":["Effect of renal injury-induced neurogenic hypertension on NO synthase, caveolin-1, AKt, calmodulin and soluble guanylate cyclase expressions in the kidney"],"prefix":"10.1152","volume":"292","author":[{"given":"Y.","family":"Bai","sequence":"first","affiliation":[]},{"given":"S.","family":"Ye","sequence":"additional","affiliation":[]},{"given":"R.","family":"Mortazavi","sequence":"additional","affiliation":[]},{"given":"V.","family":"Campese","sequence":"additional","affiliation":[]},{"given":"N. D.","family":"Vaziri","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.0600031083.x"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115849"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.57.s75.11.x"},{"key":"R4","unstructured":"Gabbai FB, Blantz RC. Role of nitric oxide in renal hemodynamics. Semin Nephrol 19: 242\u2013250, 1999."},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(90)80489-6"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.31.1.266"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2004.04.002"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00728.x"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00747.x"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1016\/S0378-1119(98)00303-5"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1994.266.5.H1918"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.28.2.297"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1590\/S0100-879X1999001100006"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200107001"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.34.4.552"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1016\/S0895-7061(00)01234-6"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.31.1.189"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.20.3.298"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.00463.2004"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00281.x"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.88.2.365"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.270.6.F1027"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1998.8769"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.264"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.36.1.142"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1998.274.2.H642"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.31.6.1248"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00670.x"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00465.x"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1046\/j.1432-1327.1998.2550391.x"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00317.2002"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1016\/S0895-7061(98)00030-2"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.103"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.275.1.F18"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1021\/bi00501a002"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.300.3.762"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00157.2006","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T23:28:12Z","timestamp":1567985292000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00157.2006"}},"issued":{"date-parts":[[2007,3]]},"references-count":36,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2007,3]]}},"alternative-id":["10.1152\/ajprenal.00157.2006"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00157.2006","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2007,3]]}},{"indexed":{"date-parts":[[2023,8,11]],"date-time":"2023-08-11T20:36:07Z","timestamp":1691786167877},"reference-count":20,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1999,4,1]]},"abstract":"<jats:p>To gain insight into the physiological role of a kidney-specific chloride channel, CLC-K2, the exact intrarenal localization was determined by in situ hybridization. In contrast to the inner medullary localization of CLC-K1, the signal of CLC-K2 in our in situ hybridization study was highly evident in the superficial cortex, moderate in the outer medulla, and absent in the inner medulla. To identify the nephron segments where CLC-K2 mRNA was expressed, we performed in situ hybridization of CLC-K2 and immunohistochemistry of marker proteins (Na<jats:sup>+<\/jats:sup>\/Ca<jats:sup>2+<\/jats:sup>exchanger, Na<jats:sup>+<\/jats:sup>-Cl<jats:sup>\u2212<\/jats:sup>cotransporter, aquaporin-2 water channel, and Tamm-Horsfall glycoprotein) in sequential sections of a rat kidney. Among the tubules of the superficial cortex, CLC-K2 mRNA was highly expressed in the distal convoluted tubules, connecting tubules, and cortical collecting ducts. The expression of CLC-K2 in the outer and inner medullary collecting ducts was almost absent. In contrast, a moderate signal of CLC-K2 mRNA was observed in the medullary thick ascending limb of Henle\u2019s loop, but the signal in the cortical thick ascending limb of Henle\u2019s loop was low. These results clearly demonstrated that CLC-K2 was not colocalized with CLC-K1 and that its localization along the nephron segments was relatively broad compared with that of CLC-K1.<\/jats:p>","DOI":"10.1152\/ajprenal.1999.276.4.f552","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T18:10:57Z","timestamp":1514052657000},"page":"F552-F558","source":"Crossref","is-referenced-by-count":24,"title":["Localization of rat CLC-K2 chloride channel mRNA in the kidney"],"prefix":"10.1152","volume":"276","author":[{"given":"Momono","family":"Yoshikawa","sequence":"first","affiliation":[{"name":"Second Department of Internal Medicine, Tokyo Medical and Dental University, Tokyo 113-8519; and"}]},{"given":"Shinichi","family":"Uchida","sequence":"additional","affiliation":[{"name":"Second Department of Internal Medicine, Tokyo Medical and Dental University, Tokyo 113-8519; and"}]},{"given":"Atsushi","family":"Yamauchi","sequence":"additional","affiliation":[{"name":"First Department of Medicine, Osaka University, School of Medicine, Osaka 565-0871, Japan"}]},{"given":"Akiko","family":"Miyai","sequence":"additional","affiliation":[{"name":"First Department of Medicine, Osaka University, School of Medicine, Osaka 565-0871, Japan"}]},{"given":"Yujiro","family":"Tanaka","sequence":"additional","affiliation":[{"name":"Second Department of Internal Medicine, Tokyo Medical and Dental University, Tokyo 113-8519; and"}]},{"given":"Sei","family":"Sasaki","sequence":"additional","affiliation":[{"name":"Second Department of Internal Medicine, Tokyo Medical and Dental University, Tokyo 113-8519; and"}]},{"given":"Fumiaki","family":"Marumo","sequence":"additional","affiliation":[{"name":"Second Department of Internal Medicine, Tokyo Medical and Dental University, Tokyo 113-8519; and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"crossref","first-page":"17677","DOI":"10.1016\/S0021-9258(17)32494-8","volume":"269","author":"Adachi S.","year":"1994","journal-title":"J. Biol. Chem."},{"issue":"36","key":"B2","first-page":"F573","volume":"267","author":"Fushimi K.","year":"1994","journal-title":"Am. J. Physiol."},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.91.15.6943"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.ph.54.030192.000333"},{"issue":"38","key":"B5","first-page":"F621","volume":"269","author":"Reeves W. B.","year":"1995","journal-title":"Am. J. Physiol."},{"issue":"28","key":"B6","first-page":"F46","volume":"259","author":"Sansom S. C.","year":"1990","journal-title":"Am. J. Physiol."},{"issue":"16","key":"B7","first-page":"F291","volume":"247","author":"Sansom S. C.","year":"1984","journal-title":"Am. J. Physiol."},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/ng1097-171"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.439"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117626"},{"key":"B11","first-page":"135","volume":"4","author":"Uchida S.","year":"1996","journal-title":"Exp. Nephrol."},{"key":"B12","doi-asserted-by":"crossref","first-page":"3821","DOI":"10.1016\/S0021-9258(18)53545-6","volume":"268","author":"Uchida S.","year":"1993","journal-title":"J. Biol. Chem."},{"issue":"41","key":"B13","first-page":"F678","volume":"272","author":"Vandewalle A.","year":"1997","journal-title":"Am. J. Physiol."},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1007\/BF01872742"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1007\/BF00231868"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1007\/BF00231440"},{"issue":"42","key":"B17","first-page":"F1030","volume":"273","author":"Winters C. J.","year":"1997","journal-title":"Am. J. Physiol."},{"issue":"32","key":"B18","first-page":"F979","volume":"263","author":"Zimniak L.","year":"1992","journal-title":"Am. J. Physiol."},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.481"},{"issue":"39","key":"B20","first-page":"F1066","volume":"270","author":"Zimniak L.","year":"1996","journal-title":"Am. J. Physiol."}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1999.276.4.F552","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:55:05Z","timestamp":1660190105000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1999.276.4.F552"}},"issued":{"date-parts":[[1999,4,1]]},"references-count":20,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1999,4,1]]}},"alternative-id":["10.1152\/ajprenal.1999.276.4.F552"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1999.276.4.f552","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1999,4,1]]}},{"indexed":{"date-parts":[[2023,1,18]],"date-time":"2023-01-18T13:15:43Z","timestamp":1674047743451},"reference-count":16,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2010,11]]},"DOI":"10.1152\/ajprenal.00485.2010","type":"journal-article","created":{"date-parts":[[2010,9,1]],"date-time":"2010-09-01T22:05:48Z","timestamp":1283378748000},"page":"F942-F943","source":"Crossref","is-referenced-by-count":2,"title":["Targeting B-Raf as a treatment strategy for polycystic kidney disease"],"prefix":"10.1152","volume":"299","author":[{"given":"Kelli M.","family":"Sas","sequence":"first","affiliation":[{"name":"Department of Medicine, Medical University of South Carolina, Charleston, South Carolina"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa060655"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.med.60.101707.125712"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1007\/978-3-642-01222-8_5"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1677\/erc.0.0080219"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1002\/bies.20069"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004090800"},{"key":"B7","author":"Renken C","journal-title":"Nephrol Dial Transplant"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1053\/j.ackd.2010.01.006"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1038\/nm1004"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0711741105"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa1003491"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1158\/0008-5472.CAN-04-1443"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005060645"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(97)90496-0"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00023.x"},{"key":"B16","author":"Yamaguchi T","journal-title":"Am J Physiol Renal Physiol"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00485.2010","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:16:59Z","timestamp":1567973819000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00485.2010"}},"issued":{"date-parts":[[2010,11]]},"references-count":16,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2010,11]]}},"alternative-id":["10.1152\/ajprenal.00485.2010"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00485.2010","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2010,11]]}},{"indexed":{"date-parts":[[2022,3,30]],"date-time":"2022-03-30T09:35:35Z","timestamp":1648632935378},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1987,10,1]]},"abstract":"<jats:p> The present study used free-flow micropuncture and whole-kidney clearance studies to determine the renal response to normocalcemic vs. hypocalcemic acute volume expansion (AVE) in anesthetized Munich-Wistar rats. Animals received AVE with Ringer bicarbonate to 10% body weight; half of these animals were supplemented with calcium to maintain normocalcemia (VE + Ca2+) and half were allowed to become hypocalcemic (VE). Filtered load of chloride and total CO2 (TCO2) to the superficial proximal tubule and delivered load to the superficial loop segment were not different between groups. Superficial proximal tubule absolute Cl reabsorption was not different, but superficial loop segment absolute Cl reabsorption was less in the VE + Ca2+ animals (2,221+\/- 106 vs. 2,651+\/- 125 pmol\/min, P less than 0.05) and whole-kidney fractional chloride excretion was greater (10.5+\/- 1.6 vs. 4.3+\/- 0.5%, P less than 0.05). When indomethacin (I) was administered to hypocalcemic (VE + I) and normocalcemic (VE + Ca2+ + I) AVE animals, both groups of animals had tubular and whole-kidney chloride reabsorption similar to VE animals. TCO2 reabsorption was not influenced by Ca2+ or I. The data indicate that normocalcemic vs. hypocalcemic AVE results in reduced superficial loop segment chloride reabsorption and greater whole-kidney fractional chloride excretion in the absence but not in the presence of prostaglandin inhibition. The data are compatible with an effect of hypocalcemia during AVE to limit superficial loop segment and whole-kidney chloride excretion by inhibiting renal prostaglandin synthesis. <\/jats:p>","DOI":"10.1152\/ajprenal.1987.253.4.f726","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T23:04:15Z","timestamp":1513983855000},"page":"F726-F733","source":"Crossref","is-referenced-by-count":0,"title":["Hypocalcemia-associated modulation of renal response to acute volume expansion in rats"],"prefix":"10.1152","volume":"253","author":[{"given":"D. E.","family":"Wesson","sequence":"first","affiliation":[{"name":"Department of Medicine, Veterans Administration Medical Center, Houston, Texas 77211."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1987.253.4.F726","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:51:51Z","timestamp":1567957911000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1987.253.4.F726"}},"issued":{"date-parts":[[1987,10,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1987,10,1]]}},"alternative-id":["10.1152\/ajprenal.1987.253.4.F726"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1987.253.4.f726","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1987,10,1]]}},{"indexed":{"date-parts":[[2022,3,30]],"date-time":"2022-03-30T10:57:07Z","timestamp":1648637827769},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1992,8,1]]},"abstract":"<jats:p> The postnatal development of mitochondrial ATP-producing pathways and Na-K-adenosinetriphosphatase (ATPase) in the rat medullary thick ascending limb of Henle (MTAL) was studied by measuring the activities of 3-ketoacid-CoA transferase, fumarase, citrate synthase, and Na-K-ATPase in microdissected MTAL of 16, 21, and 30-day-old pups and in adults. The role of adrenal steroids in the development of these four markers was also investigated by studying 21-day-old rats adrenalectomized on day 16 and given dexamethasone or aldosterone or NaCl injections from day 16 to day 21. There were large and correlated increases in the activities of the oxidative enzymes in the MTAL of control rat kidneys between 16 and 30 days after birth; Na-K-ATPase activity in the MTAL also greatly increased during the same period. Adrenalectomy completely prevented the developmental increases in MTAL oxidative enzymes and Na-K-ATPase; dexamethasone restored the development of all four enzymes, whereas aldosterone had no effect. We conclude that the postnatal maturation of Na+ reabsorption functions in MTAL cells involves coordinated increases in the capacity to produce ATP by oxidative metabolism and in Na-K-ATPase activity. This maturation process is probably triggered by the rise in circulating glucocorticoids that occurs during the weaning period. <\/jats:p>","DOI":"10.1152\/ajprenal.1992.263.2.f237","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T05:14:44Z","timestamp":1514006084000},"page":"F237-F242","source":"Crossref","is-referenced-by-count":3,"title":["Coordinate development of oxidative enzymes and Na-K-ATPase in thick ascending limb: role of corticosteroids"],"prefix":"10.1152","volume":"263","author":[{"given":"F.","family":"Djouadi","sequence":"first","affiliation":[{"name":"Institut National de la Sante et de la Recherche Medicale Unite 319, Universite Paris 7, France."}]},{"given":"A.","family":"Wijkhuisen","sequence":"additional","affiliation":[{"name":"Institut National de la Sante et de la Recherche Medicale Unite 319, Universite Paris 7, France."}]},{"given":"J.","family":"Bastin","sequence":"additional","affiliation":[{"name":"Institut National de la Sante et de la Recherche Medicale Unite 319, Universite Paris 7, France."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1992.263.2.F237","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:27:18Z","timestamp":1567960038000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1992.263.2.F237"}},"issued":{"date-parts":[[1992,8,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1992,8,1]]}},"alternative-id":["10.1152\/ajprenal.1992.263.2.F237"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1992.263.2.f237","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1992,8,1]]}},{"indexed":{"date-parts":[[2022,4,5]],"date-time":"2022-04-05T14:33:47Z","timestamp":1649169227627},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1992,1,1]]},"abstract":"<jats:p> The objective of this study was to test the hypothesis that the vasodilator prostaglandins E2 (PGE2) and PGI2) participate in the mechanisms involved in the increased renal vascular reactivity (RVR) observed in genetic hypertension. Studies were performed on anesthetized young and adult spontaneously hypertensive (SHR) and Wistar-Kyoto rats (WKY). Renal blood flow (RBF) was measured during bolus injections into the renal artery of different doses of viprostol and iloprost (stable receptor agonists of PGE2 and PGI2, respectively) before and during inhibition of prostaglandin synthesis by indomethacin. Under control conditions, PGE2 increased RBF equally in young SHR and WKY. However, after cyclooxygenase inhibition the PGE2-induced increase in RBF was larger in young SHR than in WKY. Adult SHR displayed reduced reactivity to PGE2 relative to age-matched WKY under control conditions. This strain difference was abolished after indomethacin administration. PGI2 increased RBF slightly in young rats before and after indomethacin administration. In contrast, both strains of older animals displayed significant increases in RBF in response to PGI2 injections. Indomethacin administration enhanced this PGI2-induced relaxation in adult SHR but not WKY. We propose that the action of vasodilator PGs in the renal vasculature of rats developing hypertension may be limited by low density of their renal receptors and\/or the opposing action of vasoconstrictor PGs. As age advances, PGI2 seems to be activated, possibly as part of a regulatory response to counterbalance the increased renal vascular resistance following the establishment of the disease. <\/jats:p>","DOI":"10.1152\/ajprenal.1992.262.1.f124","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T09:14:20Z","timestamp":1514020460000},"page":"F124-F130","source":"Crossref","is-referenced-by-count":3,"title":["Renal vascular reactivity to vasodilator prostaglandins in genetically hypertensive rats"],"prefix":"10.1152","volume":"262","author":[{"given":"C.","family":"Chatziantoniou","sequence":"first","affiliation":[{"name":"Department of Physiology, University of North Carolina, Chapel Hill27599-7545."}]},{"given":"W. J.","family":"Arendshorst","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of North Carolina, Chapel Hill27599-7545."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1992.262.1.F124","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:18:19Z","timestamp":1567973899000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1992.262.1.F124"}},"issued":{"date-parts":[[1992,1,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1992,1,1]]}},"alternative-id":["10.1152\/ajprenal.1992.262.1.F124"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1992.262.1.f124","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1992,1,1]]}},{"indexed":{"date-parts":[[2022,4,2]],"date-time":"2022-04-02T05:31:21Z","timestamp":1648877481204},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1993,6,1]]},"abstract":"<jats:p> Renal insulin-like growth factor (IGF)-I expression is enhanced in tissue that remains following removal of kidney mass. To characterize the expression of renal IGF-I after reduction of kidney mass by partial unilateral infarction, we measured levels of IGF-I extracted from noninfarcted (remnant) renal tissue that remained after one-half unilateral kidney infarction that was performed without (1\/2NX) or with (1 1\/2NX) contralateral nephrectomy. Levels of IGF-I extracted from remnant renal tissue after 1\/2NX increased significantly, peaking on day 3 after renal mass reduction, and then returned toward baseline. Steady-state levels of IGF-I mRNA were also elevated on day 3, suggesting that the increase in IGF-I results from enhanced synthesis. A similar pattern of increased extracted IGF-I and elevated IGF-I mRNA occurred after 1 1\/2NX. Levels of IGF-I extracted from remnant renal tissue 3 days after 1 1\/2NX were not higher than levels extracted from remnant tissue 3 days after 1\/2NX, and both were higher than levels of IGF-I extracted from contralateral kidneys 3 days after unilateral nephrectomy. Therefore, levels of IGF-I did not correlate with the extent of reduction of renal mass per se. We conclude that partial renal infarction provides a stimulus to enhance IGF-I expression. Increased renal IGF-I must be considered in the interpretation of findings originating from use of remnant kidney models of chronic renal failure. <\/jats:p>","DOI":"10.1152\/ajprenal.1993.264.6.f963","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T05:19:31Z","timestamp":1514006371000},"page":"F963-F967","source":"Crossref","is-referenced-by-count":2,"title":["Enhanced renal IGF-I expression following partial kidney infarction"],"prefix":"10.1152","volume":"264","author":[{"given":"S. A.","family":"Rogers","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, George M. O'Brien Kidney andUrological Diseases Center, Washington University School of Medicine, St.Louis, Missouri 63110."}]},{"given":"S. B.","family":"Miller","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, George M. O'Brien Kidney andUrological Diseases Center, Washington University School of Medicine, St.Louis, Missouri 63110."}]},{"given":"M. R.","family":"Hammerman","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, George M. O'Brien Kidney andUrological Diseases Center, Washington University School of Medicine, St.Louis, Missouri 63110."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1993.264.6.F963","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:28:36Z","timestamp":1567960116000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1993.264.6.F963"}},"issued":{"date-parts":[[1993,6,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1993,6,1]]}},"alternative-id":["10.1152\/ajprenal.1993.264.6.F963"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1993.264.6.f963","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1993,6,1]]}},{"indexed":{"date-parts":[[2022,4,5]],"date-time":"2022-04-05T15:46:18Z","timestamp":1649173578835},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1981,6,1]]},"abstract":"<jats:p> Urate transport was studied in isolated perfused S2 segments of the superficial proximal tubule of the rabbit. When urate was present in identical concentrations of 290 microM in the perfusing and bathing solutions, there was a net secretory flux of urate of 775.0 +\/- 152.8 fmol.min-1.mm-1. When urate was present in varying concentrations in the bathing solution only, the bath-to-lumen flux of urate increased as the concentration of urate in the bathing solution was increased from 60 to 595 microM, but tended toward a plateau at higher concentrations. After correction of the net secretory flux for the contribution of passive permeation, an apparent Km of 238 microM and Vmax of 950 fmol.min-1.mm-1 for the secretory flux of urate was calculated. When urate was present only in the luminal perfusion solution, the lumen-to-bath flux of urate was significantly less than the bath-to-lumen flux at a similar bath concentration of urate. The lumen-to-bath flux of urate was not significantly affected by cooling the bath to 25 degrees C. These studies provide evidence for both passive and facilitated mechanisms for urate secretion in the rabbit S2 segment. The absorptive flux for urate, however, appears to be primarily a passive mechanism. <\/jats:p>","DOI":"10.1152\/ajprenal.1981.240.6.f530","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T14:21:36Z","timestamp":1513952496000},"page":"F530-F535","source":"Crossref","is-referenced-by-count":0,"title":["Urate transport by the isolated perfused S2 segment of the rabbit"],"prefix":"10.1152","volume":"240","author":[{"given":"H. O.","family":"Senekjian","sequence":"first","affiliation":[]},{"given":"T. F.","family":"Knight","sequence":"additional","affiliation":[]},{"given":"E. J.","family":"Weinman","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1981.240.6.F530","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:21:37Z","timestamp":1567966897000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1981.240.6.F530"}},"issued":{"date-parts":[[1981,6,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1981,6,1]]}},"alternative-id":["10.1152\/ajprenal.1981.240.6.F530"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1981.240.6.f530","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1981,6,1]]}},{"indexed":{"date-parts":[[2022,3,29]],"date-time":"2022-03-29T19:19:33Z","timestamp":1648581573263},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1990,4,1]]},"abstract":"<jats:p> Patients with obstructive jaundice are at a high risk for acute renal failure after surgery. Direct toxic membrane effects of bile acids or bilirubin have been discussed as possible causes. Therefore, we investigated the influence of bile acids and conjugated bilirubin on Na(+)-H+ antiport and ion permeabilities in brush-border membrane vesicles isolated from the human kidney. Brush-border membrane vesicles were prepared by Mg2+ precipitation. These were highly purified as estimated from the 14-fold enrichment in the specific activity of alanine aminopeptidase. The pH-sensitive dye acridine orange was used to study the properties of proton uptake under different conditions. The brush-border membrane vesicles from human kidney cortex exhibited Na+ and K+ conductances, which were small compared with H+ conductance. Furthermore, these membranes possess an Na(+)-H+ antiporter that is sensitive to amiloride. Various bile acids (30 microM) had no significant effect on Na(+)-H+ antiport. However, the addition of sulfated bile acids resulted in a significant inhibition (greater than 50%) of the Na(+)-H+ antiporter. A nonspecific effect of sulfated bile acids on the vesicles was excluded by the use of ionophores to determine vesicle integrity and to estimate the various ion conductances. Therefore specific inhibition of the human renal Na(+)-H+ antiporter by sulfated bile acids occurs. This could result in an impaired cellular pH regulation and might play a role in postoperative acute renal failure in patients with obstructive jaundice. <\/jats:p>","DOI":"10.1152\/ajprenal.1990.258.4.f986","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T23:20:11Z","timestamp":1513984811000},"page":"F986-F991","source":"Crossref","is-referenced-by-count":2,"title":["Sulfated bile acids inhibit Na(+)-H+ antiport in human kidney brush-border membrane vesicles"],"prefix":"10.1152","volume":"258","author":[{"given":"M.","family":"Sellinger","sequence":"first","affiliation":[{"name":"Department of Medicine, University of Freiburg, Federal Republic ofGermany."}]},{"given":"K.","family":"Haag","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Freiburg, Federal Republic ofGermany."}]},{"given":"G.","family":"Burckhardt","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Freiburg, Federal Republic ofGermany."}]},{"given":"W.","family":"Gerok","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Freiburg, Federal Republic ofGermany."}]},{"given":"H.","family":"Knauf","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Freiburg, Federal Republic ofGermany."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1990.258.4.F986","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:22:18Z","timestamp":1567970538000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1990.258.4.F986"}},"issued":{"date-parts":[[1990,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1990,4,1]]}},"alternative-id":["10.1152\/ajprenal.1990.258.4.F986"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1990.258.4.f986","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1990,4,1]]}},{"indexed":{"date-parts":[[2022,4,2]],"date-time":"2022-04-02T22:32:53Z","timestamp":1648938773186},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1989,12,1]]},"abstract":"<jats:p> The effects of phorbol myristate acetate (PMA) on acid secretion by the turtle urinary bladder were examined to evaluate the importance of protein phosphorylation in modulating the distal acidification system. In HCO3-free PO4 buffer 0.2 mM mucosal PMA inhibited reverse short-circuit current (RSCC) by 42%. The inhibition of RSCC was dose dependent, and RSCC approached zero at high concentrations of PMA. PMA also inhibited acid secretion measured titrimetrically but had no effect on RSCC from bladders in which proton secretion was selectively inhibited by an adverse pH gradient or serosal 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid. The inhibition by PMA was duplicated by 1-oleoyl-2-acetyl-rac-glycerol, but not by an inactive phorbol ester. The PMA inhibition was much more potent with mucosal compared with serosal application. The PMA inhibition caused a significant 0.15 pH unit reduction of carbonic anhydrase (CA) cell cytoplasmic pH and a change in the CA cell morphology. Unlike the inhibition of proton transport induced by acetazolamide, the PMA inhibition was neither reversed nor prevented by sodium azide. We conclude that PMA decreases basal acid secretion and blocks the stimulatory effects of CO2 by an azide-insensitive mechanism distinct from that of acetazolamide. In view of recent findings that PMA stimulates HCO3 secretion by the turtle bladder, these results suggest that kinase C-mediated protein phosphorylation may be a central event in the transition from the secretion of acid to the secretion of base. <\/jats:p>","DOI":"10.1152\/ajprenal.1989.257.6.f1124","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T21:40:14Z","timestamp":1513978814000},"page":"F1124-F1131","source":"Crossref","is-referenced-by-count":0,"title":["Phorbol myristate acetate inhibits acidification by turtle urinary bladder"],"prefix":"10.1152","volume":"257","author":[{"given":"M.","family":"Graber","sequence":"first","affiliation":[{"name":"Northport Veterans Administration Medical Center 11768."}]},{"given":"P.","family":"Devine","sequence":"additional","affiliation":[{"name":"Northport Veterans Administration Medical Center 11768."}]},{"given":"T.","family":"Dixon","sequence":"additional","affiliation":[{"name":"Northport Veterans Administration Medical Center 11768."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1989.257.6.F1124","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:12:41Z","timestamp":1567969961000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1989.257.6.F1124"}},"issued":{"date-parts":[[1989,12,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1989,12,1]]}},"alternative-id":["10.1152\/ajprenal.1989.257.6.F1124"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1989.257.6.f1124","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1989,12,1]]}},{"indexed":{"date-parts":[[2022,4,3]],"date-time":"2022-04-03T12:22:50Z","timestamp":1648988570420},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1986,1,1]]},"abstract":"<jats:p> Experiments were performed to compare the tubuloglomerular feedback response to native and artificial tubular fluid. The change in early proximal flow rate produced by changes in loop of Henle flow rate was measured in anesthetized rats using micropuncture techniques. Loop perfusion fluid was either an artificial solution with an electrolyte composition similar to that of proximal fluid (ATF) or native tubular fluid (NTF) collected from the late proximal tubule. In control rats, in rats on a low NaCl diet, in rats on restricted food intake, and in acutely saline-expanded rats no differences were detected between ATF- and NTF-perfused nephrons. In rats receiving 10 g NaCl\/100 g, diet, responses with ATF and NTF to a flow change from 0 to 15 nl\/min did not differ significantly; maximum feedback responses (flow change from 0 to 40 nl\/min) were, however, significantly greater with ATF (-25.4%) than NTF (-12.9%). Chloride absorption was not different with the two perfusates. With both ATF and NTF a significant negative correlation was found between maximum responses and NaCl intake, with the slope being steeper with NTF. We conclude that some unidentified constituent of tubular fluid affects maximum feedback responses during very high NaCl intake, but feedback responses to physiological flow rate changes appear to be independent of luminal factors. <\/jats:p>","DOI":"10.1152\/ajprenal.1986.250.1.f16","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T20:37:17Z","timestamp":1513975037000},"page":"F16-F21","source":"Crossref","is-referenced-by-count":1,"title":["Tubuloglomerular feedback responses with native and artificial tubular fluid"],"prefix":"10.1152","volume":"250","author":[{"given":"J.","family":"Schnermann","sequence":"first","affiliation":[]},{"given":"G.","family":"Schubert","sequence":"additional","affiliation":[]},{"given":"J.","family":"Briggs","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1986.250.1.F16","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:37:36Z","timestamp":1567957056000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1986.250.1.F16"}},"issued":{"date-parts":[[1986,1,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1986,1,1]]}},"alternative-id":["10.1152\/ajprenal.1986.250.1.F16"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1986.250.1.f16","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1986,1,1]]}},{"indexed":{"date-parts":[[2022,4,3]],"date-time":"2022-04-03T01:42:23Z","timestamp":1648950143213},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1987,11,1]]},"abstract":"<jats:p> We studied the metabolism of calcitriol in renal failure achieved by nephrectomy in three groups of rats. Group 1 (n = 7) had sham operation of nephrectomy. Group 2 (n = 8) had unilateral nephrectomy. Group 3 (n = 7) had 5\/6 nephrectomy. Metabolic clearance rate (MCR) and production rate (PR) of calcitriol were studied 3 wk after the surgery. Serum creatinine concentrations were increased after nephrectomy for groups 2 and 3. Endogenous plasma levels of calcitriol were not different between the rats with renal failure and the controls. MCR of calcitriol were decreased in renal failure rats compared with controls (group 1, 0.24 +\/- 0.01; group 2, 0.20 +\/- 0.01, P less than 0.01; group 3, 0.16 +\/- 0.01 ml.min-1.kg-1, P less than 0.001). The MCR of calcitriol was correlated with the endogenous creatinine clearance by linear regression analysis (r = 0.72, P less than 0.001). The PR of calcitriol were also decreased in renal failure; however, the decreases were much less than the amount of renal tissue removed. We concluded that production of calcitriol is decreased in the remnant kidney. The decreased synthesis is associated with decreased degradation of calcitriol resulting in normal concentrations of calcitriol in mild to moderately severe renal failure. <\/jats:p>","DOI":"10.1152\/ajprenal.1987.253.5.f1015","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T23:14:24Z","timestamp":1513984464000},"page":"F1015-F1019","source":"Crossref","is-referenced-by-count":1,"title":["Production and degradation of calcitriol in renal failure rats"],"prefix":"10.1152","volume":"253","author":[{"given":"C. H.","family":"Hsu","sequence":"first","affiliation":[{"name":"Department of Internal Medicine and Pharmacology, University ofMichigan, Ann Arbor 48109."}]},{"given":"S.","family":"Patel","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine and Pharmacology, University ofMichigan, Ann Arbor 48109."}]},{"given":"E. W.","family":"Young","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine and Pharmacology, University ofMichigan, Ann Arbor 48109."}]},{"given":"R. U.","family":"Simpson","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine and Pharmacology, University ofMichigan, Ann Arbor 48109."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1987.253.5.F1015","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:54:44Z","timestamp":1567958084000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1987.253.5.F1015"}},"issued":{"date-parts":[[1987,11,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1987,11,1]]}},"alternative-id":["10.1152\/ajprenal.1987.253.5.F1015"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1987.253.5.f1015","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1987,11,1]]}},{"indexed":{"date-parts":[[2023,10,27]],"date-time":"2023-10-27T07:19:45Z","timestamp":1698391185813},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1991,11,1]]},"abstract":"<jats:p> The Gs alpha and Gi alpha 1-3 subunits of GTP-binding proteins were localized in sections of rat kidney using antibodies against unique synthetic decapeptides from the different G alpha subunits. All of the G alpha subunits were found to have a polarized distribution on renal tubule epithelial cells, and staining was typically found on either basolateral or apical membranes in a given cell type. Gi alpha 1 was localized to the apical pole of both thick ascending limb cells and cells forming the papillary epithelium, Gi alpha 2 labeled the basolateral plasma membrane and the cytoplasm of collecting duct principal cells, and Gi alpha 3 was most abundant in the apical region of proximal tubule cells of the S1 segment, where it was concentrated in sub-brush-border invaginations. It was also found in the perinuclear Golgi complex in these cells. Gs alpha was heavily concentrated on the basolateral plasma membranes of thick ascending limb cells and both principal and intercalated cells of the collecting duct. Less intense subapical staining of G alpha s was also found in proximal tubule cells. The cells of the macula densa had a unique G protein distribution that was distinct from the surrounding cells of the thick ascending limb of Henle. Antibodies specific for the Gi alpha 1 and Gi alpha 3 subunits both stained intracellular vesicles clustered at the basal pole of the cell. A heterogeneous distribution of G alpha subunits was also found by Western blotting on isolated cortical membrane fractions. <\/jats:p>","DOI":"10.1152\/ajprenal.1991.261.5.f831","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T09:17:21Z","timestamp":1514020641000},"page":"F831-F840","source":"Crossref","is-referenced-by-count":9,"title":["Heterogeneous localization of G protein alpha-subunits in rat kidney"],"prefix":"10.1152","volume":"261","author":[{"given":"J. L.","family":"Stow","sequence":"first","affiliation":[{"name":"Renal Unit, Massachusetts General Hospital, Boston."}]},{"given":"I.","family":"Sabolic","sequence":"additional","affiliation":[{"name":"Renal Unit, Massachusetts General Hospital, Boston."}]},{"given":"D.","family":"Brown","sequence":"additional","affiliation":[{"name":"Renal Unit, Massachusetts General Hospital, Boston."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1991.261.5.F831","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:20:12Z","timestamp":1567974012000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1991.261.5.F831"}},"issued":{"date-parts":[[1991,11,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1991,11,1]]}},"alternative-id":["10.1152\/ajprenal.1991.261.5.F831"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1991.261.5.f831","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1991,11,1]]}},{"indexed":{"date-parts":[[2022,3,29]],"date-time":"2022-03-29T21:49:59Z","timestamp":1648590599877},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1979,3,1]]},"abstract":"<jats:p> The regulation of cell volume was studied in separated renal tubules (SRT) whose basement membrane had been removed by collagenase. Regulation occurred when SRT were immersed in a hypotonic medium, the increase in cellular water content being half that expected in the absence of regulation. Regulation was immediate, with no initial swelling, and was accompanied by a loss of NaCl, with no change in cellular K. This regulation was eliminated by 10(-3) M ouabain. We conclude that: 1) Cell volume regulation which occurs in a hypotonic medium is due to an immediate loss of NaCl. 2) Loss of NaCl might be due to blocking of the net passive NaCl entry into the cells resulting from the drop in the transmembrane NaCl electrochemical gradient. The high membrane sodium permeability, probably located on the luminal side of the tubular cells, might explain why regulation was instantaneous. 3) Elimination of volume regulation by ouabain suggests there is no need to assume that a ouabain-insensitive pump regulates cell volume. <\/jats:p>","DOI":"10.1152\/ajprenal.1979.236.3.f226","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T15:43:17Z","timestamp":1513957397000},"page":"F226-F231","source":"Crossref","is-referenced-by-count":0,"title":["Regulation of cell volume in separated renal tubules incubated in hypotonic medium"],"prefix":"10.1152","volume":"236","author":[{"given":"M.","family":"Paillard","sequence":"first","affiliation":[]},{"given":"F.","family":"Leviel","sequence":"additional","affiliation":[]},{"given":"J. P.","family":"Gardin","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1979.236.3.F226","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:02:56Z","timestamp":1567954976000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1979.236.3.F226"}},"issued":{"date-parts":[[1979,3,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1979,3,1]]}},"alternative-id":["10.1152\/ajprenal.1979.236.3.F226"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1979.236.3.f226","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1979,3,1]]}},{"indexed":{"date-parts":[[2022,6,30]],"date-time":"2022-06-30T18:05:24Z","timestamp":1656612324834},"reference-count":12,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,9,1]]},"DOI":"10.1152\/ajprenal.00300.2013","type":"journal-article","created":{"date-parts":[[2013,6,6]],"date-time":"2013-06-06T04:46:35Z","timestamp":1370493995000},"page":"F641-F642","source":"Crossref","is-referenced-by-count":2,"title":["Activation of the sympathetic nervous system, is it key to the developmental origins of enhanced cardiovascular risk?"],"prefix":"10.1152","volume":"305","author":[{"given":"Barbara T.","family":"Alexander","sequence":"first","affiliation":[{"name":"Department of Physiology, University of Mississippi Medical Center, Jackson, Mississippi"}]},{"given":"Suttira","family":"Intapad","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Mississippi Medical Center, Jackson, Mississippi"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000153319.20340.2a"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00123.2008"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00241.2012"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00647.2009"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1515\/jpm-2012-0020"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00725.2006"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.111.00645"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00008.2013."},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.109.145391"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.107.092890"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.109.139402"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1002\/bdrb.10013"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00300.2013","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T23:44:38Z","timestamp":1567986278000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00300.2013"}},"issued":{"date-parts":[[2013,9,1]]},"references-count":12,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2013,9,1]]}},"alternative-id":["10.1152\/ajprenal.00300.2013"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00300.2013","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2013,9,1]]}},{"indexed":{"date-parts":[[2023,7,5]],"date-time":"2023-07-05T19:23:09Z","timestamp":1688584989049},"reference-count":11,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2018,5,1]]},"DOI":"10.1152\/ajprenal.00607.2017","type":"journal-article","created":{"date-parts":[[2018,1,8]],"date-time":"2018-01-08T18:33:31Z","timestamp":1515436411000},"page":"F879-F880","source":"Crossref","is-referenced-by-count":2,"title":["Deep-sea diving into the renal transcriptome of high-fat-fed mice nets unique catch"],"prefix":"10.1152","volume":"314","author":[{"given":"Carolyn M.","family":"Ecelbarger","sequence":"first","affiliation":[{"name":"Department of Medicine, Georgetown University, Washington, District of Columbia"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00446.2012"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00345.2017"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1007\/BF00281307"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014111067"},{"key":"B5","first-page":"1","author":"Ogden CL","year":"2015","journal-title":"NCHS Data Brief"},{"key":"B6","first-page":"92","volume":"14","author":"Oudar O","year":"1991","journal-title":"Ren Physiol Biochem"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0b013e328354a6bd"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0812859106"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1186\/s13104-017-2435-x"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2017030295"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1039\/b902356a"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00607.2017","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:42:39Z","timestamp":1567960959000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00607.2017"}},"issued":{"date-parts":[[2018,5,1]]},"references-count":11,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2018,5,1]]}},"alternative-id":["10.1152\/ajprenal.00607.2017"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00607.2017","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2018,5,1]]}},{"indexed":{"date-parts":[[2022,4,5]],"date-time":"2022-04-05T14:41:17Z","timestamp":1649169677151},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1989,9,1]]},"abstract":"<jats:p> We tested the hypothesis that changes in extracellular fluid volume are reflected by pressure changes within structures of the inner ear and that through neural pathways, a control mechanism exerts an influence on antidiuretic hormone (ADH) release and Na excretion. The study was performed on 35 guinea pigs. In protocol 1, 13 animals were studied before and after decompression of the inner ear by bilateral fluid withdrawal in an experimental setting of sustained isotonic expansion that kept the osmoreceptor partially activated and the intrathoracic volume receptors suppressed. A group of six sham-operated animals served as control. In protocol 2, nine animals were studied before and after a unilateral rise in their inner ear pressure during slightly hypertonic low-rate infusions that kept the osmoreceptor and thoracic volume receptors stimulated. A group of seven sham-operated guinea pigs served as controls. Decompression of the inner ear was attended by a rise in plasma ADH from 11.9 +\/- 2.4 to 29.1 +\/- 6.9 pg\/ml, in urine osmolality (Uosmol) from 470 +\/- 48 to 712 +\/- 46 mosmol\/kg (P less than 0.001), and a fall in urine flow rate (V) from 184 +\/- 47 to 71 +\/- 11 microliters\/min (P less than 0.01), whereas plasma Na (PNa) and osmolality (Posmol) did not change. During inner ear hypertension, plasma ADH fell from 25.6 +\/- 3.9 to 18.4 +\/- 3.1, Uosmol from 829 +\/- 58 to 627 +\/- 43 (P less than 0.001), and V rose from 51 +\/- 11 to 130 +\/- 23 (P less than 0.001), whereas glomerular filtration rate, PNa, and Posmol did not change.(ABSTRACT TRUNCATED AT 250 WORDS) <\/jats:p>","DOI":"10.1152\/ajprenal.1989.257.3.f341","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T22:10:00Z","timestamp":1513980600000},"page":"F341-F346","source":"Crossref","is-referenced-by-count":3,"title":["Volume receptors in guinea pig labyrinth: relevance with respect to ADH and Na control"],"prefix":"10.1152","volume":"257","author":[{"given":"E.","family":"Bartoli","sequence":"first","affiliation":[{"name":"Institute of Physiology, University of Sassari Medical School,Italy."}]},{"given":"A.","family":"Satta","sequence":"additional","affiliation":[{"name":"Institute of Physiology, University of Sassari Medical School,Italy."}]},{"given":"F.","family":"Melis","sequence":"additional","affiliation":[{"name":"Institute of Physiology, University of Sassari Medical School,Italy."}]},{"given":"M. A.","family":"Caria","sequence":"additional","affiliation":[{"name":"Institute of Physiology, University of Sassari Medical School,Italy."}]},{"given":"W.","family":"Masala","sequence":"additional","affiliation":[{"name":"Institute of Physiology, University of Sassari Medical School,Italy."}]},{"given":"G.","family":"Vargiu","sequence":"additional","affiliation":[{"name":"Institute of Physiology, University of Sassari Medical School,Italy."}]},{"given":"F.","family":"Meloni","sequence":"additional","affiliation":[{"name":"Institute of Physiology, University of Sassari Medical School,Italy."}]},{"given":"G. P.","family":"Teatini","sequence":"additional","affiliation":[{"name":"Institute of Physiology, University of Sassari Medical School,Italy."}]},{"given":"G. B.","family":"Azzena","sequence":"additional","affiliation":[{"name":"Institute of Physiology, University of Sassari Medical School,Italy."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1989.257.3.F341","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:15:57Z","timestamp":1567970157000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1989.257.3.F341"}},"issued":{"date-parts":[[1989,9,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1989,9,1]]}},"alternative-id":["10.1152\/ajprenal.1989.257.3.F341"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1989.257.3.f341","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1989,9,1]]}},{"indexed":{"date-parts":[[2022,3,29]],"date-time":"2022-03-29T00:22:31Z","timestamp":1648513351156},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1995,11,1]]},"abstract":"<jats:p> The pharmacological properties and signaling of angiotensin IV (ANG IV) receptors were studied in opossum kidney cell line OK7A. Saturation binding experiments with 125I-labeled ANG IV demonstrated the presence of high-affinity ANG IV binding sites in OK7A cell membranes with a dissociation constant (Kd) of 0.40 +\/- 0.08 nM and a maximal amount of binding sites (Bmax) of 180 +\/- 50 fmol\/mg protein. In competition experiments, unlabeled ANG IV inhibited 125I-ANG IV binding biphasically: 20% of binding sites had high affinity [inhibition constant (Ki) = 0.44 +\/- 0.04 nM] and 80% had low affinity (Ki = 130 +\/- 10 nM). ANG III displaced 125I-ANG IV from binding sites with low affinity (Ki = 205 +\/- 10 nM), and ANG II did not compete with 125I-ANG IV at concentrations up to 10 microM. The binding of ANG IV to OK7A cell membranes was significantly enhanced in the presence of 5 mM EDTA and completely blocked by 5 mM dithiothreitol. Guanosine 5'-O-(3-thiotriphosphate) inhibited the binding of 125I-ANG IV, indicating the G protein coupling of ANG IV receptors in OK7A cells. In signaling studies, ANG IV induced transient increase in intracellular calcium concentration ([Ca2+]i) from 49 +\/- 3 to 280 +\/- 45 nM. ANG IV failed to influence phosphoinositol metabolism, indicating that Ca2+ mobilization is not linked to ANG IV signaling. Ethylene glycol-bis(beta-aminoethylether)-N,N,N',N'-tetraacetic acid completely abolished ANG IV-induced increase in [Ca2+]i, consistent with Ca2+ influx. The voltage-sensitive Ca2+ channel blocking agents verapamil and nifedipine attenuated the effect of ANG IV on [Ca2+]i to 133 +\/- 33 and 174 +\/- 32 nM, respectively. These data suggest that ANG IV induces Ca2+ influx in OK7A cells, at least partially, through the voltage-sensitive Ca2+ channels. <\/jats:p>","DOI":"10.1152\/ajprenal.1995.269.5.f644","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T00:49:10Z","timestamp":1513990150000},"page":"F644-F652","source":"Crossref","is-referenced-by-count":4,"title":["Angiotensin IV receptors and signaling in opossum kidney cells"],"prefix":"10.1152","volume":"269","author":[{"given":"N.","family":"Dulin","sequence":"first","affiliation":[{"name":"Department of Medicine, Case Western Reserve University School ofMedicine, Cleveland, Ohio 44106-4982, USA."}]},{"given":"Z. T.","family":"Madhun","sequence":"additional","affiliation":[{"name":"Department of Medicine, Case Western Reserve University School ofMedicine, Cleveland, Ohio 44106-4982, USA."}]},{"given":"C. H.","family":"Chang","sequence":"additional","affiliation":[{"name":"Department of Medicine, Case Western Reserve University School ofMedicine, Cleveland, Ohio 44106-4982, USA."}]},{"given":"L.","family":"Berti-Mattera","sequence":"additional","affiliation":[{"name":"Department of Medicine, Case Western Reserve University School ofMedicine, Cleveland, Ohio 44106-4982, USA."}]},{"given":"D.","family":"Dickens","sequence":"additional","affiliation":[{"name":"Department of Medicine, Case Western Reserve University School ofMedicine, Cleveland, Ohio 44106-4982, USA."}]},{"given":"J. G.","family":"Douglas","sequence":"additional","affiliation":[{"name":"Department of Medicine, Case Western Reserve University School ofMedicine, Cleveland, Ohio 44106-4982, USA."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1995.269.5.F644","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:57:12Z","timestamp":1567958232000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1995.269.5.F644"}},"issued":{"date-parts":[[1995,11,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1995,11,1]]}},"alternative-id":["10.1152\/ajprenal.1995.269.5.F644"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1995.269.5.f644","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1995,11,1]]}},{"indexed":{"date-parts":[[2022,4,2]],"date-time":"2022-04-02T18:51:23Z","timestamp":1648925483316},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1977,12,1]]},"abstract":"<jats:p> The postnatal development of renal diluting capacity was studied by free-flow micropuncture and by microdissection of single superficial loops of Henle in rats kept on a high salt diet. Total renal filtration rate, sodium absorption, total solute excretion, and systemic arterial pressure were monitored during single nephron evaluation at two maturational stages (12\u201315 days and 27\u201335 days postnatal). Nephron filtration rates were identical when measured in early distal and late proximal segments of the same nephron. Absolute fluid absorption between these sites increased by a factor of 2.5, whereas loop fractional absorption of the volume load changed from 38.1 +\/- 6.9 to 49.8 +\/- 4.8% (SD), while proximal volume delivery to the loop increased from 4.33 +\/- 1.12 to 7.14 +\/- 0.65 nl\/min. Simultaneously, the osmolarity of early distal fluid (8.8% of distal length) decreased significantly from 284 + 19.8 to 180.9 +\/- 18.2 mosmol\/liter during maturation. This study suggests that the ability of the loop of Henle to generate hypotonic fluid is attained only gradually during ontogeny. Volume absorption in the loop of Henle increases disproportionately to the loop volume load. <\/jats:p>","DOI":"10.1152\/ajprenal.1977.233.6.f519","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T19:56:21Z","timestamp":1513972581000},"page":"F519-F524","source":"Crossref","is-referenced-by-count":3,"title":["Maturation of diluting capacity in loop of Henle of rat superficial nephrons"],"prefix":"10.1152","volume":"233","author":[{"given":"H.","family":"Zink","sequence":"first","affiliation":[]},{"given":"M.","family":"Horster","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1977.233.6.F519","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:55:24Z","timestamp":1567968924000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1977.233.6.F519"}},"issued":{"date-parts":[[1977,12,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1977,12,1]]}},"alternative-id":["10.1152\/ajprenal.1977.233.6.F519"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1977.233.6.f519","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1977,12,1]]}},{"indexed":{"date-parts":[[2022,4,2]],"date-time":"2022-04-02T19:14:36Z","timestamp":1648926876415},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1991,3,1]]},"abstract":"<jats:p> This study investigates the definite location of peptide YY (PYY) binding sites on the basolateral membranes in proximal tubules. S1, S2, and S3 segments were dissected, perfused in vitro, and exposed to [125I-Tyr36]monoiodo-PYY either in the bath fluid or in the perfusate. S1 segments exposed to [125I-Tyr36]PYY in the bath fluid were fixed and prepared for electron microscope autoradiography. The results demonstrated a high degree of axial heterogeneity of basolateral binding of PYY, since only S1 bound PYY, 0.59 +\/- 0.09 pg\/mm after 15 min; 89.1% could be displaced with unlabeled PYY. PYY was not internalized, 90% of the grains were associated with the basolateral membranes, and no accumulation of grains was observed over the vacuolar apparatus. After luminal perfusion with PYY, 79.3 +\/- 7.2% was processed, 61.7 +\/- 6.3% was degraded at the brush border, and no tubular accumulation was detected. Thus PYY is not taken up by endocytosis. Unexpectedly, a very large fraction of processed PYY was transported from lumen to bath as trichloroacetic acid (TCA)-precipitable label constituting 41.6 +\/- 4.7%. There was no axial heterogeneity in the luminal handling of PYY. In conclusion, this study reveals a high density of PYY binding sites at the basolateral membranes from S1 segments, indicating a selective function of S1 segments on stimulation with PYY. In contrast to other proteins PYY was not internalized from the basolateral membranes. <\/jats:p>","DOI":"10.1152\/ajprenal.1991.260.3.f359","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T23:43:36Z","timestamp":1513986216000},"page":"F359-F367","source":"Crossref","is-referenced-by-count":0,"title":["Peptide YY luminal processing and axial heterogeneity of basolateral binding in renal proximal tubules"],"prefix":"10.1152","volume":"260","author":[{"given":"S.","family":"Nielsen","sequence":"first","affiliation":[{"name":"Department of Cell Biology, University of Aarhus, Denmark."}]},{"given":"S. P.","family":"Sheikh","sequence":"additional","affiliation":[{"name":"Department of Cell Biology, University of Aarhus, Denmark."}]},{"given":"M. I.","family":"Sheikh","sequence":"additional","affiliation":[{"name":"Department of Cell Biology, University of Aarhus, Denmark."}]},{"given":"E. I.","family":"Christensen","sequence":"additional","affiliation":[{"name":"Department of Cell Biology, University of Aarhus, Denmark."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1991.260.3.F359","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:26:26Z","timestamp":1567970786000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1991.260.3.F359"}},"issued":{"date-parts":[[1991,3,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1991,3,1]]}},"alternative-id":["10.1152\/ajprenal.1991.260.3.F359"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1991.260.3.f359","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1991,3,1]]}},{"indexed":{"date-parts":[[2022,4,4]],"date-time":"2022-04-04T00:47:10Z","timestamp":1649033230434},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1994,3,1]]},"abstract":"<jats:p> The regulation of glycogen degradation and synthesis in canine inner medullary collecting ducts (IMCD) was investigated using IMCD tubules suspensions prepared from dog papilla. A small but significant amount of glycogen was found in dog IMCD. Under aerobic condition and especially when no exogenous substrate is available, glycogen breakdown can support IMCD glycolysis for a short period of time. Increasing concentration of exogenous glucose but not lactate was able to reduce and even to suppress (20 mM glucose) the glycogen breakdown. A net synthesis of glycogen was observed only when the endogenous glycogen pool was previously partially or totally depleted. Under anaerobic condition, glycogenolysis was stimulated. The addition of up to 20 mM glucose now reduced but never suppressed this process. Glycogen metabolism responded to variation in the cells energy needs, since the net glycogen breakdown was diminished and glycogen synthesis increased when the cellular ATP turnover was reduced. The reverse effects were observed when the ATP turnover was increased. At all times, glycogen metabolism correlated well with changes in tissue glucose 6-phosphate concentration. The energy requirement of IMCD cells and the availability of alternative energy sources (active mitochondria, exogenous glucose) are therefore capable of eliciting an integrated and appropriate response of glycogen phosphorylase and synthase in IMCD tubules in suspension studied in vitro. <\/jats:p>","DOI":"10.1152\/ajprenal.1994.266.3.f375","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T11:02:48Z","timestamp":1514026968000},"page":"F375-F383","source":"Crossref","is-referenced-by-count":0,"title":["Glycogen metabolism in dog inner medullary collecting ducts"],"prefix":"10.1152","volume":"266","author":[{"given":"L.","family":"Meury","sequence":"first","affiliation":[{"name":"Departement de Physiologie, Universite de Montreal, Quebec,Canada."}]},{"given":"J.","family":"Senecal","sequence":"additional","affiliation":[{"name":"Departement de Physiologie, Universite de Montreal, Quebec,Canada."}]},{"given":"J.","family":"Noel","sequence":"additional","affiliation":[{"name":"Departement de Physiologie, Universite de Montreal, Quebec,Canada."}]},{"given":"P.","family":"Vinay","sequence":"additional","affiliation":[{"name":"Departement de Physiologie, Universite de Montreal, Quebec,Canada."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1994.266.3.F375","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:31:36Z","timestamp":1567974696000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1994.266.3.F375"}},"issued":{"date-parts":[[1994,3,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1994,3,1]]}},"alternative-id":["10.1152\/ajprenal.1994.266.3.F375"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1994.266.3.f375","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1994,3,1]]}},{"indexed":{"date-parts":[[2022,4,1]],"date-time":"2022-04-01T07:21:55Z","timestamp":1648797715709},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1990,4,1]]},"abstract":"<jats:p> Basolateral membrane vesicles (BLMV) isolated from both red outer medulla or from thick ascending limb segments isolated from the dog kidney were used to examine the process of lactate transport in this nephron segment. The BLMV preparation was enriched in Na(+)-K(+)-adenosinetriphosphatase (Na(+)-K(+)-ATPase) that represented 96% of the total ATPase activity of this preparation and the vesicles were largely under the right side-out orientation. On application of a OH- or HCO3- gradient (inside greater than outside), a secondary active lactate accumulation was observed, with characteristic transient overshoot. This phenomenon was shown to occur irrespective of the presence or absence of Na+, K+, or Cl-. The pH, but not the bicarbonate-driven, overshoot was abolished by nigericin (in presence of K+). Studies with valinomycin and K+ demonstrated that the generation of a membrane potential was not responsible for the acceleration of lactate transport, even if the amplitude of lactate accumulation was reduced in the presence of a bicarbonate gradient and valinomycin. A significant trans-stimulation of [14C]lactate transport by cold lactate was observed (under voltage-clamp condition). The transport was 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid insensitive but sensitive to furosemide (IC50 = 0.1 mM) and alpha-hydroxycyanocinnamate (IC50 = 1 mM). The kinetic parameters of the transporter revealed a single carrier with an apparent Michaelis constant of 1.7 mM and an apparent Vmax of 9.7 nmol.mg protein-1.30 s-1. The transporter was shown to be distinct from that of proximal tubule brush-border membrane or mitochondria (pyruvate). Thus thick ascending limbs possess a carrier-mediated lactate transport that can be used for lactate uptake (aerobic condition) or for lactate release (anaerobic glycolysis) according to metabolic processes imposed by the local oxygenation condition. <\/jats:p>","DOI":"10.1152\/ajprenal.1990.258.4.f1042","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T23:20:11Z","timestamp":1513984811000},"page":"F1042-F1053","source":"Crossref","is-referenced-by-count":0,"title":["Basolateral transport of lactate in dog thick ascending limbs"],"prefix":"10.1152","volume":"258","author":[{"given":"P.","family":"Vinay","sequence":"first","affiliation":[{"name":"Groupe de Recherche en Transport Membranaire, Hopital Notre-Dame deMontreal, Quebec, Canada."}]},{"given":"J.","family":"Senecal","sequence":"additional","affiliation":[{"name":"Groupe de Recherche en Transport Membranaire, Hopital Notre-Dame deMontreal, Quebec, Canada."}]},{"given":"J.","family":"Noel","sequence":"additional","affiliation":[{"name":"Groupe de Recherche en Transport Membranaire, Hopital Notre-Dame deMontreal, Quebec, Canada."}]},{"given":"A.","family":"Tejedor","sequence":"additional","affiliation":[{"name":"Groupe de Recherche en Transport Membranaire, Hopital Notre-Dame deMontreal, Quebec, Canada."}]},{"given":"A.","family":"Berteloot","sequence":"additional","affiliation":[{"name":"Groupe de Recherche en Transport Membranaire, Hopital Notre-Dame deMontreal, Quebec, Canada."}]},{"given":"A.","family":"Gougoux","sequence":"additional","affiliation":[{"name":"Groupe de Recherche en Transport Membranaire, Hopital Notre-Dame deMontreal, Quebec, Canada."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1990.258.4.F1042","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:22:21Z","timestamp":1567970541000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1990.258.4.F1042"}},"issued":{"date-parts":[[1990,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1990,4,1]]}},"alternative-id":["10.1152\/ajprenal.1990.258.4.F1042"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1990.258.4.f1042","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1990,4,1]]}},{"indexed":{"date-parts":[[2022,4,2]],"date-time":"2022-04-02T15:10:38Z","timestamp":1648912238029},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1980,4,1]]},"abstract":"<jats:p> In vitro microperfusion was used to study the effect of low and high extracellular sodium concentrations on the transport capacity of the proximal convoluted tubule (PCT). Tubules from rabbit kidney were perfused with luminal and peritubular solutions containing 80, 115, 190, and 225 mM sodium. Control solutions contained 150 mM sodium. No ionic substitution was made and the proximal convoluted tubules were studied under hypo- or hypertonic conditions after a 20-min equilibration period. Sodium concentration was measured at 80, 150, and 225 mM sodium in the perfused and collected fluids and no significant difference was observed. Net sodium transport (JNa) remained relatively constant between 115 and 150 mM sodium. It decreased progressively at high sodium concentrations. Depression in JNa was also observed at 80 mM sodium. Fractional sodium reabsorption increased to 125.0% of control at 115 mM sodium and decreased to 69.4 and 40.1% at 190 and 225 mM sodium, respectively. At 80 mM, the results were not different from control. These findings indicate that at concentrations of 115-225 mM sodium the proximal convoluted tubule has the intrinsic capacity to regulate sodium transport. <\/jats:p>","DOI":"10.1152\/ajprenal.1980.238.4.f256","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T13:22:56Z","timestamp":1513948976000},"page":"F256-F260","source":"Crossref","is-referenced-by-count":0,"title":["Proximal tubular response to variations in extracellular sodium concentration"],"prefix":"10.1152","volume":"238","author":[{"given":"B.","family":"Corman","sequence":"first","affiliation":[]},{"given":"S.","family":"Carriere","sequence":"additional","affiliation":[]},{"given":"C.","family":"Le Grimellec","sequence":"additional","affiliation":[]},{"given":"J.","family":"Cardinal","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1980.238.4.F256","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:17:37Z","timestamp":1567966657000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1980.238.4.F256"}},"issued":{"date-parts":[[1980,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1980,4,1]]}},"alternative-id":["10.1152\/ajprenal.1980.238.4.F256"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1980.238.4.f256","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1980,4,1]]}},{"indexed":{"date-parts":[[2022,4,4]],"date-time":"2022-04-04T20:42:17Z","timestamp":1649104937189},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1997,6,1]]},"abstract":"<jats:p> The effect of chronic hypoxia on the proliferation and dedifferentiation of LLC-PK1 cells was examined. Cultures were exposed either to hypoxia (3% O2) or normoxia (18% O2), and [3H]thymidine incorporation, cell number, and sodium-dependent glucose (Na\/Glc) uptakes were assessed. Cultures exposed to hypoxia for 16 h significantly increased [3H]thymidine incorporation followed by a significant increase in cell number both at 24 and 48 h in comparison with respective normoxic controls. Cultures exposed to 24 and 72 h of hypoxia exhibited significant inhibition of Na\/Glc uptake when compared with their respective normoxic counterparts. Significant inhibition of cell ATP levels were observed under hypoxic conditions. Acute reoxygenation of hypoxic cells normalized cell ATP levels without any effect on the Na\/Glc uptake. Hypoxia also activated protein kinase C (PKC) at 1 and 4 h followed by a subsequent return to baseline with reactivation at 24 h, which remained sustained up to 72 h, suggesting both acute and sustained activation of PKC. Furthermore, the hypoxia-induced alterations in [3H]thymidine incorporation as well as Na\/Glc uptake were mitigated by inhibitors of PKC. These results indicate that chronic hypoxia induces both proliferation and dedifferentiation of LLC-PK1 cells mediated, in part, by the activation of PKC. <\/jats:p>","DOI":"10.1152\/ajprenal.1997.272.6.f809","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T07:50:33Z","timestamp":1514015433000},"page":"F809-F815","source":"Crossref","is-referenced-by-count":2,"title":["Chronic hypoxia induces LLC-PK1 cell proliferation and dedifferentiation by the activation of protein kinase C"],"prefix":"10.1152","volume":"272","author":[{"given":"A.","family":"Sahai","sequence":"first","affiliation":[{"name":"Department of Medicine, University of Southern California School of Medicine, Los Angeles 90033, USA."}]},{"given":"C.","family":"Mei","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Southern California School of Medicine, Los Angeles 90033, USA."}]},{"given":"A.","family":"Zavosh","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Southern California School of Medicine, Los Angeles 90033, USA."}]},{"given":"R. L.","family":"Tannen","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Southern California School of Medicine, Los Angeles 90033, USA."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1997.272.6.F809","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:12:06Z","timestamp":1567973526000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1997.272.6.F809"}},"issued":{"date-parts":[[1997,6,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1997,6,1]]}},"alternative-id":["10.1152\/ajprenal.1997.272.6.F809"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1997.272.6.f809","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1997,6,1]]}},{"indexed":{"date-parts":[[2022,3,29]],"date-time":"2022-03-29T07:05:34Z","timestamp":1648537534255},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1989,3,1]]},"abstract":"<jats:p> The effects of renal perfusion pressure and reflex sympathetic nerve stimulation on sodium excretion were studied in six conscious foxhounds on a normal sodium diet. This was done before, during common carotid occlusion (CCO), and during a recovery period following CCO. Three protocols were used 1) control (n = 6), 2) converting-enzyme inhibition (CEI, n = 6), and 3) CEI combined with a constant renal artery pressure (RAP, n = 5). In protocol 1, CCO increased RAP markedly (140.5 +\/- 5.1 vs. 103.0 +\/- 4.4 mmHg; P less than 0.001) along with a considerable natriuresis (128.4 +\/- 20.1 vs. 86.3 +\/- 15.1 mumol Na+\/min; P less than 0.05). In protocol 2, CEI increased control sodium excretion but did not impair the natriuresis by CCO. Maintaining RAP at control levels in protocol 3 lead to an antinatriuresis (53.1 +\/- 16.8 vs. 128.3 +\/- 32.2 mumol Na+\/min; P less than 0.05). Creatinine clearance was unaffected by all procedures. In conclusion, a change in ANG II formation shifts but does not impair the natriuretic response to CCO. A moderate sympathetic activation has a pronounced pressure-independent antinatriuretic effect, which is not mediated by angiotensin II. <\/jats:p>","DOI":"10.1152\/ajprenal.1989.256.3.f485","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T16:04:32Z","timestamp":1513958672000},"page":"F485-F489","source":"Crossref","is-referenced-by-count":1,"title":["Modulation of natriuresis by sympathetic nerves and angiotensin II in conscious dogs"],"prefix":"10.1152","volume":"256","author":[{"given":"P. B.","family":"Persson","sequence":"first","affiliation":[{"name":"I. Physiologisches Institut Heidelberg, Federal Republic ofGermany."}]},{"given":"H.","family":"Ehmke","sequence":"additional","affiliation":[{"name":"I. Physiologisches Institut Heidelberg, Federal Republic ofGermany."}]},{"given":"U.","family":"Kogler","sequence":"additional","affiliation":[{"name":"I. Physiologisches Institut Heidelberg, Federal Republic ofGermany."}]},{"given":"H.","family":"Kirchheim","sequence":"additional","affiliation":[{"name":"I. Physiologisches Institut Heidelberg, Federal Republic ofGermany."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1989.256.3.F485","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:07:46Z","timestamp":1567955266000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1989.256.3.F485"}},"issued":{"date-parts":[[1989,3,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1989,3,1]]}},"alternative-id":["10.1152\/ajprenal.1989.256.3.F485"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1989.256.3.f485","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1989,3,1]]}},{"indexed":{"date-parts":[[2022,4,4]],"date-time":"2022-04-04T23:05:34Z","timestamp":1649113534554},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1984,6,1]]},"abstract":"<jats:p> The transport of L-malate was evaluated in basolateral and brush border membrane vesicles isolated from the rat renal cortex. In both types of membrane vesicles, an inwardly directed sodium gradient stimulated transport and caused an overshoot of the equilibrium concentration. In basolateral membrane vesicles, the presence of sodium, but without a sodium gradient, stimulated the uptake of L-malate. Sodium gradient-stimulated L-malate uptake was stimulated and inhibited by maneuvers designed to render the inside of the basolateral membrane vesicles more electronegative or electropositive, respectively. The tricarboxylic acid cycle intermediates citrate, alpha-ketoglutarate, succinate, fumarate, L-malate, and oxaloacetate and the monocarboxylic acid pyruvate inhibited the sodium gradient-stimulated uptake of L-[14C]malate in basolateral membrane vesicles. Maleate, gluconate, formate, acetate, L-lactate, and beta-hydroxybutyrate did not inhibit uptake. These results indicate that basolateral membrane vesicles from the rat renal cortex contain a sodium-L-malate cotransport system that may be shared by the other tricarboxylic acid cycle intermediates and by pyruvate. Such a transport system, together with a similar sodium-tricarboxylic acid cycle intermediate cotransport system located in the brush border membrane, would ensure high concentrations of tricarboxylic acid cycle intermediates within the cells of the proximal tubule. <\/jats:p>","DOI":"10.1152\/ajprenal.1984.246.6.f779","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T11:45:27Z","timestamp":1513943127000},"page":"F779-F784","source":"Crossref","is-referenced-by-count":0,"title":["Mechanism of L-malate transport in rat renal basolateral membrane vesicles"],"prefix":"10.1152","volume":"246","author":[{"given":"A. M.","family":"Kahn","sequence":"first","affiliation":[]},{"given":"S.","family":"Branham","sequence":"additional","affiliation":[]},{"given":"E. J.","family":"Weinman","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1984.246.6.F779","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T14:34:49Z","timestamp":1567953289000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1984.246.6.F779"}},"issued":{"date-parts":[[1984,6,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1984,6,1]]}},"alternative-id":["10.1152\/ajprenal.1984.246.6.F779"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1984.246.6.f779","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1984,6,1]]}},{"indexed":{"date-parts":[[2024,5,13]],"date-time":"2024-05-13T11:14:18Z","timestamp":1715598858019},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1992,5,1]]},"abstract":"<jats:p> To investigate the pulsatile nature of basal and stimulated renin and aldosterone secretion, we sampled blood for plasma renin activity (PRA) and plasma aldosterone concentration at 10-min intervals for 24 h in nine normal supine human male subjects after equilibration in high- and low-sodium balance states. We evaluated serial hormonal measures by a quantitative waveform-independent deconvolution technique designed to compute the number, amplitude, and mass of underlying secretory bursts and simultaneously to estimate the presence and extent of basal secretion. For both PRA and aldosterone: 1) burstlike release accounted for greater than or equal to 60% of total secretion and tonic release for less than 40%; 2) there was an 80- to 85-min interpulse interval unchanged by sodium intake; 3) sodium restriction engendered an increase in plasma hormone concentrations by increasing the amount and maximal rate of hormone secreted per burst; 4) low dietary sodium also induced increases in basal hormone secretory rates, suggesting that there may be two regulatory processes driving renin and aldosterone secretion; and 5) PRA was significantly coupled to plasma aldosterone concentration by a 0-, 10-, or 20-min aldosterone lag time in both high- and low-sodium balance. We conclude that both renin and aldosterone are released via a predominantly burstlike mode of secretion; PRA and plasma aldosterone concentrations are positively coupled by a short time lag (0-20 min); and sodium restriction achieves an increase in mean PRA and plasma aldosterone concentration by selective amplitude enhancement of individual hormone secretory bursts and by increased tonic (interburst) basal secretory rates. <\/jats:p>","DOI":"10.1152\/ajprenal.1992.262.5.f871","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T08:53:48Z","timestamp":1514019228000},"page":"F871-F877","source":"Crossref","is-referenced-by-count":3,"title":["Temporal pattern of renin and aldosterone secretion in men: effects of sodium balance"],"prefix":"10.1152","volume":"262","author":[{"given":"W. V.","family":"Vieweg","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, University of Virginia School ofMedicine, Charlottesville."}]},{"given":"J. D.","family":"Veldhuis","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Virginia School ofMedicine, Charlottesville."}]},{"given":"R. M.","family":"Carey","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Virginia School ofMedicine, Charlottesville."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1992.262.5.F871","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:16:52Z","timestamp":1567973812000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1992.262.5.F871"}},"issued":{"date-parts":[[1992,5,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1992,5,1]]}},"alternative-id":["10.1152\/ajprenal.1992.262.5.F871"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1992.262.5.f871","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1992,5,1]]}},{"indexed":{"date-parts":[[2022,11,17]],"date-time":"2022-11-17T09:54:44Z","timestamp":1668678884165},"reference-count":56,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1998,5,1]]},"abstract":"<jats:p>The visceral glomerular epithelial cells (GECs) or podocytes of the renal glomerulus constitute a highly specialized epithelium. To study the nature of podocytes, we established mouse monoclonal antibodies against GEC. Clone P-31 reacted exclusively with the cytoplasm of GEC by immunofluorescence. Immunoblot analysis with P-31 showed that a single band of 250 kDa was detectable in a glomerular lysate. The 250-kDa polypeptide (p250) was recovered from Triton X-100-insoluble fractions of isolated glomeruli, suggesting that this molecule is associated with the cytoskeleton. Immunogold staining with P-31 demonstrated that the gold particles were located at the intersections of vimentin-type intermediate filaments of podocytes. In developing kidney, this protein first appeared in immature GECs during the S-shaped body stage. In puromycin aminonucleoside nephrosis, p250 was dramatically increased in glomeruli where enhanced desmin expression was observed in GECs. These results indicate that p250 is a novel intermediate filament-associated protein and plays a role in the organization of the intermediate filament network in both normal and diseased conditions.<\/jats:p>","DOI":"10.1152\/ajprenal.1998.274.5.f986","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T15:41:04Z","timestamp":1514043664000},"page":"F986-F997","source":"Crossref","is-referenced-by-count":5,"title":["Monoclonal antibody P-31 recognizes a novel intermediate filament-associated protein (p250) in rat podocytes"],"prefix":"10.1152","volume":"274","author":[{"given":"Hidetake","family":"Kurihara","sequence":"first","affiliation":[{"name":"Shionogi Research Laboratories, Osaka 553, Japan"}]},{"given":"Norio","family":"Sunagawa","sequence":"additional","affiliation":[{"name":"Shionogi Research Laboratories, Osaka 553, Japan"}]},{"given":"Tatsuo","family":"Kobayashi","sequence":"additional","affiliation":[{"name":"Shionogi Research Laboratories, Osaka 553, Japan"}]},{"given":"Kazuhiro","family":"Kimura","sequence":"additional","affiliation":[{"name":"Shionogi Research Laboratories, Osaka 553, Japan"}]},{"given":"Nobuo","family":"Takasu","sequence":"additional","affiliation":[{"name":"Shionogi Research Laboratories, Osaka 553, Japan"}]},{"given":"Tsutomu","family":"Shike","sequence":"additional","affiliation":[{"name":"Shionogi Research Laboratories, Osaka 553, Japan"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1981.176"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1007\/BF00490899"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.99.4.1424"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.92.3.795"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1002\/cm.970170105"},{"key":"B6","first-page":"43","volume":"34","author":"Caulfield J. P.","year":"1976","journal-title":"Lab. Invest."},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(94)90553-3"},{"key":"B8","first-page":"673","volume":"59","author":"Drenckhahn D.","year":"1988","journal-title":"Lab. Invest."},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1096\/fasebj.3.10.2666230"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.106.3.723"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1016\/0955-0674(91)90168-X"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.bi.63.070194.002021"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118671"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/0955-0674(91)90170-4"},{"key":"B15","first-page":"552","volume":"50","author":"Holthofer H.","year":"1984","journal-title":"Lab. Invest."},{"key":"B16","first-page":"548","volume":"65","author":"Holthofer H.","year":"1991","journal-title":"Lab. Invest."},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.113.1.155"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/0955-0674(91)90175-X"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1006\/dbio.1994.1248"},{"key":"B20","first-page":"430","volume":"39","author":"Kerjaschki D.","year":"1978","journal-title":"Lab. Invest."},{"key":"B21","first-page":"343","volume":"118","author":"Kerjaschki D.","year":"1985","journal-title":"Am. J. Pathol."},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/256495a0"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.47"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.89.15.7075"},{"key":"B25","first-page":"805","volume":"141","author":"Kurihara H.","year":"1992","journal-title":"Am. J. Pathol."},{"issue":"37","key":"B26","first-page":"F514","volume":"268","author":"Kurihara H.","year":"1995","journal-title":"Am. J. Physiol."},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.97.6.1891"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1038\/283249a0"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.96.3.703"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.115.2.397"},{"key":"B31","first-page":"220","volume":"126","author":"Messina A","year":"1987","journal-title":"Am. J. Pathol."},{"key":"B32","first-page":"929","volume":"137","author":"Miettinen A.","year":"1990","journal-title":"Am. J. Pathol."},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1177\/39.8.1856454"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1007\/BF00195765"},{"key":"B35","first-page":"277","volume":"57","author":"Norgaad J. O. R.","year":"1987","journal-title":"Lab. Invest."},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.cb.02.110186.002225"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.108.3.1009"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.97.6.1860"},{"key":"B39","first-page":"90","volume":"39","author":"Reeves W.","year":"1978","journal-title":"Lab. Invest."},{"key":"B41","first-page":"313","volume":"48","author":"Schnabel E.","year":"1989","journal-title":"Eur. J. Cell Biol."},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.111.3.1255"},{"key":"B43","first-page":"138","volume":"59","author":"Seifert G. J.","year":"1992","journal-title":"Eur. J. Cell Biol."},{"key":"B44","doi-asserted-by":"crossref","first-page":"1131","DOI":"10.1681\/ASN.V351131","volume":"3","author":"Sharma R.","year":"1992","journal-title":"J. Am. Soc. Nephrol."},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.125.1.159"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1038\/ng0896-450"},{"key":"B47","first-page":"465","volume":"125","author":"Stamenkovic I.","year":"1986","journal-title":"Am. J. Pathol."},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1007\/BF01007491"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1126\/science.7505952"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1002\/ar.1092100104"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.97.5.1507"},{"key":"B52","doi-asserted-by":"crossref","first-page":"1279","DOI":"10.1681\/ASN.V361279","volume":"3","author":"Weinstein T.","year":"1992","journal-title":"J. Am. Soc. Nephrol."},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.97.3.887"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1016\/0014-4827(84)90766-3"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.100.2.620"},{"key":"B56","first-page":"899","volume":"136","author":"Yaoita E.","year":"1990","journal-title":"Am. J. Pathol."},{"key":"B57","first-page":"319","volume":"149","author":"Yaoita E.","year":"1996","journal-title":"Am. J. Pathol."}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1998.274.5.F986","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:49:17Z","timestamp":1660189757000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1998.274.5.F986"}},"issued":{"date-parts":[[1998,5,1]]},"references-count":56,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1998,5,1]]}},"alternative-id":["10.1152\/ajprenal.1998.274.5.F986"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1998.274.5.f986","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1998,5,1]]}},{"indexed":{"date-parts":[[2022,11,9]],"date-time":"2022-11-09T20:48:51Z","timestamp":1668026931884},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1983,8,1]]},"abstract":"<jats:p> The renal handling of potassium is generally thought to involve proximal reabsorption and distal secretion. To evaluate transport in the pars recta, we perfused S2 and S3 segments from superficial and juxtamedullary proximal straight tubules isolated from the rabbit kidney. The data indicate net potassium secretion in the isolated perfused perfused proximal straight tubule (PST). K+ secretion (JK, pmol X mm-1 X min-1) was -2.51 +\/- 0.53 in superficial PST S2 segments, -2.80 +\/- 1.05 in superficial PST S3 segments, and -1.36 +\/- 0.84 in juxtamedullary PST. Secretion was inhibited by 10(-5) M ouabain in the bath in superficial S2 and S3 segments. When a solution resembling late proximal tubular fluid was perfused in superficial PST, JK fell from -3.86 +\/- 1.77 to -0.45 +\/- 0.63 pmol X mm-1 X min-1. When luminal flow rate was varied in the physiologic range in individual superficial S2 and S3 segments, JK varied directly; K+ secretion increased by -0.5 pmol X mm-1 X min-1 per 1 nl X min-1 increment in luminal flow, while collected K+ concentration did not vary significantly. When a favorable bath-to-lumen K+ gradient (10 vs. 5 mM) was imposed, K+ secretion was markedly enhanced; when an equal but oppositely directed gradient was imposed, net K+ reabsorption was observed. These data are consistent with a gradient-limited process. In midcortical tubule segments (S2 and S3), 10(-3) M amiloride in perfusate inhibited net K+ secretion from -2.77 +\/- 0.52 to -0.18 +\/- 1.08 pmol X mm-1 X min-1 and fluid absorption from 0.42 +\/- 0.10 to 0.18 +\/- 0.05 nl X mm-1 X min-1. Net K+ secretion in S2 and S3 segments of PST may contribute to previously reported K+ secretion prior to the bend of Henle's loop. The magnitude of this process in vivo is uncertain in the absence of measurements of interstitial K+ concentration in the milieu of the PST. <\/jats:p>","DOI":"10.1152\/ajprenal.1983.245.2.f167","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T09:39:38Z","timestamp":1513935578000},"page":"F167-F174","source":"Crossref","is-referenced-by-count":2,"title":["Potassium secretion in the rabbit proximal straight tubule"],"prefix":"10.1152","volume":"245","author":[{"given":"A. G.","family":"Wasserstein","sequence":"first","affiliation":[]},{"given":"Z. S.","family":"Agus","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1983.245.2.F167","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T14:23:21Z","timestamp":1567952601000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1983.245.2.F167"}},"issued":{"date-parts":[[1983,8,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1983,8,1]]}},"alternative-id":["10.1152\/ajprenal.1983.245.2.F167"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1983.245.2.f167","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1983,8,1]]}},{"indexed":{"date-parts":[[2022,3,29]],"date-time":"2022-03-29T04:32:25Z","timestamp":1648528345229},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1995,4,1]]},"abstract":"<jats:p> The permeabilities of the basolateral membrane of rabbit proximal convoluted tubule (PCT) to taurine (PTau) and glucose (PGlc) were estimated under control and hypotonic conditions using the initial rate of increase in cellular volume (CV) induced on isotonic replacement of 40 mM mannitol by one or the other of these substrates. Under control conditions, addition of taurine led to an increase in CV at an initial rate of 7.1 +\/- 1.7%\/min, leading to a cell swelling of 30.2 +\/- 4.8% after 5 min (n = 6). Addition of glucose led to an increase in CV at an initial rate of 30.0 +\/- 3.8%\/min, leading to a cell swelling of 25.7 +\/- 3.1% after 5 min (n = 7). After a period of recovery of 5 min in the absence of taurine or glucose, a 40 mosmol\/kg hypotonic shock induced a cell swelling of 14.2 +\/- 1.3 and 16.1 +\/- 5.2%, respectively, followed by an almost complete volume regulatory decrease after 5 min. At that time, addition of taurine under continuous hypotonicity induced an increase in CV at an initial rate 2.57 +\/- 0.17 times larger than that observed under the isotonic condition (P &lt; 0.005), while addition of glucose induced an initial increase in CV identical to that observed under the isotonic condition. The increases in CV observed on addition of taurine were completely abolished in the absence of sodium under both isotonic and hypotonic conditions. The permeability to K+ was also estimated, in the absence of sodium, using the initial rate of increase in CV induced on isotonic replacement of 40 mM N-methyl-D-glucamine by K+.(ABSTRACT TRUNCATED AT 250 WORDS) <\/jats:p>","DOI":"10.1152\/ajprenal.1995.268.4.f595","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T06:23:42Z","timestamp":1514010222000},"page":"F595-F603","source":"Crossref","is-referenced-by-count":2,"title":["Hypotonicity increases basolateral taurine permeability in rabbit proximal convoluted tubule"],"prefix":"10.1152","volume":"268","author":[{"given":"S.","family":"Breton","sequence":"first","affiliation":[{"name":"Groupe de Recherche en Transport Membranaire, Universite de Montreal, Quebec, Canada."}]},{"given":"M.","family":"Marsolais","sequence":"additional","affiliation":[{"name":"Groupe de Recherche en Transport Membranaire, Universite de Montreal, Quebec, Canada."}]},{"given":"R.","family":"Laprade","sequence":"additional","affiliation":[{"name":"Groupe de Recherche en Transport Membranaire, Universite de Montreal, Quebec, Canada."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1995.268.4.F595","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:02:13Z","timestamp":1567972933000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1995.268.4.F595"}},"issued":{"date-parts":[[1995,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1995,4,1]]}},"alternative-id":["10.1152\/ajprenal.1995.268.4.F595"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1995.268.4.f595","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1995,4,1]]}},{"indexed":{"date-parts":[[2022,3,29]],"date-time":"2022-03-29T14:54:34Z","timestamp":1648565674732},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1987,12,1]]},"abstract":"<jats:p> To further characterize the mechanism of Cl- transport across the hamster thin ascending limb (TAL) of Henle's loop, we examined effects of pH on Cl- permeability as determined by either the choline chloride diffusion voltage or the lumen-to-bath 36Cl flux in the isolated segments perfused in vitro. When pH of the bathing fluid or the perfusate was reduced from 7.4 to 5.8, the Cl(-)-Na+ permeability ratio (PCl\/PNa) was reduced from 2.77 +\/- 0.21 to 0.48 +\/- 0.02 (n = 7, P less than 0.01) or from 2.55 +\/- 0.15 to 0.81 +\/- 0.11 (n = 6, P less than 0.01), respectively. At 37 degrees C, when the pH of the bathing fluid was reduced from 7.4 to 6.2, the lumen-to-bath flux coefficient for 36Cl (X10(-7) cm2\/s) was reduced from 84.8 +\/- 7.5 to 20.4 +\/- 3.2 (n = 7, P less than 0.01), whereas the value for 22Na was unchanged (27.3 +\/- 2.9 vs. 25.3 +\/- 2.5, n = 5). From the pH titration curves for PCl\/PNa, pKa values for proton binding were 6.31 and 5.78, and Hill's coefficients were 2.1 and 2.3 on the basolateral side and on the luminal side, respectively. Alkalinization had little or no effect on the Cl- permeability. At room temperature, the acid pH did not affect the Cl- permeability. Intracellular acidification with o-nitrophenylacetate also decreased the Cl- permeability.(ABSTRACT TRUNCATED AT 250 WORDS) <\/jats:p>","DOI":"10.1152\/ajprenal.1987.253.6.f1216","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T03:25:22Z","timestamp":1513999522000},"page":"F1216-F1222","source":"Crossref","is-referenced-by-count":1,"title":["Effect of pH on Cl- transport in TAL of Henle's loop"],"prefix":"10.1152","volume":"253","author":[{"given":"Y.","family":"Kondo","sequence":"first","affiliation":[{"name":"Department of Pharmacology, National Cardiovascular Center ResearchInstitute, Osaka, Japan."}]},{"given":"K.","family":"Yoshitomi","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, National Cardiovascular Center ResearchInstitute, Osaka, Japan."}]},{"given":"M.","family":"Imai","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, National Cardiovascular Center ResearchInstitute, Osaka, Japan."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1987.253.6.F1216","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:51:19Z","timestamp":1567972279000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1987.253.6.F1216"}},"issued":{"date-parts":[[1987,12,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1987,12,1]]}},"alternative-id":["10.1152\/ajprenal.1987.253.6.F1216"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1987.253.6.f1216","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1987,12,1]]}},{"indexed":{"date-parts":[[2022,3,29]],"date-time":"2022-03-29T06:08:20Z","timestamp":1648534100137},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1993,12,1]]},"abstract":"<jats:p> 11 beta-Hydroxysteroid dehydrogenase (11-OHSD) plays a critical role in conferring aldosterone specificity to mineralocorticoid target cells. We have recently described a novel isoform of 11-OHSD in the collecting duct (11-OHSD\/CD), which differs from the previously characterized isoform (11-OHSD-1) in kinetic parameters, cofactor dependency, and reversibility of the reaction. Unlike 11-OHSD-1, the collecting duct enzyme catalyzes irreversible dehydrogenation of endogenous glucocorticoids, has a very high affinity for its substrate, and is located in mineralocorticoid target cells; it thus appears well suited to \"protect\" the mineralocorticoid receptors from occupancy by glucocorticoids. As a first step in attempting to isolate the cDNA for the 11-OHSD\/CD isoform, we isolated mRNA from immunodissected cortical collecting duct (CCD) cells and characterized the 11-OHSD in oocytes injected with this mRNA. Water-injected oocytes had no measurable 11-OHSD activity. In contrast, oocytes injected with as little as 1 ng CCD mRNA expressed detectable 11-OHSD activity. Expression of 11-OHSD activity was dependent on the amount of mRNA injected and was maximal with 30 ng mRNA. Similar to the findings in CCD cells, the expressed enzyme preferred NAD over NADP (activity was 0.46 +\/- 0.04 and 0.011 +\/- 0.01 fmol.min-1.oocyte-1 with 0.1 mM NAD and NADP, respectively). The Michaelis constant (Km) for corticosterone was 11.5 +\/- 3.7 nM. Similar to the findings in CCD cells, the expressed enzyme worked predominantly in the oxidative direction, as back-conversion of [3H]dehydrocorticosterone to corticosterone was negligible. (ABSTRACT TRUNCATED AT 250 WORDS) <\/jats:p>","DOI":"10.1152\/ajprenal.1993.265.6.f896","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T11:20:49Z","timestamp":1514028049000},"page":"F896-F900","source":"Crossref","is-referenced-by-count":5,"title":["Expression and characterization of a new species of 11 beta-hydroxysteroid dehydrogenase in Xenopus oocytes"],"prefix":"10.1152","volume":"265","author":[{"given":"A.","family":"Naray-Fejes-Toth","sequence":"first","affiliation":[{"name":"Department of Physiology, Dartmouth Medical School, Lebanon, NewHampshire 03756."}]},{"given":"E.","family":"Rusvai","sequence":"additional","affiliation":[{"name":"Department of Physiology, Dartmouth Medical School, Lebanon, NewHampshire 03756."}]},{"given":"D. L.","family":"Denault","sequence":"additional","affiliation":[{"name":"Department of Physiology, Dartmouth Medical School, Lebanon, NewHampshire 03756."}]},{"given":"D. L.","family":"St Germain","sequence":"additional","affiliation":[{"name":"Department of Physiology, Dartmouth Medical School, Lebanon, NewHampshire 03756."}]},{"given":"G.","family":"Fejes-Toth","sequence":"additional","affiliation":[{"name":"Department of Physiology, Dartmouth Medical School, Lebanon, NewHampshire 03756."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1993.265.6.F896","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:34:36Z","timestamp":1567974876000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1993.265.6.F896"}},"issued":{"date-parts":[[1993,12,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1993,12,1]]}},"alternative-id":["10.1152\/ajprenal.1993.265.6.F896"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1993.265.6.f896","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1993,12,1]]}},{"indexed":{"date-parts":[[2022,3,30]],"date-time":"2022-03-30T06:40:27Z","timestamp":1648622427279},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1983,10,1]]},"abstract":"<jats:p> Micropuncture experiments were performed in thyroparathyroidectomized dogs to examine the influence of changes in filtered calcium load on segmental tubular calcium reabsorption. Filtered calcium load was changed either by reducing glomerular filtration rate (GFR) by aortic clamping (group I) or by progressive calcium infusion (group II) to increase plasma ultrafilterable calcium concentration (UFCa). The results suggest that fractional proximal calcium reabsorption responds similarly to altered filtered load, whether produced by changes in GFR or UFCa. In contrast, fractional reabsorption by the loop segment is progressively reduced as UFCa is increased but is relatively unchanged by alterations in filtered load secondary to altered GFR. These data indicate a specific parathyroid hormone-independent reciprocal effect of UFCa on calcium reabsorption in the loop segment, which may be an important determinant of urinary calcium excretion. <\/jats:p>","DOI":"10.1152\/ajprenal.1983.245.4.f515","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T14:43:17Z","timestamp":1513953797000},"page":"F515-F520","source":"Crossref","is-referenced-by-count":0,"title":["Renal tubular calcium transport: effects of changes in filtered calcium load"],"prefix":"10.1152","volume":"245","author":[{"given":"R. A.","family":"Sutton","sequence":"first","affiliation":[]},{"given":"N. L.","family":"Wong","sequence":"additional","affiliation":[]},{"given":"G. A.","family":"Quamme","sequence":"additional","affiliation":[]},{"given":"J. H.","family":"Dirks","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1983.245.4.F515","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:24:39Z","timestamp":1567967079000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1983.245.4.F515"}},"issued":{"date-parts":[[1983,10,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1983,10,1]]}},"alternative-id":["10.1152\/ajprenal.1983.245.4.F515"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1983.245.4.f515","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1983,10,1]]}},{"indexed":{"date-parts":[[2022,4,4]],"date-time":"2022-04-04T01:40:25Z","timestamp":1649036425128},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1987,4,1]]},"abstract":"<jats:p> It is generally assumed that electrolytes equilibrate readily across renal cortical brush-border membrane vesicles (BBMV). This assumption was tested by use of two new methods in rat BBMV prepared with free-flow electrophoresis (FFE), Mg aggregation, or Ca aggregation. Intravesicular KCl and RbCl concentrations, as well as the conductance of Cl relative to K (GCl\/GK) and GNa\/GK were determined with the fluorescent, potential-sensitive probe 3,3'-dipropylthiadicarbocyanine iodide [diS-C3-(5)]; intravesicular KCl concentration was also approximated utilizing the response of Na-dependent [3H]glucose uptake to variations in the membrane potential. These studies demonstrated that KCl fails to attain electrochemical equilibrium in BBMV prepared by the three methods, despite prolonged incubation at 22 degrees C; a significant, inwardly directed electrolyte gradient was sustained in all cases. The intravesicular electrolyte concentration was lower in BBMV prepared with FFE than in those prepared with Mg or Ca. GCl\/GK was lowest in BBMV prepared with FFE and highest in those prepared with Ca; GNa\/GK was comparable in all preparations. The apparent impermeance of BBMV may impact significantly in interpreting data from studies that require knowledge of the precise concentration of intravesicular electrolytes. <\/jats:p>","DOI":"10.1152\/ajprenal.1987.252.4.f700","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T21:13:31Z","timestamp":1513977211000},"page":"F700-F711","source":"Crossref","is-referenced-by-count":0,"title":["Ionic permeabilities of rat renal cortical brush-border membrane vesicles"],"prefix":"10.1152","volume":"252","author":[{"given":"M. S.","family":"Lipkowitz","sequence":"first","affiliation":[]},{"given":"R. G.","family":"Abramson","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1987.252.4.F700","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:44:45Z","timestamp":1567957485000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1987.252.4.F700"}},"issued":{"date-parts":[[1987,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1987,4,1]]}},"alternative-id":["10.1152\/ajprenal.1987.252.4.F700"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1987.252.4.f700","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1987,4,1]]}},{"indexed":{"date-parts":[[2022,3,30]],"date-time":"2022-03-30T20:56:00Z","timestamp":1648673760008},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1986,11,1]]},"abstract":"<jats:p> Dexamethasone has been reported to stimulate Na-K-ATPase activity in the medullary thick ascending limb of adrenalectomized animals within a few hours. The present study was aimed at characterizing the mechanism of this action by investigating the stimulatory effect of the hormone in vitro. Dexamethasone (10(-8) M) added in vitro to segments of the medullary thick ascending limb of Henle's loop, which were microdissected from adrenalectomized rats, restored in a dose-dependent manner the depressed Na-K-ATPase activity within one h of incubation. This stimulation of Na-K-ATPase was inhibited by cycloheximide and actinomycin D. Dexamethasone also stimulated the component of oxidative metabolism coupled to sodium transport. These results, which confirm previous in vivo observations, demonstrate that dexamethasone-induced stimulation of Na-K-ATPase is a direct tubular action of the hormone mediated by protein synthesis. They suggest that this short-term effect of dexamethasone corresponds to the stimulation of sodium reabsorption by the dilution segment. <\/jats:p>","DOI":"10.1152\/ajprenal.1986.251.5.f851","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T00:52:48Z","timestamp":1513990368000},"page":"F851-F857","source":"Crossref","is-referenced-by-count":3,"title":["In vitro stimulation of Na-K-ATPase in rat thick ascending limb by dexamethasone"],"prefix":"10.1152","volume":"251","author":[{"given":"A.","family":"Doucet","sequence":"first","affiliation":[]},{"given":"A.","family":"Hus-Citharel","sequence":"additional","affiliation":[]},{"given":"F.","family":"Morel","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1986.251.5.F851","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:34:27Z","timestamp":1567971267000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1986.251.5.F851"}},"issued":{"date-parts":[[1986,11,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1986,11,1]]}},"alternative-id":["10.1152\/ajprenal.1986.251.5.F851"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1986.251.5.f851","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1986,11,1]]}},{"indexed":{"date-parts":[[2022,3,29]],"date-time":"2022-03-29T14:14:00Z","timestamp":1648563240086},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1984,9,1]]},"abstract":"<jats:p> It has been shown that acute respiratory acidosis in dogs results in enhanced renal extraction of L-glutamine from plasma and increased ammonia excretion per nephron. To determine whether a component of the enhanced L-glutamine extraction results from increased transport of L-glutamine across the basolateral membrane into the renal proximal tubular cell, we measured Na+ gradient-dependent L-[3H]glutamine transport in proximal tubular basolateral membrane vesicles isolated from kidneys of normal dogs and from kidneys of dogs following 2 h of acute respiratory acidosis. The initial rate of Na+ gradient-dependent L-[3H] glutamine uptake (15 s) was increased significantly in basolateral membrane vesicles from the acidotic compared with normal dogs. Increased uptake could be measured under conditions in which changes in membrane potential resulting from fluxes of solute were minimized. We conclude that an adaptation occurs in the basolateral membrane of the renal proximal tubular cell during acute respiratory acidosis that allows increased transport of L-glutamine across the membrane into the proximal tubular cell. This adaptation may permit increased ammonia production per nephron. <\/jats:p>","DOI":"10.1152\/ajprenal.1984.247.3.f403","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T16:17:14Z","timestamp":1513959434000},"page":"F403-F407","source":"Crossref","is-referenced-by-count":1,"title":["Glutamine transport in basolateral vesicles from dogs with acute respiratory acidosis"],"prefix":"10.1152","volume":"247","author":[{"given":"D. W.","family":"Windus","sequence":"first","affiliation":[]},{"given":"S.","family":"Klahr","sequence":"additional","affiliation":[]},{"given":"M. R.","family":"Hammerman","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1984.247.3.F403","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:30:53Z","timestamp":1567967453000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1984.247.3.F403"}},"issued":{"date-parts":[[1984,9,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1984,9,1]]}},"alternative-id":["10.1152\/ajprenal.1984.247.3.F403"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1984.247.3.f403","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1984,9,1]]}},{"indexed":{"date-parts":[[2022,3,29]],"date-time":"2022-03-29T14:15:09Z","timestamp":1648563309807},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1988,8,1]]},"DOI":"10.1152\/ajprenal.1988.255.2.f205","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T03:15:30Z","timestamp":1513998930000},"page":"F205-F205","source":"Crossref","is-referenced-by-count":0,"title":["A new journal"],"prefix":"10.1152","volume":"255","author":[{"given":"P. C.","family":"Johnson","sequence":"first","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1988.255.2.F205","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:48:26Z","timestamp":1567972106000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1988.255.2.F205"}},"issued":{"date-parts":[[1988,8,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1988,8,1]]}},"alternative-id":["10.1152\/ajprenal.1988.255.2.F205"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1988.255.2.f205","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1988,8,1]]}},{"indexed":{"date-parts":[[2022,4,5]],"date-time":"2022-04-05T22:41:21Z","timestamp":1649198481777},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2018,9,1]]},"DOI":"10.1152\/ajprenal-zh2-8577-corr.2018","type":"journal-article","created":{"date-parts":[[2018,9,6]],"date-time":"2018-09-06T22:21:57Z","timestamp":1536272517000},"page":"F746-F746","source":"Crossref","is-referenced-by-count":0,"title":["CORRIGENDUM"],"prefix":"10.1152","volume":"315","member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal-zh2-8577-corr.2018","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T02:49:33Z","timestamp":1567997373000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal-zh2-8577-corr.2018"}},"issued":{"date-parts":[[2018,9,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2018,9,1]]}},"alternative-id":["10.1152\/ajprenal-zh2-8577-corr.2018"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal-zh2-8577-corr.2018","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2018,9,1]]}},{"indexed":{"date-parts":[[2023,4,24]],"date-time":"2023-04-24T20:30:55Z","timestamp":1682368255593},"reference-count":18,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2007,1]]},"abstract":"<jats:p>Transgenic mice facilitate mechanistic studies of altered peritoneal transport, but the majority of transport studies have been carried out in rats. We hypothesized that mouse transport parameters, normalized to the peritoneal contact area, would be similar to those of the rat. To address this, we affixed small (\u223c10-mm diameter) plastic chambers to the serosa of the abdominal wall of anesthetized CD1 and C57BL mice. The chamber constrained transfer across the area of the chamber base and facilitated mixing, volumetric, and concentration measurements vs. time for mannitol, serum albumin, and osmotic and hydrostatic pressure-driven convection. The mass transfer coefficient of mannitol (MTC<jats:sub>M<\/jats:sub>) and of serum albumin (MTC<jats:sub>BSA<\/jats:sub>), hydrostatic pressure-driven flux ( J<jats:sub>P<\/jats:sub>), and osmotic filtration ( J<jats:sub>osm<\/jats:sub>) were calculated from the time-dependent volume and concentration data. The units of all parameters (\u03bcl\u00b7min<jats:sup>\u22121<\/jats:sup>\u00b7cm<jats:sup>\u22122<\/jats:sup>) were compared with previously derived parameters from SD rats with a one-way ANOVA. Results indicated small but significant differences in MTC<jats:sub>BSA<\/jats:sub>(x10<jats:sup>2<\/jats:sup>): CD1, 9.72 \u00b1 1.97, n = 6; C57BL, 7.13 \u00b1 1.52, n = 10; rat, 12.5 \u00b1 1.6, n = 17 ( P = 0.03). ANOVAs of all other parameters were not significant and confirmed our hypothesis: MTC<jats:sub>M<\/jats:sub>(CD1, 3.20 \u00b1 0.38, n = 7; C57BL, 2.34 \u00b1 0.41, n = 6; rat, 2.72 \u00b1 0.23 n = 19), J<jats:sub>P<\/jats:sub>(CD1, 0.77 \u00b1 0.15, n = 10; C57BL, 0.33 \u00b1 0.13, n = 15; rat, 0.51 \u00b1 0.16, n = 9), or J<jats:sub>osm<\/jats:sub>(CD1, 0.92 \u00b1 0.35, n = 6; C57BL, 0.49 \u00b1 0.35, n = 6; rat 1.72 \u00b1 0.35, n = 6). We conclude that elimination of the variable peritoneal transfer area normalizes calculated transport characteristics and facilitates comparison between species.<\/jats:p>","DOI":"10.1152\/ajprenal.00169.2006","type":"journal-article","created":{"date-parts":[[2006,7,19]],"date-time":"2006-07-19T00:59:40Z","timestamp":1153270780000},"page":"F495-F499","source":"Crossref","is-referenced-by-count":4,"title":["Similitude of transperitoneal permeability in different rodent species"],"prefix":"10.1152","volume":"292","author":[{"given":"Michael F.","family":"Flessner","sequence":"first","affiliation":[]},{"given":"Kimberly","family":"Credit","sequence":"additional","affiliation":[]},{"given":"Xiarong","family":"Li","sequence":"additional","affiliation":[]},{"given":"Jarred","family":"Tanksley","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-201x.2000.00685.x"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000026492.83560.81"},{"key":"R3","unstructured":"Chagnac A, Herskovitz P, Weinstein T, Elyashiv S, Hirsh J, Hamel I, Gafter U.The peritoneal membrane in peritoneal dialysis patients: estimation of its functional surface area by applying stereologic methods to computerized tomography scans.J Am Soc Nephrol10: 342\u2013346, 1999."},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1002\/jps.2600751106"},{"key":"R5","doi-asserted-by":"crossref","unstructured":"Flessner MF, Henegar J, Bigler S, Genous L.Is the peritoneum a significant transport barrier in peritoneal dialysis?Perit Dial Int23: 542\u2013549, 2003.","DOI":"10.1177\/089686080302300605"},{"key":"R6","unstructured":"Flessner MF.Transport of Water-Soluble Solutes Between the Peritoneal Cavity and Plasma in the Rat.Ann Arbor, MI: Univ. of Michigan, 1981."},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.267.5.F861"},{"key":"R8","doi-asserted-by":"crossref","unstructured":"Flessner MF.Small-solute transport across specific peritoneal tissue surfaces in the rat.J Am Soc Nephrol7: 225\u2013233, 1996.","DOI":"10.1681\/ASN.V72225"},{"key":"R9","doi-asserted-by":"crossref","unstructured":"Flessner MF, Choi J, Vanpelt H, He Z, Credit K, Henegar J, Hughson M.Correlating structure with solute and water transport in a chronic model of peritoneal inflammation.Am J Physiol Renal Physiol290: F232\u2013F240, 2006.","DOI":"10.1152\/ajprenal.00211.2005"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00062.2006"},{"key":"R11","doi-asserted-by":"crossref","unstructured":"Flessner MF, Lofthouse J, Williams A.Increasing peritoneal contact area during dialysis improves mass transfer.J Am Soc Nephrol12: 2139\u20132145, 2001.","DOI":"10.1681\/ASN.V12102139"},{"key":"R12","doi-asserted-by":"crossref","unstructured":"Flessner MF, Lofthouse J, Zakaria EL.Improving contact area between the peritoneum and intraperitoneal therapeutic solutions.J Am Soc Nephrol12: 807\u2013813, 2001.","DOI":"10.1681\/ASN.V124807"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.270.2.F377"},{"key":"R14","doi-asserted-by":"crossref","unstructured":"Keshaviah P, Emerson PF, Vonesh EF, Brandes JC.Relationship between body size, fill volume, and mass transfer area coefficient in peritoneal dialysis.J Am Soc Nephrol4: 1820\u20131826, 1994.","DOI":"10.1681\/ASN.V4101820"},{"key":"R15","doi-asserted-by":"crossref","unstructured":"Mortier S, Lameire NH, deVriese AS.The effects of peritoneal dialysis solutions on peritoneal host defense.Perit Dial Int24: 123\u2013138, 2004.","DOI":"10.1177\/089686080402400203"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000285"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00815.x"},{"key":"R18","doi-asserted-by":"crossref","unstructured":"Zweers MM, Splint LJ, Krediet RT, Struijk DG.Effect of fluid supplementation and modality on peritoneal permeability in a rat peritoneal dialysis model.Perit Dial Int21: 58\u201364, 2001.","DOI":"10.1177\/089686080102100109"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00169.2006","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,7,29]],"date-time":"2021-07-29T22:16:45Z","timestamp":1627597005000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00169.2006"}},"issued":{"date-parts":[[2007,1]]},"references-count":18,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2007,1]]}},"alternative-id":["10.1152\/ajprenal.00169.2006"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00169.2006","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2007,1]]}},{"indexed":{"date-parts":[[2024,8,8]],"date-time":"2024-08-08T11:55:23Z","timestamp":1723118123477},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1994,12,1]]},"abstract":"<jats:p> Renal hypertrophy is an early feature of diabetes, and it may predispose the kidney to the eventual development of parenchymal dysfunction. Since we have previously demonstrated that short-term culture in high glucose concentration stimulates production of transforming growth factor-beta 1 (TGF-beta 1) in proximal tubular and glomerular mesangial cells, we postulated that this cytokine, which has potent regulatory effects on cellular growth and extracellular matrix production, is important in mediating diabetic renal disease. In this study we evaluated the gene and protein expression of TGF-beta 1 in the kidney of two rodent models of spontaneous insulin-dependent diabetes mellitus [the biobreeding (BB) rat and the nonobese diabetic (NOD) mouse]. In association with the appearance in both models of significant renal hypertrophy, TGF-beta 1 mRNA levels were increased threefold in the kidney of the diabetic BB rat after 3 days of diabetes and also threefold after 7\u20139 days in the NOD mouse. There was no increase in TGF-beta 1 transcripts in the livers of the diabetic animals, suggesting that this response is tissue specific. Immunohistochemical studies revealed that TGF-beta 1 protein is concordantly elevated in the cortical tubular cells of the diabetic kidney in both models. These results suggest that the stimulated expression of renal TGF-beta is an early manifestation of the involvement of the kidney by diabetes. Whether increased TGF-beta production in the diabetic kidney is a key promoter of diabetic renal manifestations (e.g., hypertrophy) deserves additional studies. <\/jats:p>","DOI":"10.1152\/ajprenal.1994.267.6.f1094","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T23:54:01Z","timestamp":1513986841000},"page":"F1094-F1001","source":"Crossref","is-referenced-by-count":23,"title":["Renal hypertrophy is associated with upregulation of TGF-beta 1 gene expression in diabetic BB rat and NOD mouse"],"prefix":"10.1152","volume":"267","author":[{"given":"K.","family":"Sharma","sequence":"first","affiliation":[{"name":"Penn Center for Molecular Studies of Kidney Diseases, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia 19104\u20136144."}]},{"given":"F. N.","family":"Ziyadeh","sequence":"additional","affiliation":[{"name":"Penn Center for Molecular Studies of Kidney Diseases, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia 19104\u20136144."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1994.267.6.F1094","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:55:53Z","timestamp":1567958153000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1994.267.6.F1094"}},"issued":{"date-parts":[[1994,12,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1994,12,1]]}},"alternative-id":["10.1152\/ajprenal.1994.267.6.F1094"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1994.267.6.f1094","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1994,12,1]]}},{"indexed":{"date-parts":[[2022,4,5]],"date-time":"2022-04-05T16:23:51Z","timestamp":1649175831018},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1978,8,1]]},"abstract":"<jats:p> In the perfused Necturus kidney, the ratio of transepithelial sodium-to-chloride permeabilities (PNa\/PCl) was estimated from dilution potentials at 1:7. The ratio of transepithelial permeabilities PHCO3\/cl was estimated from bi-ionic potentials at 1:4 and that of Plact\/PCl at 1:12. The permeability sequence, therefore, is PCl greater than PHCO3 greater than than PNa or PnaCl greater than PNaHCO3. The latter is similar to the situation in the rat. However, because of the low Na permeability, passive NaCl absorption by solvent drag is probably less important in Necturus than in the rat. The measurement of transepithelial input conductance during replacement of extracellular chloride by either bicarbonate or lactate shows that the former reduces the transmural conductance to 31% of control values as compared with 40% for the latter. Such discrepancies between permeability and conductance sequences are consistent either with an interference of the test anion with chloride permeation or with the presence of positive fixed changes within the shunt pathway. <\/jats:p>","DOI":"10.1152\/ajprenal.1978.235.2.f89","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T20:45:56Z","timestamp":1513975556000},"page":"F89-F95","source":"Crossref","is-referenced-by-count":0,"title":["Further studies on ion permeation in proximal tubule of necturus kidney"],"prefix":"10.1152","volume":"235","author":[{"given":"A.","family":"Edelman","sequence":"first","affiliation":[]},{"given":"T.","family":"Anagnostopoulos","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1978.235.2.F89","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:03:38Z","timestamp":1567969418000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1978.235.2.F89"}},"issued":{"date-parts":[[1978,8,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1978,8,1]]}},"alternative-id":["10.1152\/ajprenal.1978.235.2.F89"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1978.235.2.f89","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1978,8,1]]}},{"indexed":{"date-parts":[[2022,4,5]],"date-time":"2022-04-05T16:17:31Z","timestamp":1649175451762},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1978,2,1]]},"abstract":"<jats:p> There is evidence for the endogenous generation of [des-Asp1]angiotensin II (AIII) from a nonapeptide precursor, [des-Asp1]angiotensin I ([des-Asp1]AI). In the present study, the effects of equipressor doses of exogeneously administered [des-Asp1]AI and AIII on renal function and plasma aldosterone concentration were compared. Intravenous infusion of [des-Asp1]AI (75 ng\/kg min-1 for 40 min) decreased renin secretion, renal blood flow, creatinine clearance, and sodium and potassium excretion in dogs. Infusion of AIII at one-third of the rate of [des-Asp1]AI (25 ng\/kg min-1) produced comparable decreases in these same parameters. Filtration fraction was increased with both peptides. Both peptides also increased plasma aldosterone concentration to the same extent. A bolus injection (5 mg i.v.) of the converting enzyme inhibitor SQ 20,881 completely reversed the mean arterial pressure and renal blood flow responses to [des-Asp1]AI, but did not alter these responses to AIII. These data are consistent with the concept that endogenous generation of AIII from [des-Asp1]AI can occur via the action of converting enzyme on this substance. <\/jats:p>","DOI":"10.1152\/ajprenal.1978.234.2.f130","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T19:59:39Z","timestamp":1513972779000},"page":"F130-F134","source":"Crossref","is-referenced-by-count":2,"title":["Renal and adrenal responses to [des-Asp1]angiotensin I in the dog"],"prefix":"10.1152","volume":"234","author":[{"given":"R. H.","family":"Freeman","sequence":"first","affiliation":[]},{"given":"J. O.","family":"Davis","sequence":"additional","affiliation":[]},{"given":"M. C.","family":"Khosla","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1978.234.2.F130","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:55:50Z","timestamp":1567968950000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1978.234.2.F130"}},"issued":{"date-parts":[[1978,2,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1978,2,1]]}},"alternative-id":["10.1152\/ajprenal.1978.234.2.F130"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1978.234.2.f130","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1978,2,1]]}},{"indexed":{"date-parts":[[2022,4,5]],"date-time":"2022-04-05T16:16:30Z","timestamp":1649175390281},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1989,10,1]]},"abstract":"<jats:p> Phosphate transport was studied in brush-border membrane vesicles prepared from outer medullary tissue of the porcine kidney. Phosphate uptake studies were performed in the absence of sodium at 21 degrees C. A 1.2- to 12-fold overshoot, above equilibrium values, was present with intracellular pH (pHin) equal to 8.0 and extracellular pH (pHout) equal to 6.5, which was not evident at pHin = pHout. Concentration-dependence of the pH-stimulate uptake was determined by the difference of uptake in the absence of a pH gradient (pHin = pHout) from that in the presence of a pH gradient over a large range of phosphate concentrations. The uptake was consistent with a single facilitative system characterized by apparent kinetic parameters; with Michaelis constant 149 +\/- 11 microM and maximal velocity 4.9 +\/- 0.4 nmol.mg protein-1.min-1, n = 3. Phosphate uptake was inhibited by the stilbene derivative 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid with a mean inhibition constant (Ki) value of 0.15 mM (n = 2). In addition, pH gradient-stimulated phosphate uptake was sensitive to furosemide and bumetanide; Ki values of 0.50 +\/- 0.05 and 0.11 +\/- 0.04 mM, respectively. Arsenate (1 mM) and phosphonoformate (1 mM) inhibited pH-dependent phosphate uptake, whereas sulfate (5 mM), bicarbonate (25 mM), and chloride (100 mM) were without effect, indicating that the transport system is relatively specific to phosphate and its close analogues. pH gradient-stimulated phosphate uptake was not influenced by potassium-diffusional gradients. The data provide evidence for a facilitative process in brush-border membrane vesicles isolated from outer medullary tissue of the pig kidney that is capable of transporting phosphate in the absence of sodium. <\/jats:p>","DOI":"10.1152\/ajprenal.1989.257.4.f639","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T16:53:58Z","timestamp":1513961638000},"page":"F639-F648","source":"Crossref","is-referenced-by-count":0,"title":["pH gradient-stimulated phosphate transport in outer medullary brush-border membranes"],"prefix":"10.1152","volume":"257","author":[{"given":"G. A.","family":"Quamme","sequence":"first","affiliation":[{"name":"Department of Medicine, University Hospital, University of British Columbia, Vancouver, Canada."}]},{"given":"J. J.","family":"Walker","sequence":"additional","affiliation":[{"name":"Department of Medicine, University Hospital, University of British Columbia, Vancouver, Canada."}]},{"given":"T. S.","family":"Yan","sequence":"additional","affiliation":[{"name":"Department of Medicine, University Hospital, University of British Columbia, Vancouver, Canada."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1989.257.4.F639","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:14:47Z","timestamp":1567955687000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1989.257.4.F639"}},"issued":{"date-parts":[[1989,10,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1989,10,1]]}},"alternative-id":["10.1152\/ajprenal.1989.257.4.F639"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1989.257.4.f639","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1989,10,1]]}},{"indexed":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T04:10:59Z","timestamp":1660191059694},"reference-count":25,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1998,2,1]]},"abstract":"<jats:p>Sorbitol content was determined in porcine urinary bladder epithelial cells immediately after death of the animals and after primary culture of the cells at different osmolalities. In both instances, sorbitol content increased with urine and medium osmolality, respectively. For example, at 300 mosmol\/kg the cultured cells contained 0.84 \u00b1 0.02 nmol\/mg protein, at 600 mosmol\/kg contained 21.7 \u00b1 0.95 nmol\/mg protein, and at 900 mosmol\/kg contained 59.5 \u00b1 2.8 nmol\/mg protein. Similarly, aldose reductase activity rose from 0.27 \u00b1 0.04 \u03bcmol \u22c5 h<jats:sup>\u22121<\/jats:sup>\u22c5 mg protein<jats:sup>\u22121<\/jats:sup>at 300 mosmol\/kg to 1.81 \u00b1 0.16 at 600 mosmol\/kg and to 3.02 \u00b1 0.33 at 900 mosmol\/kg. These changes were, however, only observed when NaCl but not when urea was used to augment the medium osmolality, since urea equilibrated across the cell membrane. In contrast, sorbitol release from cells cultured at 900 mosmol\/kg was slowest into a 900 mosmol\/kg medium and fastest into a 300 mosmol\/kg medium (63 \u00b1 16 nmol\/10 min compared with 389 \u00b1 52 nmol\/10 min). These studies demonstrate that the sorbitol content of porcine urinary bladder epithelium is regulated by changes both in sorbitol synthesis and sorbitol release. Thus the regulatory mechanisms in the urinary bladder seem to be similar to those present in the embryological related collecting duct.<\/jats:p>","DOI":"10.1152\/ajprenal.1998.274.2.f342","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T14:28:38Z","timestamp":1514039318000},"page":"F342-F347","source":"Crossref","is-referenced-by-count":2,"title":["Regulation of sorbitol content in cultured porcine urinary bladder epithelial cells"],"prefix":"10.1152","volume":"274","author":[{"given":"Solveigh","family":"M\u00e4hler","sequence":"first","affiliation":[{"name":"Institut f\u00fcr Arbeitsphysiologie an der Universit\u00e4t Dortmund, and"}]},{"given":"Evamaria","family":"Kinne-Saffran","sequence":"additional","affiliation":[{"name":"Max-Planck-Institut f\u00fcr molekulare Physiologie, 44139 Dortmund, Germany"}]},{"given":"Hiroshi","family":"Fujisue","sequence":"additional","affiliation":[{"name":"Max-Planck-Institut f\u00fcr molekulare Physiologie, 44139 Dortmund, Germany"}]},{"given":"Rolf K. H.","family":"Kinne","sequence":"additional","affiliation":[{"name":"Max-Planck-Institut f\u00fcr molekulare Physiologie, 44139 Dortmund, Germany"}]},{"given":"Wolfram","family":"F\u00f6llmann","sequence":"additional","affiliation":[{"name":"Institut f\u00fcr Arbeitsphysiologie an der Universit\u00e4t Dortmund, and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1988.254.6.C788"},{"key":"B2","first-page":"132","volume":"4","author":"Beck F. X.","year":"1990","journal-title":"Comp. Physiol."},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1994.267.5.C1483"},{"key":"B4","first-page":"361","volume":"33","author":"Crocker C. L.","year":"1967","journal-title":"Am. J. Med. Technol."},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/0003-9861(85)90213-9"},{"key":"B6","first-page":"709","volume":"1","author":"D\u00f6rrenhaus A.","year":"1997","journal-title":"Arch. Toxicol."},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/0887-2333(94)90062-0"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1007\/s002040050171"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1991.71.4.1081"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1007\/BF01868535"},{"issue":"36","key":"B11","first-page":"F13","volume":"267","author":"Grunewald J. M.","year":"1994","journal-title":"Am. J. Physiol."},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1007\/BF00580961"},{"issue":"35","key":"B13","first-page":"F298","volume":"266","author":"Guhe C.","year":"1994","journal-title":"Am. J. Physiol."},{"key":"B14","first-page":"599","volume":"70","author":"Guhe C.","year":"1996","journal-title":"Toxicol."},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.248"},{"issue":"40","key":"B16","first-page":"F230","volume":"271","author":"Kwon E. D.","year":"1996","journal-title":"Am. J. Physiol."},{"key":"B17","doi-asserted-by":"crossref","first-page":"265","DOI":"10.1016\/S0021-9258(19)52451-6","volume":"193","author":"Lowry O. H.","year":"1951","journal-title":"J. Biol. Chem."},{"key":"B18","first-page":"775","volume":"374","author":"M\u00e4hler S.","year":"1993","journal-title":"Hoppe Seylers Z. Physiol. Chem."},{"issue":"40","key":"B19","first-page":"F886","volume":"271","author":"Negrete H. O.","year":"1996","journal-title":"Am. J. Physiol."},{"key":"B20","first-page":"241","volume":"8","author":"Pirke K. M.","year":"1970","journal-title":"Z. Klin. Chem. Klin. Biochem."},{"issue":"25","key":"B22","first-page":"F128","volume":"256","author":"Wirthensohn G.","year":"1989","journal-title":"Am. J. Physiol."},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1007\/BF00695336"},{"issue":"26","key":"B24","first-page":"F602","volume":"257","author":"Yancey P. H.","year":"1989","journal-title":"Am. J. Physiol."},{"issue":"27","key":"B25","first-page":"R198","volume":"258","author":"Yancey P. H.","year":"1990","journal-title":"Am. J. Physiol."},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1126\/science.7112124"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1998.274.2.F342","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:46:28Z","timestamp":1660189588000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1998.274.2.F342"}},"issued":{"date-parts":[[1998,2,1]]},"references-count":25,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1998,2,1]]}},"alternative-id":["10.1152\/ajprenal.1998.274.2.F342"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1998.274.2.f342","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1998,2,1]]}},{"indexed":{"date-parts":[[2022,3,31]],"date-time":"2022-03-31T12:15:11Z","timestamp":1648728911252},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1983,9,1]]},"abstract":"<jats:p> The effect of epinephrine on renal potassium excretion was examined in the rat. In group I KCl was infused acutely to increase plasma K (PK) by 2.0 meq\/liter; urinary K excretion (UKV) rose by 1.22 mueq\/min. In group II rats, which received a similar dose of KCl but with epinephrine, the increase in PK (delta = 0.8 meq\/liter, P less than 0.001) was blunted and UKV was reduced (delta = 0.23 mueq\/min, P less than 0.001). To determine whether the reduction in UKV resulted from the smaller increase in PK or from a direct action of epinephrine on renal K transport, a third group of animals received a lower dose of KCl. Despite similar PK levels, the epinephrine group excreted significantly less K in the urine (0.61 vs. 0.93 mueq\/min). In group IV propranolol was infused with KCl; UKV was modestly increased. The effects of epinephrine on UKV were unrelated to changes in glomerular filtration rate, urine flow, or UNaV. Micropuncture results showed that at comparable PK levels epinephrine had no direct effect on K secretion by the distal tubule but indirectly inhibited K secretion in this nephron segment by reducing PK. In addition, epinephrine reduced K addition at tubular sites beyond the late distal tubule, most likely in the collecting tubule. <\/jats:p>","DOI":"10.1152\/ajprenal.1983.245.3.f303","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T14:38:37Z","timestamp":1513953517000},"page":"F303-F311","source":"Crossref","is-referenced-by-count":2,"title":["Inhibitory effect of epinephrine on renal potassium secretion: a micropuncture study"],"prefix":"10.1152","volume":"245","author":[{"given":"R. A.","family":"DeFronzo","sequence":"first","affiliation":[]},{"given":"B.","family":"Stanton","sequence":"additional","affiliation":[]},{"given":"G.","family":"Klein-Robbenhaar","sequence":"additional","affiliation":[]},{"given":"G.","family":"Giebisch","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1983.245.3.F303","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:23:23Z","timestamp":1567967003000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1983.245.3.F303"}},"issued":{"date-parts":[[1983,9,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1983,9,1]]}},"alternative-id":["10.1152\/ajprenal.1983.245.3.F303"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1983.245.3.f303","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1983,9,1]]}},{"indexed":{"date-parts":[[2023,10,24]],"date-time":"2023-10-24T21:38:58Z","timestamp":1698183538536},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1989,4,1]]},"abstract":"<jats:p> Phospholipase activation with resulting phospholipid breakdown and lipid byproduct accumulation may play a critical role in hypoxic cell injury. To explore this role, mildly hypoxic rabbit renal proximal tubules (PT) in suspension were treated in vitro with exogenous phospholipase A2 (PLA2). This treatment produced severe tubule cell injury measured by alterations in tubule cation homeostasis, respiratory rates, and adenosine nucleotide metabolism. This injury was associated with loss of the major membrane phospholipids, phosphatidylcholine (PC) and phosphatidylethanolamine (PE), with accumulation of lipid byproducts, lysophosphatidylcholine (LPC), lysophosphatidylethanolamine (LPE), and free fatty acids (FFA). Addition of fatty acid-free bovine serum albumin (BSA) to PTs reduced markedly FFA levels and improved significantly derangements in metabolic parameters of hypoxic PTs treated with exogenous PLA2, suggesting that FFA accumulation was a critical factor in this injury process. Effects of increasing durations of hypoxia (30, 45, and 60 min) with or without reoxygenation recovery demonstrated increased FFA levels, especially polyunsaturated FFA, which correlated better with the degree of hypoxic injury than alterations in membrane phospholipid and lysophospholipid levels. PTs undergoing hypoxia and reoxygenation recovery exposed to BSA were not protected. Although 60 min of hypoxia with 60 min reoxygenation produced accumulation of FFA to levels nearly identical to those seen in hypoxic PTs treated with exogenous PLA2 and BSA, with a similar distribution of various FFA species, hypoxia\/reoxygenation produced a more severe degree of cell injury than that observed with hypoxia plus exogenous PLA and BSA.(ABSTRACT TRUNCATED AT 250 WORDS) <\/jats:p>","DOI":"10.1152\/ajprenal.1989.256.4.f688","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T20:49:08Z","timestamp":1513975748000},"page":"F688-F696","source":"Crossref","is-referenced-by-count":4,"title":["The role of free fatty acids in hypoxia-induced injury to renal proximal tubule cells"],"prefix":"10.1152","volume":"256","author":[{"given":"H. D.","family":"Humes","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, Veterans Administration MedicalCenter, Ann Arbor, Michigan."}]},{"given":"V. D.","family":"Nguyen","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Veterans Administration MedicalCenter, Ann Arbor, Michigan."}]},{"given":"D. A.","family":"Cieslinski","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Veterans Administration MedicalCenter, Ann Arbor, Michigan."}]},{"given":"J. M.","family":"Messana","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Veterans Administration MedicalCenter, Ann Arbor, Michigan."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1989.256.4.F688","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:05:53Z","timestamp":1567969553000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1989.256.4.F688"}},"issued":{"date-parts":[[1989,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1989,4,1]]}},"alternative-id":["10.1152\/ajprenal.1989.256.4.F688"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1989.256.4.f688","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1989,4,1]]}},{"indexed":{"date-parts":[[2022,4,4]],"date-time":"2022-04-04T16:55:10Z","timestamp":1649091310955},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1979,9,1]]},"abstract":"<jats:p> Differences in the rate of renin release by superficial and deep areas of the cat kidney cortex were studied in vitro and in vivo. Renin release in vitro by outer cortical slices was significantly higher than by their inner counterparts: 19.6 +\/- 2.3 vs. 12.8 +\/- 1.95 ng angiotensin I-h-1-mg fresh tissue-1-h of incubation-1. In vivo blood was sampled from subcapsular (outer cortical) and deep (inner cortical and medullary) renal venous circulation from anesthetized cats. Renal venous minus arterial plasma renin concentration was respectively, 4.3 +\/- 1.12 and 1.9 +\/- 1.04 ng angiotensin I-ml-1-h-1 (P less than 0.01). By assuming that in these experiments renal blood flow distribution was approximately equal to each of the two areas of venous drainage, as reported in the isolated perfused cat kidney, we infer from the regional differences in arteriovenous concentration that the rate of renin release of the outer cortex is higher than that of the innder cortex in the cat kidney in vivo. Tissue content of renin was found to decrease toward the deep cortex. The results support the concept that the rate of regional renin release correlates with tissue renin content, at least under the conditions of the present experiments. <\/jats:p>","DOI":"10.1152\/ajprenal.1979.237.3.f188","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T20:22:48Z","timestamp":1513974168000},"page":"F188-F195","source":"Crossref","is-referenced-by-count":0,"title":["Regional renin release by the cat kidney in vitro and in vivo"],"prefix":"10.1152","volume":"237","author":[{"given":"S. M.","family":"Jones","sequence":"first","affiliation":[]},{"given":"J.","family":"Torretti","sequence":"additional","affiliation":[]},{"given":"J. S.","family":"Williams","sequence":"additional","affiliation":[]},{"given":"S. F.","family":"Weinberger","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1979.237.3.F188","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:59:19Z","timestamp":1567969159000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1979.237.3.F188"}},"issued":{"date-parts":[[1979,9,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1979,9,1]]}},"alternative-id":["10.1152\/ajprenal.1979.237.3.F188"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1979.237.3.f188","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1979,9,1]]}},{"indexed":{"date-parts":[[2024,7,4]],"date-time":"2024-07-04T00:31:00Z","timestamp":1720053060136},"reference-count":50,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1998,10,1]]},"abstract":"<jats:p>Three classes of high-affinity Na<jats:sup>+<\/jats:sup>-P<jats:sub>i<\/jats:sub>cotransporters are expressed in mammalian kidney. These include Npt1 (type I), Npt2 (type II), and the cellular receptors for gibbon ape leukemia virus (Glvr-1) and amphotropic murine retrovirus (Ram-1) (type III). We defined the tissue distribution as well as the relative renal abundance of Npt1, Npt2, Glvr-1, and Ram-1 mRNAs and examined the effects of low-P<jats:sub>i<\/jats:sub>diet, the Hyp mutation, and growth hormone (GH) on their renal expression by ribonuclease protection assay. In normal mouse kidney, Npt1, Npt2, Glvr-1, and Ram-1 accounted for 15 \u00b1 1.0, 84 \u00b1 1.0, 0.5 \u00b1 0.2, and 0.5 \u00b1 0.3% of total Na<jats:sup>+<\/jats:sup>-P<jats:sub>i<\/jats:sub>cotransporter mRNAs, respectively. Evidence was obtained for low-abundance Npt1 mRNA expression in liver and Npt2 mRNA expression in intestine, whereas Glvr-1 and Ram-1 mRNAs were also detected in bone, intestine, heart, and liver. Npt2 mRNA was localized to proximal tubules in the renal outer cortex, whereas Glvr-1 transcripts were detected throughout the kidney by in situ hybridization. The Hyp mutation elicited a significant reduction in renal Npt1 and Npt2 mRNAs (78 \u00b1 8 and 57 \u00b1 3% of normal, respectively), whereas neither low-P<jats:sub>i<\/jats:sub>diet nor GH influenced the renal abundance of Npt1 and Npt2 transcripts. Renal Glvr-1 mRNA expression was significantly increased in Hyp mice and GH-treated mice (145 \u00b1 6 and 165 \u00b1 5% of control, respectively), whereas the renal abundance of Ram-1 transcript was unaffected by either the Hyp mutation, low-P<jats:sub>i<\/jats:sub>diet, or GH treatment. In summary, we demonstrate that Npt2 is the predominant Na<jats:sup>+<\/jats:sup>-P<jats:sub>i<\/jats:sub>cotransporter in mouse kidney, that Npt2 and Glvr-1 have distinct patterns of renal expression, and that the Hyp mutation modulates the renal expression of Npt1, Npt2, and Glvr-1 mRNAs. Our results suggest that increased renal Glvr-1 mRNA may contribute to GH stimulation of renal Na<jats:sup>+<\/jats:sup>-P<jats:sub>i<\/jats:sub>cotransport.<\/jats:p>","DOI":"10.1152\/ajprenal.1998.275.4.f527","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T16:39:30Z","timestamp":1514047170000},"page":"F527-F534","source":"Crossref","is-referenced-by-count":12,"title":["Differential expression, abundance, and regulation of Na<sup>+<\/sup>-phosphate cotransporter genes in murine kidney"],"prefix":"10.1152","volume":"275","author":[{"given":"Harriet S.","family":"Tenenhouse","sequence":"first","affiliation":[{"name":"Medical Research Council Genetics Group, McGill University-Montreal Children\u2019s Hospital Research Institute, Departments of Pediatrics and Biology, McGill University, Montreal, Quebec, Canada H3H 1P3"}]},{"given":"St\u00e9phane","family":"Roy","sequence":"additional","affiliation":[{"name":"Medical Research Council Genetics Group, McGill University-Montreal Children\u2019s Hospital Research Institute, Departments of Pediatrics and Biology, McGill University, Montreal, Quebec, Canada H3H 1P3"}]},{"given":"Jos\u00e9e","family":"Martel","sequence":"additional","affiliation":[{"name":"Medical Research Council Genetics Group, McGill University-Montreal Children\u2019s Hospital Research Institute, Departments of Pediatrics and Biology, McGill University, Montreal, Quebec, Canada H3H 1P3"}]},{"given":"Claude","family":"Gauthier","sequence":"additional","affiliation":[{"name":"Medical Research Council Genetics Group, McGill University-Montreal Children\u2019s Hospital Research Institute, Departments of Pediatrics and Biology, McGill University, Montreal, Quebec, Canada H3H 1P3"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.9.5372"},{"key":"B2","first-page":"936","volume":"431","author":"Beck L.","year":"1996","journal-title":"Pfl\u00fcgers Arch."},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119276"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1007\/BF00384344"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1007\/BF00584576"},{"issue":"37","key":"B7","first-page":"F1038","volume":"268","author":"Chong S. S.","year":"1995","journal-title":"Am. J. Physiol."},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1006\/geno.1993.1476"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1096\/fasebj.8.11.8070635"},{"key":"B10","first-page":"115","volume":"16","author":"Cross H. S.","year":"1990","journal-title":"Miner. Electrolyte Metab."},{"issue":"35","key":"B11","first-page":"F767","volume":"266","author":"Custer M.","year":"1994","journal-title":"Am. J. Physiol."},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1007\/BF00384343"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.73.12.4667"},{"key":"B15","first-page":"1259","volume":"76","author":"Goodyer C. G.","year":"1993","journal-title":"J. Clin. Endocrinol. Metab."},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2736(80)90378-8"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1007\/BF00386183"},{"key":"B18","first-page":"927","volume":"228","author":"Helps C.","year":"1995","journal-title":"J. Biochem."},{"issue":"43","key":"B19","first-page":"F197","volume":"274","author":"Hilfiker H.","year":"1998","journal-title":"Am. J. Physiol."},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1210\/endo.139.1.5664"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.135"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.91.15.7071"},{"issue":"37","key":"B23","first-page":"F784","volume":"268","author":"Kempson S. A.","year":"1995","journal-title":"Am. J. Physiol."},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1007\/BF00374664"},{"issue":"36","key":"B25","first-page":"F900","volume":"267","author":"Levi M.","year":"1994","journal-title":"Am. J. Physiol."},{"issue":"34","key":"B26","first-page":"E1021","volume":"271","author":"Li H.","year":"1996","journal-title":"Am. J. Physiol."},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119289"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.90.13.5979"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1042\/bj3270735"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1985.65.2.431"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.ph.58.030196.003135"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1991.260.5.C885"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1002\/jbmr.5650100909"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1007\/s002329900183"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1007\/s004240050573"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1359\/jbmr.1997.12.10.1672"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1210\/endo.137.7.8770917"},{"key":"B38","doi-asserted-by":"crossref","first-page":"6615","DOI":"10.1016\/S0021-9258(17)37417-3","volume":"269","author":"Sorribas V.","year":"1994","journal-title":"J. Biol. Chem."},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/6.2.165"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1359\/jbmr.1997.12.2.159"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1359\/jbmr.1998.13.4.590"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1172\/JCI114590"},{"issue":"24","key":"B43","first-page":"R373","volume":"255","author":"Tenenhouse H. S.","year":"1988","journal-title":"Am. J. Physiol."},{"issue":"37","key":"B44","first-page":"F1062","volume":"268","author":"Tenenhouse H. S.","year":"1995","journal-title":"Am. J. Physiol."},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1038\/281225a0"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1978.115"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117019"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1038\/ng1095-130"},{"issue":"37","key":"B49","first-page":"F626","volume":"268","author":"Verri T.","year":"1995","journal-title":"Am. J. Physiol."},{"key":"B50","doi-asserted-by":"crossref","first-page":"6637","DOI":"10.1016\/S0021-9258(17)37420-3","volume":"269","author":"Werner A.","year":"1994","journal-title":"J. Biol. Chem."},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.88.21.9608"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.109.2.217"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1998.275.4.F527","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:51:19Z","timestamp":1660189879000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1998.275.4.F527"}},"issued":{"date-parts":[[1998,10,1]]},"references-count":50,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1998,10,1]]}},"alternative-id":["10.1152\/ajprenal.1998.275.4.F527"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1998.275.4.f527","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1998,10,1]]}},{"indexed":{"date-parts":[[2023,12,15]],"date-time":"2023-12-15T15:00:41Z","timestamp":1702652441265},"reference-count":20,"publisher":"American Physiological Society","issue":"4","funder":[{"name":"National Institute of Health","award":["R01DK089066"],"award-info":[{"award-number":["R01DK089066"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2017,4,1]]},"DOI":"10.1152\/ajprenal.00648.2016","type":"journal-article","created":{"date-parts":[[2017,1,19]],"date-time":"2017-01-19T02:41:23Z","timestamp":1484793683000},"page":"F671-F672","source":"Crossref","is-referenced-by-count":6,"title":["A new microscope for the kidney: mathematics"],"prefix":"10.1152","volume":"312","author":[{"given":"Anita T.","family":"Layton","sequence":"first","affiliation":[{"name":"Department of Mathematics, Duke University, Durham, North Carolina"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00577.2014"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00681.2009"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00600.2014"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00334.2015"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00149.2014"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00230.2016"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00203.2010"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00263.2011"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00294.2016"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00007.2015"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00293.2016"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00543.2015"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00500.2013"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00539.2014"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-3495(83)84287-8"},{"key":"B16","first-page":"F860","volume":"250","author":"Weinstein AM","year":"1986","journal-title":"Am J Physiol"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00231.2009"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00232.2009"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00504.2014"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00505.2014"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00648.2016","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T06:09:12Z","timestamp":1568009352000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00648.2016"}},"issued":{"date-parts":[[2017,4,1]]},"references-count":20,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2017,4,1]]}},"alternative-id":["10.1152\/ajprenal.00648.2016"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00648.2016","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2017,4,1]]}},{"indexed":{"date-parts":[[2023,10,31]],"date-time":"2023-10-31T05:05:16Z","timestamp":1698728716077},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1996,5,1]]},"abstract":"<jats:p> The mechanism of tubular Mg transport was investigated in membrane vesicles (MV) of trout kidneys prepared by differential centrifugation with sucrose. MV consisted largely of brush-border membranes, as indicated by high enrichments of brush-border membrane enzymes. Although measured transport of 28 Mg included a binding component, most membrane transport was into or out of an osmotically active space. There was no evidence for amiloride-sensitive Na\/Mg exchange, nor was Mg uptake affected by the carboxyl group reagents trimethyloxonium tetrafluoroborate, glycine methyl ester.HCl-1-ethyl-3- (3-dimethyl-aminopropyl)carbodiimide, and N,N'-dicyclohexyl carbodiimide or the Ca channel modulators D-600, verapamil, diltiazem, and BAY K 8644. However, Mg uptake increased in the presence of inside-negative voltages generated by inward gradients of the permeant anions NO3, SCN, and Cl or by outward gradients of K (plus valinomycin). Alkaline-earth cations displayed the selectivity sequence VII (Mg &gt; Ca &gt; Sr &gt; Ba) for cis-inhibition of 28 Mg uptake. Mg efflux was trans-inhibited by La and Gd, and Mg uptake was cis-inhibited by Mn. The sulfhydryl group reagents p- chloromercuribenzoic acid and p-chloromercuriphenylsulfonate stimulated Mg uptake and efflux. These results reveal an electrodiffusive pathway for Mg transport in trout renal MV. <\/jats:p>","DOI":"10.1152\/ajprenal.1996.270.5.f739","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T01:59:33Z","timestamp":1513994373000},"page":"F739-F748","source":"Crossref","is-referenced-by-count":7,"title":["Electrodiffusive transport of Mg across renal membrane vesicles of the rainbow trout Oncorhynchus mykiss"],"prefix":"10.1152","volume":"270","author":[{"given":"C. A.","family":"Freire","sequence":"first","affiliation":[{"name":"Department of Epithelial Physiology, Max-Planck-Institute forMolecular Physiology, Dortmund, Germany."}]},{"given":"R. K.","family":"Kinne","sequence":"additional","affiliation":[{"name":"Department of Epithelial Physiology, Max-Planck-Institute forMolecular Physiology, Dortmund, Germany."}]},{"given":"E.","family":"Kinne-Saffran","sequence":"additional","affiliation":[{"name":"Department of Epithelial Physiology, Max-Planck-Institute forMolecular Physiology, Dortmund, Germany."}]},{"given":"K. W.","family":"Beyenbach","sequence":"additional","affiliation":[{"name":"Department of Epithelial Physiology, Max-Planck-Institute forMolecular Physiology, Dortmund, Germany."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1996.270.5.F739","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:08:20Z","timestamp":1567958900000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1996.270.5.F739"}},"issued":{"date-parts":[[1996,5,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1996,5,1]]}},"alternative-id":["10.1152\/ajprenal.1996.270.5.F739"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1996.270.5.f739","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1996,5,1]]}},{"indexed":{"date-parts":[[2022,4,4]],"date-time":"2022-04-04T10:18:55Z","timestamp":1649067535401},"reference-count":40,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2006,10]]},"abstract":"<jats:p>We used the mouse nephrin promoter to express a constitutively active G\u03b1q [G\u03b1q(Q&gt;L)] transgene in mice. As previously reported, the transgene was expressed in kidney, pancreas, and brain, and the kidney phenotype was characterized by albuminuria and reduced nephron mass. Additional studies revealed a second phenotype characterized by polyuria and polydipsia. The polyuric phenotype was not caused by abnormal glucose metabolism or hypercalcemia but was accompanied by reduced urinary concentrating ability. Additional studies found that 1) water restriction was associated with an appropriate increase in serum vasopressin levels in transgenic (TG) mice; 2) the urinary concentrating defect was not corrected by administration of desamino-d-arginine vasopressin (DDAVP); and 3) papillary length was similar in TG and non-TG mice. To examine the renal response to DDAVP at the molecular level, we monitored aquaporin 2 (AQP2) and vasopressin V2 receptor (V2R) mRNA levels in mouse kidney. Consistent with the known effects of vasopressin, administration of DDAVP caused a decrease in V2R mRNA levels and an increase in AQP2 mRNA levels in both TG and non-TG animals, suggesting an appropriate renal response to DDAVP in the TG mice. To determine whether the urine concentrating abnormality was the result of primary polydipsia, water intake by TG mice was restricted to the amount ingested by non-TG animals. After 5 days, urinary concentrating ability was similar in TG mice and non-TG littermate controls. These data are consistent with the notion that expression of the G\u03b1q(Q&gt;L) transgene in the brain induced primary polydipsia in the TG mice.<\/jats:p>","DOI":"10.1152\/ajprenal.00401.2005","type":"journal-article","created":{"date-parts":[[2006,4,12]],"date-time":"2006-04-12T01:53:55Z","timestamp":1144806835000},"page":"F781-F789","source":"Crossref","is-referenced-by-count":3,"title":["G\u03b1q-dependent signaling cascades stimulate water-seeking behavior"],"prefix":"10.1152","volume":"291","author":[{"given":"Liming","family":"Wang","sequence":"first","affiliation":[]},{"given":"Patrick J.","family":"Flannery","sequence":"additional","affiliation":[]},{"given":"Krairerk","family":"Athirakul","sequence":"additional","affiliation":[]},{"given":"Stephen R.","family":"Dunn","sequence":"additional","affiliation":[]},{"given":"Wissam M.","family":"Kourany","sequence":"additional","affiliation":[]},{"given":"Robert F.","family":"Spurney","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1081\/JDI-100101958"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1985.249.6.R643"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.17.5.720"},{"key":"R4","unstructured":"Carpenter MB.The hypothalamus. In:Core Text of Neuroanatomy, edited by Carpenter MB. Baltimore, MD: Williams and Wilkins, 1978."},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1997.272.1.H299"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/13.12.3043"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1172\/JCI23378"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1172\/JCI10022"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.bi.60.070191.003253"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00600.x"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1172\/JCI103462"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.86.8.2952"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.8.3521"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(92)80071-N"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.1996.tb02594.x"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1006\/frne.1997.0153"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.12.10.4687"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(12)80920-6"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1172\/JCI104567"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00450.x"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000019782.37851.BF"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1007\/978-3-642-55532-9_1"},{"key":"R23","doi-asserted-by":"crossref","unstructured":"McKinley MJand Johnson A.The physiological regulation of thirst and fluid intake.News Physiol Sci19: 1\u20136, 2004.","DOI":"10.1152\/nips.01470.2003"},{"key":"R24","unstructured":"Moeller JM, Kovari IA, and Holzman LB.Evaluation of a new tool for exploring podocyte biology: mouse Nphs1 5\u2032 flanking region drives LacZ expression in podocytes.J Am Soc Nephrol11: 2306\u20132314, 2000."},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1038\/351233a0"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.1.F75"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.ph.49.030187.002213"},{"key":"R28","unstructured":"Qadri FJ, Culman J, Veltmar A, Mass K, Rascher W, and Unger T.Angiotensin II-induced vasopressin release is mediated through alpha-1 adrenoceptors and angiotensin II AT1receptors in the supraoptic nucleus.J Pharmacol Exp Ther267: 567\u2013574, 1993."},{"key":"R29","doi-asserted-by":"crossref","unstructured":"Sandberg K, Ji H, Clark AJ, Shapira H, and Catt KJ.Cloning and expression of a novel angiotensin II receptor subtype.J Biol Chem267: 9455\u20139458, 1991.","DOI":"10.1016\/S0021-9258(19)50109-0"},{"key":"R30","unstructured":"Sanderberg KJH.Kidney angiotensin receptors, and their role in renal pathophysiology.Semin Nephrol20: 402\u2013416, 2000."},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1038\/351230a0"},{"key":"R32","doi-asserted-by":"crossref","unstructured":"Schmidt-Nielson Band O'Dell R.Structure and concentrating mechanism in the mammalian kidney.Am J Physiol200: 1119\u20131124, 1961.","DOI":"10.1152\/ajplegacy.1961.200.6.1119"},{"key":"R33","unstructured":"Schrier RWand Berl T.Disorders of water metabolism. In:Renal and Electrolyte Disorders, edited by Schrier RW. Boston, MA: Little, Brown, 1976."},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1988.254.3.C404"},{"key":"R35","doi-asserted-by":"crossref","unstructured":"Stork JE, Rahman MA, and Dunn MJ.Eicosanoids in experimental human renal disease.Am J Med80: 34\u201345, 1986.","DOI":"10.1016\/0002-9343(86)90930-7"},{"key":"R36","unstructured":"Streeten DH, Moses AM, and Miller M.Disorders of the neurohypophysis. In:Harrison's Principal of Internal Medicine(11th ed.), edited by Braunwald E, Isselbacher KJ, Petersdorf RG, Wilson JD, Martin JB, and Fauci AS. New York: McGraw-Hill, 1987."},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1172\/JCI116838"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1677\/jme.0.0200281"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005020167"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.01089.2003"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00401.2005","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,7,25]],"date-time":"2021-07-25T15:58:27Z","timestamp":1627228707000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00401.2005"}},"issued":{"date-parts":[[2006,10]]},"references-count":40,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2006,10]]}},"alternative-id":["10.1152\/ajprenal.00401.2005"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00401.2005","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2006,10]]}},{"indexed":{"date-parts":[[2022,4,4]],"date-time":"2022-04-04T15:14:12Z","timestamp":1649085252182},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1986,1,1]]},"abstract":"<jats:p> To assess the concept of compartmentalization of renal prostaglandins (PG), we compared entry of PGE2 and the PGI2 metabolite 6-keto-PGF1 alpha into the renal vascular and tubular compartments, in sodium pentobarbital-anesthetized dogs. Renal arterial 6-keto-PGF1 alpha infusion increased both renal venous and urinary 6-keto-PGF1 alpha outflow. In contrast, renal arterial infusion of arachidonic acid (AA) or bradykinin (BK) increased renal venous 6-keto-PGF1 alpha outflow but had no effect on its urinary outflow. Both urinary and renal venous PGE2 outflows increased during AA or BK infusion. Ureteral stopped-flow studies revealed no postglomerular 6-keto-PGF1 alpha entry into tubular fluid. During renal arterial infusion of [3H]PGI2 and inulin, first-pass 3H clearance was 40% of inulin clearance; 35% of urinary 3H was 6-keto-PGF1 alpha, and two other urinary metabolites were found. During renal arterial infusion of [3H]6-keto-PGF1 alpha and inulin, first-pass 3H clearance was 150% of inulin clearance; 75% of urinary 3H was 6-keto-PGF1 alpha, and only one other metabolite was found. We conclude that in the dog PGE2 synthesized in the kidney enters directly into both the renal vascular and tubular compartments, but 6-keto-PGF1 alpha of renal origin enters directly into only the renal vascular compartment. <\/jats:p>","DOI":"10.1152\/ajprenal.1986.250.1.f58","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T01:37:17Z","timestamp":1513993037000},"page":"F58-F65","source":"Crossref","is-referenced-by-count":0,"title":["PGI2 synthesis and excretion in dog kidney: evidence for renal PG compartmentalization"],"prefix":"10.1152","volume":"250","author":[{"given":"R. M.","family":"Boyd","sequence":"first","affiliation":[]},{"given":"A.","family":"Nasjletti","sequence":"additional","affiliation":[]},{"given":"P. M.","family":"Heerdt","sequence":"additional","affiliation":[]},{"given":"P. G.","family":"Baer","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1986.250.1.F58","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:37:41Z","timestamp":1567971461000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1986.250.1.F58"}},"issued":{"date-parts":[[1986,1,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1986,1,1]]}},"alternative-id":["10.1152\/ajprenal.1986.250.1.F58"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1986.250.1.f58","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1986,1,1]]}},{"indexed":{"date-parts":[[2022,4,4]],"date-time":"2022-04-04T16:11:08Z","timestamp":1649088668332},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1982,7,1]]},"abstract":"<jats:p> Changes in plasma potassium ([K+]p) and insulin levels were monitored during K+ infusion in awake and anesthetized nephrectomized, splenectomized dogs. In dogs studied while anesthetized with pentobarbital, the increase in [K+]p was linear, reflecting a nearly constant rate of cellular uptake of the infused K+. In contrast, in dogs studied 18 h after nephrectomy while awake, [K+]p oscillated during infusion, reflecting an inconstant rate of cellular K+ uptake. Although these oscillations in [K+]p were associated with parallel oscillations in plasma insulin levels (suggesting the possibility of a physiological feedback control loop involving K+ and insulin), when the oscillations in insulin levels were blunted by somatostatin infusion or abolished by pancreatectomy plus insulin replacement, oscillations in [K+]p persisted and the average rate of cellular K+ uptake was not diminished. The observed oscillations of [K+]p during K+ infusion suggest the possibility of regulatory control of cellular K+ uptake within the pathophysiologic range of [K+]p. The putative control system is independent of and quantitatively more important than K+-induced insulin secretion and is obscured by pentobarbital anesthesia. <\/jats:p>","DOI":"10.1152\/ajprenal.1982.243.1.f44","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T08:49:57Z","timestamp":1513932597000},"page":"F44-F52","source":"Crossref","is-referenced-by-count":2,"title":["Oscillations of plasma K+ and insulin during K+ infusion in awake anephric dogs"],"prefix":"10.1152","volume":"243","author":[{"given":"R. H.","family":"Sterns","sequence":"first","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1982.243.1.F44","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T14:15:45Z","timestamp":1567952145000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1982.243.1.F44"}},"issued":{"date-parts":[[1982,7,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1982,7,1]]}},"alternative-id":["10.1152\/ajprenal.1982.243.1.F44"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1982.243.1.f44","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1982,7,1]]}},{"indexed":{"date-parts":[[2022,4,6]],"date-time":"2022-04-06T03:13:34Z","timestamp":1649214814225},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1982,6,1]]},"abstract":"<jats:p> The formalism of linear nonequilibrium thermodynamics for a three-flow system was applied to the isolated frog corneal epithelium to study the coupling between metabolism and the Na-K transport system across this layer. There is little or no net ion transport across the isolated frog corneal epithelium bathed in Na2SO4 Ringer. Addition of amphotericin B to the tear side solution increases apical membrane permeability, which results in a net Na transport (from tear to stroma) and a net K transport in the opposite direction. Corneas were mounted in a modified Ussing chamber that permitted the simultaneous measurements of electrical parameters and O2 consumption by means of Clark-type oxygen electrodes. The overall degree of coupling, q, of the Na-K transport system to metabolism was calculated from measuring the suprabasal O2 consumption rate at \"static head\" and \"level flow\" conditions and by a second independent technique. Measurements of electrical conductance used in conjunction with other previously measured parameters allowed the calculation of the affinity, A, of the metabolic reaction driving transport, all phenomenological coefficients, and the electromotive forces of sodium (ENa) and potassium transport (EK). Values of q determined by the two techniques agreed (q = 0.80 and 0.84, respectively). This indicates incomplete coupling and a variable stoichiometric relationship among O2 consumption rate, net Na transport, and net K transport. The value calculated for A was 70.5 kcal.mol-1, for ENa 142.5 mV, and for EK -34.9 mV. <\/jats:p>","DOI":"10.1152\/ajprenal.1982.242.6.f690","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T13:27:56Z","timestamp":1513949276000},"page":"F690-F698","source":"Crossref","is-referenced-by-count":0,"title":["Thermodynamic analysis of active sodium and potassium transport in the frog corneal epithelium"],"prefix":"10.1152","volume":"242","author":[{"given":"O. A.","family":"Candia","sequence":"first","affiliation":[]},{"given":"P. S.","family":"Reinach","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1982.242.6.F690","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:16:03Z","timestamp":1567966563000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1982.242.6.F690"}},"issued":{"date-parts":[[1982,6,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1982,6,1]]}},"alternative-id":["10.1152\/ajprenal.1982.242.6.F690"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1982.242.6.f690","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1982,6,1]]}},{"indexed":{"date-parts":[[2024,5,12]],"date-time":"2024-05-12T21:26:28Z","timestamp":1715549188780},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1993,4,1]]},"abstract":"<jats:p> The present study examined the effects of atrial, brain, and C-type natriuretic peptides (ANP, BNP, and CNP, respectively) on endothelin-1 (ET-1) secretion after stimulation with arginine vasopressin (AVP), using cultured rat glomerular mesangial cells. AVP stimulated immunoreactive (ir) ET-1 secretion in a concentration-dependent manner via a receptor-mediated process. Rat ANP-(1-28) and rat BNP-45 potently inhibited this stimulated secretion in a concentration-dependent manner. Inhibition by ANP and BNP of AVP-stimulated ET-1 secretion was paralleled by an increase in the medium level of guanosine 3',5'-cyclic monophosphate (cGMP). The addition of a cGMP analogue, 8-bromo-cGMP, reduced the stimulated ET-1 secretion. CNP was much less effective than rat ANP-(1-28) or rat BNP-45 with respect to inhibiting irET-1 secretion and increasing cGMP levels. High-performance liquid chromatography indicated that the major component of irET-1 in the culture medium corresponds to ET-1-(1-21). These findings indicate that AVP stimulates ET-1 secretion in cultured rat mesangial cells and that rat ANP and BNP inhibit this stimulated secretion, probably through a cGMP-dependent process. <\/jats:p>","DOI":"10.1152\/ajprenal.1993.264.4.f678","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T10:24:58Z","timestamp":1514024698000},"page":"F678-F683","source":"Crossref","is-referenced-by-count":0,"title":["Natriuretic peptides inhibit mesangial cell production of endothelin induced by arginine vasopressin"],"prefix":"10.1152","volume":"264","author":[{"given":"M.","family":"Kohno","sequence":"first","affiliation":[{"name":"First Department of Internal Medicine, Osaka City University MedicalSchool, Japan."}]},{"given":"T.","family":"Horio","sequence":"additional","affiliation":[{"name":"First Department of Internal Medicine, Osaka City University MedicalSchool, Japan."}]},{"given":"M.","family":"Ikeda","sequence":"additional","affiliation":[{"name":"First Department of Internal Medicine, Osaka City University MedicalSchool, Japan."}]},{"given":"K.","family":"Yokokawa","sequence":"additional","affiliation":[{"name":"First Department of Internal Medicine, Osaka City University MedicalSchool, Japan."}]},{"given":"T.","family":"Fukui","sequence":"additional","affiliation":[{"name":"First Department of Internal Medicine, Osaka City University MedicalSchool, Japan."}]},{"given":"K.","family":"Yasunari","sequence":"additional","affiliation":[{"name":"First Department of Internal Medicine, Osaka City University MedicalSchool, Japan."}]},{"given":"K.","family":"Murakawa","sequence":"additional","affiliation":[{"name":"First Department of Internal Medicine, Osaka City University MedicalSchool, Japan."}]},{"given":"N.","family":"Kurihara","sequence":"additional","affiliation":[{"name":"First Department of Internal Medicine, Osaka City University MedicalSchool, Japan."}]},{"given":"T.","family":"Takeda","sequence":"additional","affiliation":[{"name":"First Department of Internal Medicine, Osaka City University MedicalSchool, Japan."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1993.264.4.F678","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:30:47Z","timestamp":1567974647000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1993.264.4.F678"}},"issued":{"date-parts":[[1993,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1993,4,1]]}},"alternative-id":["10.1152\/ajprenal.1993.264.4.F678"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1993.264.4.f678","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1993,4,1]]}},{"indexed":{"date-parts":[[2024,5,12]],"date-time":"2024-05-12T17:58:17Z","timestamp":1715536697830},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1988,9,1]]},"abstract":"<jats:p> This study examined whether the renal effects of atrial natriuretic factor (ANF) are mediated by dopamine1 (DA1) receptor activation. Intravenous infusion of low-dose ANF (0.0025 micrograms.kg-1.min-1) in euvolemic, pentobarbital sodium-anesthetized male mongrel dogs enhanced urine flow (V) by 71 +\/- 14% (mean +\/- SE) and urinary sodium excretion (UNaV) by 457 +\/- 172% (P less than 0.05). Renal blood flow (RBF) was unchanged. Administration of pharmacological doses of ANF (0.1 microgram.kg-1.min-1) into the renal artery in volume-expanded dogs increased RBF by 26 +\/- 6, V by 56 +\/- 15, and UNaV by 101 +\/- 42%. The selective DA1 receptor antagonist SCH-23390 (0.5 microgram.kg-1.min-1 iv) did not affect the response to ANF at either dose. The selective DA1 agonist, fenoldopam, increased RBF by 45 +\/- 3, V by 94 +\/- 27, and UNaV by 61 +\/- 15% in volume-expanded dogs. With SCH-23390, fenoldopam increased RBF by only 16 +\/- 6% whereas V and UNaV decreased by 16 +\/- 10 and 17 +\/- 10%, respectively. Accordingly, the failure of DA1 receptor-blocking doses of SCH-23390 to antagonize the response to ANF, at pharmacological or physiological doses, indicates that the renal effects of ANF, in the dog, are independent of DA1 receptor activation. <\/jats:p>","DOI":"10.1152\/ajprenal.1988.255.3.f494","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T16:21:03Z","timestamp":1513959663000},"page":"F494-F499","source":"Crossref","is-referenced-by-count":0,"title":["Renal effects of atrial natriuretic factor are independent of dopamine1 receptors"],"prefix":"10.1152","volume":"255","author":[{"given":"M. B.","family":"Murphy","sequence":"first","affiliation":[{"name":"Department of Pharmacological and Physiological Sciences, University of Chicago, Illinois 60637."}]},{"given":"A. S.","family":"Bass","sequence":"additional","affiliation":[{"name":"Department of Pharmacological and Physiological Sciences, University of Chicago, Illinois 60637."}]},{"given":"L. I.","family":"Goldberg","sequence":"additional","affiliation":[{"name":"Department of Pharmacological and Physiological Sciences, University of Chicago, Illinois 60637."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1988.255.3.F494","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:09:27Z","timestamp":1567955367000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1988.255.3.F494"}},"issued":{"date-parts":[[1988,9,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1988,9,1]]}},"alternative-id":["10.1152\/ajprenal.1988.255.3.F494"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1988.255.3.f494","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1988,9,1]]}},{"indexed":{"date-parts":[[2024,5,12]],"date-time":"2024-05-12T17:53:08Z","timestamp":1715536388189},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1986,10,1]]},"abstract":"<jats:p> Animals and humans undergoing a chronic treatment with cyclosporin A (CyA) show a reduction in glomerular filtration rate (GFR). The cause of this abnormality has not been established. Since CyA interferes with arachidonic acid (AA) metabolism in various cells, we wished to determine whether alterations in renal AA metabolites contribute to deteriorating renal function in rats on CyA. We show that chronic CyA treatment induces a progressive increase in the renal synthesis of thromboxane (TX) A2. This is a selective abnormality in that CyA does not influence the renal synthesis of prostaglandin E2 (PGE2) and prostacyclin (PGI2). A significant negative correlation has been found between TXB2 urinary excretion rate and inulin clearance. No correlation has been observed between TXB2 excretion and p-aminohippuric acid clearance. The withdrawal of CyA is followed by a normalization of both TXB2 urinary excretion rate and GFR. The administration of a selective TXA2 inhibitor, UK-38,485, resulted in a significant reduction in urinary excretion of TXB2 accompanied by a significant increase in GFR. We conclude that chronic treatment with CyA in rats is associated with a selective increase in renal TXA2 synthesis and suggest that this abnormality may play a role in the reduction of GFR. <\/jats:p>","DOI":"10.1152\/ajprenal.1986.251.4.f581","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T00:55:07Z","timestamp":1513990507000},"page":"F581-F587","source":"Crossref","is-referenced-by-count":1,"title":["Functional significance of exaggerated renal thromboxane A2 synthesis induced by cyclosporin A"],"prefix":"10.1152","volume":"251","author":[{"given":"N.","family":"Perico","sequence":"first","affiliation":[]},{"given":"A.","family":"Benigni","sequence":"additional","affiliation":[]},{"given":"C.","family":"Zoja","sequence":"additional","affiliation":[]},{"given":"F.","family":"Delaini","sequence":"additional","affiliation":[]},{"given":"G.","family":"Remuzzi","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1986.251.4.F581","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:34:07Z","timestamp":1567971247000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1986.251.4.F581"}},"issued":{"date-parts":[[1986,10,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1986,10,1]]}},"alternative-id":["10.1152\/ajprenal.1986.251.4.F581"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1986.251.4.f581","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1986,10,1]]}},{"indexed":{"date-parts":[[2024,5,12]],"date-time":"2024-05-12T17:30:48Z","timestamp":1715535048331},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1979,5,1]]},"abstract":"<jats:p> Experiments were designed to clarify the factors affecting renin released during in vitro experiments. Kidneys from rat, dog, and pig were used. Experiments were done in which the gas phase was either bubbled through the incubation medium or layered above it. Renin released into the incubation medium disappeared very rapidly when gas was bubbled through the medium. The decline was similar in mediums bubbled with oxygen-CO2 (95%--5%) or nitrogen-CO2 (95%--5%). The half-life of renin activity in the bubbled medium was approximately 15 min in both cases. However, in experiments in which nonbubbled medium was used throughout, renin released into the incubation medium did not disappear after removal of slices. These data are interpreted to mean that the renin released into the incubation medium is inactivated at the air-water interface. <\/jats:p>","DOI":"10.1152\/ajprenal.1979.236.5.f501","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T20:34:10Z","timestamp":1513974850000},"page":"F501-F504","source":"Crossref","is-referenced-by-count":0,"title":["Renin inactivation during in vitro experiments"],"prefix":"10.1152","volume":"236","author":[{"given":"K. W.","family":"Cho","sequence":"first","affiliation":[]},{"given":"R. L.","family":"Malvin","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1979.236.5.F501","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:00:56Z","timestamp":1567969256000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1979.236.5.F501"}},"issued":{"date-parts":[[1979,5,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1979,5,1]]}},"alternative-id":["10.1152\/ajprenal.1979.236.5.F501"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1979.236.5.f501","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1979,5,1]]}},{"indexed":{"date-parts":[[2024,5,12]],"date-time":"2024-05-12T18:14:57Z","timestamp":1715537697724},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1988,4,1]]},"abstract":"<jats:p> Previous studies have shown that renal interstitial volume expansion (RIVE) increases renal interstitial hydrostatic pressure and urinary sodium excretion. In the present study we investigated whether blockade of prostaglandin synthesis inhibits the increase in fractional sodium excretion induced by RIVE. Expansion of the renal interstitial volume was achieved by injecting 50 microliters of 2.5% albumin solution into a polyethylene matrix chronically implanted in the left kidney. Fractional sodium excretion (FENa), renal interstitial hydrostatic pressure (PI), and urinary prostaglandin excretion (UPGE2) were measured before and after RIVE in eight control, seven meclofenamate-treated, and eight indomethacin-treated rats. RIVE in the control animals resulted in significant increases in PI (delta + 4.2 +\/- 0.8 mmHg), in FENa (delta + 1.02 +\/- 0.27%), and in UPGE2 (% delta + 150 +\/- 38%) without significant changes in glomerular filtration rate. Inhibition of prostaglandin synthesis with meclofenamate or indomethacin attenuated the natriuretic response and blocked the increase in UPGE2 associated with RIVE. In summary, direct increases in renal interstitial hydrostatic pressure increase UPGE2 and urinary sodium excretion. This natriuretic response is markedly diminished by inhibition of prostaglandin synthesis. These studies suggest that prostaglandin synthesis may have an important role in mediating the natriuretic effect of increased renal interstitial hydrostatic pressure during renal interstitial volume expansion. <\/jats:p>","DOI":"10.1152\/ajprenal.1988.254.4.f507","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T03:22:12Z","timestamp":1513999332000},"page":"F507-F511","source":"Crossref","is-referenced-by-count":1,"title":["Prostaglandin blockade blunts the natriuresis of elevated renal interstitial hydrostatic pressure"],"prefix":"10.1152","volume":"254","author":[{"given":"D.","family":"Pawlowska","sequence":"first","affiliation":[{"name":"Department of Physiology and Biophysics, Mayo Clinic and Foundation, Rochester, Minnesota 55905."}]},{"given":"J. A.","family":"Haas","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, Mayo Clinic and Foundation, Rochester, Minnesota 55905."}]},{"given":"J. P.","family":"Granger","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, Mayo Clinic and Foundation, Rochester, Minnesota 55905."}]},{"given":"J. C.","family":"Romero","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, Mayo Clinic and Foundation, Rochester, Minnesota 55905."}]},{"given":"F. G.","family":"Knox","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, Mayo Clinic and Foundation, Rochester, Minnesota 55905."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1988.254.4.F507","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:50:04Z","timestamp":1567972204000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1988.254.4.F507"}},"issued":{"date-parts":[[1988,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1988,4,1]]}},"alternative-id":["10.1152\/ajprenal.1988.254.4.F507"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1988.254.4.f507","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1988,4,1]]}},{"indexed":{"date-parts":[[2024,5,12]],"date-time":"2024-05-12T18:15:09Z","timestamp":1715537709038},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1985,10,1]]},"abstract":"<jats:p> The contribution of the renal nerves in maintaining blood pressure and modulating renal prostanoid synthesis was examined in established (less than 8 wk in duration) one-kidney, one-clip (1K,1C) hypertension in the rat. Systolic blood pressure was measured for 7 days after renal denervation, at which time the renal artery clip was removed. Twenty-four-hour urinary excretion of PGE2 and 6-keto-PGF1 alpha (stable degradation product of PGI2) was determined before and after denervation and unclipping. Compared with sham-denervated rats, denervation (n = 15) resulted in a small but significant fall in blood pressure (from 216 +\/- 4 to 182 +\/- 4 mmHg after 48 h) and an increase in urinary 6-keto-PGF1 alpha (from 31 +\/- 4 to 43 +\/- 5 ng\/24 h after 24 h). There was no change in PGE2 excretion. Seven days after surgery, blood pressures were similar in denervated (202 +\/- 4 mmHg) and sham-denervated (211 +\/- 5 mmHg) rats and fell to a similar extent 24 h after unclipping (142 +\/- 3 and 147 +\/- 4 mmHg, respectively). Urinary 6-keto-PGF1 alpha increased from 25 +\/- 5 to 74 +\/- 11 in denervated and 21 +\/- 2 to 72 +\/- 9 ng\/24 h in sham-denervated rats in the 24 h after unclipping. PGE2 excretion increased approximately twofold over this period. These findings indicate that the renal nerves have only a minor role in established hypertension in the 1K,1C rat and that the reversal of hypertension and stimulation of renal prostanoid synthesis following unclipping is not dependent on neural mechanisms. <\/jats:p>","DOI":"10.1152\/ajprenal.1985.249.4.f542","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T23:57:54Z","timestamp":1513987074000},"page":"F542-F545","source":"Crossref","is-referenced-by-count":1,"title":["Renal prostanoids after unclipping the denervated one-kidney, one-clip hypertensive rat"],"prefix":"10.1152","volume":"249","author":[{"given":"R.","family":"Vandongen","sequence":"first","affiliation":[]},{"given":"H.","family":"McGowan","sequence":"additional","affiliation":[]},{"given":"H.","family":"Anderson","sequence":"additional","affiliation":[]},{"given":"A.","family":"Barden","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1985.249.4.F542","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:29:30Z","timestamp":1567970970000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1985.249.4.F542"}},"issued":{"date-parts":[[1985,10,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1985,10,1]]}},"alternative-id":["10.1152\/ajprenal.1985.249.4.F542"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1985.249.4.f542","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1985,10,1]]}},{"indexed":{"date-parts":[[2024,5,12]],"date-time":"2024-05-12T19:19:40Z","timestamp":1715541580872},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1980,8,1]]},"DOI":"10.1152\/ajprenal.1980.239.2.f187","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T13:17:30Z","timestamp":1513948650000},"page":"F187-F193","source":"Crossref","is-referenced-by-count":0,"title":["Nephron heterogeneity in renal excretion of sodium and potassium in the rat"],"prefix":"10.1152","volume":"239","author":[{"given":"H. J.","family":"Reineck","sequence":"first","affiliation":[]},{"given":"R.","family":"Parma","sequence":"additional","affiliation":[]},{"given":"J. L.","family":"Barnes","sequence":"additional","affiliation":[]},{"given":"R. W.","family":"Osgood","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1980.239.2.F187","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:14:44Z","timestamp":1567966484000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1980.239.2.F187"}},"issued":{"date-parts":[[1980,8,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1980,8,1]]}},"alternative-id":["10.1152\/ajprenal.1980.239.2.F187"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1980.239.2.f187","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1980,8,1]]}},{"indexed":{"date-parts":[[2024,5,12]],"date-time":"2024-05-12T17:54:03Z","timestamp":1715536443417},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1980,8,1]]},"DOI":"10.1152\/ajprenal.1980.239.2.f97","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T13:17:30Z","timestamp":1513948650000},"page":"F97-F106","source":"Crossref","is-referenced-by-count":1,"title":["The renal sodium pump and vanadate"],"prefix":"10.1152","volume":"239","author":[{"given":"J. J.","family":"Grantham","sequence":"first","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1980.239.2.F97","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:14:36Z","timestamp":1567966476000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1980.239.2.F97"}},"issued":{"date-parts":[[1980,8,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1980,8,1]]}},"alternative-id":["10.1152\/ajprenal.1980.239.2.F97"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1980.239.2.f97","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1980,8,1]]}},{"indexed":{"date-parts":[[2024,7,18]],"date-time":"2024-07-18T09:48:54Z","timestamp":1721296134644},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1985,6,1]]},"abstract":"<jats:p> The effects of arachidonic acid, prostaglandins (PG) I2, E2, D2, and F2 alpha on norepinephrine- (NE) and angiotensin II- (ANG II) induced tone were examined in interlobular arteries and afferent and efferent arterioles isolated from rabbit kidney. Arachidonic acid at 10(-5) M produced a rapid relaxation of NE-induced tone in all three vessel types. The vasodilatory effect of arachidonic acid but not acetylcholine was blocked by meclofenamate. In interlobular arteries, PGE2, and PGI2 caused a dose-dependent relaxation of NE-induced tone with a concentration causing the half-maximal response (ED50) of 1.2 and 4.6 X 10(-8) M, respectively. PGD2 caused a small but significant relaxation at 10(-7) M and above, whereas PGF2 alpha was inactive. In afferent arterioles contracted with NE, PGE2 and PGI2 caused identical dose-dependent relaxations. Significant effects were observed at concentrations between 10(-11) and 10(-10) M with ED50 values of 1.7 X 10(-8) M for PGE2 and 8.7 X 10(-9) M for PGI2. PGD2 had significant effects only at 10(-5) M, whereas PGF2 alpha was without effect. In contrast to the preglomerular vessels, efferent arterioles responded only to PGI2 (ED50, 9.7 X 10(-9) M), and the other arachidonic acid metabolites had no effect on lumen diameter. PGI2 antagonized the vasoconstrictive effects of both NE and ANG II in this vessel segment. The results demonstrate that of the prostanoids tested only PGE2 and PGI2 were effective in antagonizing vasoconstrictor stimuli in isolated renal microvessels. Furthermore, the rabbit renal microvasculature displays segmental heterogeneity for the vasodilatory PGs in that PGI2 affected both pre- and postglomerular arterioles, whereas PGE2 was effective only on the preglomerular microvessels. <\/jats:p>","DOI":"10.1152\/ajprenal.1985.248.6.f779","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T00:41:19Z","timestamp":1513989679000},"page":"F779-F784","source":"Crossref","is-referenced-by-count":22,"title":["Effects of prostaglandins on vasoconstrictor action in isolated renal arterioles"],"prefix":"10.1152","volume":"248","author":[{"given":"R. M.","family":"Edwards","sequence":"first","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1985.248.6.F779","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:32:26Z","timestamp":1567971146000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1985.248.6.F779"}},"issued":{"date-parts":[[1985,6,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1985,6,1]]}},"alternative-id":["10.1152\/ajprenal.1985.248.6.F779"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1985.248.6.f779","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1985,6,1]]}},{"indexed":{"date-parts":[[2023,11,21]],"date-time":"2023-11-21T20:59:08Z","timestamp":1700600348171},"reference-count":33,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1998,6,1]]},"abstract":"<jats:p>Effects of extracellular ATP on intracellular free calcium concentration ([Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>) were examined in rat single nephron segments using the fura 2-AM. ATP (10 \u03bcM) induced a significant transient increase in [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>in the glomerulus, the early proximal convoluted tubule (S1), the cortical collecting tubule (CCT), and the outer medullary collecting tubule (OMCT). The magnitude of the response was the greatest in the OMCT among four segments. ATP induced an increase in the [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>in a dose-dependent manner in S1 and OMCT. In the OMCT, ATP caused a biphasic increase in [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>consisting of an initial rapid rise and a sustained phase. Removal of calcium from the medium resulted in an attenuation of the sustained phase of [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>and an \u223c30% reduction in the height of the initial [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>peak in response to 10 \u03bcM ATP. Effects of ATP, its analogs, and its metabolites were tested in the S1 and OMCT. ATP, 2-methylthio-ATP (2-MeS-ATP), ADP, and UTP increased [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>dose dependently. AMP and adenosine did not affect [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>in the S1 and OMCT. The ATP- or 2-MeS-ATP-induced [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>increase was inhibited by the pretreatment of the S1 and OMCT with suramin or reactive blue 2. Neomycin, a phospholipase C inhibitor, attenuated the ATP-induced [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>increase. To investigate the hormonelike action of ATP in OMCT, a heterologous cross desensitization was performed. The pretreatment of OMCT with ATP inhibited increases in vasopressin-, ANG II-, endothelin-1-, or bradykinin-induced [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>increase. These findings suggest that ATP might affect the above peptidyl agonist-activated calcium mobilizations.<\/jats:p>","DOI":"10.1152\/ajprenal.1998.274.6.f1006","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T15:24:19Z","timestamp":1514042659000},"page":"F1006-F1014","source":"Crossref","is-referenced-by-count":20,"title":["P2 purinoceptor localization along rat nephron and evidence suggesting existence of subtypes P2Y<sub>1<\/sub>and P2Y<sub>2<\/sub>"],"prefix":"10.1152","volume":"274","author":[{"given":"Seok Ho","family":"Cha","sequence":"first","affiliation":[{"name":"Department of Pharmacology and Toxicology, Kyorin University School of Medicine, Mitaka, Tokyo 181, Japan"}]},{"given":"Takashi","family":"Sekine","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, Kyorin University School of Medicine, Mitaka, Tokyo 181, Japan"}]},{"given":"Hitoshi","family":"Endou","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, Kyorin University School of Medicine, Mitaka, Tokyo 181, Japan"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115191"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.25.6.1224"},{"issue":"35","key":"B3","first-page":"F210","volume":"266","author":"Briner V. A.","year":"1994","journal-title":"Am. J. Physiol."},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.1990.tb37657.x"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1995.1835"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2760(82)90252-1"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1929.sp002608"},{"issue":"36","key":"B8","first-page":"F998","volume":"267","author":"Ecelbarger C. A.","year":"1994","journal-title":"Am. J. Physiol."},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/0167-4889(92)90025-7"},{"key":"B10","doi-asserted-by":"crossref","first-page":"20351","DOI":"10.1016\/S0021-9258(17)30510-0","volume":"265","author":"Fasolato C.","year":"1990","journal-title":"J. Biol. Chem."},{"issue":"40","key":"B11","first-page":"F610","volume":"271","author":"Firestein B. L.","year":"1996","journal-title":"Am. J. Physiol."},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.84.16.5630"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1042\/bj2330309"},{"key":"B14","doi-asserted-by":"crossref","first-page":"3440","DOI":"10.1016\/S0021-9258(19)83641-4","volume":"260","author":"Grynkiewicz G.","year":"1985","journal-title":"J. Biol. Chem."},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1993.265.4.C966"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/0014-2999(88)90642-5"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.1991.tb12216.x"},{"issue":"23","key":"B18","first-page":"F240","volume":"254","author":"Jones S. M.","year":"1988","journal-title":"Am. J. Physiol."},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-291X(05)80078-6"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/0165-6147(91)90587-I"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/0006-291X(92)90538-V"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.90.11.5113"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.1990.tb12052.x"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1016\/S0079-6123(08)61746-X"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1016\/S0959-4388(97)80062-1"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1126\/science.272.5262.735"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1042\/bj2720469"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1995.1798"},{"key":"B29","first-page":"2962","volume":"50","author":"Umemura S.","year":"1992","journal-title":"Nihonrinsho"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1038\/371516a0"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(93)81397-I"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1007\/BF00580712"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.1995.tb13312.x"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1998.274.6.F1006","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:48:10Z","timestamp":1660189690000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1998.274.6.F1006"}},"issued":{"date-parts":[[1998,6,1]]},"references-count":33,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1998,6,1]]}},"alternative-id":["10.1152\/ajprenal.1998.274.6.F1006"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1998.274.6.f1006","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1998,6,1]]}},{"indexed":{"date-parts":[[2023,10,25]],"date-time":"2023-10-25T10:59:50Z","timestamp":1698231590700},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1989,11,1]]},"abstract":"<jats:p> Continuous-flow colorimetric methods for measurement of sodium and potassium contents in 1- to 30-nl aqueous samples are described. The methods employ macrocyclic ionophores (cryptahemispherands) that selectively bind sodium or potassium, altering the absorbance spectra of covalently attached chromophores. The potassium method is linear in the range 0-350 pmol and exhibits a high degree of precision (coefficient of variation of approximately 2% in the 150- to 350-pmol range). It can detect as little as 8 pmol of K+. The sodium method is linear in the range 0-2,700 pmol and also exhibits a high degree of precision (coefficient of variation of approximately 3% in the 1,700- to 2,700-pmol range). It can detect as little as 57 pmol of Na+. The instrumentation and reagents are available from commercial sources. These methods are proposed for measurement of K+ and Na+ fluxes in isolated perfused tubules. <\/jats:p>","DOI":"10.1152\/ajprenal.1989.257.5.f893","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T22:07:26Z","timestamp":1513980446000},"page":"F893-F898","source":"Crossref","is-referenced-by-count":2,"title":["Continuous-flow quantitation of Na+ and K+ in nanoliter samples using chromogenic macrocyclic ionophores"],"prefix":"10.1152","volume":"257","author":[{"given":"Y.","family":"Terada","sequence":"first","affiliation":[{"name":"Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lungand Blood Institute, Bethesda, Maryland 20892."}]},{"given":"M. A.","family":"Knepper","sequence":"additional","affiliation":[{"name":"Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lungand Blood Institute, Bethesda, Maryland 20892."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1989.257.5.F893","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:15:09Z","timestamp":1567970109000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1989.257.5.F893"}},"issued":{"date-parts":[[1989,11,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1989,11,1]]}},"alternative-id":["10.1152\/ajprenal.1989.257.5.F893"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1989.257.5.f893","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1989,11,1]]}},{"indexed":{"date-parts":[[2024,5,16]],"date-time":"2024-05-16T05:09:23Z","timestamp":1715836163013},"reference-count":43,"publisher":"American Physiological Society","issue":"7","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2012,4,1]]},"abstract":"<jats:p>Recent anatomic findings indicate that in the upper inner medulla of the rodent kidney, tubules, and vessels are organized around clusters of collecting ducts (CDs). Within CD clusters, CDs and some of the ascending vasa recta (AVR) and ascending thin limbs (ATLs), when viewed in transverse sections, form interstitial nodal spaces, which are arrayed at structured intervals throughout the inner medulla. These spaces, or microdomains, are bordered on one side by a single CD, on the opposite side by one or more ATLs, and on the other two sides by AVR. To study the interactions among these CDs, ATLs, and AVR, we have developed a mathematical compartment model, which simulates steady-state solute exchange through the microdomain at a given inner medullary level. Fluid in all compartments contains Na<jats:sup>+<\/jats:sup>, Cl<jats:sup>\u2212<\/jats:sup>, urea and, in the microdomain, negative fixed charges that represent macromolecules (e.g., hyaluronan) balanced by Na<jats:sup>+<\/jats:sup>. Fluid entry into AVR is assumed to be driven by hydraulic and oncotic pressures. Model results suggest that the isolated microdomains facilitate solute and fluid mixing among the CDs, ATLs, and AVR, promote water withdrawal from CDs, and consequently may play an important role in generating the inner medullary osmotic gradient.<\/jats:p>","DOI":"10.1152\/ajprenal.00539.2011","type":"journal-article","created":{"date-parts":[[2011,12,8]],"date-time":"2011-12-08T05:05:28Z","timestamp":1323320728000},"page":"F830-F839","source":"Crossref","is-referenced-by-count":13,"title":["Isolated interstitial nodal spaces may facilitate preferential solute and fluid mixing in the rat renal inner medulla"],"prefix":"10.1152","volume":"302","author":[{"given":"Anita T.","family":"Layton","sequence":"first","affiliation":[{"name":"Department of Mathematics, Duke University, Durham, North Carolina; and"}]},{"given":"Rebecca L.","family":"Gilbert","sequence":"additional","affiliation":[{"name":"Department of Physiology, College of Medicine, University of Arizona, Tuscon, Arizona"}]},{"given":"Thomas L.","family":"Pannabecker","sequence":"additional","affiliation":[{"name":"Department of Physiology, College of Medicine, University of Arizona, Tuscon, Arizona"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1007\/BF00583730"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1002\/aja.1001180302"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1172\/JCI105898"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.263.3.F417"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.264.2.F337"},{"key":"B6","doi-asserted-by":"crossref","first-page":"970.","DOI":"10.1096\/fasebj.23.1_supplement.970.3","volume":"23","author":"Dantzler WH","year":"2009","journal-title":"FASEB J"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.2010.02214.x"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00218.x"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.256.1.F63"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1978.235.3.F192"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1084\/jem.171.6.2063"},{"key":"B12","first-page":"1677- 1688","volume":"2","author":"Han JS","year":"1992","journal-title":"J Am Soc Nephrol"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2000.00378.x"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.53.3.401"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1172\/JCI108633"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00072.2010"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1977.118"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00067.2002"},{"key":"B19","first-page":"587","volume-title":"The Kidney: Physiology and Pathophysiology (3rd ed.)","author":"Kriz W","year":"2000"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1007\/BF01870733"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00203.2010"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8240(03)00045-4"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00346.2003"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/physiol.00013.2009"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.1998.529bw.x"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1113\/expphysiol.1998.sp004089"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1995.sp020869"},{"key":"B28","doi-asserted-by":"crossref","first-page":"824","DOI":"10.1152\/ajplegacy.1970.218.3.824","volume":"218","author":"Marsh DJ","year":"1970","journal-title":"Am J Physiol"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1172\/JCI116948"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00285.2003"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00481.2005"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00231.2007"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90252.2008"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00068.2008"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1981.104"},{"key":"B36","doi-asserted-by":"crossref","first-page":"1921","DOI":"10.1152\/ajplegacy.1975.228.6.1921","volume":"228","author":"Sanjana VM","year":"1975","journal-title":"Am J Physiol"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1982.220"},{"key":"B38","first-page":"70","volume":"25","author":"Schmidt-Nielsen B","year":"1985","journal-title":"Bull MDIBL"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1007\/BF00313964"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1038\/nrc1391"},{"key":"B41","doi-asserted-by":"crossref","first-page":"694","DOI":"10.1152\/ajplegacy.1964.206.4.694","volume":"206","author":"Windhager EE","year":"1964","journal-title":"Am J Physiol"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00071.2010"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.281.3.F478"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00539.2011","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,12,19]],"date-time":"2021-12-19T08:27:16Z","timestamp":1639902436000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00539.2011"}},"issued":{"date-parts":[[2012,4,1]]},"references-count":43,"journal-issue":{"issue":"7","published-print":{"date-parts":[[2012,4,1]]}},"alternative-id":["10.1152\/ajprenal.00539.2011"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00539.2011","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2012,4,1]]}},{"indexed":{"date-parts":[[2024,4,10]],"date-time":"2024-04-10T05:13:18Z","timestamp":1712725998946},"reference-count":14,"publisher":"American Physiological Society","issue":"7","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2014,4,1]]},"DOI":"10.1152\/ajprenal.00681.2013","type":"journal-article","created":{"date-parts":[[2014,1,16]],"date-time":"2014-01-16T05:08:36Z","timestamp":1389848916000},"page":"F721-F723","source":"Crossref","is-referenced-by-count":2,"title":["Two Rhesus protein ammonia transporters team up to eliminate ammonium into urine"],"prefix":"10.1152","volume":"306","author":[{"given":"Carsten A.","family":"Wagner","sequence":"first","affiliation":[{"name":"Institute of Physiology, University of Zurich, Zurich, Switzerland"}]},{"given":"Soline","family":"Bourgeois","sequence":"additional","affiliation":[{"name":"Institute of Physiology, University of Zurich, Zurich, Switzerland"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00301.2012"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/nature07518"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M112.441782"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00172.2005"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/B978-012088488-9.50059-0"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1007\/s00232-013-9593-0"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00176.2013"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/81656"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1217775110"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2010.386"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-009-0657-z"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.6.F866"},{"key":"B13","doi-asserted-by":"crossref","first-page":"827","DOI":"10.1681\/ASN.V134827","volume":"13","author":"Wall SM","year":"2002","journal-title":"J Am Soc Nephrol"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00554.2010"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00681.2013","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,3,23]],"date-time":"2022-03-23T19:40:32Z","timestamp":1648064432000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00681.2013"}},"issued":{"date-parts":[[2014,4,1]]},"references-count":14,"journal-issue":{"issue":"7","published-print":{"date-parts":[[2014,4,1]]}},"alternative-id":["10.1152\/ajprenal.00681.2013"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00681.2013","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2014,4,1]]}},{"indexed":{"date-parts":[[2024,6,17]],"date-time":"2024-06-17T19:55:54Z","timestamp":1718654154618},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1995,3,1]]},"abstract":"<jats:p> An apical, hormone-regulated, calcium entry channel in the distal convoluted tubule and\/or connecting tubule (DCT\/CNT) is thought to play an important role in controlling renal calcium excretion. We previously identified a gene transcript encoding the pore-forming alpha 1-subunit of a calcium channel (alpha 1A, or CaCh4) which may be a candidate for such a molecule. The properties of voltage-dependent calcium channels are known to be modulated by their beta-subunits. To identify the accessory beta-subunit of DCT\/CNT calcium channels, degenerate primers based on published beta-subunit sequences were used to amplify rat kidney cDNA by the polymerase chain reaction (PCR), and the products were subcloned and sequenced. Alternatively spliced transcripts of three beta-subunit genes (beta 2, beta 3, and beta 4) were identified. Northern blot analysis indicated that beta 4-subunit is preferentially expressed in kidney cortex. Transcripts of all three beta-subunit genes were detected by PCR in microdissected nephron segments, but only beta 4-subunit was found in DCT\/CNT. As the beta 4- and alpha 1A-subunits colocalize to the DCT\/CNT, we hypothesize that they may be constituent subunits of a renal calcium channel regulated by a hormone(s). <\/jats:p>","DOI":"10.1152\/ajprenal.1995.268.3.f525","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T04:08:46Z","timestamp":1514002126000},"page":"F525-F531","source":"Crossref","is-referenced-by-count":6,"title":["Molecular characterization of renal calcium channel beta-subunit transcripts"],"prefix":"10.1152","volume":"268","author":[{"given":"A. S.","family":"Yu","sequence":"first","affiliation":[{"name":"Department of Medicine, Brigham and Women's Hospital, Boston,Massachusetts 02115."}]},{"given":"M.","family":"Boim","sequence":"additional","affiliation":[{"name":"Department of Medicine, Brigham and Women's Hospital, Boston,Massachusetts 02115."}]},{"given":"S. C.","family":"Hebert","sequence":"additional","affiliation":[{"name":"Department of Medicine, Brigham and Women's Hospital, Boston,Massachusetts 02115."}]},{"given":"A.","family":"Castellano","sequence":"additional","affiliation":[{"name":"Department of Medicine, Brigham and Women's Hospital, Boston,Massachusetts 02115."}]},{"given":"E.","family":"Perez-Reyes","sequence":"additional","affiliation":[{"name":"Department of Medicine, Brigham and Women's Hospital, Boston,Massachusetts 02115."}]},{"given":"J.","family":"Lytton","sequence":"additional","affiliation":[{"name":"Department of Medicine, Brigham and Women's Hospital, Boston,Massachusetts 02115."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1995.268.3.F525","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:54:26Z","timestamp":1567972466000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1995.268.3.F525"}},"issued":{"date-parts":[[1995,3,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1995,3,1]]}},"alternative-id":["10.1152\/ajprenal.1995.268.3.F525"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1995.268.3.f525","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1995,3,1]]}},{"indexed":{"date-parts":[[2024,6,17]],"date-time":"2024-06-17T19:55:54Z","timestamp":1718654154856},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1979,6,1]]},"abstract":"<jats:p> The in vivo microperfusion technique was employed to examine urate absorption in the proximal convoluted tubule of the rat kidney using [2\u201314C]urate as the marker for fractional urate absorption. With NaCl as the perfusion solution, water absorption averaged 2.53 +\/- 0.16 nl.min-1.mm tubule-1, and the fractional absorption of [2\u201314C]urate averages 11.6 +\/- 1.0%\/mm tubule. The addition of D-glucose (50 mg\/100 ml) enhanced water absorption to 3.62 +\/- 0.19 nl.min-1.mm tubule-1, but inhibited fractional urate absorption to 6.6 +\/- 1.2%\/mm tubule. Phloridzin (4.4 mg\/100 ml), 2-deoxy-D-glucose (45.6 mg\/100 ml), and 3-O-methyl-D-glucose (53.9 mg\/100 ml) also inhibited the absorption of [2\u201314C]urate to the same degree as did D-glucose despite differing effects on water absorption. The addition of probenecid (2.8 mg\/100 ml) to the NaCl perfusion solution had no effect on water absorption but inhibited [2\u201314C]urate absorption to 6.4 +\/- 0.6%\/mm tubule. The addition of both probenecid and phloridzin further reduced [2\u201314C-A1urate absorption to 3.8 +\/- 0.7%\/mm tubule. Probenecid alone had no effect on glucose transport. These studies suggest that the presence of either certain hexose sugars, phloridzin, or probenecid in the lumen of the proximal convoluted tubule inhibits the tubular absorption of urate. <\/jats:p>","DOI":"10.1152\/ajprenal.1979.236.6.f526","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T15:35:14Z","timestamp":1513956914000},"page":"F526-F529","source":"Crossref","is-referenced-by-count":4,"title":["Effects of intraluminal D-glucose and probenecid on urate absorption in the rat proximal tubule"],"prefix":"10.1152","volume":"236","author":[{"given":"T. F.","family":"Knight","sequence":"first","affiliation":[]},{"given":"H. O.","family":"Senekjian","sequence":"additional","affiliation":[]},{"given":"S.","family":"Sansom","sequence":"additional","affiliation":[]},{"given":"E. J.","family":"Weinman","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1979.236.6.F526","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:01:54Z","timestamp":1567954914000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1979.236.6.F526"}},"issued":{"date-parts":[[1979,6,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1979,6,1]]}},"alternative-id":["10.1152\/ajprenal.1979.236.6.F526"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1979.236.6.f526","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1979,6,1]]}},{"indexed":{"date-parts":[[2024,6,17]],"date-time":"2024-06-17T17:24:40Z","timestamp":1718645080872},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1996,9,1]]},"abstract":"<jats:p> We recently cloned extracellular Ca(2+)-sensing receptors (CaRs) from bovine parathyroid and rat kidney that play key roles in Ca2+ homeostasis. Inactivating mutations of the CaR in the inherited human disorder, familial hypocalciuric hypercalcemia, cause reduced responsiveness of the parathyroid to extracellular Ca2+ (Cao2+), as well as abnormally avid renal tubular reabsorption of both Ca2+ and Mg2+ in the distal tubule, suggesting an important role for the CaR in regulating parathyroid hormone (PTH) secretion and renal handling of divalent cations. High Cao2+ also inhibits vasopressinstimulated adenosine 3',5'-cyclic monophosphate accumulation in the medullary thick ascending limb (MTAL) and water reabsorption in the collecting duct (CD) and modulates various other aspects of renal function. The relevance of the CaR to these processes, however, is uncertain. Reduced responsiveness of vasopressin-and PTH-mediated actions on the kidney have been described in the newborn that could potentially reflect effects of the CaR on these aspects of renal function. To define further the role of the CaR in regulating renal function, including the above-mentioned changes during the perinatal period, therefore, we have studied its ontogeny in rat kidney. Northern and Western blot analyses, as well as immunohistochemistry with CaR-specific probes, demonstrate that there is little prenatal expression of the extracellular Ca(2+)-sensing receptor, except in large tubules and branching ureteric buds of developing nephrons. Postnatally, CaR mRNA and protein increase markedly during the 1st wk, related principally to expression of the receptor in the developing TAL and, to a lesser extent, in the CD. The level of expression of the receptor remains nearly constant after postnatal day 14. These results demonstrate that the perinatal increases in expression of CaR mRNA and protein parallel its tissue-specific renal expression. Furthermore, it is possible that some of the previously described changes in renal handling of divalent cations and water in the perinatal and immediate postnatal period are related, in part, to the increasing levels of expression of the CaR and resultant inhibitory effects on the actions of PTH and antidiuretic hormone on the developing nephron. <\/jats:p>","DOI":"10.1152\/ajprenal.1996.271.3.f736","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T06:31:13Z","timestamp":1514010673000},"page":"F736-F743","source":"Crossref","is-referenced-by-count":16,"title":["Ontogeny of the extracellular calcium-sensing receptor in rat kidney"],"prefix":"10.1152","volume":"271","author":[{"given":"N.","family":"Chattopadhyay","sequence":"first","affiliation":[{"name":"Department of Medicine, Brigham and Women's Hospital, Boston,Massachusetts, USA."}]},{"given":"M.","family":"Baum","sequence":"additional","affiliation":[{"name":"Department of Medicine, Brigham and Women's Hospital, Boston,Massachusetts, USA."}]},{"given":"M.","family":"Bai","sequence":"additional","affiliation":[{"name":"Department of Medicine, Brigham and Women's Hospital, Boston,Massachusetts, USA."}]},{"given":"D.","family":"Riccardi","sequence":"additional","affiliation":[{"name":"Department of Medicine, Brigham and Women's Hospital, Boston,Massachusetts, USA."}]},{"given":"S. C.","family":"Hebert","sequence":"additional","affiliation":[{"name":"Department of Medicine, Brigham and Women's Hospital, Boston,Massachusetts, USA."}]},{"given":"H. W.","family":"Harris","sequence":"additional","affiliation":[{"name":"Department of Medicine, Brigham and Women's Hospital, Boston,Massachusetts, USA."}]},{"given":"E. M.","family":"Brown","sequence":"additional","affiliation":[{"name":"Department of Medicine, Brigham and Women's Hospital, Boston,Massachusetts, USA."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1996.271.3.F736","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:06:06Z","timestamp":1567973166000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1996.271.3.F736"}},"issued":{"date-parts":[[1996,9,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1996,9,1]]}},"alternative-id":["10.1152\/ajprenal.1996.271.3.F736"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1996.271.3.f736","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1996,9,1]]}},{"indexed":{"date-parts":[[2024,6,17]],"date-time":"2024-06-17T20:37:56Z","timestamp":1718656676822},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1990,2,1]]},"abstract":"<jats:p> We examined the effect of cell swelling on intracellular free calcium concentration ([Ca]i) in cultured toad bladder cells (TB-M) grown as a polarized monolayer on collagen-coated filters. [Ca]i was measured by use of fura-2, fluorescence microscopy, and simple video imaging. In preliminary experiments we determined that reducing ionic strength by 15% had no effect on the Kd of fura-2, indicating that the dye could be used to examine the effects of cell swelling on [Ca]i. Reducing the osmolality of the serosal bathing medium by 15% caused [Ca]i to increase within 10 s from 97 +\/- 9 to 354 +\/- 88 nM (n = 5). By 2 min [Ca]i had declined to 163 +\/- 22 nM. The increase in [Ca]i was not caused by a fall in Na concentration ([Na]) because isosmotic reduction of serosal [Na] did not result in an increase in [Ca]i. The swelling-induced increase in [Ca]i could be abolished by lowering serosal [Ca] to 200 nM and by addition of lanthanum. The calcium-channel blockers nitrendipine and verapamil also inhibited the swelling-induced increase in [Ca]i, although to different degrees. These experiments demonstrate that swelling of cultured toad bladder cells results in a significant increase in [Ca]i by enhancing the rate of calcium entry across the basolateral membrane, possibly through a calcium channel. <\/jats:p>","DOI":"10.1152\/ajprenal.1990.258.2.f292","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T21:33:17Z","timestamp":1513978397000},"page":"F292-F296","source":"Crossref","is-referenced-by-count":6,"title":["Cell swelling increases intracellular free [Ca] in cultured toad bladder cells"],"prefix":"10.1152","volume":"258","author":[{"given":"S. M.","family":"Wong","sequence":"first","affiliation":[{"name":"Department of Medicine, Columbia University, College of Physicians andSurgeons, New York, New York 10032."}]},{"given":"M. C.","family":"DeBell","sequence":"additional","affiliation":[{"name":"Department of Medicine, Columbia University, College of Physicians andSurgeons, New York, New York 10032."}]},{"suffix":"Jr","given":"H. S.","family":"Chase","sequence":"additional","affiliation":[{"name":"Department of Medicine, Columbia University, College of Physicians andSurgeons, New York, New York 10032."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1990.258.2.F292","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:11:48Z","timestamp":1567969908000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1990.258.2.F292"}},"issued":{"date-parts":[[1990,2,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1990,2,1]]}},"alternative-id":["10.1152\/ajprenal.1990.258.2.F292"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1990.258.2.f292","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1990,2,1]]}},{"indexed":{"date-parts":[[2024,6,17]],"date-time":"2024-06-17T20:38:01Z","timestamp":1718656681533},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1988,5,1]]},"abstract":"<jats:p> The present in vitro microperfusion study examined whether apical membrane chloride transport is mediated by chloride-base exchange in the rabbit proximal convoluted (PCT) and proximal straight tubule (PST) by examining the effect of the addition of luminal chloride on intracellular pH. Intracellular pH was measured fluorometrically using the pH-sensitive dye 2',7'-bis(carboxyethyl)-5,6-carboxyfluorescein. In PCT initially perfused without chloride, changing the luminal perfusate to a high chloride (148 mM)-low bicarbonate (5 mM) solution simulating late proximal tubular fluid produced a cell acidification (7.56 +\/- 0.06 to 7.52 +\/- 0.06, P less than 0.02) when 1 mM formate was present in the perfusate and bathing solution. This acidification was inhibited by 0.5 mM 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid. This chloride-base exchange was not observed in the absence of formate, and neither acetate nor lactate produced the cell acidification observed with formate. Because the Na+-H+ antiporter could blunt a pH change, 2 mM amiloride was added to the luminal perfusate. While addition of luminal chloride produced a small cell acidification in the absence of formate (7.63 +\/- 0.06 to 7.60 +\/- 0.05, P less than 0.05), a much greater cell acidification was observed in the presence of 1 mM formate (7.69 +\/- 0.05 to 7.58 +\/- 0.06, P less than 0.01). Chloride-base exchange was only detected in the presence of formate in the PST. These studies demonstrate apical membrane chloride-base exchange in the presence of formate in the rabbit proximal tubule consistent with chloride-formate exchange. <\/jats:p>","DOI":"10.1152\/ajprenal.1988.254.5.f677","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T03:22:43Z","timestamp":1513999363000},"page":"F677-F683","source":"Crossref","is-referenced-by-count":3,"title":["Effect of luminal chloride on cell pH in rabbit proximal tubule"],"prefix":"10.1152","volume":"254","author":[{"given":"M.","family":"Baum","sequence":"first","affiliation":[{"name":"Department of Pediatrics, University of Texas Health Science Center,Dallas 75235."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1988.254.5.F677","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:51:08Z","timestamp":1567972268000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1988.254.5.F677"}},"issued":{"date-parts":[[1988,5,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1988,5,1]]}},"alternative-id":["10.1152\/ajprenal.1988.254.5.F677"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1988.254.5.f677","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1988,5,1]]}},{"indexed":{"date-parts":[[2024,6,17]],"date-time":"2024-06-17T20:38:50Z","timestamp":1718656730780},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1993,1,1]]},"abstract":"<jats:p> The Shaker gene family encodes voltage-gated K channels. Five partial-length Shaker-like cDNAs (KC2, 4, 10, 19, and 22) were previously isolated from rabbit kidney using polymerase chain reaction (PCR) [G. V. Desir, E. Hamlin, A.H. Puente, R.F. Reilly, F. Hiledebrandt, and P. Igarashi. Am. J. Physiol. 262 (Renal Fluid Electrolyte Physiol. 31): F151-F157, 1992]. We now report the cloning of another Shaker-like cDNA (KC6) from rabbit kidney and the identification of one isoform that is highly expressed in rabbit distal tubule cells grown in culture. A partial-length cDNA (859 bp) for KC6 was isolated by PCR amplification of rabbit kidney cDNA using Shaker-specific degenerate primers. KC6 was most similar to the rat brain clone RBK2 (77% amino acid identity) and to the rabbit clone KC19 (78% amino acid identity). Transcript levels for KC2, 4, 6, 10, 19, and 22 were quantified using the ribonuclease protection assay. Transcripts for all six isoforms were detected in renal tissues. KC22 was the most abundant isoform in kidney cortex and medulla (20- to 40-fold greater than the other isoforms). Furthermore, KC22 expression levels were fivefold higher in primary cultures of rabbit distal convoluted tubules and connecting tubules than in whole kidney cortex. Although the partial-length sequence for KC22 represents the most conserved regions in the Shaker gene family it only has 35-88% amino acid identity with other Shaker channels, suggesting that KC22 represents a novel isoform. In contrast, KC4 and KC19 (less abundant in kidney than KC22) are highly homologous to the rat brain clones RBK1 and RBK2, respectively (97% amino acid identity).(ABSTRACT TRUNCATED AT 250 WORDS) <\/jats:p>","DOI":"10.1152\/ajprenal.1993.264.1.f128","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T09:34:43Z","timestamp":1514021683000},"page":"F128-F133","source":"Crossref","is-referenced-by-count":3,"title":["Identification of a novel K-channel gene (KC22) that is highly expressed in distal tubule of rabbit kidney"],"prefix":"10.1152","volume":"264","author":[{"given":"G. V.","family":"Desir","sequence":"first","affiliation":[{"name":"Department of Medicine, Yale University School of Medicine, New Haven,Connecticut 06510."}]},{"given":"H.","family":"Velazquez","sequence":"additional","affiliation":[{"name":"Department of Medicine, Yale University School of Medicine, New Haven,Connecticut 06510."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1993.264.1.F128","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:22:48Z","timestamp":1567974168000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1993.264.1.F128"}},"issued":{"date-parts":[[1993,1,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1993,1,1]]}},"alternative-id":["10.1152\/ajprenal.1993.264.1.F128"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1993.264.1.f128","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1993,1,1]]}},{"indexed":{"date-parts":[[2024,6,17]],"date-time":"2024-06-17T20:35:33Z","timestamp":1718656533874},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1989,6,1]]},"abstract":"<jats:p> Prostaglandin (PG) activation of the phosphoinositol transduction pathway in MDCK cells and modulation of this process by phorbol esters was studied by monitoring changes in cytosolic free Ca2+ concentration, [Cai2+], with the Ca2+-sensitive fluorescent probe, fura-2 and measurement of stimulation of inositol phosphates by anion-exchange chromatography. Cells challenged with PGE1 or PGE2 responded with a prompt and transient increase in [Cai2+] that was independent of extracellular Ca2+. The K0.5 for PGE2 for the process was 6.1 X 10(-7) M. PGE1 and PGE2 appeared to be recognized by a common receptor. PGF2 alpha was without effect. 8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate (TMB-8) but not verapamil, a Ca2+ channel inhibitor, blocked the PGE2-evoked Ca2+ transient. Under identical conditions PGE2 increased inositol phosphate accumulation by 54 +\/- 8% (inositol-1-monophosphate), 23 +\/- 6% (inositol-1,4-bisphosphate), and 49 +\/- 3% (total inositol trisphosphate), above control values. Brief (30-60 s) exposure of cells to phorbol-12,13-myristate (PMA) or phorbol-12,13-dibutyrate (PDB) completely blocked the PGE2-induced Ca2+ transient. The K0.5 for the process for PMA and PDB was 0.3 +\/- 0.1 and 4.5 +\/- 2.2 nM, respectively. Neither 4 alpha-nor 4 beta-phorbol, which lack the ability to activate protein kinase C, were effective in this regard. In contrast to complete blockade by 10(-8) PMA of the PGE2 (10(-5) M)-elicited Ca2+ transient, this concentration of PMA inhibited the Ca2+ transient evoked by 10(-9) M bradykinin (BK) by 50%. In fact 10(-4) M PMA only partially blocked the BK-elicited Ca2+ transient. In summary, in MDCK cells, the PG receptor is coupled both to the adenylate cyclase system and inositol phospholipid transduction pathway. The PG receptor appears to be regulated by protein kinase C. In addition to protein kinase C other factors regulate the BK receptor. <\/jats:p>","DOI":"10.1152\/ajprenal.1989.256.6.f1135","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T15:49:59Z","timestamp":1513957799000},"page":"F1135-F1143","source":"Crossref","is-referenced-by-count":2,"title":["Differential effects of phorbol esters on PGE2 and bradykinin-induced elevation of [Cai2+] in MDCK cells"],"prefix":"10.1152","volume":"256","author":[{"given":"A.","family":"Aboolian","sequence":"first","affiliation":[{"name":"Department of Medicine, School of Medicine, State University of NewYork, Stony Brook 11794."}]},{"given":"M.","family":"Vander Molen","sequence":"additional","affiliation":[{"name":"Department of Medicine, School of Medicine, State University of NewYork, Stony Brook 11794."}]},{"given":"E. P.","family":"Nord","sequence":"additional","affiliation":[{"name":"Department of Medicine, School of Medicine, State University of NewYork, Stony Brook 11794."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1989.256.6.F1135","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:06:11Z","timestamp":1567955171000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1989.256.6.F1135"}},"issued":{"date-parts":[[1989,6,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1989,6,1]]}},"alternative-id":["10.1152\/ajprenal.1989.256.6.F1135"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1989.256.6.f1135","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1989,6,1]]}},{"indexed":{"date-parts":[[2024,6,17]],"date-time":"2024-06-17T20:33:45Z","timestamp":1718656425833},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1987,5,1]]},"abstract":"<jats:p> Volume regulation in the perfused proximal nephron of the rabbit was examined quantitatively with a computer-based method for estimating cell volume from differential interference-contrast microscopic images of isolated nephron segments. Following a hyperosmotic challenge (290-390 mosmol), the cells shrank as simple osmometers without a subsequent regulatory volume increase. Conversely, cell swelling induced by a hyposmotic challenge (290-190 mosmol) was completely reversed with a triphasic time course in which a rapid (less than 2 min) initial volume decline was followed by secondary swelling and shrinking phases. A similar regulatory volume decrease was observed following isosmotic cell swelling that was induced by exposure to 290 mosmol, urea-containing solutions. In addition, the cells partially reversed isosmotic swelling that was induced by the luminal replacement of a relatively impermeant cation (i.e., choline) with Na+ and a concomitant increase in luminal solute entry. Our results support two conclusions. First, there exist quantitative differences between the volume regulatory behaviors of perfused and nonperfused proximal tubules, the latter of which exhibit an incomplete and monotonic reversal of hyposmotic cell swelling (M. Dellasega and J. Grantham, Am. J. Physiol. 224: 1288-1294, 1973). Second, the primary physiological role of cell volume regulation in the proximal nephron may be to minimize isosmotic cell swelling associated with acute imbalances in the rates of cell solute entry and exit. <\/jats:p>","DOI":"10.1152\/ajprenal.1987.252.5.f922","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T21:33:29Z","timestamp":1513978409000},"page":"F922-F932","source":"Crossref","is-referenced-by-count":4,"title":["Cell volume regulation in rabbit proximal straight tubule perfused in vitro"],"prefix":"10.1152","volume":"252","author":[{"given":"K. L.","family":"Kirk","sequence":"first","affiliation":[]},{"given":"J. A.","family":"Schafer","sequence":"additional","affiliation":[]},{"given":"D. R.","family":"DiBona","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1987.252.5.F922","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:45:15Z","timestamp":1567957515000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1987.252.5.F922"}},"issued":{"date-parts":[[1987,5,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1987,5,1]]}},"alternative-id":["10.1152\/ajprenal.1987.252.5.F922"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1987.252.5.f922","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1987,5,1]]}},{"indexed":{"date-parts":[[2024,6,17]],"date-time":"2024-06-17T20:31:34Z","timestamp":1718656294133},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1990,7,1]]},"abstract":"<jats:p> Sustained exposure to aldosterone (Aldo) increases the abundance and activity of the Na-K pump in cortical collecting tubules (CCT). However, the onset and mechanism of the early interaction of Aldo with the CCT pump, especially in adrenal-intact animals, are unclear. We evaluated the short-term effects of the hormone on Na-K-adenosinetriphosphatase (ATPase) activity and on ouabain-sensitive 86Rb uptake, a measure of the transporting rate of the pump, in microdissected CCT from adrenal-intact rats. Incubation with Aldo (10(-8) M, 2 h) had no effect on Na-K-ATPase activity (Vmax), whereas it produced at least a twofold increase in 86Rb uptake. This effect was generated by physiological concentrations of the hormone (threshold 10(-10) M; apparent K1\/2 approximately 10(-9) M), after a short lag of less than or equal to 30 min. Incubation with Aldo in the presence of amiloride or nystatin or in a Na-free medium (choline chloride) did not prevent the enhanced 86Rb uptake seen after Aldo alone; possible interpretations of these observations are discussed. We conclude that Aldo produces a rapid stimulation of pump function in CCT that precedes its induction of new pump synthesis; the physiological significance of this effect is suggested by its occurrence in tubules from adrenal-intact animals within the time frame and concentration range of the hormone's effects on electrolyte transport. <\/jats:p>","DOI":"10.1152\/ajprenal.1990.259.1.f40","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T17:23:09Z","timestamp":1513963389000},"page":"F40-F45","source":"Crossref","is-referenced-by-count":15,"title":["Early effects of aldosterone on Na-K pump in rat cortical collecting tubules"],"prefix":"10.1152","volume":"259","author":[{"given":"Y.","family":"Fujii","sequence":"first","affiliation":[{"name":"Department of Medicine, University of Chicago Pritzker School of Medicine, Illinois 60637."}]},{"given":"F.","family":"Takemoto","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Chicago Pritzker School of Medicine, Illinois 60637."}]},{"given":"A. I.","family":"Katz","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Chicago Pritzker School of Medicine, Illinois 60637."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1990.259.1.F40","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:17:05Z","timestamp":1567955825000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1990.259.1.F40"}},"issued":{"date-parts":[[1990,7,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1990,7,1]]}},"alternative-id":["10.1152\/ajprenal.1990.259.1.F40"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1990.259.1.f40","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1990,7,1]]}},{"indexed":{"date-parts":[[2024,6,17]],"date-time":"2024-06-17T19:54:12Z","timestamp":1718654052484},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1997,6,1]]},"abstract":"<jats:p> Previous studies from this laboratory have demonstrated that the 3\u201334 analog of parathyroid hormone (PTH) causes a 15\u201330% inhibition of Na(+)-K(+)-adenosinetriphosphatase (Na(+)-K(+)-ATPase) activity in rat renal proximal tubules through the generation of an increase in intracellular arachidonic acid, followed by its conversion to 20-hydroxyeicosatetraenoic acid (20-HETE) [C. P. Ribeiro and L. J. Mandel. Am. J. Physiol. 262 (Renal Fluid Electrolyte Physiol. 31): F209-F216, 1992; and C. P. Ribeiro, G. Dubay, J. R. Falk, and L. J. Mandel. Am. J. Physiol. 266 (Renal Fluid Electrolyte Physiol. 35): F497-F505, 1994]. The present study also uses proximal tubule suspensions to further elucidate this signaling pathway. Guanosine 5'-O-(2-thiodiphosphate), 500 microM, an inhibitor of heterotrimeric GTP-binding proteins (G proteins), and an anti-Gq\/G11 antibody (1:500) both blocked the inhibition of the Na(+)-K(+)-ATPase by PTH-(3\u201334). Furthermore, a 42-kDa protein was identified in proximal tubules by the anti-Gq\/G11 antibody (1:1,000). Bromoenol lactone (BEL), 1 microM, a suicide inhibitor of the calcium-independent 40-kDa phospholipase A2 (PLA2), prevented PTH-(3\u201334) inhibition of the Na(+)-K(+)-ATPase, unless exogenous 10 microM 20-HETE was added. In addition, BEL blocked the PTH-(3\u201334)-induced increase in arachidonic acid release in the proximal tubules. We conclude that a member of the Gq family and the calcium-independent 40-kDa PLA2 participate in the PTH-(3\u201334) signaling pathway in rat proximal tubules by mediating the steps between the binding of PTH-(3\u201334) to its receptor and the subsequent generation of arachidonic acid. <\/jats:p>","DOI":"10.1152\/ajprenal.1997.272.6.f781","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T07:50:33Z","timestamp":1514015433000},"page":"F781-F788","source":"Crossref","is-referenced-by-count":13,"title":["Parathyroid hormone inhibits Na(+)-K(+)-ATPase through Gq\/G11 and the calcium-independent phospholipase A2"],"prefix":"10.1152","volume":"272","author":[{"given":"B. H.","family":"Derrickson","sequence":"first","affiliation":[{"name":"Department of Cell Biology, Duke University, Durham, North Carolina 27710, USA."}]},{"given":"L. J.","family":"Mandel","sequence":"additional","affiliation":[{"name":"Department of Cell Biology, Duke University, Durham, North Carolina 27710, USA."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1997.272.6.F781","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:12:05Z","timestamp":1567973525000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1997.272.6.F781"}},"issued":{"date-parts":[[1997,6,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1997,6,1]]}},"alternative-id":["10.1152\/ajprenal.1997.272.6.F781"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1997.272.6.f781","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1997,6,1]]}},{"indexed":{"date-parts":[[2024,7,3]],"date-time":"2024-07-03T15:13:11Z","timestamp":1720019591880},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1980,11,1]]},"abstract":"<jats:p> Synthesis of prostaglandin E2 (PGE2) by rabbit bladder was examined. PGE2 synthesis was assessed by thin-layer chromatographic analysis after conversion of [14C]-arachidonic acid to [14C]PGE2 or by a specific radioimmunoassay technique. Intact bladder and microsomes prepared from the bladder transitional epithelium (mucosal) layer and the outer vesicular layer demonstrated synthesis of PGE2. PGE2 synthesis was increased by arachidonic acid and blocked by indomethacin. When the inside medium (bathing the transitional epithelium) contained [14C]arachidonic acid, no detectable radioactivity was observed in the outside medium (bathing the outer layer). Conversely, when the outside medium contained [14C]arachidonic acid, no detectable radioactivity was observed in the inside medium. In addition, [14C]arachidonic acid was incorporated only into tissue directly exposed to bathing media containing the label. These results demonstrate that the rabbit bladder can synthesize PGE2 and that the PGE2- synthesizing systems of the transitional epithelium and outer layer of bladder may be distinct. <\/jats:p>","DOI":"10.1152\/ajprenal.1980.239.5.f452","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T13:01:10Z","timestamp":1513947670000},"page":"F452-F458","source":"Crossref","is-referenced-by-count":5,"title":["Prostaglandin E2 production by rabbit urinary bladder"],"prefix":"10.1152","volume":"239","author":[{"given":"W. W.","family":"Brown","sequence":"first","affiliation":[]},{"given":"T. V.","family":"Zenser","sequence":"additional","affiliation":[]},{"given":"B. B.","family":"Davis","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1980.239.5.F452","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:15:09Z","timestamp":1567966509000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1980.239.5.F452"}},"issued":{"date-parts":[[1980,11,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1980,11,1]]}},"alternative-id":["10.1152\/ajprenal.1980.239.5.F452"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1980.239.5.f452","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1980,11,1]]}},{"indexed":{"date-parts":[[2023,9,28]],"date-time":"2023-09-28T04:56:29Z","timestamp":1695876989718},"reference-count":13,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2008,11]]},"DOI":"10.1152\/ajprenal.90506.2008","type":"journal-article","created":{"date-parts":[[2008,9,4]],"date-time":"2008-09-04T00:24:23Z","timestamp":1220487863000},"page":"F1301-F1302","source":"Crossref","is-referenced-by-count":9,"title":["Shuttling of calcium between endoplasmic reticulum and mitochondria in the renal vasculature"],"prefix":"10.1152","volume":"295","author":[{"given":"Yashpal S.","family":"Kanwar","sequence":"first","affiliation":[]},{"given":"Lin","family":"Sun","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1993.sp019489"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1126\/science.1083628"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1152\/physiol.00017.2007"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1990.70.2.391"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.07716.x"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.03254"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90343.2008"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(93)81423-W"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1016\/j.ceca.2006.08.015"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M505024200"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1097\/01.mog.0000239863.96833.c0"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2007.01.008"},{"key":"R13","unstructured":"Ziyadeh FN. Mediators of diabetic renal disease: the case for TGF-\u03b2 as the major mediator. J Am Soc Nephrol 1: S55\u2013S57, 2004."}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.90506.2008","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T23:02:37Z","timestamp":1567983757000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.90506.2008"}},"issued":{"date-parts":[[2008,11]]},"references-count":13,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2008,11]]}},"alternative-id":["10.1152\/ajprenal.90506.2008"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.90506.2008","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2008,11]]}},{"indexed":{"date-parts":[[2024,7,2]],"date-time":"2024-07-02T18:33:54Z","timestamp":1719945234791},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1995,4,1]]},"abstract":"<jats:p> The role of prostanoids in renal function remains unclear, as inhibitors of cyclooxygenase (COX) have contrasting effects. We postulated that these inconsistencies were related to differential effects of the prevailing chloride concentration on COX-dependent mechanisms. In oncotically perfused rat kidneys, in the presence of either high (117 mM) or low (87 mM) chloride with sodium held constant, low chloride resulted in a higher glomerular filtration rate (GFR) than with high chloride, i.e., 1.2 +\/- 0.2 and 0.5 +\/- 0.1 ml\/min, respectively, for the last clearance period. Water and electrolyte excretion and levels of immunoassayable prostaglandins were higher with low chloride. Indomethacin (10 microM) had opposite effects on renal function depending on the chloride levels, although prostaglandin release was inhibited similarly. For example, indomethacin substantially reduced the elevated urine flow and sodium excretion in the low-chloride group, which, by the last period, were reduced from 111 +\/- 32 to 37 +\/- 3 microliters\/min and 8.3 +\/- 2.9 to 3.1 +\/- 0.6 mu eq\/min, respectively, whereas the lower urine flow and sodium excretion in the high-chloride group increased from 32 +\/- 8 to 109 +\/- 15 microliters\/min and 2.5 +\/- 0.8 to 7.1 +\/- 1.6 mu eq\/min, respectively. In summary, inhibition of COX has differential effects depending on the prevailing chloride concentration, or conversely, high and low chloride have contrasting effects on renal function, which are reversed by COX inhibition. We suggest that prohypertensive and antihypertensive COX-dependent mechanisms are linked to chloride; the latter is an integral component in the development of salt-sensitive hypertension. <\/jats:p>","DOI":"10.1152\/ajprenal.1995.268.4.f561","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T06:23:42Z","timestamp":1514010222000},"page":"F561-F568","source":"Crossref","is-referenced-by-count":2,"title":["Role of chloride in the variable response of the kidney to cyclooxygenase inhibition"],"prefix":"10.1152","volume":"268","author":[{"given":"K.","family":"Yin","sequence":"first","affiliation":[{"name":"Department of Pharmacology, New York Medical College, Valhalla 10595, USA."}]},{"given":"J. C.","family":"McGiff","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, New York Medical College, Valhalla 10595, USA."}]},{"given":"C. P.","family":"Bell-Quilley","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, New York Medical College, Valhalla 10595, USA."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1995.268.4.F561","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:02:06Z","timestamp":1567972926000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1995.268.4.F561"}},"issued":{"date-parts":[[1995,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1995,4,1]]}},"alternative-id":["10.1152\/ajprenal.1995.268.4.F561"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1995.268.4.f561","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1995,4,1]]}},{"indexed":{"date-parts":[[2024,7,18]],"date-time":"2024-07-18T01:33:46Z","timestamp":1721266426585},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1990,8,1]]},"abstract":"<jats:p> We investigated effects of various agents on proliferation, intracellular pH (pHi), and intracellular calcium [( Ca2+]i) of rat mesangial cells (MCs) in early passages (2-5). Serum-starved MCs incubated in HCO3- were exposed to one of the following: fetal calf serum (FCS), serotonin, angiotensin II (ANG II), arginine vasopressin (AVP), bombesin (Bom), bradykinin (BK), epidermal growth factor (EGF), epinephrine (Epi), interleukin 1 (IL-1), norepinephrine (NE), neuropeptide Y, oxytocin, substance P (SP), platelet-derived growth factor, or 12-O-tetradecanoylphorbol-13-acetate (TPA). We assessed DNA synthesis from [3H]thymidine uptake during exposure to test agent. All agents except ANG II, NE, Bom, and SP were mitogenic. When MCs were incubated in a HCO3(-) -free N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid-buffered medium, maximal mitogenic responses to FCS, AVP, and EGF were 41, 44, and 55% (P less than 0.01) lower, respectively, than those in presence of HCO3-. In absence of HCO3-, agents other than BK and IL-1 produced a biphasic pHi response characterized by a transient acidification followed by a prolonged alkalinization that was both Na(+)-dependent and amiloride-sensitive. In presence of HCO3-, agents produced only a small and gradual acidification, except for IL-1 and Epi. Addition of all agonists except IL-1, EGF, and TPA produced significant transient increases in [Ca2+]i, the magnitudes of which were similar in HCO3- and non-HCO3- buffers. These results demonstrate that, in presence of HCO3-, agents (i.e., NE and ANG II) can produce typical [Ca2+]i transients and still not cause MC proliferation. Conversely, an agent may cause proliferation without eliciting a short-term change in either [Ca2+]i or pHi (i.e., IL-1), a change in [Ca2+]i but not pHi (i.e., Epi), or a change in pHi but not [Ca2+]i (i.e., TPA). Thus, at least for MCs, proliferation in HCO3- can be dissociated from early agonist-induced changes in pHi and [Ca2+]i. <\/jats:p>","DOI":"10.1152\/ajprenal.1990.259.2.f269","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T17:26:51Z","timestamp":1513963611000},"page":"F269-F278","source":"Crossref","is-referenced-by-count":7,"title":["Effects of mitogens and other agents on rat mesangial cell proliferation, pH, and Ca2+"],"prefix":"10.1152","volume":"259","author":[{"given":"M. B.","family":"Ganz","sequence":"first","affiliation":[{"name":"Renal Division, West Haven Veterans Administration Medical Center,Connecticut 06516."}]},{"given":"M. C.","family":"Perfetto","sequence":"additional","affiliation":[{"name":"Renal Division, West Haven Veterans Administration Medical Center,Connecticut 06516."}]},{"given":"W. F.","family":"Boron","sequence":"additional","affiliation":[{"name":"Renal Division, West Haven Veterans Administration Medical Center,Connecticut 06516."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1990.259.2.F269","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:18:58Z","timestamp":1567955938000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1990.259.2.F269"}},"issued":{"date-parts":[[1990,8,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1990,8,1]]}},"alternative-id":["10.1152\/ajprenal.1990.259.2.F269"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1990.259.2.f269","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1990,8,1]]}},{"indexed":{"date-parts":[[2024,8,7]],"date-time":"2024-08-07T11:54:40Z","timestamp":1723031680355},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1996,9,1]]},"abstract":"<jats:p> Transforming growth factor-beta 1 (TGF-beta 1) treatment (0.2-2.0 ng\/ml, 8-80 M) of confluent primary cultures of rabbit renal proximal bular cells (RPTC) for 6 consecutive days resulted in both a benotypic transformation of the monolayer into solid clus- rs of cells and apoptosis. TGF-beta 1 treatment stimulated glycolysis before any effect on monolayer DNA content or morphology. TGF-beta 1 treatment also resulted in a 35% decrease in oxygen consumption, 50% inhibition of Na(+)-K(+)- ATPase activity, and a 57% decrease in gluconeogenesis. A concentration of 0.06 ng\/ml TGF-beta 1 decreased oxygen consumption and induced glycolysis but had no effect on morphology and viability of RPTC. Endogenous production of TGF-beta 1 by RPTC increased 2.6-fold during 10 days of culture. Control RPTC treated with anti-TGF-beta antibodies exhibited decreased glycolysis, and lactate metabolism shifted from net production to net consumption. These results show that TGF-beta 1 stimulates glycolysis, decreases respiration, and, at higher concentrations, induces RPTC apoptosis and phenopic changes. Inhibition of net lactate production in cells grown in the presence of anti-TGF-beta antibodies suggests that increased endogenous production of TGF-beta is responsible for the stimulation of glycolysis in long-term cultures of RPTC. <\/jats:p>","DOI":"10.1152\/ajprenal.1996.271.3.f689","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T06:31:13Z","timestamp":1514010673000},"page":"F689-F697","source":"Crossref","is-referenced-by-count":9,"title":["Autocrine production and TGF-beta 1-mediated effects on metabolism and viability in renal cells"],"prefix":"10.1152","volume":"271","author":[{"given":"G.","family":"Nowak","sequence":"first","affiliation":[{"name":"Department of Pharmacology and Toxicology, University of Arkansas forMedical Sciences, Little Rock 72205-7199, USA."}]},{"given":"R. G.","family":"Schnellmann","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, University of Arkansas forMedical Sciences, Little Rock 72205-7199, USA."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1996.271.3.F689","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:06:02Z","timestamp":1567973162000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1996.271.3.F689"}},"issued":{"date-parts":[[1996,9,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1996,9,1]]}},"alternative-id":["10.1152\/ajprenal.1996.271.3.F689"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1996.271.3.f689","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1996,9,1]]}},{"indexed":{"date-parts":[[2024,8,7]],"date-time":"2024-08-07T11:57:12Z","timestamp":1723031832865},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1990,6,1]]},"abstract":"<jats:p> The glutathione (GSH) content of rat kidney decreases after cessation of blood flow, falling to 40% of control levels 35 min after renal artery occlusion [R. C. Scaduto, Jr., V. H. Gattone II, L. W. Grotyohann, J. Wertz, and L. F. Martin. Am. J. Physiol. 255 ( Renal Fluid Electrolyte Physiol. 24): F911-F921, 1988]. Renal GSH levels remained depressed for at least 2 h after resumption of blood flow. Because GSH functions in the removal of free radicals, and lipid peroxidation is a free radical-initiated process that occurs in the ischemic kidney, we investigated the fate of this GSH pool in the ischemic kidney. Using high-performance liquid chromatography to measure thiols, we found the loss of GSH to be associated with a stoichiometric accumulation of cysteine in the kidney. Moreover, preischemic labeling of the renal GSH pool with <jats:sup>35<\/jats:sup>S led to accumulation of [<jats:sup>35<\/jats:sup>S]cysteine during ischemia that had the same specific activity as that of tissue GSH. Formation of cysteine during ischemia was suppressed in rats pretreated with acivicin, an inhibitor of \u0263-glutamyltransferase (\u0263-GT), although the degree of suppression was small in comparison to the extent of \u0263-GT inhibition. During the initial 2 min of blood reflow after ischemia, tissue cysteine returned to control levels, and a transient increase in the cysteine content of renal venous blood was observed. After ischemia, renal GSH levels remained depressed, but postischemic GSH levels could be increased by administration of N-acetylcysteine during the ischemic period. We conclude that renal ischemia leads to marked catabolism of GSH to cysteine, which is flushed from the tissue upon resumption of renal blood flow. The data are consistent with a pathway involving initial hydrolysis of GSH by \u0263-GT under conditions in which GSH synthesis is suppressed. Resynthesis of GSH after ischemia is limited by the availability of cysteine. <\/jats:p><jats:p> ischemia; cysteine; plasma thiols; kidney thiols <\/jats:p><jats:p> Submitted on August 7, 1989 <\/jats:p><jats:p> Accepted on November 20, 1989 <\/jats:p>","DOI":"10.1152\/ajprenal.1990.258.6.f1547","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T23:11:03Z","timestamp":1513984263000},"page":"F1547-F1553","source":"Crossref","is-referenced-by-count":7,"title":["Glutathione catabolism by the ischemic rat kidney"],"prefix":"10.1152","volume":"258","author":[{"given":"Stephen O.","family":"Slusser","sequence":"first","affiliation":[{"name":"Departments of Surgery and Cellular and Molecular Physiology, The Milton S. Hershey Medical Center, Pennsylvania State University, Hershey, Pennsylvania 17033"}]},{"given":"Lee W.","family":"Grotyohann","sequence":"additional","affiliation":[{"name":"Departments of Surgery and Cellular and Molecular Physiology, The Milton S. Hershey Medical Center, Pennsylvania State University, Hershey, Pennsylvania 17033"}]},{"given":"Louis F.","family":"Martin","sequence":"additional","affiliation":[{"name":"Departments of Surgery and Cellular and Molecular Physiology, The Milton S. Hershey Medical Center, Pennsylvania State University, Hershey, Pennsylvania 17033"}]},{"suffix":"Jr.","given":"Russell C.","family":"Scaduto","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1990.258.6.F1547","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:20:46Z","timestamp":1567970446000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1990.258.6.F1547"}},"issued":{"date-parts":[[1990,6,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1990,6,1]]}},"alternative-id":["10.1152\/ajprenal.1990.258.6.F1547"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1990.258.6.f1547","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1990,6,1]]}},{"indexed":{"date-parts":[[2022,4,4]],"date-time":"2022-04-04T08:17:24Z","timestamp":1649060244315},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1982,6,1]]},"abstract":"<jats:p> Previous studies have shown that organic bases, including some drugs, are secreted by renal proximal tubules. The present studies examined the transport of the organic bases cimetidine and procainamide by rabbit proximal straight tubules perfused in vitro. Both drugs were secreted into the tubule lumen. [3H]cimetidine secretion was reduced by quinidine, procainamide, and N-acetylprocainamide. Previous studies showed that cimetidine secretion was reduced by other organic bases. Hypothermia and ouabain inhibited [3H]procainamide secretion as was shown previously for cimetidine secretion. [3H]procainamide secretion was also reduced by quinidine, cimetidine, procainamide, and N-acetylprocainamide but not by probenecid. High concentrations of cimetidine (10(-3) M) had no effect on the rates of fluid or total CO2 absorption. When analyzed in terms of Michaelis-Menten kinetics, the effect of cimetidine on procainamide secretion and procainamide on cimetidine secretion was consistent with competitive inhibition. The results suggest that both cimetidine and procainamide are secreted into the lumen of proximal straight tubules predominately by an organic base transport mechanism. These studies raise the possibility that some of these drugs might compete for a common secretory mechanism in renal tubules and reduce the elimination of each other. <\/jats:p>","DOI":"10.1152\/ajprenal.1982.242.6.f672","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T13:27:56Z","timestamp":1513949276000},"page":"F672-F680","source":"Crossref","is-referenced-by-count":2,"title":["Cimetidine and procainamide secretion by proximal tubules in vitro"],"prefix":"10.1152","volume":"242","author":[{"given":"T. D.","family":"McKinney","sequence":"first","affiliation":[]},{"suffix":"Jr","given":"K. V.","family":"Speeg","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1982.242.6.F672","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:16:02Z","timestamp":1567966562000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1982.242.6.F672"}},"issued":{"date-parts":[[1982,6,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1982,6,1]]}},"alternative-id":["10.1152\/ajprenal.1982.242.6.F672"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1982.242.6.f672","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1982,6,1]]}},{"indexed":{"date-parts":[[2024,7,24]],"date-time":"2024-07-24T16:30:17Z","timestamp":1721838617803},"reference-count":88,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1997,10,1]]},"abstract":"<jats:p>X-linked hypophosphatemic rickets (HYP) is the most common form of hereditary renal phosphate wasting. The hallmarks of this disease are isolated renal phosphate wasting with inappropriately normal calcitriol concentrations and a mineralization defect in bone. Studies in the Hyp mouse, one of the murine models of the human disease, suggest that there is an \u223c50% decrease in both message and protein of NPT-2, the predominant sodium-phosphate cotransporter in the proximal tubule. However, human NPT-2 maps to chromosome 5q35, indicating that it is not the disease gene. Positional cloning studies have led to the identification of a gene, PEX, which is responsible for the disorder. Further studies have led to identification of the murine Pex gene, which is mutated in the murine models of the disorder. These studies, in concert with other studies, have led to improved understanding of the pathophysiology of HYP and a new appreciation for the complexity of normal phosphate homeostasis.<\/jats:p>","DOI":"10.1152\/ajprenal.1997.273.4.f489","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T14:56:01Z","timestamp":1514040961000},"page":"F489-F498","source":"Crossref","is-referenced-by-count":9,"title":["Positional cloning of the PEX gene: new insights into the pathophysiology of X-linked hypophosphatemic rickets"],"prefix":"10.1152","volume":"273","author":[{"given":"Michael J.","family":"Econs","sequence":"first","affiliation":[{"name":"Department of Medicine, Duke University Medical Center and the Durham Veterans Affairs Medical Center, Durham, North Carolina 27710; and"}]},{"given":"Fiona","family":"Francis","sequence":"additional","affiliation":[{"name":"Max-Planck Institut f\u00fcr Molekulare Genetik, 14195 Berlin, Germany"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.87.11.4256"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1126\/science.173.3999.845"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119276"},{"key":"B4","first-page":"314","volume":"32","author":"Botstein D.","year":"1980","journal-title":"Am. J. Hum. Genet."},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.88.9.4005"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199406093302304"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199412293312603"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/ng0495-347"},{"issue":"38","key":"B9","first-page":"F439","volume":"269","author":"Collins J. F.","year":"1995","journal-title":"Am. J. Physiol."},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1096\/fasebj.10.7.8635692"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1172\/JCI109415"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1210\/endo-112-2-633"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.86.18.7103"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1172\/JCI114442"},{"key":"B15","first-page":"S136","volume":"11","author":"Dixon P. H.","year":"1996","journal-title":"J. Bone Miner. Res."},{"key":"B16","first-page":"435","volume":"300","author":"Drezner M. K.","year":"1979","journal-title":"N. Engl. J. Med."},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1006\/geno.1996.0421"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1002\/jbmr.5650100313"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1002\/jbmr.5650070213"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1210\/endo-123-2-768"},{"key":"B21","first-page":"201","volume":"75","author":"Econs M. J.","year":"1992","journal-title":"J. Clin. Endocrinol. Metab."},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199406093302310"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1002\/jbmr.5650080916"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/3.4.680"},{"key":"B26","first-page":"1351","volume":"79","author":"Econs M. J.","year":"1994","journal-title":"J. Clin. Endocrinol. Metab."},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.73.12.4667"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.25.15262"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1006\/geno.1994.1247"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1101\/gr.7.6.573"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM198010303031802"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1997.6153"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1172\/JCI111900"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-4613-4217-5_24"},{"key":"B35","first-page":"790","volume":"60","author":"Holm I. A.","year":"1997","journal-title":"Am. J. Hum. Genet."},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(94)01079-X"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1126\/science.1188357"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1038\/ng1095-130"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1016\/0888-7543(91)90072-M"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1006\/geno.1994.1034"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/15.20.8125"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.115.4.887"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.468"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.88.10.4123"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.88.14.6353"},{"key":"B46","doi-asserted-by":"crossref","first-page":"15670","DOI":"10.1016\/S0021-9258(18)98459-0","volume":"266","author":"Le Moual H.","year":"1991","journal-title":"J. Biol. Chem."},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1111\/j.1432-1033.1994.tb18760.x"},{"key":"B48","first-page":"397","volume":"44","author":"Litt M.","year":"1989","journal-title":"Am. J. Hum. Genet."},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1172\/JCI110783"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.88.21.9628"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1210\/jcem-60-4-711"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1007\/BF02411222"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1210\/jcem-54-2-307"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.83.13.4899"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1007\/BF00401243"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1210\/endo-107-5-1577"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1002\/jbmr.5650040407"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1002\/jor.1100130107"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1016\/8756-3282(95)00420-3"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1001\/archinte.1974.00320210159025"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115735"},{"key":"B62","doi-asserted-by":"crossref","first-page":"1","DOI":"10.1002\/jbmr.5650101302","volume":"10","author":"Nesbitt T.","year":"1995","journal-title":"J. Bone Miner. Res."},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.93.5.1792"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1172\/JCI112304"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1017\/S0016672300031542"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1007\/BF00401242"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1981.54"},{"key":"B69","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/22.23.5135"},{"key":"B70","doi-asserted-by":"publisher","DOI":"10.1007\/BF02185769"},{"key":"B71","doi-asserted-by":"publisher","DOI":"10.1007\/BF00205082"},{"key":"B72","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/6.4.539"},{"key":"B73","doi-asserted-by":"publisher","DOI":"10.1007\/BF00219180"},{"key":"B74","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(94)01277-6"},{"key":"B75","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM197811022991803"},{"key":"B76","doi-asserted-by":"publisher","DOI":"10.1007\/BF01799618"},{"key":"B77","doi-asserted-by":"publisher","DOI":"10.1159\/000385992"},{"key":"B78","first-page":"491","volume":"94","author":"Sonin N. V.","year":"1996","journal-title":"Mouse Genome"},{"key":"B79","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/6.2.165"},{"key":"B80","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.149"},{"key":"B81","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2736(89)90218-6"},{"key":"B82","doi-asserted-by":"publisher","DOI":"10.1210\/endo.131.1.1612032"},{"key":"B83","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1978.115"},{"key":"B84","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117019"},{"key":"B85","doi-asserted-by":"publisher","DOI":"10.1172\/JCI113342"},{"key":"B86","doi-asserted-by":"publisher","DOI":"10.1136\/jmg.24.12.756"},{"key":"B87","first-page":"388","volume":"44","author":"Weber J. L.","year":"1989","journal-title":"Am. J. Hum. Genet."},{"key":"B88","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.88.21.9608"},{"key":"B89","first-page":"4075","volume":"81","author":"Whyte M. P.","year":"1996","journal-title":"J. Clin. Endocrinol. Metab."},{"key":"B90","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(94)90425-1"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1997.273.4.F489","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:47:40Z","timestamp":1660189660000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1997.273.4.F489"}},"issued":{"date-parts":[[1997,10,1]]},"references-count":88,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1997,10,1]]}},"alternative-id":["10.1152\/ajprenal.1997.273.4.F489"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1997.273.4.f489","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1997,10,1]]}},{"indexed":{"date-parts":[[2022,4,4]],"date-time":"2022-04-04T14:08:56Z","timestamp":1649081336415},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2005,7]]},"DOI":"10.1152\/ajprenal.00155.2005","type":"journal-article","created":{"date-parts":[[2005,6,10]],"date-time":"2005-06-10T18:33:16Z","timestamp":1118428396000},"page":"F1-F1","source":"Crossref","is-referenced-by-count":0,"title":["Processing color figures: that was then, this is now"],"prefix":"10.1152","volume":"289","author":[{"given":"Eric J.","family":"Pesanelli","sequence":"first","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00155.2005","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T21:57:12Z","timestamp":1567979832000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00155.2005"}},"issued":{"date-parts":[[2005,7]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2005,7]]}},"alternative-id":["10.1152\/ajprenal.00155.2005"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00155.2005","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2005,7]]}},{"indexed":{"date-parts":[[2024,8,4]],"date-time":"2024-08-04T05:16:00Z","timestamp":1722748560085},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1990,6,1]]},"abstract":"<jats:p> Agents that inhibit or stimulate Na+ transport were tested for their effects on the ionic composition and volume of the in vivo choroid plexus (CP) epithelium. Ketamine-anesthetized adult Sprague-Dawley rats treated 1 h with acetazolamide or insulin were analyzed for choroid cell [Na+]i, [HCO3-]i, and pHi (dimethadione method); for transmembrane Na+ and H+ gradients; and for the kinetics of penetration of 22Na from plasma to plexus epithelium to CSF. Acetazolamide (25 mg\/kg) reduced [Na+]i by 5-10 mmol\/l and substantially elevated [HCO3-]i and pHi; the concurrent 22Na uptake by the in vivo choroid plexus and CSF, as quantified by the transfer coefficient, Kin (ml.g-1.h-1), was curtailed by 55-60%. Such effects on Na+ transport and distribution are likely secondary to the alkalinization of pHi induced by carbonic anhydrase inhibition. Conversely, insulin (3 U\/kg ip) stimulated Na+ transport, i.e., manifested as enhanced uptake of 22Na from plasma to choroid cell and increased [Na+]i. For various treatments altering the basolateral membrane H+ gradient, the regression analysis of the 22Na Kin vs. log [H+]i\/[H+]ISF (where ISF is interstitial fluid) was significant at P less than 0.01. This is consistent with effects mediated by Na(+)-H+ exchange. K+ and Cl- redistribution phenomena were coincident with altered Na+ transport, as choroidal cells retained K+, Cl-, and H2O after acetazolamide but lost K+, Cl-, and H2O with insulin treatment. A model is presented relating alterations in CP Na+ transport, KCl content, and cell volume. Overall, the findings encourage the postulate for effects of these drugs on Na+ transport basolaterally, either indirectly by attenuating [H+]i\/[H+]ISF (acetazolamide) or directly by accelerating Na+ transport (insulin). <\/jats:p>","DOI":"10.1152\/ajprenal.1990.258.6.f1538","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T18:11:03Z","timestamp":1513966263000},"page":"F1538-F1546","source":"Crossref","is-referenced-by-count":12,"title":["Acetazolamide and insulin alter choroid plexus epithelial cell [Na+], pH, and volume"],"prefix":"10.1152","volume":"258","author":[{"given":"C. E.","family":"Johanson","sequence":"first","affiliation":[{"name":"Department of Clinical Neurosciences, Brown University\/Rhode Island Hospital, Providence 02902."}]},{"given":"V. A.","family":"Murphy","sequence":"additional","affiliation":[{"name":"Department of Clinical Neurosciences, Brown University\/Rhode Island Hospital, Providence 02902."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1990.258.6.F1538","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:20:45Z","timestamp":1567956045000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1990.258.6.F1538"}},"issued":{"date-parts":[[1990,6,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1990,6,1]]}},"alternative-id":["10.1152\/ajprenal.1990.258.6.F1538"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1990.258.6.f1538","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1990,6,1]]}},{"indexed":{"date-parts":[[2024,8,16]],"date-time":"2024-08-16T05:09:31Z","timestamp":1723784971770},"reference-count":32,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1998,5,1]]},"abstract":"<jats:p>Elevations of arginine vasopressin (AVP) binding to renal vasopressin V<jats:sub>2<\/jats:sub>receptors (V<jats:sub>2<\/jats:sub>R) enhance water and urea reabsorption in the collecting duct epithelium. This study was designed to quantify the levels of V<jats:sub>2<\/jats:sub>R mRNA and protein within the distinct regions of the Sprague-Dawley rat kidney (i.e., the cortex and outer and inner medulla) during 24 and 48 h of water restriction. A competitive reverse transcription-polymerase chain reaction (RT-PCR) assay was developed to quantify changes in the V<jats:sub>2<\/jats:sub>R mRNA, in which a deletion mutant RNA transcript was used to control for the efficiency of RT-PCR. Western blot analysis was utilized for the quantification of the V<jats:sub>2<\/jats:sub>R protein. The results showed that the steady-state levels of the V<jats:sub>2<\/jats:sub>R mRNA decreased in a time-dependent manner in the cortex and outer and inner medulla throughout 48 h of water restriction. Western blot analysis revealed that the V<jats:sub>2<\/jats:sub>R protein in the renal cortex decreased after the initial 24 h of water restriction and remained decreased at 48 h. In contrast, outer medullary V<jats:sub>2<\/jats:sub>R protein decreased significantly only after 48 h of water restriction, whereas no significant change in the inner medullary V<jats:sub>2<\/jats:sub>R protein was observed throughout the 48 h of water restriction. These results suggest that water restriction leads to a regional time-dependent downregulation of the V<jats:sub>2<\/jats:sub>R mRNA and protein within the rat kidney. The stability of the plasma membrane V<jats:sub>2<\/jats:sub>R protein within the inner medulla may allow for the optimization of urine concentration and minimize water loss during periods of water restriction.<\/jats:p>","DOI":"10.1152\/ajprenal.1998.274.5.f906","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T15:41:04Z","timestamp":1514043664000},"page":"F906-F913","source":"Crossref","is-referenced-by-count":9,"title":["Regional time-dependent changes in vasopressin V<sub>2<\/sub>receptor expression in the rat kidney during water restriction"],"prefix":"10.1152","volume":"274","author":[{"given":"Frank","family":"Park","sequence":"first","affiliation":[{"name":"Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226"}]},{"given":"George","family":"Koike","sequence":"additional","affiliation":[{"name":"Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226"}]},{"suffix":"Jr.","given":"Allen W.","family":"Cowley","sequence":"additional","affiliation":[{"name":"Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226"}]}],"member":"24","reference":[{"issue":"37","key":"B1","first-page":"F103","volume":"268","author":"Baudouin-Legros M.","year":"1995","journal-title":"Am. J. Physiol."},{"issue":"20","key":"B2","first-page":"F271","volume":"251","author":"Besseghir K.","year":"1986","journal-title":"Am. J. Physiol."},{"key":"B3","doi-asserted-by":"crossref","first-page":"11783","DOI":"10.1016\/S0021-9258(19)49766-4","volume":"267","author":"Birnbaumer M.","year":"1992","journal-title":"J. Biol. Chem."},{"issue":"29","key":"B4","first-page":"F46","volume":"260","author":"Carmelo C.","year":"1991","journal-title":"Am. J. Physiol."},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.1041380311"},{"issue":"27","key":"B6","first-page":"F1173","volume":"258","author":"Chou C.-L.","year":"1990","journal-title":"Am. J. Physiol."},{"issue":"29","key":"B7","first-page":"F656","volume":"260","author":"Dublineau I.","year":"1991","journal-title":"Am. J. Physiol."},{"issue":"38","key":"B8","first-page":"F663","volume":"269","author":"Ecelbarger C. A.","year":"1995","journal-title":"Am. J. Physiol."},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1007\/BF02584033"},{"issue":"39","key":"B10","first-page":"R1257","volume":"270","author":"Franchini K. G.","year":"1996","journal-title":"Am. J. Physiol."},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.87.7.2725"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117525"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.108.2.389"},{"key":"B14","doi-asserted-by":"crossref","first-page":"11783","DOI":"10.1016\/S0021-9258(19)49766-4","volume":"267","author":"Innamorati G.","year":"1992","journal-title":"J. Biol. Chem."},{"issue":"34","key":"B15","first-page":"F214","volume":"265","author":"Knepper M. A.","year":"1993","journal-title":"Am. J. Physiol."},{"key":"B16","first-page":"357","volume":"14","author":"Kumar R.","year":"1994","journal-title":"Semin. Nephrol."},{"issue":"30","key":"B17","first-page":"F554","volume":"261","author":"Lankford S. P.","year":"1991","journal-title":"Am. J. Physiol."},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/0303-7207(85)90175-3"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1038\/357336a0"},{"issue":"33","key":"B20","first-page":"F228","volume":"264","author":"Lutz W.","year":"1993","journal-title":"Am. J. Physiol."},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1995.269.3.C655"},{"issue":"34","key":"B22","first-page":"F225","volume":"265","author":"Nielsen S.","year":"1993","journal-title":"Am. J. Physiol."},{"issue":"34","key":"B23","first-page":"F204","volume":"265","author":"Nielsen S.","year":"1993","journal-title":"Am. J. Physiol."},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118222"},{"issue":"42","key":"B25","first-page":"R243","volume":"273","author":"Park F.","year":"1997","journal-title":"Am. J. Physiol."},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.1981.tb15463.x"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1124\/mol.52.1.21"},{"issue":"41","key":"B28","first-page":"F183","volume":"272","author":"Saito T.","year":"1997","journal-title":"Am. J. Physiol."},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/0006-2952(93)90585-K"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1007\/BF00595690"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1988.254.3.C404"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1172\/JCI116838"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1998.274.5.F906","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:49:04Z","timestamp":1660189744000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1998.274.5.F906"}},"issued":{"date-parts":[[1998,5,1]]},"references-count":32,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1998,5,1]]}},"alternative-id":["10.1152\/ajprenal.1998.274.5.F906"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1998.274.5.f906","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1998,5,1]]}},{"indexed":{"date-parts":[[2024,8,13]],"date-time":"2024-08-13T20:09:56Z","timestamp":1723579796874},"reference-count":38,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2003,9]]},"abstract":"<jats:p>Polyamines are involved in the control of the cell cycle and cell growth. In murine kidney, testosterone enhances gene expression of ornithine decarboxylase (ODC), the first enzyme in polyamine biosynthesis. In this study, we document the time course effect of testosterone on 1) gene expression of ODC, antizyme 1 (AZ1), and spermidine\/spermine- N<jats:sup>1<\/jats:sup>-acetyltransferase ( N<jats:sup>1<\/jats:sup>-SSAT); 2) ODC activity in proximal convoluted tubules (PCT) and cortical proximal straight tubules (CPST); and 3) renal polyamine levels. Female mice were treated with testosterone for a period of 1, 2, 3, and 5 consecutive days. ODC gene expression was extremely low in kidneys of untreated female mice compared with that of males. Consequently, the renal putrescine level was sevenfold lower in females than in males, whereas spermidine and spermine levels did not differ between sexes. In female kidneys, testosterone treatment sharply increased ODC mRNA and protein levels as well as ODC activity. Testosterone increased the expression of ODC in PCT and CPST over different time courses, which suggests that ODC activity is differentially regulated in distinct tubules. The expression of AZ1 and N<jats:sup>1<\/jats:sup>-SSAT mRNA was similar in male and female mouse kidneys. Testosterone treatment enhanced AZ1 and N<jats:sup>1<\/jats:sup>-SSAT mRNA levels in a time-dependent manner by unknown molecular mechanisms. Putrescine and spermidine levels increased after testosterone treatment in female kidneys. Surprisingly, although ODC protein and activity were undetectable in female kidneys, the levels of AZ1 mRNA and protein were similar to those in males. Therefore, one may propose that ODC protein could be continuously degraded by AZ1 in female kidneys.<\/jats:p>","DOI":"10.1152\/ajprenal.00407.2002","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:39:09Z","timestamp":1425415149000},"page":"F498-F506","source":"Crossref","is-referenced-by-count":16,"title":["Influence of testosterone on regulation of ODC, antizyme, and<i>N<\/i><sup>1<\/sup>-SSAT gene expression in mouse kidney"],"prefix":"10.1152","volume":"285","author":[{"given":"Olivier","family":"Levillain","sequence":"first","affiliation":[]},{"given":"Anna","family":"Greco","sequence":"additional","affiliation":[]},{"given":"Jean-Jacques","family":"Diaz","sequence":"additional","affiliation":[]},{"given":"Roger","family":"Augier","sequence":"additional","affiliation":[]},{"given":"Anne","family":"Didier","sequence":"additional","affiliation":[]},{"given":"Karine","family":"Kindbeiter","sequence":"additional","affiliation":[]},{"given":"Fr\u00e9d\u00e9ric","family":"Catez","sequence":"additional","affiliation":[]},{"given":"Myriam","family":"Cayre","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"REF1","doi-asserted-by":"crossref","unstructured":"Berger FG, Szymanski P, Read E, and Watson G.Androgen-regulated ornithine decarboxylase mRNAs of mouse kidney.J Biol Chem259: 7941-7946, 1984.","DOI":"10.1016\/S0021-9258(17)42883-3"},{"key":"REF2","unstructured":"Besson MT, Delbecque JP, Mathelin J, Boisson AM, and Delachambre J.Epidermal polyamine levels related to cell cycle events during the metamorphosis ofTenebrio molitor L. (Insecta, Coleoptera): effect of juvenoid application.Comp Biochem Physiol83B: 589-593, 1986."},{"key":"REF3","doi-asserted-by":"publisher","DOI":"10.1139\/o01-001"},{"key":"REF4","doi-asserted-by":"publisher","DOI":"10.1016\/0020-1790(88)90110-2"},{"key":"REF5","doi-asserted-by":"publisher","DOI":"10.1016\/0003-2697(76)90527-3"},{"key":"REF6","unstructured":"Cohen SS.Pathways of polyamine metabolism in animals. In:A Guide to the Polyamines, edited by Cohen SS. New York: Oxford Univ. Press, 1998, p. 207-230."},{"key":"REF7","doi-asserted-by":"crossref","unstructured":"Crozat A, Palvimo JJ, Julkunen M, and J\u00e4nne OA.Comparison of androgen regulation of ornithine decarboxylase andS-adenosylmethionine decarboxylase gene expression in rodent kidney and accessory sex organs.Endocrinology130: 1131-1144, 1992.","DOI":"10.1210\/en.130.3.1131"},{"key":"REF8","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-2836(83)80284-8"},{"key":"REF9","unstructured":"Hayashi S-I.Multiple mechanisms for the regulation of mammalian ornithine decarboxylase. In:Ornithine Decarboxylase: Biology, Enzymology, and Molecular Genetics, edited by Hayashi S-I. New York: Pergamon, 1989, p. 35-45."},{"key":"REF10","doi-asserted-by":"publisher","DOI":"10.1111\/j.1432-0436.1981.tb01123.x"},{"key":"REF11","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.73.6.1858"},{"key":"REF12","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1978.tb06085.x"},{"key":"REF13","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.1984.tb38277.x"},{"key":"REF14","doi-asserted-by":"publisher","DOI":"10.1007\/BF01366925"},{"key":"REF15","doi-asserted-by":"publisher","DOI":"10.1042\/bj3240807"},{"key":"REF16","doi-asserted-by":"publisher","DOI":"10.1016\/0006-291X(88)90614-6"},{"key":"REF17","doi-asserted-by":"publisher","DOI":"10.1507\/endocrj1954.37.555"},{"key":"REF18","doi-asserted-by":"publisher","DOI":"10.1007\/BF00268930"},{"key":"REF19","doi-asserted-by":"publisher","DOI":"10.1038\/227680a0"},{"key":"REF20","doi-asserted-by":"publisher","DOI":"10.1007\/s004240000340"},{"key":"REF21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.6.F1020"},{"key":"REF22","doi-asserted-by":"publisher","DOI":"10.1016\/0304-4165(92)90113-9"},{"key":"REF23","doi-asserted-by":"publisher","DOI":"10.1093\/oxfordjournals.jbchem.a123018"},{"key":"REF24","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.10.6175"},{"key":"REF25","doi-asserted-by":"publisher","DOI":"10.1210\/mend-1-3-266"},{"key":"REF26","doi-asserted-by":"publisher","DOI":"10.1042\/bj3170811"},{"key":"REF27","doi-asserted-by":"publisher","DOI":"10.1042\/bst0260591"},{"key":"REF28","doi-asserted-by":"publisher","DOI":"10.1042\/bj2990019"},{"key":"REF29","doi-asserted-by":"crossref","unstructured":"Pajunen AEI, Isomaa VV, J\u00e4nne OA, and Bardin CW.Androgenic regulation of ornithine decarboxylase activity in mouse kidney and its relationship to changes in cytosol and nuclear androgen receptor concentrations.J Biol Chem257: 8190-8198, 1982.","DOI":"10.1016\/S0021-9258(18)34316-3"},{"key":"REF30","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1982.243.5.C212"},{"key":"REF31","doi-asserted-by":"publisher","DOI":"10.1126\/science.6806900"},{"key":"REF32","doi-asserted-by":"publisher","DOI":"10.1016\/0304-4165(81)90378-0"},{"key":"REF33","doi-asserted-by":"publisher","DOI":"10.1159\/000014144"},{"key":"REF34","doi-asserted-by":"publisher","DOI":"10.1016\/0303-7207(91)90057-Y"},{"key":"REF35","doi-asserted-by":"publisher","DOI":"10.1016\/0303-7207(91)90056-X"},{"key":"REF36","doi-asserted-by":"publisher","DOI":"10.1177\/002215549904701106"},{"key":"REF37","doi-asserted-by":"crossref","unstructured":"Seiler N.Use of the dansyl reaction in biochemical analysis.Methods Biochem Anal18: 259-337, 1970.","DOI":"10.1002\/9780470110362.ch5"},{"key":"REF38","unstructured":"Seiler N, Bolkenius FN, and Rennert OM.Interconversion, catabolism and elimination of the polyamines.Med Biol59: 334-346, 1981."}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00407.2002","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,5,1]],"date-time":"2022-05-01T09:38:16Z","timestamp":1651397896000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00407.2002"}},"issued":{"date-parts":[[2003,9]]},"references-count":38,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2003,9]]}},"alternative-id":["10.1152\/ajprenal.00407.2002"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00407.2002","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2003,9]]}},{"indexed":{"date-parts":[[2025,2,21]],"date-time":"2025-02-21T11:59:23Z","timestamp":1740139163530,"version":"3.37.3"},"reference-count":27,"publisher":"American Physiological Society","issue":"8","funder":[{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)","doi-asserted-by":"publisher","award":["DK-094905","DK-090006","DK-102427","DK-091253"],"award-info":[{"award-number":["DK-094905","DK-090006","DK-102427","DK-091253"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2015,4,15]]},"abstract":"<jats:p> This study examined the role of spinal metabotropic glutamate receptor 5 (mGluR5) in the nociceptive C-fiber afferent-mediated spinal bladder reflex and in the inhibtion of this reflex by pudendal nerve stimulation (PNS). In \u03b1-chloralose-anesthetized cats after spinal cord transection at the T9\/T10 level, intravesical infusion of 0.25% acetic acid irritated the bladder, activated nociceptive C-fiber afferents, and induced spinal reflex bladder contractions of low amplitude (&lt;50 cmH<jats:sub>2<\/jats:sub>O) and short duration (&lt;20 s) at a smaller bladder capacity \u223c80% of saline control capacity. PNS significantly ( P &lt; 0.01) increased bladder capacity from 85.5 \u00b1 10.1 to 137.3 \u00b1 14.1 or 148.2 \u00b1 11.2% at 2T or 4T stimulation, respectively, where T is the threshold intensity for PNS to induce anal twitch. MTEP {3-[(2-methyl-4-thiazolyl)ethynyl]pyridine; 3 mg\/kg iv, a selective mGluR5 antagonist} completely removed the PNS inhibition and significantly ( P &lt; 0.05) increased bladder capacity from 71.8 \u00b1 9.9 to 94.0 \u00b1 13.9% of saline control, but it did not change the bladder contraction amplitude. After propranolol (3 mg\/kg iv, a \u03b21\/\u03b22-adrenergic receptor antagonist) treatment, PNS inhibition remained but MTEP significantly ( P &lt; 0.05) reduced the bladder contraction amplitude from 18.6 \u00b1 2.1 to 6.6 \u00b1 1.2 cmH<jats:sub>2<\/jats:sub>O and eliminated PNS inhibition. At the end of experiments, hexamethonium (10 mg\/kg iv, a ganglionic blocker) significantly ( P &lt; 0.05) reduced the bladder contraction amplitude from 20.9 \u00b1 3.2 to 8.1 \u00b1 1.5 cmH<jats:sub>2<\/jats:sub>O on average demonstrating that spinal reflexes were responsible for a major component of the contractions. This study shows that spinal mGluR5 plays an important role in the nociceptive C-fiber afferent-mediated spinal bladder reflex and in pudendal inhibition of this spinal reflex. <\/jats:p>","DOI":"10.1152\/ajprenal.00623.2014","type":"journal-article","created":{"date-parts":[[2015,2,12]],"date-time":"2015-02-12T00:38:04Z","timestamp":1423701484000},"page":"F832-F838","source":"Crossref","is-referenced-by-count":7,"title":["Role of spinal metabotropic glutamate receptor 5 in pudendal inhibition of the nociceptive bladder reflex in cats"],"prefix":"10.1152","volume":"308","author":[{"given":"Jeremy N.","family":"Reese","sequence":"first","affiliation":[{"name":"Department of Urology, University of Pittsburgh, Pittsburgh, Pennsylvania;"}]},{"given":"Marc J.","family":"Rogers","sequence":"additional","affiliation":[{"name":"Department of Urology, University of Pittsburgh, Pittsburgh, Pennsylvania;"}]},{"given":"Zhiying","family":"Xiao","sequence":"additional","affiliation":[{"name":"Department of Urology, University of Pittsburgh, Pittsburgh, Pennsylvania;"},{"name":"Department of Urology, The Second Hospital, Shandong University, Jinan, People's Republic of China; and"}]},{"given":"Bing","family":"Shen","sequence":"additional","affiliation":[{"name":"Department of Urology, University of Pittsburgh, Pittsburgh, Pennsylvania;"}]},{"given":"Jicheng","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Urology, University of Pittsburgh, Pittsburgh, Pennsylvania;"}]},{"given":"Zeyad","family":"Schwen","sequence":"additional","affiliation":[{"name":"Department of Urology, University of Pittsburgh, Pittsburgh, Pennsylvania;"}]},{"given":"James R.","family":"Roppolo","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Chemical Biology, University of Pittsburgh, Pittsburgh, Pennsylvania"}]},{"given":"William C.","family":"de Groat","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Chemical Biology, University of Pittsburgh, Pittsburgh, Pennsylvania"}]},{"given":"Changfeng","family":"Tai","sequence":"additional","affiliation":[{"name":"Department of Urology, University of Pittsburgh, Pittsburgh, Pennsylvania;"},{"name":"Department of Pharmacology and Chemical Biology, University of Pittsburgh, Pittsburgh, Pennsylvania"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1002\/nau.10052"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.2165\/00003495-200363230-00003"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1038\/86075"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/j.eururo.2008.06.047"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1038\/sc.2014.157"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/S0165-6147(00)01635-7"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/0165-1838(90)90105-R"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1972.sp009985"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/0165-1838(81)90059-X"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1969.sp008683"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1972.sp009708"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1038\/nrn2401"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1111\/j.1464-410X.2008.07748.x"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1990.sp018117"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1186\/1471-2490-14-65"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2011.215657"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(17)52127-8"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.1998.531bb.x"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1002\/nau.20174"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1002\/nau.20823"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1159\/000356063"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00368.2014"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1002\/ana.21814"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1016\/j.juro.2007.07.032"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1097\/00001756-199412300-00053"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/S0028-3908(00)00113-1"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00308.2014"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00623.2014","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T21:13:57Z","timestamp":1567977237000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00623.2014"}},"issued":{"date-parts":[[2015,4,15]]},"references-count":27,"journal-issue":{"issue":"8","published-print":{"date-parts":[[2015,4,15]]}},"alternative-id":["10.1152\/ajprenal.00623.2014"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00623.2014","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2015,4,15]]}},{"indexed":{"date-parts":[[2025,2,21]],"date-time":"2025-02-21T11:58:48Z","timestamp":1740139128834,"version":"3.37.3"},"reference-count":9,"publisher":"American Physiological Society","issue":"1","funder":[{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["R01DK117913-01","R01DK129467","1R01DK133912"],"award-info":[{"award-number":["R01DK117913-01","R01DK129467","1R01DK133912"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["R01DK109683","R01DK122980","R01DK129467"],"award-info":[{"award-number":["R01DK109683","R01DK122980","R01DK129467"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000738","name":"U.S. Department of Veterans Affairs","doi-asserted-by":"publisher","award":["I01BX000345"],"award-info":[{"award-number":["I01BX000345"]}],"id":[{"id":"10.13039\/100000738","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2024,1,1]]},"DOI":"10.1152\/ajprenal.00344.2023","type":"journal-article","created":{"date-parts":[[2023,11,30]],"date-time":"2023-11-30T09:00:33Z","timestamp":1701334833000},"page":"F118-F119","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Injury in nonaged podocytes as an accelerator of glomerular aging"],"prefix":"10.1152","volume":"326","author":[{"given":"Zhengying","family":"Fang","sequence":"first","affiliation":[{"name":"Barbara T. Murphy Division of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9756-1765","authenticated-orcid":false,"given":"Kyung","family":"Lee","sequence":"additional","affiliation":[{"name":"Barbara T. Murphy Division of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1502-2849","authenticated-orcid":false,"given":"John Cijiang","family":"He","sequence":"additional","affiliation":[{"name":"Barbara T. Murphy Division of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, United States"},{"name":"Renal Section, James J. Peters Veterans Affair Medical Center, Bronx, New York, United States"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.28"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014080752"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00497.2015"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/s41581-022-00648-y"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2021050614"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2015.157"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00255.2017"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00261.2023"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1038\/s41581-022-00601-z"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00344.2023","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,2,7]],"date-time":"2024-02-07T14:07:00Z","timestamp":1707314820000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00344.2023"}},"issued":{"date-parts":[[2024,1,1]]},"references-count":9,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2024,1,1]]}},"alternative-id":["10.1152\/ajprenal.00344.2023"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00344.2023","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2024,1,1]]},"assertion":[{"value":"2023-10-26","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2023-11-15","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2023-11-22","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2023-12-20","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2025,6,15]],"date-time":"2025-06-15T04:40:07Z","timestamp":1749962407567,"version":"3.41.0"},"reference-count":50,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2017,5,1]]},"abstract":"<jats:p>Our aim was to investigate whether blockade of calcium channels (CCs) or angiotensin II type 1 receptors (AT1R) modulates renal responses to nitric oxide synthesis inhibition (NOSI) in humans. Fourteen sodium-replete, healthy volunteers underwent 90-min infusions of 3.0 \u03bcg\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7min<jats:sup>\u22121<\/jats:sup>N<jats:sup>G<\/jats:sup>-nitro-l-arginine methyl ester (l-NAME) on 3 occasions, preceded by 3 days of either placebo (PL), 10 mg of manidipine (MANI), or 50 mg of losartan (LOS). At each phase, mean arterial pressure (MAP), glomerular filtration rate (GFR; inulin), renal blood flow (RBF; p-aminohippurate), urinary sodium (UNaV), and 8-isoprostane (U8-iso-PGF2\u03b1V; an oxidative stress marker) were measured. With PL + l -NAME, the following changes were observed: +6% MAP ( P &lt; 0.005 vs. baseline), \u221210% GFR, \u221220% RBF, \u221249% UNaV ( P &lt; 0.001), and +120% U8-iso-PGF2\u03b1V ( P &lt; 0.01). In contrast, MAP did not increase during LOS + l-NAME or MANI + l-NAME ( P &gt; 0.05 vs. baseline), whereas renal changes were the same during LOS + l-NAME vs. PL + l-NAME (ANOVA, P &gt; 0.05). However, during MANI + l-NAME, changes vs. baseline in GFR (\u22126%), RBF (\u221212%), and UNaV (\u221234%) were blunted vs. PL + l-NAME and LOS + l-NAME ( P &lt; 0.005), and the rise in U8-iso-PGF2\u03b1V was almost abolished (+37%, P &gt; 0.05 vs. baseline; P &lt; 0.01 vs. PL + l-NAME or LOS + l-NAME). We conclude that, since MANI blunted l-NAME-induced renal hemodynamic changes, CCs participate in the renal responses to NOSI in healthy, sodium-replete humans independent of changes in MAP and without the apparent contribution of the AT1R. Because the rise in U8-iso-PGF2\u03b1V was essentially prevented during MANI + l-NAME, CC blockade may oppose the renal effects of NOSI in part by counteracting oxidative stress responses to acutely impaired renal NO bioavailability.<\/jats:p>","DOI":"10.1152\/ajprenal.00568.2016","type":"journal-article","created":{"date-parts":[[2017,2,9]],"date-time":"2017-02-09T01:10:25Z","timestamp":1486602625000},"page":"F870-F878","source":"Crossref","is-referenced-by-count":2,"title":["Calcium channel blockade blunts the renal effects of acute nitric oxide synthase inhibition in healthy humans"],"prefix":"10.1152","volume":"312","author":[{"given":"Alberto","family":"Montanari","sequence":"first","affiliation":[{"name":"Department of Clinical and Experimental Medicine, University of Parma Medical School, Parma, Italy;"}]},{"given":"Davide","family":"Lazzeroni","sequence":"additional","affiliation":[{"name":"Prevention and Rehabilitation Unit at the Don Gnocchi Foundation and Department of Clinical and Experimental Medicine, University of Parma Medical School, Parma, Italy; and"}]},{"given":"Giovanna","family":"Pel\u00e0","sequence":"additional","affiliation":[{"name":"Department of Clinical and Experimental Medicine, University of Parma Medical School, Parma, Italy;"}]},{"given":"Antonio","family":"Crocamo","sequence":"additional","affiliation":[{"name":"Department of Clinical and Experimental Medicine, University of Parma Medical School, Parma, Italy;"}]},{"given":"Yuliya","family":"Lytvyn","sequence":"additional","affiliation":[{"name":"Division of Nephrology, University Health Network, University of Toronto, Toronto, Ontario, Canada"}]},{"given":"Luisa","family":"Musiari","sequence":"additional","affiliation":[{"name":"Department of Clinical and Experimental Medicine, University of Parma Medical School, Parma, Italy;"}]},{"given":"Aderville","family":"Cabassi","sequence":"additional","affiliation":[{"name":"Department of Clinical and Experimental Medicine, University of Parma Medical School, Parma, Italy;"}]},{"given":"David Z. I.","family":"Cherney","sequence":"additional","affiliation":[{"name":"Division of Nephrology, University Health Network, University of Toronto, Toronto, Ontario, Canada"}]}],"member":"24","reference":[{"key":"B1","first-page":"R1472","volume":"267","author":"Alberola AM","year":"1994","journal-title":"Am J Physiol Renal Physiol"},{"key":"B2","doi-asserted-by":"crossref","first-page":"693","DOI":"10.1016\/S0022-3565(24)38008-5","volume":"288","author":"Baylis C","year":"1999","journal-title":"J Pharmacol Exp Ther"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-199801000-00010"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00424.2007"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.270.5.F845"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/j.cardfail.2013.10.001"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/14.3.641"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.275.6.F870"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.37.1.34"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.87.10.840"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-199209000-00017"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00286.2012"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00260.x"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfh187"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200409000-00002"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.2165\/00003495-199958030-00002"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.29.5.1192"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/S0008-6363(98)00124-2"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00292.2006"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00042.2005"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1146\/annurev-physiol-012110-142247"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.2174\/157016112798829823"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1097\/00005344-199204002-00045"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1111\/apha.12070"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.2174\/1573402110666140131160617"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.3945\/ajcn.2008.27131"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-200203000-00029"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00332.2006"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.4.F561"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.275.6.F849"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.3109\/10641963.2012.681727"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1007\/s00228-003-0662-7"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-200302000-00026"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.2007.04642.x"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1159\/000064285"},{"key":"B36","doi-asserted-by":"crossref","first-page":"109","DOI":"10.1016\/S0031-6997(25)06663-3","volume":"43","author":"Moncada S","year":"1991","journal-title":"Pharmacol Rev"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.30.3.557"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00109.2013"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1038\/clpt.1992.56"},{"key":"B40","doi-asserted-by":"crossref","first-page":"1706","DOI":"10.1681\/ASN.V1281706","volume":"12","author":"Perinotto P","year":"2001","journal-title":"J Am Soc Nephrol"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2008.10.041"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.33.4.937"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5001745"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1097\/HJH.0b013e3282f1a93e"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.2337\/dc06-1551"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2012111112"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.2174\/157340210903140415124048"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1007\/s11906-011-0207-x"},{"key":"B49","first-page":"251","volume":"19","author":"Welch WJ","year":"1999","journal-title":"Semin Nephrol"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00250.2005"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00568.2016","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,6,15]],"date-time":"2025-06-15T04:19:27Z","timestamp":1749961167000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00568.2016"}},"issued":{"date-parts":[[2017,5,1]]},"references-count":50,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2017,5,1]]}},"alternative-id":["10.1152\/ajprenal.00568.2016"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00568.2016","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2017,5,1]]}},{"indexed":{"date-parts":[[2025,6,18]],"date-time":"2025-06-18T12:26:20Z","timestamp":1750249580048},"reference-count":34,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2004,12]]},"abstract":"<jats:p>RET, a tyrosine kinase receptor essential for kidney development, has recently been shown to be important for the formation of the urinary tract. When RET is overexpressed in the HoxB7\/Ret transgenic mouse, kidneys are small and cystic, and in some of the mice, the ureters are grossly dilated. Here, we report that the observed ureteral dilatation is associated with the urinary tract abnormality vesicoureteric reflux (VUR), in which urine flows retrogradely from the bladder to the ureter. Reflux was determined in vitro by injecting methylene blue into the bladders of HoxB7\/Ret and wild-type mice. At postnatal day 1, 30% of HoxB7\/Ret mice had VUR compared with 4% of wild-type mice ( P &lt; 0.05). The length of the intravesical ureteral tunnel was shorter in HoxB7\/Ret mice compared with wild-type mice, on both the right and the left sides ( P &lt; 0.05), suggesting a basis for the higher incidence of VUR in these mutants. At embryonic day 11, the ureteric bud was found to exit more caudally from the mesonephric duct in HoxB7\/Ret mice, and this may predispose them to VUR ( P &lt; 0.05). Wild-type and HoxB7\/Ret mice were tested for reflux at embryonic day 17, and both showed a high frequency of VUR (59 and 75%, respectively). These results suggest that VUR may occur transiently during normal urinary tract development before the ureter has completed its insertion into the bladder. In the HoxB7\/Ret mouse, overexpression of RET appears to delay the maturation of the distal ureter, resulting in postnatal VUR. The HoxB7\/Ret mouse is thus an important model in which to examine how vesicoureteric reflux arises during urinary tract development.<\/jats:p>","DOI":"10.1152\/ajprenal.00444.2003","type":"journal-article","created":{"date-parts":[[2004,8,25]],"date-time":"2004-08-25T00:24:00Z","timestamp":1093393440000},"page":"F1123-F1130","source":"Crossref","is-referenced-by-count":39,"title":["Overexpression of RET leads to vesicoureteric reflux in mice"],"prefix":"10.1152","volume":"287","author":[{"given":"O. H.","family":"Yu","sequence":"first","affiliation":[]},{"given":"I. J.","family":"Murawski","sequence":"additional","affiliation":[]},{"given":"D. B.","family":"Myburgh","sequence":"additional","affiliation":[]},{"given":"I. R.","family":"Gupta","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1038\/ng952"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/19.15.4056"},{"key":"R3","doi-asserted-by":"crossref","unstructured":"Brophy PD, Ostrom L, Lang KM, and Dressler GR.Regulation of ureteric bud outgrowth by Pax2-dependent activation of the glial derived neurotrophic factor gene.Development12: 4747\u20134756, 2001.","DOI":"10.1242\/dev.128.23.4747"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/5.Supplement_1.1425"},{"key":"R5","unstructured":"Eccles Mand Jacobs G.The genetics of primary vesico-ureteric reflux.Ann Acad Med Singapore29: 337\u2013345, 2000."},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1086\/302864"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(96)03419-8"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1016\/S1534-5807(04)00108-X"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00715.x"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1007\/s004670050589"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.151.5.961"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00703.x"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1002\/nau.10074"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1159\/000020795"},{"key":"R15","doi-asserted-by":"crossref","unstructured":"Kress C, Vogels R, Graaff WD, Bonnerot C, Meijlink F, Nicolas JF, and Deschamps J.Hox-2 upstream sequences mediate lacz expression in intermediate mesoderm derivatives of transgenic mice.Development109: 775\u2013786, 1990.","DOI":"10.1242\/dev.109.4.775"},{"key":"R16","doi-asserted-by":"crossref","unstructured":"Kume T, Deng K, and Hogan B.Murine forkhead\/winged helix genes Foxc1 (Mf1) and Foxc2 (Mfh1) are required for the early organogenesis of the kidney and urinary tract.Development127: 1387\u20131395, 2000.","DOI":"10.1242\/dev.127.7.1387"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(17)62184-0"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(17)67007-1"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1172\/JCI8256"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1002\/pd.207"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1016\/S1097-2765(00)80169-0"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1007\/s004670100634"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(05)65703-5"},{"key":"R24","doi-asserted-by":"crossref","unstructured":"Pachnis V, Mankoo B, and Costantini F.Expression of the c-ret proto-oncogene during mouse embryogenesis.Development119: 1005\u20131017, 1993.","DOI":"10.1242\/dev.119.4.1005"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1046\/j.1469-0705.2001.00333.x"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1038\/ng0495-358"},{"key":"R27","doi-asserted-by":"crossref","unstructured":"Schuchardt A, D'Agati V, Pachnis V, and Costantini F.Renal agenesis and hypodysplasia inret-k\u2212mutant mice result from defects in ureteric bud development.Development122: 1919\u20131929, 1996.","DOI":"10.1242\/dev.122.6.1919"},{"key":"R28","unstructured":"Schwarz R, Stephens F, and Cussen L.The pathogenesis of renal dysplasia. II. The significance of lateral and medial ectopy of the ureteric orifice.Invest Urol19: 97\u2013100, 1981."},{"key":"R29","doi-asserted-by":"crossref","unstructured":"Srinivas S, Wu Z, Chen CM, D'Agati V, and Costantini F.Dominant effects of RET receptor misexpression and ligand-independent RET signaling on ureteric bud development.Development126: 1375\u20131386, 1999.","DOI":"10.1242\/dev.126.7.1375"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(17)62433-9"},{"key":"R31","doi-asserted-by":"crossref","unstructured":"Theiler K.The House Mouse: Atlas of Embryonic Development.New York: Springer-Verlag, 1989.","DOI":"10.1007\/978-3-642-88418-4"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(17)60484-1"},{"key":"R33","unstructured":"Walsh P.Campbell's Urology.Philadelphia, PA: Saunders, vol. 1\u20133, 1998."},{"key":"R34","unstructured":"Wilkinson D.Essential Developmental Biology: A Practical Approach.Oxford, UK: Oxford University Press, 1993."}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00444.2003","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,6,25]],"date-time":"2021-06-25T05:18:37Z","timestamp":1624598317000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00444.2003"}},"issued":{"date-parts":[[2004,12]]},"references-count":34,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2004,12]]}},"alternative-id":["10.1152\/ajprenal.00444.2003"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00444.2003","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2004,12]]}},{"indexed":{"date-parts":[[2025,8,23]],"date-time":"2025-08-23T05:06:56Z","timestamp":1755925616390},"reference-count":9,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2011,8]]},"DOI":"10.1152\/ajprenal.00286.2011","type":"journal-article","created":{"date-parts":[[2011,6,3]],"date-time":"2011-06-03T09:51:26Z","timestamp":1307094686000},"page":"F295-F296","source":"Crossref","is-referenced-by-count":2,"title":["A new mouse model for Bartter's syndrome"],"prefix":"10.1152","volume":"301","author":[{"given":"Jacques","family":"Teulon","sequence":"first","affiliation":[{"name":"Universit\u00e9 Paris Descartes, Institut National de la Sant\u00e9 et de la Recherche M\u00e9dicale UMRS 872, Equipe 3; and Centre de Recherche des Cordeliers,"},{"name":"Universit\u00e9 Pierre et Marie Curie and Centre National de la Recherche Scientifique ERL7226, and"}]},{"given":"Dominique","family":"Eladari","sequence":"additional","affiliation":[{"name":"Universit\u00e9 Paris Descartes, Institut National de la Sant\u00e9 et de la Recherche M\u00e9dicale UMRS 872, Equipe 3; and Centre de Recherche des Cordeliers,"},{"name":"Universit\u00e9 Pierre et Marie Curie and Centre National de la Recherche Scientifique ERL7226, and"},{"name":"D\u00e9partement de Physiologie, Hopital Europ\u00e9en Georges Pompidou, Assistance Publique-Hopitaux de Paris, Paris, France"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfn689"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.3389\/fphys.2010.00155"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1007\/s00418-003-0535-2"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008010102"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1172\/JCI40145"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M205627200"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1172\/JCI4074"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1038\/emboj.2008.203"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.090091297"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00286.2011","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T00:14:33Z","timestamp":1567988073000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00286.2011"}},"issued":{"date-parts":[[2011,8]]},"references-count":9,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2011,8]]}},"alternative-id":["10.1152\/ajprenal.00286.2011"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00286.2011","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2011,8]]}},{"indexed":{"date-parts":[[2024,5,13]],"date-time":"2024-05-13T08:29:32Z","timestamp":1715588972990},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1977,11,1]]},"abstract":"<jats:p> The administration of corticosterone for 5 consecutive days to normal rats on a standard sodium intake induced negative sodium and water balance. These effects were opposite those observed under DOCA treatment. However, not only under DOCA but also under corticosterone treatment extracellular fluid volume (ECFV) and plasma volume (PV) increased, and blood pressure (BP) rose in parallel. Plasma renin and angiotensin II concentrations declined under the influence of both steroids. Plasma arginine vasopressin concentrations increased under DOCA, whereas they transiently decreased under corticosterone administration. These data suggest that the common mediator for BP elevation due to steroid excess would be an increase in ECFV and PV. The pathways by which this increase is achieved seem to be different. Under DOCA treatment ECFV and PV increased subsequent to renal sodium and water retention. Under corticosterone, however, sodium and water were shifted from intra- to extracellular compartments, and a fraction of this shifted sodium and water was conserved in extracellular space, most likely because corticosterone also affected renal sodium handling. <\/jats:p>","DOI":"10.1152\/ajprenal.1977.233.5.f403","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T15:08:13Z","timestamp":1513955293000},"page":"F403-F411","source":"Crossref","is-referenced-by-count":11,"title":["Comparative study on development of corticosterone and DOCA hypertension in rats"],"prefix":"10.1152","volume":"233","author":[{"given":"D.","family":"Haack","sequence":"first","affiliation":[]},{"given":"J.","family":"Mohring","sequence":"additional","affiliation":[]},{"given":"B.","family":"Mohring","sequence":"additional","affiliation":[]},{"given":"M.","family":"Petri","sequence":"additional","affiliation":[]},{"given":"E.","family":"Hackenthal","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1977.233.5.F403","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T14:56:06Z","timestamp":1567954566000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1977.233.5.F403"}},"issued":{"date-parts":[[1977,11,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1977,11,1]]}},"alternative-id":["10.1152\/ajprenal.1977.233.5.F403"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1977.233.5.f403","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1977,11,1]]}},{"indexed":{"date-parts":[[2024,9,6]],"date-time":"2024-09-06T02:10:02Z","timestamp":1725588602103},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1993,8,1]]},"abstract":"<jats:p> This study examined the interaction of 1 alpha,25-dihydroxyvitamin D3 [1,25(OH)2D3] and parathyroid hormone (PTH) on Ca2+ uptake, intracellular Ca2+ ([Ca2+]i) and membrane voltage in transformed mouse distal convoluted tubule (DCT) cells. 1,25(OH)2D3 increased PTH-dependent 45Ca2+ uptake by 2 h and was maximally stimulated at 5 h over the range of 10(-11) to 10(-9) M 1,25(OH)2D3. [Ca2+]i was measured in single cells grown on cover slips and loaded with fura-2. In control cells [Ca2+]i averaged 109 nM and was not changed by acute addition of 1,25(OH)2D3 (10(-7) M) alone or by pretreatment with 1,25(OH)2D3 for 5 h. The magnitude of the bPTH-(1-34)-stimulated increase of [Ca2+]i was similar in control cells and in cells pretreated with 1,25(OH)2D3. In cells pretreated with 1,25(OH)2D3 the latency before [Ca2+]i increased, following addition of PTH, was reduced from 8.6 min to 3.5 +\/- 0.9 min (P &lt; 0.01). 1,25(OH)2D3 alone had no effect on 45Ca2+ uptake but shortened the time course of PTH-dependent 45Ca2+ uptake. The inactive vitamin D analogue, 25-hydroxyvitamin D3 (10(-7) M) (with or without PTH), did not affect 45Ca2+ uptake. Inhibition of transcription with 5-6-dichloro-1-beta-D- ribofuranosylbenzimidazole abolished the effect of 1,25(OH)2D3, but not that of PTH. Treatment with 1,25(OH)2D3 also decreased the latency but not the magnitude of membrane hyperpolarization induced by PTH. Nifedipine abolished PTH-induced increases of [Ca2+]i and 45Ca2+ entry in cells pretreated with 1,25(OH)2D3.(ABSTRACT TRUNCATED AT 250 WORDS) <\/jats:p>","DOI":"10.1152\/ajprenal.1993.265.2.f300","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T05:16:32Z","timestamp":1514006192000},"page":"F300-F308","source":"Crossref","is-referenced-by-count":16,"title":["Vitamin D3 accelerates PTH-dependent calcium transport in distal convoluted tubule cells"],"prefix":"10.1152","volume":"265","author":[{"given":"P. A.","family":"Friedman","sequence":"first","affiliation":[{"name":"Department of Pharmacology and Toxicology, Dartmouth Medical School,Hanover, New Hampshire 03755-3835."}]},{"given":"F. A.","family":"Gesek","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, Dartmouth Medical School,Hanover, New Hampshire 03755-3835."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1993.265.2.F300","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:27:12Z","timestamp":1567960032000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1993.265.2.F300"}},"issued":{"date-parts":[[1993,8,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1993,8,1]]}},"alternative-id":["10.1152\/ajprenal.1993.265.2.F300"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1993.265.2.f300","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1993,8,1]]}},{"indexed":{"date-parts":[[2024,9,15]],"date-time":"2024-09-15T22:44:14Z","timestamp":1726440254900},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1988,7,1]]},"abstract":"<jats:p> Cells of the medullary segment of the thick ascending limb of Henle's loop (TALH) convert arachidonic acid (AA) via the cytochrome P-450 monooxygenase pathway to biologically active metabolites: P1, a vasorelaxant, and P2, an inhibitor of Na+-K+-ATPase activity. These AA metabolites may contribute to the renal vascular and metabolic adjustments in response to renal hypoperfusion and the attendant elevation of blood pressure produced by suprarenal aortic coarctation. On the eighth postoperative day, the blood pressures of hypertensive and sham-operated control rabbits were 105 (90-115) and 63 (60-64) mmHg (medians with semiquartile values), respectively (P less than 0.01). Formation of P1 and P2 was increased twofold in TALH cells obtained from hypertensive rabbits: 2.35 (1.79-4.83) and 1.28 (1.56-4.56) micrograms AA converted.mg protein-1.30 min-1 compared with sham-operated rabbits: 1.27 (1.03-1.53) and 0.64 (0.58-1.10) micrograms AA converted.mg protein-1.30 min-1 (P less than 0.05). The profile of biological activity of AA metabolites contained within P1 and P2 was unaffected by aortic coarctation. The cytochrome P-450 monooxygenase-derived AA metabolites may exert a defensive function to limit the degree of TALH cell injury in response to renal hypoperfusion and associated zonal anoxia by reducing energy-dependent Na+-K+-ATPase activity and affecting local vasodilatation. <\/jats:p>","DOI":"10.1152\/ajprenal.1988.255.1.f151","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T03:07:22Z","timestamp":1513998442000},"page":"F151-F157","source":"Crossref","is-referenced-by-count":2,"title":["Renal cytochrome P-450-related arachidonate metabolism in rabbit aortic coarctation"],"prefix":"10.1152","volume":"255","author":[{"given":"M. A.","family":"Carroll","sequence":"first","affiliation":[{"name":"Department of Pharmacology, New York Medical College, Valhalla10595."}]},{"given":"M.","family":"Schwartzman","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, New York Medical College, Valhalla10595."}]},{"given":"M.","family":"Baba","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, New York Medical College, Valhalla10595."}]},{"given":"M. J.","family":"Miller","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, New York Medical College, Valhalla10595."}]},{"given":"J. C.","family":"McGiff","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, New York Medical College, Valhalla10595."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1988.255.1.F151","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:48:39Z","timestamp":1567972119000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1988.255.1.F151"}},"issued":{"date-parts":[[1988,7,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1988,7,1]]}},"alternative-id":["10.1152\/ajprenal.1988.255.1.F151"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1988.255.1.f151","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[1988,7,1]]}},{"indexed":{"date-parts":[[2024,9,15]],"date-time":"2024-09-15T22:44:41Z","timestamp":1726440281662},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1992,5,1]]},"abstract":"<jats:p> The present study was undertaken to determine the time courses and kinetics of the subcellular processing of 125I-insulin in isolated and in vitro perfused proximal tubules. Morphometric analysis demonstrated well-preserved ultrastructure after 90 min of perfusion. After luminal perfusion for 90 min the absorption was constant with time and reached steady state within 5 min (177 +\/- 7 fg.min-1.mm-1). Also the hydrolysis rate and tubular accumulation rate were constant and averaged 84 +\/- 8 and 93 +\/- 10 fg.min-1.mm-1, respectively. Free 125I appeared already within 5 min of perfusion and reached steady state within 10 min. From proximal tubules perfused with 125I-insulin for 30 min and chased for 60 min, a compartmental analysis revealed two compartments; half time (t1\/2) for delivery of insulin to the lysosomes was determined to be 8.5 min, and t1\/2 for lysosomal degradation was 72 min. The results demonstrated that internalization by endocytic invaginations, incorporation in endocytic vacuoles, fusion with lysosomes, and hydrolysis were rapid processes and reached maximum rates within few minutes. A significant transtubular transport of insulin to the peritubular compartment was determined to be a constant rate of 11.2 +\/- 0.7 fg.min-1.mm-1. Perfusion of tubules with insulin at high concentrations in the perfusate revealed that the transport was dependent on the absorbed amount and not on the perfused load, compatible with transport through the cells and not via a paracellular mechanism. The intactness of the tight junctions was supported by the following: 1) [14C]inulin leak did not increase with time and 2) enzyme-free intercellular spaces were evident after perfusion for only 5 min with microperoxidase (mol wt of 1,700). The transported 125I-insulin was trichloroacetic acid precipitable and immunoprecipitable. <\/jats:p>","DOI":"10.1152\/ajprenal.1992.262.5.f813","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T03:53:48Z","timestamp":1514001228000},"page":"F813-F822","source":"Crossref","is-referenced-by-count":2,"title":["Time course and kinetics of proximal tubular processing of insulin"],"prefix":"10.1152","volume":"262","author":[{"given":"S.","family":"Nielsen","sequence":"first","affiliation":[{"name":"Department of Cell Biology, University of Aarhus, Denmark."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1992.262.5.F813","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:16:43Z","timestamp":1567959403000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1992.262.5.F813"}},"issued":{"date-parts":[[1992,5,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1992,5,1]]}},"alternative-id":["10.1152\/ajprenal.1992.262.5.F813"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1992.262.5.f813","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[1992,5,1]]}},{"indexed":{"date-parts":[[2024,7,30]],"date-time":"2024-07-30T23:18:23Z","timestamp":1722381503866},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1990,1,1]]},"abstract":"<jats:p> Sorbitol accumulates in renal medullary cells by synthesis from glucose in a reaction catalyzed by aldose reductase. Medullary sodium and urea are high and vary with urinary concentration. Sorbitol varies similarly, consistent with its role as a compatible intracellular organic osmolyte. We measured renal medullary sodium, urea, sorbitol, aldose reductase (protein and activity), and aldose reductase mRNA in rats treated to change medullary sodium and urea. In untreated Brattleboro rats all measurements were low and increased after 7 days of treatment with arginine vasopressin. In contrast, when normal rats were water deprived for 3 days, urea increased out of proportion to sodium, and sorbitol, aldose reductase, and aldose reductase mRNA were unchanged. After 2 h of diuresis, normal rats had lower medullary sodium and urea and reduced mRNA and sorbitol; however aldose reductase did not change. These data are consistent with previous results from cultured cells in which altered extracellular sodium, but not urea, leads to rapid changes in aldose reductase mRNA and slow changes (days) in aldose reductase. In addition, acute decreases in extracellular sodium increase leakage of sorbitol from cells. We also confirm previous results showing medullary glycerophosphorylcholine correlates best with urea, whereas the sum of all compatible osmolytes correlates best with sodium. <\/jats:p>","DOI":"10.1152\/ajprenal.1990.258.1.f154","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T16:46:30Z","timestamp":1513961190000},"page":"F154-F161","source":"Crossref","is-referenced-by-count":5,"title":["In vivo osmoregulation of aldose reductase mRNA, protein, and sorbitol in renal medulla"],"prefix":"10.1152","volume":"258","author":[{"suffix":"Jr","given":"B. D.","family":"Cowley","sequence":"first","affiliation":[{"name":"National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892."}]},{"given":"J. D.","family":"Ferraris","sequence":"additional","affiliation":[{"name":"National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892."}]},{"given":"D.","family":"Carper","sequence":"additional","affiliation":[{"name":"National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892."}]},{"given":"M. B.","family":"Burg","sequence":"additional","affiliation":[{"name":"National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1990.258.1.F154","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:12:58Z","timestamp":1567955578000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1990.258.1.F154"}},"issued":{"date-parts":[[1990,1,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1990,1,1]]}},"alternative-id":["10.1152\/ajprenal.1990.258.1.F154"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1990.258.1.f154","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1990,1,1]]}},{"indexed":{"date-parts":[[2025,3,28]],"date-time":"2025-03-28T19:10:04Z","timestamp":1743189004288,"version":"3.40.3"},"reference-count":39,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2012,8,1]]},"abstract":"<jats:p>Temporal adaptation of tubuloglomerular feedback (TGF) permits readjustment of the relationship of nephron filtration rate [single nephron glomerular filtration rate (SNGFR)] and early distal tubular flow rate (V<jats:sub>ED<\/jats:sub>) while maintaining TGF responsiveness. We used closed-loop assessment of TGF in hydropenia and after acute saline volume expansion (SE; 10% body wt over 1 h) to determine whether 1) temporal adaptation of TGF occurs, 2) adenosine A<jats:sub>1<\/jats:sub>receptors (A<jats:sub>1<\/jats:sub>R) mediate TGF responsiveness, and 3) inhibition of TGF affects SNGFR, V<jats:sub>ED<\/jats:sub>, or urinary excretion under these conditions. SNGFR was evaluated in Fromter-Wistar rats by micropuncture in 1) early distal tubules (ambient flow at macula densa), 2) recollected from early distal tubules while 12 nl\/min isotonic fluid was added to late proximal tubule (increased flow to macula densa), and 3) from proximal tubules of same nephrons (zero flow to macula densa). SE increased both ambient SNGFR and V<jats:sub>ED<\/jats:sub>compared with hydropenia, whereas TGF responsiveness (proximal-distal difference in SNGFR, distal SNGFR response to adding fluid to proximal tubule) was maintained, demonstrating TGF adaptation. A<jats:sub>1<\/jats:sub>R blockade completely inhibited TGF responsiveness during SE and made V<jats:sub>ED<\/jats:sub>more susceptible to perturbation in proximal tubular flow, but did not alter ambient SNGFR or V<jats:sub>ED<\/jats:sub>. Greater urinary excretion of fluid and Na<jats:sup>+<\/jats:sup>with A<jats:sub>1<\/jats:sub>R blockade may reflect additional effects on the distal nephron in hydropenia and SE. In conclusion, A<jats:sub>1<\/jats:sub>R-independent mechanisms adjust SNGFR and V<jats:sub>ED<\/jats:sub>to higher values after SE, which facilitates fluid and Na<jats:sup>+<\/jats:sup>excretion. Concurrently, TGF adapts and stabilizes early distal delivery at the new setpoint in an A<jats:sub>1<\/jats:sub>R-dependent mechanism.<\/jats:p>","DOI":"10.1152\/ajprenal.00329.2011","type":"journal-article","created":{"date-parts":[[2012,5,24]],"date-time":"2012-05-24T03:17:24Z","timestamp":1337829444000},"page":"F405-F411","source":"Crossref","is-referenced-by-count":9,"title":["Acute saline expansion increases nephron filtration and distal flow rate but maintains tubuloglomerular feedback responsiveness: role of adenosine A<sub>1<\/sub>receptors"],"prefix":"10.1152","volume":"303","author":[{"given":"Roland C.","family":"Blantz","sequence":"first","affiliation":[{"name":"Division of Nephrology-Hypertension and O'Brien Kidney Center for Acute Kidney Injury, University of California, San Diego, School of Medicine and the Veterans Affairs San Diego Health Care System, San Diego, California"}]},{"given":"Prabhleen","family":"Singh","sequence":"additional","affiliation":[{"name":"Division of Nephrology-Hypertension and O'Brien Kidney Center for Acute Kidney Injury, University of California, San Diego, School of Medicine and the Veterans Affairs San Diego Health Care System, San Diego, California"}]},{"given":"Aihua","family":"Deng","sequence":"additional","affiliation":[{"name":"Division of Nephrology-Hypertension and O'Brien Kidney Center for Acute Kidney Injury, University of California, San Diego, School of Medicine and the Veterans Affairs San Diego Health Care System, San Diego, California"}]},{"given":"Scott C.","family":"Thomson","sequence":"additional","affiliation":[{"name":"Division of Nephrology-Hypertension and O'Brien Kidney Center for Acute Kidney Injury, University of California, San Diego, School of Medicine and the Veterans Affairs San Diego Health Care System, San Diego, California"}]},{"given":"Volker","family":"Vallon","sequence":"additional","affiliation":[{"name":"Division of Nephrology-Hypertension and O'Brien Kidney Center for Acute Kidney Injury, University of California, San Diego, School of Medicine and the Veterans Affairs San Diego Health Care System, San Diego, California"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-4684-9252-1_17"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.260.5.F749"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.267.2.F223"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.3.F409"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00509.x"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1111\/j.2042-7158.1991.tb06651.x"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1988.sp016934"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1007\/BF00585122"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00682.x"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00343.2005"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.66033.x"},{"key":"B12","doi-asserted-by":"crossref","first-page":"527","DOI":"10.1016\/S0031-6997(24)01511-4","volume":"53","author":"Fredholm BB","year":"2001","journal-title":"Pharmacol Rev"},{"key":"B13","doi-asserted-by":"crossref","first-page":"69","DOI":"10.1152\/ajplegacy.1954.180.1.69","volume":"180","author":"Goodyer AV","year":"1955","journal-title":"Am J Physiol"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1007\/BF00362733"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00113.2005"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00061.2008"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1159\/000108625"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1007\/BF00582339"},{"key":"B19","first-page":"263","author":"Rector FC","year":"1971","journal-title":"Rec Advan Renal Physiol Int Symp Renal Handling of Sodium, Brestenberg"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1096\/fj.07-8807com"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002369"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.259.4.F565"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.145"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.258.3.F553"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1172\/JCI108527"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.171317998"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1172\/JCI8761"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.6.F1123"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1172\/JCI5156"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.264.6.F930"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.270.3.F461"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00340.2003"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1172\/JCI26092"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1997.273.4.R1414"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.06713.x"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00031.2005"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-004-1239-8"},{"key":"B38","doi-asserted-by":"crossref","first-page":"1297","DOI":"10.1152\/ajplegacy.1971.221.5.1297","volume":"221","author":"Wallin JD","year":"1971","journal-title":"Am J Physiol"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1987.198"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00329.2011","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,3,28]],"date-time":"2025-03-28T18:29:42Z","timestamp":1743186582000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00329.2011"}},"issued":{"date-parts":[[2012,8,1]]},"references-count":39,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2012,8,1]]}},"alternative-id":["10.1152\/ajprenal.00329.2011"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00329.2011","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2012,8,1]]}},{"indexed":{"date-parts":[[2025,9,26]],"date-time":"2025-09-26T16:58:27Z","timestamp":1758905907070,"version":"3.38.0"},"reference-count":45,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2011,6]]},"abstract":"<jats:p>Increased aortic pulse-wave velocity (PWV) reflects increased arterial stiffness and is a strong predictor of cardiovascular risk in chronic kidney disease (CKD). We examined functional and structural correlations among PWV, aortic calcification, and vascular remodeling in a rodent model of CKD, the Lewis polycystic kidney (LPK) rat. Hemodynamic parameters and beat-to-beat aortic PWV were recorded in urethane-anesthetized animals [12-wk-old hypertensive female LPK rats ( n = 5)] before the onset of end-stage renal disease and their age- and sex-matched normotensive controls (Lewis, n = 6). Animals were euthanized, and the aorta was collected to measure calcium content by atomic absorption spectrophotometry. A separate cohort of animals ( n = 5\/group) were anesthetized with pentobarbitone sodium and pressure perfused with formalin, and the aorta was collected for histomorphometry, which allowed calculation of aortic wall thickness, medial cross-sectional area (MCSA), elastic modulus (EM), and wall stress (WS), size and density of smooth muscle nuclei, and relative content of lamellae, interlamellae elastin, and collagen. Mean arterial pressure (MAP) and PWV were significantly greater in the LPK compared with Lewis (72 and 33%, respectively) animals. The LPK group had 6.8-fold greater aortic calcification, 38% greater aortic MCSA, 56% greater EM\/WS, 13% greater aortic wall thickness, 21% smaller smooth muscle cell area, and 20% less elastin density with no difference in collagen fiber density. These findings demonstrate vascular remodeling and increased calcification with a functional increase in PWV and therefore aortic stiffness in hypertensive LPK rats.<\/jats:p>","DOI":"10.1152\/ajprenal.00079.2011","type":"journal-article","created":{"date-parts":[[2011,4,7]],"date-time":"2011-04-07T01:38:37Z","timestamp":1302140317000},"page":"F1431-F1436","source":"Crossref","is-referenced-by-count":52,"title":["Aortic stiffness is associated with vascular calcification and remodeling in a chronic kidney disease rat model"],"prefix":"10.1152","volume":"300","author":[{"given":"Keith","family":"Ng","sequence":"first","affiliation":[{"name":"Australian School of Advanced Medicine, Macquarie University, Sydney, New South Wales, Australia"}]},{"given":"Cara M.","family":"Hildreth","sequence":"additional","affiliation":[{"name":"Australian School of Advanced Medicine, Macquarie University, Sydney, New South Wales, Australia"}]},{"given":"Jacqueline K.","family":"Phillips","sequence":"additional","affiliation":[{"name":"Australian School of Advanced Medicine, Macquarie University, Sydney, New South Wales, Australia"}]},{"given":"Alberto P.","family":"Avolio","sequence":"additional","affiliation":[{"name":"Australian School of Advanced Medicine, Macquarie University, Sydney, New South Wales, Australia"}]}],"member":"24","reference":[{"key":"B1","first-page":"36","volume":"11","author":"Abramoff MD","year":"2004","journal-title":"Biophoton Int"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/ajh.2010.192"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1097\/01.hjh.0000334602.71005.52"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.29.3.770"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1111\/j.1447-0594.2009.00528.x"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.71.2.202"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00932.x"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1097\/HJH.0b013e32833c2177"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1159\/000101369"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.01271.2004"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.3109\/0886022X.2010.502607"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00732.2006"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1932554100"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1093\/cvr\/cvn022"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2006.04.083"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/j.autneu.2009.09.019"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1093\/eurheartj\/ehq237"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1159\/000113013"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1097\/HJH.0b013e32833f5e68"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1001\/archinte.164.6.659"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/S0024-3205(00)00567-1"},{"key":"B22","doi-asserted-by":"crossref","first-page":"1063","DOI":"10.1016\/S0022-3565(25)22510-1","volume":"270","author":"Kost CK","year":"1994","journal-title":"J Pharmacol Exp Ther"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.37.5.1236"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.63.1.227"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1990.19"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.09008.x"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.108.126615"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000239206.64270.5f"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000165310.84801.e0"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000114581.77705.29"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/jappl.1997.82.1.203"},{"volume-title":"McDonald's Blood Flow in Arteries: Theoretical, Experimental and Clinical Principles","year":"1998","author":"Nichols WW","key":"B32"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1159\/000159247"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.29.4.999"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1038\/ajh.2007.89"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000168052.00426.65"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1159\/000101828"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000069826.36125.B4"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000240346.42873.f6"},{"key":"B40","doi-asserted-by":"crossref","first-page":"2117","DOI":"10.1681\/ASN.V12102117","volume":"12","author":"Shoji T","year":"2001","journal-title":"J Am Soc Nephrol"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1097\/HJH.0b013e328331b81e"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1797.2008.01056.x"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.107.089391"},{"key":"B44","first-page":"133","volume":"68","author":"Wimmer NJ","year":"2007","journal-title":"Clin Nephrol"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.28.6.622"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00079.2011","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,3,4]],"date-time":"2025-03-04T22:56:12Z","timestamp":1741128972000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00079.2011"}},"issued":{"date-parts":[[2011,6]]},"references-count":45,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2011,6]]}},"alternative-id":["10.1152\/ajprenal.00079.2011"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00079.2011","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2011,6]]}},{"indexed":{"date-parts":[[2025,10,21]],"date-time":"2025-10-21T15:22:10Z","timestamp":1761060130800},"reference-count":38,"publisher":"American Physiological Society","issue":"3","funder":[{"name":"National Institutes of Helath","award":["dk38432"],"award-info":[{"award-number":["dk38432"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2016,9,1]]},"abstract":"<jats:p> \u03b1<jats:sub>1<\/jats:sub>-Microglobulin (A1M) is a low-molecular-weight heme-binding antioxidant protein that is readily filtered by the glomerulus and reabsorbed by proximal tubules. Given these properties, recombinant A1M (rA1M) has been proposed as a renal antioxidant and therapeutic agent. However, little direct evidence to support this hypothesis exists. Hence, we have sought \u201cproof of concept\u201d in this regard. Cultured proximal tubule (HK-2) cells or isolated mouse proximal tubule segments were challenged with a variety of prooxidant insults: 1) hemin, 2) myoglobin; 3) \u201ccatalytic\u201d iron, 4) H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>\/Fenton reagents, 5) a Ca<jats:sup>2+<\/jats:sup> ionophore, 6) antimycin A, or 7) hypoxia (with or without rA1M treatment). HK-2 injury was gauged by the percent lactate dehydrogenase release and 4,5-(dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide uptake. In vivo protection was sought in rA1M-treated mice subjected to 1) graded myohemoglobinura (2, 4, 8, or 9 ml\/kg glycerol injection), 2) purified myoglobinemia\/uria, or 3) endotoxemia. In vivo injury was assessed by blood urea nitrogen, creatinine, and the expression of redox-sensitive genes (heme oxygenase-1, neutrophil gelatinase-associated lipocalin, and monocyte chemoattractant protein-1 mRNAs). Although rA1M totally blocked in vitro hemin toxicity, equimolar albumin (another heme binder) or 10% serum induced equal protection. rA1M failed to mitigate any nonhemin forms of either in vitro or in vivo injury. A1M appeared to be rapidly degraded within proximal tubules (by Western blot analysis). Surprisingly, rA1M exerted select injury-promoting effects (increased in vitro catalytic iron\/antimycin toxicities and increased in vivo monocyte chemoattractant protein-1\/neutrophil gelatinase-associated lipocalin mRNA expression after glycerol or endotoxin injection). We conclude that rA1M has questionable utility as a renal antioxidant\/cytoprotective agent, particularly in the presence of larger amounts of competitive free heme (e.g., albumin) binders. <\/jats:p>","DOI":"10.1152\/ajprenal.00264.2016","type":"journal-article","created":{"date-parts":[[2016,5,11]],"date-time":"2016-05-11T22:35:32Z","timestamp":1463006132000},"page":"F640-F651","source":"Crossref","is-referenced-by-count":9,"title":["An evaluation of the antioxidant protein \u03b1<sub>1<\/sub>-microglobulin as a renal tubular cytoprotectant"],"prefix":"10.1152","volume":"311","author":[{"given":"Richard A.","family":"Zager","sequence":"first","affiliation":[{"name":"Fred Hutchinson Cancer Center, Seattle, Washington; and"},{"name":"University of Washington, Seattle Washington"}]},{"given":"Ali C. M.","family":"Johnson","sequence":"additional","affiliation":[{"name":"Fred Hutchinson Cancer Center, Seattle, Washington; and"}]},{"given":"Kirsten","family":"Frostad","sequence":"additional","affiliation":[{"name":"Fred Hutchinson Cancer Center, Seattle, Washington; and"}]}],"member":"24","reference":[{"key":"B1","first-page":"333","volume":"5","author":"Ahlstedt J","year":"2015","journal-title":"Am J Nucl Med Mol Imaging"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.3390\/ijms161226234"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/j.freeradbiomed.2014.06.025"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/S0167-4838(00)00157-6"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1159\/000183608"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0090020"},{"key":"B7","doi-asserted-by":"crossref","first-page":"e0138111","DOI":"10.1371\/journal.pone.0138111","volume":"10","author":"Edstr\u00f6m-H\u00e4gerwall A","year":"2015","journal-title":"PLos One"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1136\/jcp.41.11.1176"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1021\/bi00436a045"},{"key":"B10","first-page":"S31","volume":"75","author":"Gram M","year":"2015","journal-title":"Free Radic Biol Med"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0138111"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2015.06.018"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.378"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.268.6.F1154"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.3389\/fphys.2014.00465"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1067\/mlc.2001.112957"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010060641"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0125499"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007121368"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1089\/ars.2012.4658"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbapap.2015.10.002"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.6"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1016\/S0925-4773(02)00202-2"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.3389\/fphys.2015.00187"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00502.2013"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1111\/j.1432-1033.1997.00676.x"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00654.2010"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0086353"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1136\/jcp.36.3.253"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.48"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.104"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.65.5.1263"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00426.2012"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2011121147"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0066776"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0098380"},{"key":"B37","first-page":"180","volume":"56","author":"Zager RA","year":"1987","journal-title":"Lab Invest"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00168.2012"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00264.2016","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:41:10Z","timestamp":1567975270000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00264.2016"}},"issued":{"date-parts":[[2016,9,1]]},"references-count":38,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2016,9,1]]}},"alternative-id":["10.1152\/ajprenal.00264.2016"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00264.2016","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2016,9,1]]}},{"indexed":{"date-parts":[[2025,10,8]],"date-time":"2025-10-08T16:13:46Z","timestamp":1759940026123},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1997,3,1]]},"abstract":"<jats:p> Decreases in plasma folate levels leading to folate deficiency can result from increased urinary loss of folate, due to changes in either the renal reabsorption or secretion of folate. Hence, human proximal tubule (HPT) cells were cultured on microporous membranes to separate apical (AP) and basolateral (BL) domains and to assess the transport of 5-methyltetrahydrofolate from AP-to-BL (i.e., reabsorptive) and BL-to-AP (secretory) directions. Cellular uptake of alpha-methylglucoside occurred specifically from the AP direction, and transport of p-aminohippurate occurred more readily from the BL direction, demonstrating cell polarity similar to that in vivo. Under tight monolayer conditions, binding of folate to the AP membrane occurred more readily from the AP direction, although AP binding also occurred from the BL chamber. Intracellular transport occurred equally from both AP and BL directions. When loaded from either direction, folate was effluxed from HPT cells into both AP and BL chambers. About 20-30% of the internalized substrate was converted to nonfolate catabolites. Thus HPT cells readily take up folate via both the AP and BL membranes, metabolize it intracellularly and secrete the products across both membranes. These studies suggest that renal folate homeostasis is regulated bidirectionally. <\/jats:p>","DOI":"10.1152\/ajprenal.1997.272.3.f380","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T03:08:36Z","timestamp":1513998516000},"page":"F380-F388","source":"Crossref","is-referenced-by-count":4,"title":["Reabsorptive and secretory 5-methyltetrahydrofolate transport pathways in cultured human proximal tubule cells"],"prefix":"10.1152","volume":"272","author":[{"given":"K. M.","family":"Morshed","sequence":"first","affiliation":[{"name":"Department of Pharmacology and Therapeutics, Louisiana StateUniversity Medical Center, Shreveport 71130, USA."}]},{"given":"K. E.","family":"McMartin","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Therapeutics, Louisiana StateUniversity Medical Center, Shreveport 71130, USA."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1997.272.3.F380","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:13:01Z","timestamp":1567959181000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1997.272.3.F380"}},"issued":{"date-parts":[[1997,3,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1997,3,1]]}},"alternative-id":["10.1152\/ajprenal.1997.272.3.F380"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1997.272.3.f380","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1997,3,1]]}},{"indexed":{"date-parts":[[2025,10,9]],"date-time":"2025-10-09T06:31:39Z","timestamp":1759991499674},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1985,5,1]]},"abstract":"<jats:p> A method is described for determining glomerular filtration rate (GFR) in conscious unrestrained rats without extracellular volume expansion. The glomerular marker used was 14C-labeled inulin infused in the minimal fluid volume of 1 microliter\/h by intraperitoneally implanted osmotic minipumps. The workability, reproducibility, and precision of the technique was evaluated in sham-operated (sham) and uninephrectomized (UNI-NX) rats for 6 days. In six sham-operated rats the clearance of [14C]-inulin calculated from the plasma value obtained in a blood sample taken at 10 A.M. before food consumption was (means +\/- SE): day 1 after pump implantation: 1.38 +\/- 0.05; day 2: 1.27 +\/- 0.05; day 3: 1.46 +\/- 0.16; day 4: 1.45 +\/- 0.15; day 5: 1.33 +\/- 0.08; day 6: 1.38 +\/- 0.11 ml\/min. In six UNI-NX rats the corresponding values were: day 1: 0.88 +\/- 0.04; day 2: 0.79 +\/- 0.05; day 3: 0.91 +\/- 0.03; day 4: 0.91 +\/- 0.03; day 5: 0.83 +\/- 0.06; day 6: 0.87 +\/- 0.05 ml\/min. When determined on day 2, 3, or 6 at 6 P.M., i.e., at the end of the food consumption period, [14C]inulin clearance was increased in all animals compared with the value determined at 10 A.M. in the fasted state. The use of implanted osmotic minipumps for delivering a glomerular marker such as [14C]inulin allows the determination of GFR in conscious unrestrained rats with normal fluid balance conditions. This method appears to be particularly appropriate for studying the influence of the intake and composition of food on GFR in physiological conditions. <\/jats:p>","DOI":"10.1152\/ajprenal.1985.248.5.f734","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T19:32:13Z","timestamp":1513971133000},"page":"F734-F738","source":"Crossref","is-referenced-by-count":10,"title":["Measurement of glomerular filtration rate in conscious unrestrained rats with inulin infused by implanted osmotic pumps"],"prefix":"10.1152","volume":"248","author":[{"given":"J.","family":"Jobin","sequence":"first","affiliation":[]},{"given":"J. P.","family":"Bonjour","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1985.248.5.F734","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:32:11Z","timestamp":1567956731000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1985.248.5.F734"}},"issued":{"date-parts":[[1985,5,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1985,5,1]]}},"alternative-id":["10.1152\/ajprenal.1985.248.5.F734"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1985.248.5.f734","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1985,5,1]]}},{"indexed":{"date-parts":[[2025,10,20]],"date-time":"2025-10-20T10:22:16Z","timestamp":1760955736051},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1985,11,1]]},"abstract":"<jats:p> We recently emphasized that ATP is an obligatory product of renal glutamine metabolism and that all cells must remain in ATP balance. Based on this, we suggested that the maximum rate of renal ammoniagenesis in dogs with chronic metabolic acidosis may be limited by the rate of ATP utilization in the kidney. Since a large infusion of glutamine led to a twofold increase in renal ammoniagenesis in acidotic dogs, we wished to evaluate the renal metabolic changes that permitted this increment within the constraints of renal ATP balance. A large glutamine infusion did not lead to an augmented rate of ATP hydrolysis because renal oxygen consumption was not increased. Two major metabolic changes could explain this stimulation while maintaining ATP balance: first, ATP production from lactate by the kidney was decreased following the glutamine infusion; second, the metabolic fate of glutamine was changed so that more ammonium per ATP was synthesized (i.e., the rates of amino acid release into the renal vein were markedly enhanced, and gluconeogenesis was now a quantitatively significant process). 3-Mercaptopicolinate, an inhibitor of phosphoenolpyruvate carboxykinase, when infused with glutamine, apparently decreased the calculated rate of gluconeogenesis as expected; however, ammonium production did not decline, because the rate of amino acid release increased further, as did the rate of oxygen consumption. Therefore, a large glutamine infusion increased renal ammoniagenesis in dogs with chronic metabolic acidosis while maintaining ATP balance, because ATP production from other substrates was decreased and because the fate of glutamine metabolism was altered in that less ATP was formed per glutamine utilized. <\/jats:p>","DOI":"10.1152\/ajprenal.1985.249.5.f745","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T19:00:57Z","timestamp":1513969257000},"page":"F745-F752","source":"Crossref","is-referenced-by-count":3,"title":["Regulation of renal ammoniagenesis in the dog with chronic metabolic acidosis: effect of a glutamine load"],"prefix":"10.1152","volume":"249","author":[{"given":"A.","family":"Gougoux","sequence":"first","affiliation":[]},{"given":"P.","family":"Vinay","sequence":"additional","affiliation":[]},{"given":"M. L.","family":"Halperin","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1985.249.5.F745","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:29:41Z","timestamp":1567956581000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1985.249.5.F745"}},"issued":{"date-parts":[[1985,11,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1985,11,1]]}},"alternative-id":["10.1152\/ajprenal.1985.249.5.F745"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1985.249.5.f745","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1985,11,1]]}},{"indexed":{"date-parts":[[2025,9,10]],"date-time":"2025-09-10T22:01:04Z","timestamp":1757541664365},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1989,5,1]]},"abstract":"<jats:p> Acetazolamide (ACZL) inhibits luminal acidification by the turtle urinary bladder, a process thought to be mediated by the drug's ability to inhibit carbonic anhydrase (CA) and thus elevate cell pH. To test the hypothesis that these transport changes are actually mediated by changes of cell pH, we measured this parameter in single, identifiable mucosal cells using 4-methylumbelliferone and fluorescence microscopy. In control bladders 5 X 10(-4) M ACZL inhibited proton transport by 80 +\/- 6%, and alkalinized cell pH, especially in a subpopulation of CA cells. A much larger cell alkalinization was induced by serosal HCO3- but proton transport fell only 30 +\/- 7%. When cell pH was clamped at approximately 7.0 using 50 mM dimethyloxazolidinedione, or when cell pH was acidified using 7.5 mM propionate, transport rates still declined by 74 +\/- 2, and 100 +\/- 12%, respectively, in response to ACZL. In propionate-acidified bladders, 1 mM sodium azide blocked the inhibition of transport seen with 5 X 10(-4) M ACZL and reversed the inhibition with 10(-5) M ACZL. The apical endocytosis rate was increased by ACZL in normal and propionate-acidified bladders, but was not stimulated by alkalinizing the cell with NH4Cl. We conclude that ACZL can induce cellular alkalinization in this tissue, but that this pH change is not required for the inhibition of transport, or the ACZL-associated stimulation of endocytosis. The drug's ability to inhibit acidification appears to be the result of an azide-sensitive mechanism that has yet to be defined. <\/jats:p>","DOI":"10.1152\/ajprenal.1989.256.5.f923","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T20:51:24Z","timestamp":1513975884000},"page":"F923-F931","source":"Crossref","is-referenced-by-count":1,"title":["Acetazolamide inhibits acidification by the turtle bladder independent of cell pH"],"prefix":"10.1152","volume":"256","author":[{"given":"M.","family":"Graber","sequence":"first","affiliation":[{"name":"Department of Medicine, State University of New York, Stony Brook 11794."}]},{"given":"T.","family":"Dixon","sequence":"additional","affiliation":[{"name":"Department of Medicine, State University of New York, Stony Brook 11794."}]},{"given":"D.","family":"Coachman","sequence":"additional","affiliation":[{"name":"Department of Medicine, State University of New York, Stony Brook 11794."}]},{"given":"P.","family":"Devine","sequence":"additional","affiliation":[{"name":"Department of Medicine, State University of New York, Stony Brook 11794."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1989.256.5.F923","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:06:51Z","timestamp":1567969611000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1989.256.5.F923"}},"issued":{"date-parts":[[1989,5,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1989,5,1]]}},"alternative-id":["10.1152\/ajprenal.1989.256.5.F923"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1989.256.5.f923","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1989,5,1]]}},{"indexed":{"date-parts":[[2025,9,17]],"date-time":"2025-09-17T16:52:08Z","timestamp":1758127928684},"reference-count":31,"publisher":"American Physiological Society","issue":"9","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2012,11,1]]},"abstract":"<jats:p>We previously reported that mice with experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis (MS), develop profound urinary bladder dysfunction. Because neurogenic bladder in MS patients causes marked bladder remodeling, we next examined morphometric and molecular alterations of the bladder in EAE mice. EAE was created in female SJL\/J mice by immunization with the p139\u2013151 encephalitogenic peptide of myelin proteolipid protein in complete Freund's adjuvant, along with intraperitoneal injections of Bordetella pertussis toxin. Seventy days after immunization, mice were scored for the level of neurological impairment and then killed. Spinal cord sections were assessed for demyelination, inflammation, and T cell infiltration; the composition of the bladder tissue was measured quantitatively; and gene expression of markers of tissue remodeling and fibrosis was assessed. A significant increase in the bladder weight-to-body weight ratio was observed with increasing neurological impairment, and morphometric analysis showed marked bladder remodeling with increased luminal area and tissue hypertrophy. Despite increased amounts of all tissue components (urothelium, smooth muscle, and connective tissue), the ratio of connective tissue to muscle increased significantly in EAE mice compared with control mice. Marked increases in mRNA expression of collagen type I \u03b1<jats:sub>2<\/jats:sub>, tropoelastin, transforming growth factor-\u03b23, and connective tissue growth factor (CTGF) were observed in EAE mice, as were decreased levels of mRNAs for smooth muscle myosin heavy chain, nerve growth factors, and muscarinic and purinergic receptors. Our results suggest that bladder remodeling corresponding to EAE severity may be due to enhanced expression of CTGF and increased growth of connective tissue.<\/jats:p>","DOI":"10.1152\/ajprenal.00273.2012","type":"journal-article","created":{"date-parts":[[2012,9,20]],"date-time":"2012-09-20T00:46:37Z","timestamp":1348101997000},"page":"F1363-F1369","source":"Crossref","is-referenced-by-count":37,"title":["Connective tissue and its growth factor CTGF distinguish the morphometric and molecular remodeling of the bladder in a model of neurogenic bladder"],"prefix":"10.1152","volume":"303","author":[{"given":"Cengiz Z.","family":"Altuntas","sequence":"first","affiliation":[{"name":"Urology Institute, University Hospitals Case Medical Center and Department of Urology, Case Western Reserve University School of Medicine, Cleveland, Ohio;"}]},{"given":"Firouz","family":"Daneshgari","sequence":"additional","affiliation":[{"name":"Urology Institute, University Hospitals Case Medical Center and Department of Urology, Case Western Reserve University School of Medicine, Cleveland, Ohio;"}]},{"given":"Kenan","family":"Izgi","sequence":"additional","affiliation":[{"name":"Urology Institute, University Hospitals Case Medical Center and Department of Urology, Case Western Reserve University School of Medicine, Cleveland, Ohio;"},{"name":"Department of Chemistry, Cleveland State University, Cleveland, Ohio;"}]},{"given":"Fuat","family":"Bicer","sequence":"additional","affiliation":[{"name":"Urology Institute, University Hospitals Case Medical Center and Department of Urology, Case Western Reserve University School of Medicine, Cleveland, Ohio;"},{"name":"Department of Chemistry, Cleveland State University, Cleveland, Ohio;"}]},{"given":"Ahmet","family":"Ozer","sequence":"additional","affiliation":[{"name":"Urology Institute, University Hospitals Case Medical Center and Department of Urology, Case Western Reserve University School of Medicine, Cleveland, Ohio;"},{"name":"Department of Genetics, Case Western Reserve University School of Medicine, Cleveland, Ohio;"}]},{"given":"Cagri","family":"Sakalar","sequence":"additional","affiliation":[{"name":"Department of Immunology, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio; and"}]},{"given":"Kerry O.","family":"Grimberg","sequence":"additional","affiliation":[{"name":"Urology Institute, University Hospitals Case Medical Center and Department of Urology, Case Western Reserve University School of Medicine, Cleveland, Ohio;"}]},{"given":"Ismail","family":"Sayin","sequence":"additional","affiliation":[{"name":"Urology Institute, University Hospitals Case Medical Center and Department of Urology, Case Western Reserve University School of Medicine, Cleveland, Ohio;"},{"name":"Department of Biology, Case Western Reserve University, Cleveland, Ohio"}]},{"given":"Vincent K.","family":"Tuohy","sequence":"additional","affiliation":[{"name":"Department of Immunology, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio; and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1177\/1352458509104594"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jneuroim.2008.06.038"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1191\/1352458504ms1060oa"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1007\/978-90-481-3779-4_14"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006050525"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1089\/ars.2009.2737"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.00131.2002"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M109.040444"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(05)65931-9"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00301.x"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1023\/A:1021398626846"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/j.immuni.2010.03.004"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1016\/j.immuni.2004.08.018"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1111\/j.1464-410X.1984.tb07157.x"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(01)61760-9"},{"key":"B16","doi-asserted-by":"crossref","first-page":"231","DOI":"10.1097\/00029330-200702010-00012","volume":"120","author":"Liu FY","year":"2007","journal-title":"Chin Med J (Engl)"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00917.2005"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1114\/B:ABME.0000042228.89106.48"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(01)61915-3"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/j.cytogfr.2008.01.002"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1097\/00005072-199009000-00002"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/j.it.2005.08.014"},{"key":"B23","doi-asserted-by":"crossref","first-page":"1983","DOI":"10.1002\/art.27445","volume":"62","author":"Tran CM","year":"2010","journal-title":"Arthritis Rheum"},{"key":"B24","doi-asserted-by":"crossref","first-page":"1523","DOI":"10.4049\/jimmunol.142.5.1523","volume":"142","author":"Tuohy VK","year":"1989","journal-title":"J Immunol"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(17)45138-X"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/j.immuni.2006.01.001"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1006\/exnr.1999.7254"},{"key":"B28","volume-title":"Campbell-Walsh Urology","author":"Wein AJ","year":"2007"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1038\/cr.2009.5"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1084\/jem.183.4.1777"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0025958"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00273.2012","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,4,29]],"date-time":"2024-04-29T15:34:55Z","timestamp":1714404895000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00273.2012"}},"issued":{"date-parts":[[2012,11,1]]},"references-count":31,"journal-issue":{"issue":"9","published-print":{"date-parts":[[2012,11,1]]}},"alternative-id":["10.1152\/ajprenal.00273.2012"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00273.2012","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2012,11,1]]}},{"indexed":{"date-parts":[[2025,9,19]],"date-time":"2025-09-19T11:20:24Z","timestamp":1758280824629},"reference-count":40,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2005,11]]},"abstract":"<jats:p>We previously reported that inhibition of nitric oxide (NO) synthesis by N-nitro-l-arginine methyl ester (l-NAME) during late pregnancy leads to increased production of renal vascular 20-hydroxyeicosatetraenoic acid (20-HETE), a cytochrome P-450 (CYP) 4A-derived vasoconstrictor, in pregnant rats. However, the effect of upregulation of vascular 20-HETE production on renal function after NO inhibition is not known. To test the hypothesis that increased gestational vascular 20-HETE synthesis after NO inhibition is involved in mediating blood pressure and renal functional changes, we first determined the IC<jats:sub>50<\/jats:sub>value of the effect of nitroprusside (SNP), a NO donor, on renal 20-HETE production in cortical microsomes. We then divided pregnant rats and age-matched virgin rats into a vehicle control group, an l-NAME treatment group (0.25 mg\/ml in drinking water), and a group treated with l-NAME plus N-methylsulfonyl-12,12-dibromododec-11-enamide (DDMS; CYP4A-selective inhibitor, 10 mg\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7day<jats:sup>\u22121<\/jats:sup>iv). After 4 days of treatment, we measured blood pressure, renal blood flow (RBF), renal vascular resistance (RVR), and glomerular filtration rate (GFR) in each group. The addition of SNP (IC<jats:sub>50<\/jats:sub>= 22 \u03bcM) decreased renal cortical 20-HETE production. In pregnant rats, l-NAME treatment led to significantly higher mean arterial pressure (MAP) and RVR, and lower RBF and GFR. Combined treatment with DDMS and l-NAME significantly attenuated the increases in MAP and RVR and the decrease in GFR, but not the reduction in RBF induced by l-NAME treatment. l-NAME and l-NAME plus DDMS had no significant impact on renal hemodynamics in virgin rats. In addition, chronic treatment with DDMS selectively inhibited cortical 20-HETE production without a significant effect on CYP4A expression in l-NAME-treated pregnant rats. In conclusion, NO effectively inhibits renal cortical microsomal 20-HETE production in female rats. In pregnant rats, the augmentation of renal 20-HETE production after NO inhibition is associated with increased MAP and RVR, whereas decreased GFR is negated by treatment of a selective and competitive CYP4A inhibitor. These results demonstrate that the interaction between renal 20-HETE and NO is important in the regulation of renal function and blood pressure in pregnant rats.<\/jats:p>","DOI":"10.1152\/ajprenal.00149.2005","type":"journal-article","created":{"date-parts":[[2005,7,6]],"date-time":"2005-07-06T03:24:16Z","timestamp":1120620256000},"page":"F1116-F1122","source":"Crossref","is-referenced-by-count":6,"title":["Renal 20-HETE inhibition attenuates changes in renal hemodynamics induced by<scp>l<\/scp>-NAME treatment in pregnant rats"],"prefix":"10.1152","volume":"289","author":[{"given":"Hui","family":"Huang","sequence":"first","affiliation":[]},{"given":"Yiqiang","family":"Zhou","sequence":"additional","affiliation":[]},{"given":"Venugopal T.","family":"Raju","sequence":"additional","affiliation":[]},{"given":"Juan","family":"Du","sequence":"additional","affiliation":[]},{"given":"Hsin-Hsin","family":"Chang","sequence":"additional","affiliation":[]},{"given":"Cong-Yi","family":"Wang","sequence":"additional","affiliation":[]},{"given":"Michael W.","family":"Brands","sequence":"additional","affiliation":[]},{"given":"John R.","family":"Falck","sequence":"additional","affiliation":[]},{"given":"Mong-Heng","family":"Wang","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.33.1.435"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.29.1.320"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1161\/01.STR.30.12.2727"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00664.2001"},{"key":"R5","unstructured":"Baylis C, Beinder E, Suto T, and August P.Recent insights into the roles of nitric oxide and renin-angiotensin in the pathophysiology of preeclamptic pregnancy.Semin Nephrol18: 208\u2013230, 1998."},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1998.274.3.H853"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1172\/JCI5347"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1096\/fasebj.7.6.7682524"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9378(96)70166-7"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1994.266.6.C1775"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.1998.771bs.x"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1994.266.5.H2098"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2003.049981"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000084634.97353.1A"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.6.F965"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.31.1.315"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.31.5.1065"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00762.2001"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1006\/niox.2000.0296"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1999.277.3.R607"},{"key":"R21","doi-asserted-by":"crossref","unstructured":"Minamiyama Y, Takemura S, Imaoka S, Funae Y, Tanimoto Y, and Inoue M.Irreversible inhibition of cytochrome P450 by nitric oxide.J Pharmacol Exp Ther283: 1479\u20131485, 1997.","DOI":"10.1016\/S0021-5198(19)41480-7"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1016\/0002-9378(92)91634-M"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9378(13)90488-9"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1016\/S0076-6879(96)68012-4"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119279"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0702171"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1172\/JCI6786"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.266.3.F497"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00324.2003"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000047240.33861.6B"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00021.2001"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.83.11.1069"},{"key":"R33","unstructured":"Wang MH, Brand-Schieber E, Zand BA, Nguyen X, Falck JR, Balu N, and Laniado Schwartzman M.Cytochrome P450-derived arachidonic acid metabolism in the rat kidney: characterization of selective inhibitors.J Pharmacol Exp Ther284: 966\u2013973, 1998."},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.2.F246"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000090123.55365.BA"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.00044.2003"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.106.4.727"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1016\/0002-9378(93)90299-X"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1161\/hy1201.096116"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1996.270.1.R228"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00149.2005","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,7,13]],"date-time":"2021-07-13T02:02:29Z","timestamp":1626141749000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00149.2005"}},"issued":{"date-parts":[[2005,11]]},"references-count":40,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2005,11]]}},"alternative-id":["10.1152\/ajprenal.00149.2005"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00149.2005","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2005,11]]}},{"indexed":{"date-parts":[[2025,9,20]],"date-time":"2025-09-20T20:23:35Z","timestamp":1758399815462},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1989,7,1]]},"abstract":"<jats:p> Intracellular sodium has been implicated in a variety of cellular processes including regulation of Na+-K+-ATPase activity, mitogen-induced cell growth, and proliferation and stimulation of Na+-K+-ATPase by aldosterone. In renal epithelial cells a rise in sodium uptake across the apical membrane increases intracellular sodium concentration, which in turn stimulates the turnover rate of Na+-K+-ATPase and thereby enhances sodium efflux across the basolateral membrane. A prolonged increase in sodium uptake causes dramatic hypertrophy and hyperplasia and a rise in the quantity of Na+-K+-ATPase in the basolateral membrane. These structural and functional changes occur in the kidney in the absence of alterations in plasma aldosterone and vasopressin levels. Several mitogens induce growth and proliferation by initiating a cascade of events, which include a rise in intracellular sodium. Accordingly, an increase in the sodium concentration within renal epithelial cells may elicit a \u201cmitogen-like\u201d effect by initiating the cascade at the sodium step, even in the absence of a mitogen. A rise in cell sodium may also stimulate the production of autocrine growth factors that directly or indirectly regulate cell growth and proliferation, by modifying the response to mitogens or to changes in the ionic composition of the extracellular fluid. In this review we will examine the evidence that supports a role for intracellular sodium in regulating these cellular events in renal epithelial cells. <\/jats:p>","DOI":"10.1152\/ajprenal.1989.257.1.f1","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T20:57:31Z","timestamp":1513976251000},"page":"F1-F10","source":"Crossref","is-referenced-by-count":16,"title":["Regulation of renal ion transport and cell growth by sodium"],"prefix":"10.1152","volume":"257","author":[{"given":"B. A.","family":"Stanton","sequence":"first","affiliation":[{"name":"Department of Physiology, Dartmouth Medical School, Hanover, New Hampshire 03756."}]},{"given":"B.","family":"Kaissling","sequence":"additional","affiliation":[{"name":"Department of Physiology, Dartmouth Medical School, Hanover, New Hampshire 03756."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1989.257.1.F1","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:06:40Z","timestamp":1567969600000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1989.257.1.F1"}},"issued":{"date-parts":[[1989,7,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1989,7,1]]}},"alternative-id":["10.1152\/ajprenal.1989.257.1.F1"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1989.257.1.f1","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1989,7,1]]}},{"indexed":{"date-parts":[[2025,9,21]],"date-time":"2025-09-21T16:57:52Z","timestamp":1758473872181},"reference-count":25,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2000,1,1]]},"abstract":"<jats:p>The apical small conductance (SK) channel plays a key role in K secretion in the cortical collecting duct (CCD). A high-K intake stimulates renal K secretion and involves a significant increase in the number of SK channels in the apical membrane of the CCD. We used the patch-clamp technique to examine the role of protein tyrosine kinase (PTK) in regulating the activity of SK channels in the CCD. The application of 100 \u03bcM genistein stimulated SK channels in 11 of 12 patches in CCDs from rats on a K-deficient diet, and the mean increase in NP<jats:sub>o<\/jats:sub>, a product of channel number ( N) and open probability ( P<jats:sub>o<\/jats:sub>), was 2.5. In contrast, inhibition of PTK had no effect in tubules from animals on a high-K diet in all 10 experiments. Western blot analysis further shows that the level of cSrc, a nonreceptor type of PTK, is 261% higher in the kidneys from rats on a K-deficient diet than those on a high-K diet. However, the effect of cSrc was not the result of direct inhibition of channel itself, because addition of exogenous cSrc had no effect on SK channels in inside-out patches. In cell-attached patches, application of herbimycin A increased channel activity in 14 of 16 patches, and the mean increase in NP<jats:sub>o<\/jats:sub>was 2.4 in tubules from rats on a K-deficient diet. In contrast, herbimycin A had no effect on channel activity in any of 15 tubules from rats on a high-K diet. Furthermore, herbimycin A pretreatment increased NP<jats:sub>o<\/jats:sub>per patch from the control value (0.4) to 2.25 in CCDs from rats on a K-deficient diet, whereas herbimycin failed to increase channel activity ( NP<jats:sub>o<\/jats:sub>: control, 3.10; herbimycin A, 3.25) in the CCDs from animals on a high-K diet. We conclude that PTK is involved in regulating the number of apical SK channels in the kidney.<\/jats:p>","DOI":"10.1152\/ajprenal.2000.278.1.f165","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T12:05:07Z","timestamp":1514030707000},"page":"F165-F171","source":"Crossref","is-referenced-by-count":49,"title":["Protein tyrosine kinase regulates the number of renal secretory K channels"],"prefix":"10.1152","volume":"278","author":[{"given":"Wenhui","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Pharmacology,"}]},{"given":"Kenneth M.","family":"Lerea","sequence":"additional","affiliation":[{"name":"Department of Anatomy and Cell Biology, New York Medical College, Valhalla, New York 10595; and"}]},{"given":"Mary","family":"Chan","sequence":"additional","affiliation":[{"name":"Department of Pharmacology,"}]},{"given":"Gerhard","family":"Giebisch","sequence":"additional","affiliation":[{"name":"Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut 06510"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115398"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.110.5.601"},{"key":"B3","doi-asserted-by":"crossref","first-page":"10738","DOI":"10.1016\/S0021-9258(17)44518-2","volume":"258","author":"Casnellie J. E.","year":"1983","journal-title":"J. Biol. Chem."},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1172\/JCI111598"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.8.4673"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.256.1.F143"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.3.F525"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.5.F817"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.236"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1038\/362031a0"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(93)90324-J"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1991.231"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1172\/JCI113329"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.104.4.693"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1038\/373573a0"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.41.24292"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/17.16.4723"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1172\/JCI112783"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1985.177"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.263.6.F1076"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.259.3.F494"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.59.1.413"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.48.30185"},{"key":"B24","doi-asserted-by":"crossref","first-page":"437","DOI":"10.1152\/ajplegacy.1971.221.2.437","volume":"221","author":"Wright F. S.","year":"1971","journal-title":"Am. J. Physiol."},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1997.272.3.C886"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.2000.278.1.F165","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:38:19Z","timestamp":1660189099000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.2000.278.1.F165"}},"issued":{"date-parts":[[2000,1,1]]},"references-count":25,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2000,1,1]]}},"alternative-id":["10.1152\/ajprenal.2000.278.1.F165"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.2000.278.1.f165","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2000,1,1]]}},{"indexed":{"date-parts":[[2025,5,3]],"date-time":"2025-05-03T19:28:13Z","timestamp":1746300493443},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1977,11,1]]},"DOI":"10.1152\/ajprenal.1977.233.5.f366","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T20:08:13Z","timestamp":1513973293000},"page":"F366-F372","source":"Crossref","is-referenced-by-count":19,"title":["Control of glomerular filtration rate by renin-angiotensin system"],"prefix":"10.1152","volume":"233","author":[{"given":"J. E.","family":"Hall","sequence":"first","affiliation":[]},{"given":"A. C.","family":"Guyton","sequence":"additional","affiliation":[]},{"given":"T. E.","family":"Jackson","sequence":"additional","affiliation":[]},{"given":"T. G.","family":"Coleman","sequence":"additional","affiliation":[]},{"given":"T. E.","family":"Lohmeier","sequence":"additional","affiliation":[]},{"given":"N. C.","family":"Trippodo","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1977.233.5.F366","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:56:03Z","timestamp":1567968963000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1977.233.5.F366"}},"issued":{"date-parts":[[1977,11,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1977,11,1]]}},"alternative-id":["10.1152\/ajprenal.1977.233.5.F366"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1977.233.5.f366","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1977,11,1]]}},{"indexed":{"date-parts":[[2025,5,12]],"date-time":"2025-05-12T19:22:53Z","timestamp":1747077773197},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1991,4,1]]},"abstract":"<jats:p> Two major types of intercalated cells (IC) have been previously defined in rabbit collecting duct: alpha-cells have a basolateral band 3-like anion exchanger and secrete H+, whereas beta-cells bind peanut agglutinin (PNA) apically and are believed to secrete HCO3-. To further define IC types, we double-labeled kidney sections with anti-H(+) -ATPase antibodies and with either an anti-band 3 antibody or PNA. We found four patterns of staining: 1) IC with apical H(+)-ATPase and basal band 3, a configuration consistent with ongoing H+ secretion, which prevailed in the inner stripe of outer medulla (OMCDi); 2) diffuse H(+)-ATPase labeling across the cell and basal band 3, which was most numerous in the outer stripe of outer medulla (OMCDo); 3) IC with \"bright\" apical peanut lectin, diffuse H(+)-ATPase, and no band 3, which was abundant in the cortical collecting duct (CCD) and probably represents HCO3(-)-secreting cells; and 4) \"hybrid\" cells with various staining combinations (e.g., apical lectin binding and apical H(+)-ATPase), which although they are uncommon, were seen in the CCD. Consistent with this immunocytochemical finding of hybrid cells, cell-sorting studies on isolated CCD IC showed that 6-18% of PNA-positive cells also stained positively for band 3. We conclude that 1) band 3-positive IC in the OMCD vary axially. Most OMCDi IC are probably active proton secretors, whereas up to one-half of OMCDo IC may be latent H+ secretors. 2) The diffuse H(+)-ATPase pattern in putative beta-cells differs from comparable results in the rat and is not consistent with a \"reversed\" alpha-cell. HCO3- secretion by beta-cells may be driven by an H+ extrusion mechanism other than the alpha-cell pump re-sorted to the basolateral membrane. 3) The possibility of hybrid cells that might combine alpha- and beta-cell transport proteins suggests a mechanism for functional reversal of collecting duct IC polarity. <\/jats:p>","DOI":"10.1152\/ajprenal.1991.260.4.f506","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T23:43:00Z","timestamp":1513986180000},"page":"F506-F517","source":"Crossref","is-referenced-by-count":18,"title":["Colocalization of H(+)-ATPase and band 3 anion exchanger in rabbit collecting duct intercalated cells"],"prefix":"10.1152","volume":"260","author":[{"given":"V. L.","family":"Schuster","sequence":"first","affiliation":[{"name":"Renal Division, University of Iowa, Iowa City 52242."}]},{"given":"G.","family":"Fejes-Toth","sequence":"additional","affiliation":[{"name":"Renal Division, University of Iowa, Iowa City 52242."}]},{"given":"A.","family":"Naray-Fejes-Toth","sequence":"additional","affiliation":[{"name":"Renal Division, University of Iowa, Iowa City 52242."}]},{"given":"S.","family":"Gluck","sequence":"additional","affiliation":[{"name":"Renal Division, University of Iowa, Iowa City 52242."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1991.260.4.F506","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:26:31Z","timestamp":1567970791000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1991.260.4.F506"}},"issued":{"date-parts":[[1991,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1991,4,1]]}},"alternative-id":["10.1152\/ajprenal.1991.260.4.F506"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1991.260.4.f506","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1991,4,1]]}},{"indexed":{"date-parts":[[2024,7,22]],"date-time":"2024-07-22T17:51:50Z","timestamp":1721670710931},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1989,11,1]]},"abstract":"<jats:p> Genetic hypertension in the rat is associated with abnormal renal function. This may be due to systemic hypertension or to intrinsic alterations in the kidney. Therefore, we examined intrinsic rates of oxidative metabolism in renal cortical tubules isolated from spontaneously hypertensive rats (SHR) and age-matched normotensive controls (WKY) before, during, and after the development of hypertension. We examined tubule function in SHR and WKY treated with antihypertensive agents to block the development of hypertension. During the early phase of hypertension (ages 7-8 wk), SHR tubules have intrinsic rates of oxygen consumption that are 15-25% greater than that of WKY. Ouabain-sensitive rates of oxygen consumption, an index of sodium entry, and Na+-K+-ATPase activity were not increased by 17%. Reduction of blood pressure with drugs did not abolish these differences in oxidative metabolism. Addition of exogenous arachidonic acid (1 microM) did reduce the metabolic differences between 8-wk-old SHR and WKY tubules. Norepinephrine (1 microM) had a greater stimulatory effect on oxygen consumption rates in tubules from hypertensive SHR. The relationship of these metabolic differences to the development of hypertension remains unclear. <\/jats:p>","DOI":"10.1152\/ajprenal.1989.257.5.f818","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T22:07:26Z","timestamp":1513980446000},"page":"F818-F825","source":"Crossref","is-referenced-by-count":4,"title":["Increased oxidative metabolism in renal tubules from spontaneously hypertensive rats"],"prefix":"10.1152","volume":"257","author":[{"given":"P. C.","family":"Brazy","sequence":"first","affiliation":[{"name":"Division of Nephrology, Durham Veterans Administration, NorthCarolina."}]},{"given":"P. E.","family":"Klotman","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Durham Veterans Administration, NorthCarolina."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1989.257.5.F818","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:15:03Z","timestamp":1567970103000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1989.257.5.F818"}},"issued":{"date-parts":[[1989,11,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1989,11,1]]}},"alternative-id":["10.1152\/ajprenal.1989.257.5.F818"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1989.257.5.f818","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1989,11,1]]}},{"indexed":{"date-parts":[[2024,7,12]],"date-time":"2024-07-12T04:34:15Z","timestamp":1720758855024},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1994,5,1]]},"abstract":"<jats:p> The role of intracellular Ca<jats:sup>2+<\/jats:sup> in the development and maintenance of epithelial tight junctional integrity is poorly understood. We assessed tight junctional resistance (Rj) in confluent monolayers of A6 cells that were treated with mucosal amiloride such that the transepithelial resistance (Rt) reflects Rj. Solution Ca<jats:sup>2+<\/jats:sup> concentration [Ca<jats:sup>2+<\/jats:sup>] was reduced by ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) addition to the bathing solutions. Reduction of mucosal [Ca<jats:sup>2+<\/jats:sup>] to 1 microM or reduction of serosal Ca<jats:sup>2+<\/jats:sup> to 100 microM did not significantly alter Rt. However, a further decrease of serosal Ca<jats:sup>2+<\/jats:sup> to 40 microM caused the resistance to fall to &lt; 12% of the control value. Following restoration of serosal [Ca<jats:sup>2+<\/jats:sup>], Rt increased to a new steady-state value within approximately 15 min. The magnitude of recovery of Rt was inversely correlated with the length of time the epithelium was exposed to low serosal [Ca<jats:sup>2+<\/jats:sup>]. To further test the effects of asymmetric Ca<jats:sup>2+<\/jats:sup> removal, the serosal [Ca<jats:sup>2+<\/jats:sup>] was chelated using EGTA to reduce Rt. When the Ca<jats:sup>2+<\/jats:sup> ionophore A-23187 was subsequently added to the mucosal solution, Rt increased from 20% to 60% of the control level. In addition, cells were loaded with the fluorescent Ca<jats:sup>2+<\/jats:sup> indicator, Calcium Green, and the temporal relationship between changes in Rt and intracellular Ca<jats:sup>2+<\/jats:sup> was determined. Following removal of serosal Ca<jats:sup>2+<\/jats:sup>, cell Ca<jats:sup>2+<\/jats:sup> decreased, followed by a decrease in Rt. In contrast, returning Ca<jats:sup>2+<\/jats:sup>to the serosal bathing solution resulted in a parallel increase of both Rt and cell [Ca<jats:sup>2+<\/jats:sup>]. These data strongly suggest that changes in intracellular [Ca<jats:sup>2+<\/jats:sup>] play an important role in the regulation of Rj. <\/jats:p>","DOI":"10.1152\/ajprenal.1994.266.5.f775","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T05:56:45Z","timestamp":1514008605000},"page":"F775-F784","source":"Crossref","is-referenced-by-count":5,"title":["Role of intracellular Ca2+ in modulation of tight junction resistance in A6 cells"],"prefix":"10.1152","volume":"266","author":[{"given":"B.","family":"Jovov","sequence":"first","affiliation":[{"name":"Department of Physiology and Biophysics, University of Texas Medical Branch, Galveston 77555."}]},{"given":"S. A.","family":"Lewis","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, University of Texas Medical Branch, Galveston 77555."}]},{"given":"W. E.","family":"Crowe","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, University of Texas Medical Branch, Galveston 77555."}]},{"given":"J. R.","family":"Berg","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, University of Texas Medical Branch, Galveston 77555."}]},{"given":"N. K.","family":"Wills","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, University of Texas Medical Branch, Galveston 77555."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1994.266.5.F775","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:31:18Z","timestamp":1567960278000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1994.266.5.F775"}},"issued":{"date-parts":[[1994,5,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1994,5,1]]}},"alternative-id":["10.1152\/ajprenal.1994.266.5.F775"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1994.266.5.f775","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1994,5,1]]}},{"indexed":{"date-parts":[[2025,9,26]],"date-time":"2025-09-26T22:32:31Z","timestamp":1758925951638},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1991,10,1]]},"abstract":"<jats:p> Two populations of voltage-dependent Ca2+ channels, T-type and L-type, are present in bovine adrenal glomerulosa cells. Activation of these channels by cell depolarization with the resultant increase in Ca2+ influx may be one way in which agonists regulate aldosterone secretion. In addition, these channels may be the site of antagonist action. In the present study, we have demonstrated that atrial natriuretic peptide (ANP), an antagonist of aldosterone secretion, alters only the voltage dependence of inactivation of the T-type channel while enhancing the voltage dependence of activation of a subpopulation of L-type channels. These patch-clamp data, which demonstrated contrasting effects of ANP on the activity of T- and L-type Ca2+ channels correlated with changes induced in cytosolic calcium [( Ca2+]i). In the weakly depolarized cell, ANP (greater than 30 pM) lowered [Ca2+]i, in contrast to the strongly depolarized cell, in which ANP (greater than 10 pM) raised [Ca2+]i. Similar alterations in the level of [Ca2+]i in the stimulated cell were induced by the Ca(2+)-channel blocker nitrendipine and the L-type channel agonist, (-)BAY K 8644. With increasing concentrations of extracellular K+ (3.5-60 mM) the rate of aldosterone secretion rose nonmonotonically. ANP inhibited secretion over this broad range of K+ concentrations; however, its potency as an inhibitor of secretion was diminished in the strongly depolarized cell. These data are discussed in the context of a model that proposes a role for sustained Ca2+ influx in cell activation. <\/jats:p>","DOI":"10.1152\/ajprenal.1991.261.4.f706","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T18:30:54Z","timestamp":1513967454000},"page":"F706-F719","source":"Crossref","is-referenced-by-count":7,"title":["Ca2+ channels and aldosterone secretion: modulation by K+ and atrial natriuretic peptide"],"prefix":"10.1152","volume":"261","author":[{"given":"P. Q.","family":"Barrett","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, Yale University School of Medicine,New Haven, Connecticut 06510."}]},{"given":"C. M.","family":"Isales","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Yale University School of Medicine,New Haven, Connecticut 06510."}]},{"given":"W. B.","family":"Bollag","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Yale University School of Medicine,New Haven, Connecticut 06510."}]},{"given":"R. T.","family":"McCarthy","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Yale University School of Medicine,New Haven, Connecticut 06510."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1991.261.4.F706","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:23:05Z","timestamp":1567956185000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1991.261.4.F706"}},"issued":{"date-parts":[[1991,10,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1991,10,1]]}},"alternative-id":["10.1152\/ajprenal.1991.261.4.F706"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1991.261.4.f706","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[1991,10,1]]}},{"indexed":{"date-parts":[[2025,9,23]],"date-time":"2025-09-23T13:15:30Z","timestamp":1758633330441},"reference-count":40,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2015,3,15]]},"abstract":"<jats:p>After kidney donation, the remaining kidney tends to hyperfiltrate, thus limiting the initial loss of renal function. The potential determinants of this adaptive glomerular hyperfiltration (GHF) and specifically the influence of arterial function are poorly known. In 45 normotensive healthy kidney donors [51 \u00b1 10 yr (mean \u00b1 SD), 39 females], glomerular filtration rate (GFR) was measured as the clearance of continuously infused<jats:sup>99m<\/jats:sup>Tc-DTPA and timed urine collections at baseline, i.e., before donation, and 1 yr after donation. GHF was computed as postdonation GFR minus half of baseline GFR. Arterial function was assessed as baseline carotid-femoral pulse wave velocity (PWV) and carotid augmentation index (AIx). After kidney donation, no significant change in blood pressure (BP) was observed, but two subjects developed hypertension. GFR decreased from 107 \u00b1 19 to 73 \u00b1 15 ml\u00b7min<jats:sup>\u22121<\/jats:sup>\u00b71.73 m<jats:sup>\u22122<\/jats:sup>, and mean GHF was 20 \u00b1 10 ml\u00b7min<jats:sup>\u22121<\/jats:sup>\u00b71.73 m<jats:sup>\u22122<\/jats:sup>. In univariate analysis, GHF was inversely correlated to age ( r<jats:sup>2<\/jats:sup>= 0.24, P = 0.01), baseline PWV ( r<jats:sup>2<\/jats:sup>= 0.23, P = 0.001), and Aix ( r<jats:sup>2<\/jats:sup>= 0.11, P = 0.031). Nevertheless, GHF was not correlated to baseline peripheral or central BP. In multivariate analysis, baseline PWV, but not AIx, remained inversely correlated to GHF, independently of age, baseline mean BP, and GFR (model r<jats:sup>2<\/jats:sup>= 0.34, P &lt; 0.001). In healthy subjects selected for renal donation, increased arterial stiffness is associated with decreased postdonation compensatory hyperfiltration.<\/jats:p>","DOI":"10.1152\/ajprenal.00524.2014","type":"journal-article","created":{"date-parts":[[2015,1,8]],"date-time":"2015-01-08T07:16:50Z","timestamp":1420701410000},"page":"F567-F571","source":"Crossref","is-referenced-by-count":22,"title":["Arterial stiffness: an independent determinant of adaptive glomerular hyperfiltration after kidney donation"],"prefix":"10.1152","volume":"308","author":[{"given":"Pierre","family":"Fesler","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, Hopital Lapeyronie, Montpellier, France;"},{"name":"Universit\u00e9 Montpellier 1, Montpellier, France"}]},{"given":"Georges","family":"Mourad","sequence":"additional","affiliation":[{"name":"Department of Nephrology, H\u00f4pital Lapeyronie, Montpellier, France; and"},{"name":"Universit\u00e9 Montpellier 1, Montpellier, France"}]},{"given":"Guilhem","family":"du Cailar","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Hopital Lapeyronie, Montpellier, France;"}]},{"given":"Jean","family":"Ribstein","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Hopital Lapeyronie, Montpellier, France;"},{"name":"Universit\u00e9 Montpellier 1, Montpellier, France"}]},{"given":"Albert","family":"Mimran","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Hopital Lapeyronie, Montpellier, France;"},{"name":"Universit\u00e9 Montpellier 1, Montpellier, France"}]}],"member":"24","reference":[{"key":"B1","first-page":"151","volume":"17","year":"1999","journal-title":"J Hypertens"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfr578"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1797.2010.01291.x"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1977.233.1.F13"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/0002-9343(83)90873-2"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-145-3-200608010-00006"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1097\/00007890-200211150-00025"},{"key":"B8","first-page":"617","volume":"20","author":"Esposito C","year":"2007","journal-title":"J Nephrol"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000109321.76818.14"},{"key":"B10","doi-asserted-by":"crossref","first-page":"2462","DOI":"10.1097\/HJH.0b013e32833e2a21","volume":"28","author":"Fesler P","year":"2010","journal-title":"J Hypertens"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1097\/HJH.0b013e3281fbd15e"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.0590031052.x"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5001819"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1097\/01.tp.0000277288.78771.c2"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00018.x"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa0804883"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.2169\/internalmedicine.47.0825"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008030318"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1097\/HJH.0b013e32834d0ca1"},{"key":"B20","first-page":"36","volume":"6","author":"Mimran A","year":"1983","journal-title":"Ren Physiol"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2011111080"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2796.2004.01338.x"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.37.1.101"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1993.156"},{"key":"B25","first-page":"49","volume-title":"McDonalds Blood Flow in Arteries","author":"Nichols WW","year":"2005"},{"key":"B26","first-page":"193","volume-title":"McDonalds Blood Flow in Arteries","author":"Nichols WW","year":"2005"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.23.4.567"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1097\/01.mbp.0000217998.96967.fb"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-6143.2008.02355.x"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-6143.2006.01359.x"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000240346.42873.f6"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfp559"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1291\/hypres.31.1895"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2010.128"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000158843.60830.cf"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1159\/000167051"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2796.1990.tb00251.x"},{"key":"B38","doi-asserted-by":"crossref","first-page":"1798","DOI":"10.1681\/ASN.V4101798","volume":"4","author":"Ter Wee PM","year":"1994","journal-title":"J Am Soc Nephrol"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-199816121-00033"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/15.8.1162"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00524.2014","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,4,26]],"date-time":"2022-04-26T10:19:08Z","timestamp":1650968348000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00524.2014"}},"issued":{"date-parts":[[2015,3,15]]},"references-count":40,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2015,3,15]]}},"alternative-id":["10.1152\/ajprenal.00524.2014"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00524.2014","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2015,3,15]]}},{"indexed":{"date-parts":[[2025,11,1]],"date-time":"2025-11-01T17:21:43Z","timestamp":1762017703484},"reference-count":107,"publisher":"American Physiological Society","issue":"12","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,12,15]]},"abstract":"<jats:p>The renal proximal tubule (PT) is a major site for maintaining whole body pH homeostasis and is responsible for reabsorbing \u223c80% of filtered HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup>, the major plasma buffer, into the blood. The PT adapts its rate of HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup>reabsorption ( J<jats:sub>HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup><\/jats:sub>) in response to acute acid-base disturbances. Our laboratory previously showed that single isolated perfused PTs adapt J<jats:sub>HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup><\/jats:sub>in response to isolated changes in basolateral (i.e., blood side) CO<jats:sub>2<\/jats:sub>and HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup>concentrations but, surprisingly, not to pH. The response to CO<jats:sub>2<\/jats:sub>concentration can be blocked by the ErbB family tyrosine kinase inhibitor PD-168393. In the present study, we exposed enriched rabbit PT suspensions to five acute acid-base disturbances for 5 and 20 min using a panel of phosphotyrosine (pY)-specific antibodies to determine the influence of each disturbance on pan-pY, ErbB1-specific pY (four sites), and ErbB2-specific pY (two sites). We found that each acid-base treatment generated a distinct temporal pY pattern. For example, the summated responses of the individual ErbB1\/2-pY sites to each disturbance showed that metabolic acidosis (normal CO<jats:sub>2<\/jats:sub>concentration and reduced HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup>concentration) produced a transient summated pY decrease (5 vs. 20 min), whereas metabolic alkalosis produced a transient increase. Respiratory acidosis (normal HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup>concentration and elevated CO<jats:sub>2<\/jats:sub>concentration) had little effect on summated pY at 5 min but produced an elevation at 20 min, whereas respiratory alkalosis produced a reduction at 20 min. Our data show that ErbB1 and ErbB2 in the PT respond to acute acid-base disturbances, consistent with the hypothesis that they are part of the signaling cascade.<\/jats:p>","DOI":"10.1152\/ajprenal.00307.2013","type":"journal-article","created":{"date-parts":[[2013,10,17]],"date-time":"2013-10-17T04:35:32Z","timestamp":1381984532000},"page":"F1747-F1764","source":"Crossref","is-referenced-by-count":8,"title":["Effect of acute acid-base disturbances on ErbB1\/2 tyrosine phosphorylation in rabbit renal proximal tubules"],"prefix":"10.1152","volume":"305","author":[{"given":"Lara A.","family":"Skelton","sequence":"first","affiliation":[{"name":"Department of Physiology and Biophysics, Case Western Reserve University School of Medicine, Cleveland, Ohio"}]},{"given":"Walter F.","family":"Boron","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, Case Western Reserve University School of Medicine, Cleveland, Ohio"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-5793(97)00412-2"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/nature08297"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.13.3.1497"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.14.8.5192"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.12.8335"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1159\/000341235"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2011.227132"},{"key":"B8","first-page":"613","volume-title":"Medical Physiology","author":"Boron W","year":"2012"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006060620"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1210\/en.2006-0547"},{"key":"B11","doi-asserted-by":"crossref","first-page":"33","DOI":"10.1152\/ajplegacy.1953.175.1.33","volume":"175","author":"Brazeau P","year":"1953","journal-title":"Am J Physiol"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2012010029"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1042\/BJ20100617"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1201132109"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.268.2.F193"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1126\/science.289.5479.625"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1038\/nature01392"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1038\/35014615"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1998.275.6.C1481"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000036753.50601.E9"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M406591200"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.1.F129"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-4827(03)00214-3"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1172\/JCI102874"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M708116200"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/S1097-2765(03)00047-9"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.20.12022"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1016\/B978-1-4160-3115-4.50041-X"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.ph.58.030196.002235"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1359\/jbmr.060210"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.C000716200"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1016\/j.yexcr.2004.07.003"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.105.094979"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1007\/978-3-540-79090-7_9"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1038\/ncb2158"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M407832200"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0705487105"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0912101106"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.38.24839"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1152\/jn.01269.2005"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00132.2006"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1172\/JCI200418046"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1038\/nature01905"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00075.2003"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1016\/j.ijrobp.2003.06.002"},{"key":"B46","first-page":"267","volume":"150","author":"Mitaka T","year":"1997","journal-title":"Am J Pathol"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1159\/000338486"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0813231106"},{"key":"B49","doi-asserted-by":"crossref","first-page":"379","DOI":"10.1681\/ASN.V122379","volume":"12","author":"Nakanishi K","year":"2001","journal-title":"J Am Soc Nephrol"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.92.3.395"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.102.6.1171"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1998.274.2.C543"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1016\/S0301-0082(99)00008-8"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.120.2.371"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-5793(03)00013-9"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1016\/j.gene.2005.10.018"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(02)00963-7"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00023.2012"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115739"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00406.2007"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2012.237958"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002543"},{"key":"B63","first-page":"953","volume":"5","author":"Press MF","year":"1990","journal-title":"Oncogene"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.88.24.11110"},{"key":"B65","first-page":"1273","volume":"7","author":"Prigent SA","year":"1992","journal-title":"Oncogene"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00282.2004"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1038\/ng1032"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.266.3.F459"},{"key":"B69","doi-asserted-by":"publisher","DOI":"10.1172\/JCI102823"},{"key":"B70","first-page":"1519","volume":"11","author":"Ricci A","year":"1995","journal-title":"Oncogene"},{"key":"B71","doi-asserted-by":"publisher","DOI":"10.1016\/S0169-5002(08)70101-6"},{"key":"B72","doi-asserted-by":"publisher","DOI":"10.1007\/BF02624615"},{"key":"B73","doi-asserted-by":"publisher","DOI":"10.1038\/387409a0"},{"key":"B74","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1981.61.2.296"},{"key":"B75","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.1.F27"},{"key":"B76","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.16.9660"},{"key":"B77","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.2.1032"},{"key":"B78","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1002753107"},{"key":"B79","first-page":"S4","volume":"23","author":"Skelton LA","year":"2010","journal-title":"J Nephrol"},{"key":"B80","doi-asserted-by":"publisher","DOI":"10.1172\/JCI112948"},{"key":"B81","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1096-9896(199807)185:3<236::AID-PATH118>3.0.CO;2-7"},{"key":"B82","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0812220106"},{"key":"B83","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009050477"},{"key":"B84","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1203913"},{"key":"B85","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M109.006478"},{"key":"B86","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M801330200"},{"key":"B87","doi-asserted-by":"publisher","DOI":"10.1177\/875647939000600106"},{"key":"B88","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.4.1415"},{"key":"B89","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-010-0865-6"},{"key":"B90","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00418.x"},{"key":"B91","doi-asserted-by":"publisher","DOI":"10.1016\/j.yjmcc.2008.10.024"},{"key":"B92","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.12.1.128"},{"key":"B93","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2011020160"},{"key":"B94","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00589.2001"},{"key":"B95","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuroscience.2004.02.032"},{"key":"B96","doi-asserted-by":"publisher","DOI":"10.1038\/386173a0"},{"key":"B97","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.281.6.F1117"},{"key":"B98","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.10.5603"},{"key":"B99","doi-asserted-by":"publisher","DOI":"10.1038\/onc.2013.74"},{"key":"B100","doi-asserted-by":"publisher","DOI":"10.1021\/bi00379a034"},{"key":"B101","doi-asserted-by":"publisher","DOI":"10.1038\/35052073"},{"key":"B102","doi-asserted-by":"publisher","DOI":"10.1016\/j.yexcr.2008.08.005"},{"key":"B103","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2006.05.013"},{"key":"B104","doi-asserted-by":"publisher","DOI":"10.1038\/374636a0"},{"key":"B105","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00013.2003"},{"key":"B106","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00520.2005"},{"key":"B107","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0500423102"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00307.2013","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,3,9]],"date-time":"2022-03-09T10:45:29Z","timestamp":1646822729000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00307.2013"}},"issued":{"date-parts":[[2013,12,15]]},"references-count":107,"journal-issue":{"issue":"12","published-print":{"date-parts":[[2013,12,15]]}},"alternative-id":["10.1152\/ajprenal.00307.2013"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00307.2013","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2013,12,15]]}},{"indexed":{"date-parts":[[2025,11,1]],"date-time":"2025-11-01T12:39:22Z","timestamp":1762000762611,"version":"build-2065373602"},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1991,10,1]]},"abstract":"<jats:p> Renal glomerular and cortical metabolism of endogenous arachidonic acid by cytochrome P-450 epoxygenase yields 8,9-, 11,12-, and 14,15-epoxyeicosatrienoic acids (EET). Using gas chromatography-mass spectrometry, we measured the synthesis of 8,9-EET from an endogenous pool of arachidonic acid in normal rat kidney. The (8S,9R) isomer was favored over the (8R,9S) isomer in a ratio (%) of 59 to 41 in isolated glomeruli and 68 to 32 in cortex tissue. (8S,9R)- but not (8R,9S)-EET elicited dose-dependent vasoconstriction on intrarenal administration in the euvolemic Munich-Wistar rat. Micropuncture measurements of glomerular dynamics revealed that (8S,9R)-EET increased afferent arteriolar resistance (RA) leading to reductions in single-nephron plasma flow rate (QA), net transcapillary hydraulic pressure difference (delta P), and consequently single-nephron glomerular filtration rate (SNGFR). There was no significant change in the value of the glomerular capillary ultrafiltration coefficient (Kf). In the presence of a cyclooxygenase inhibitor, indomethacin, the effects of 8,9-EET were reversed. RA fell leading to increases in QA and delta P, with resultant augmentation of SNGFR. Under these conditions, a modest reduction if Kf was noted. Thus (8S,9R)-EET is a stereoselective renal vasoconstrictor, preferentially generated over its optical isomer, (8R,9S)-EET, suggesting that it is biologically relevant and implying specific structural requirements for EET receptor activation. The principal mechanism of action of 8,9-EET is preglomerular vasoconstriction. The vasoconstrictor effect of 8,9-EET is CO dependent. <\/jats:p>","DOI":"10.1152\/ajprenal.1991.261.4.f578","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T23:30:54Z","timestamp":1513985454000},"page":"F578-F586","source":"Crossref","is-referenced-by-count":11,"title":["Glomerular stereospecific synthesis and hemodynamic actions of 8,9-epoxyeicosatrienoic acid in rat kidney"],"prefix":"10.1152","volume":"261","author":[{"given":"T.","family":"Katoh","sequence":"first","affiliation":[{"name":"Department of Medicine, Vanderbilt University, Nashville, Tennessee37232."}]},{"given":"K.","family":"Takahashi","sequence":"additional","affiliation":[{"name":"Department of Medicine, Vanderbilt University, Nashville, Tennessee37232."}]},{"given":"J.","family":"Capdevila","sequence":"additional","affiliation":[{"name":"Department of Medicine, Vanderbilt University, Nashville, Tennessee37232."}]},{"given":"A.","family":"Karara","sequence":"additional","affiliation":[{"name":"Department of Medicine, Vanderbilt University, Nashville, Tennessee37232."}]},{"given":"J. R.","family":"Falck","sequence":"additional","affiliation":[{"name":"Department of Medicine, Vanderbilt University, Nashville, Tennessee37232."}]},{"given":"H. R.","family":"Jacobson","sequence":"additional","affiliation":[{"name":"Department of Medicine, Vanderbilt University, Nashville, Tennessee37232."}]},{"given":"K. F.","family":"Badr","sequence":"additional","affiliation":[{"name":"Department of Medicine, Vanderbilt University, Nashville, Tennessee37232."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1991.261.4.F578","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:22:55Z","timestamp":1567970575000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1991.261.4.F578"}},"issued":{"date-parts":[[1991,10,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1991,10,1]]}},"alternative-id":["10.1152\/ajprenal.1991.261.4.F578"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1991.261.4.f578","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[1991,10,1]]}},{"indexed":{"date-parts":[[2025,11,5]],"date-time":"2025-11-05T14:18:09Z","timestamp":1762352289893,"version":"3.40.4"},"reference-count":74,"publisher":"American Physiological Society","issue":"12","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,12,15]]},"abstract":"<jats:p>Binding of vasopressin to its type 2 receptor in renal collecting ducts induces cAMP signaling, transcription and translocation of aquaporin (AQP)2 water channels to the plasma membrane, and water reabsorption from the prourine. Demeclocycline is currently used to treat hyponatremia in patients with the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Demeclocycline's mechanism of action, which is poorly understood, is studied here. In mouse cortical collecting duct (mpkCCD) cells, which exhibit deamino-8-d-arginine vasopressin (dDAVP)-dependent expression of endogenous AQP2, demeclocycline decreased AQP2 abundance and gene transcription but not its protein stability. Demeclocycline did not affect vasopressin type 2 receptor localization but decreased dDAVP-induced cAMP generation and the abundance of adenylate cyclase 3 and 5\/6. The addition of exogenous cAMP partially corrected the demeclocycline effect. As in patients, demeclocycline increased urine volume, decreased urine osmolality, and reverted hyponatremia in an SIADH rat model. AQP2 and adenylate cyclase 5\/6 abundances were reduced in the inner medulla but increased in the cortex and outer medulla, in the absence of any sign of toxicity. In conclusion, our in vitro and in vivo data indicate that demeclocycline mainly attenuates hyponatremia in SIADH by reducing adenylate cyclase 5\/6 expression and, consequently, cAMP generation, AQP2 gene transcription, and AQP2 abundance in the renal inner medulla, coinciding with a reduced vasopressin escape response in other collecting duct segments.<\/jats:p>","DOI":"10.1152\/ajprenal.00723.2012","type":"journal-article","created":{"date-parts":[[2013,10,24]],"date-time":"2013-10-24T02:56:45Z","timestamp":1382583405000},"page":"F1705-F1718","source":"Crossref","is-referenced-by-count":21,"title":["Demeclocycline attenuates hyponatremia by reducing aquaporin-2 expression in the renal inner medulla"],"prefix":"10.1152","volume":"305","author":[{"given":"Marleen L. A.","family":"Kortenoeven","sequence":"first","affiliation":[{"name":"Department of Physiology, Radboud University Medical Center, Nijmegen, The Netherlands;"},{"name":"Department of Biomedicine, Health, Aarhus University, Aarhus, Denmark;"}]},{"given":"Anne P.","family":"Sinke","sequence":"additional","affiliation":[{"name":"Department of Physiology, Radboud University Medical Center, Nijmegen, The Netherlands;"}]},{"given":"Niels","family":"Hadrup","sequence":"additional","affiliation":[{"name":"Department of Physiology, Radboud University Medical Center, Nijmegen, The Netherlands;"},{"name":"Division of Toxicology and Risk Assessment, National Food Institute, Technical University of Denmark, S\u00f8borg, Denmark"}]},{"given":"Christiane","family":"Trimpert","sequence":"additional","affiliation":[{"name":"Department of Physiology, Radboud University Medical Center, Nijmegen, The Netherlands;"}]},{"given":"Jack F. M.","family":"Wetzels","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Radboud University Medical Center, Nijmegen, The Netherlands; and"}]},{"given":"Robert A.","family":"Fenton","sequence":"additional","affiliation":[{"name":"Department of Biomedicine, Health, Aarhus University, Aarhus, Denmark;"}]},{"given":"Peter M. T.","family":"Deen","sequence":"additional","affiliation":[{"name":"Department of Physiology, Radboud University Medical Center, Nijmegen, The Netherlands;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1002\/hep.1840210128"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/0002-9343(67)90096-4"},{"key":"B3","doi-asserted-by":"crossref","first-page":"923","DOI":"10.1681\/ASN.V105923","volume":"10","author":"Bens M","year":"1999","journal-title":"J Am Soc Nephrol"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1093\/jn\/112.1.126"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.200409124"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.3181\/00379727-210-43927AA"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1984.247.3.R537"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1007\/s004240050345"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.0168.2001"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1126\/science.8140421"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1006\/exnr.2001.7775"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119352"},{"key":"B14","first-page":"625","volume":"101","author":"Fabre J","year":"1971","journal-title":"Schweiz Med Wochenschr"},{"key":"B15","doi-asserted-by":"crossref","first-page":"358","DOI":"10.1016\/S0022-3565(25)29928-1","volume":"190","author":"Feldman HA","year":"1974","journal-title":"J Pharmacol Exp Ther"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1172\/JCI107649"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM197801262980401"},{"key":"B18","first-page":"F926","volume":"38","author":"Fujita N","year":"1995","journal-title":"Am J Physiol"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.23.14800"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M303435200"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M111880200"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004110930"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.1.F185"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.1991.tb12466.x"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M500040200"},{"key":"B26","first-page":"281","volume":"64","author":"Horattas MC","year":"1998","journal-title":"Am Surg"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1996.270.6.C1695"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/18.9.2394"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.272.6.F816"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00284.x"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.1.F96"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2009.91"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M110.207878"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1038\/227680a0"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005080884"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1210\/endo.141.5.7465"},{"key":"B39","doi-asserted-by":"crossref","first-page":"861","DOI":"10.1681\/ASN.V86861","volume":"8","author":"Matsumura Y","year":"1997","journal-title":"J Am Soc Nephrol"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1001\/jama.1980.03300500039026"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.505"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.2000.80.4.1373"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1248\/bpb.24.897"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1248\/bpb.23.182"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.4.1013"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.94.10.5450"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118222"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1136\/pgmj.54.635.623"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2010.130"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1136\/thx.34.3.324"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1016\/S0005-8165(73)80016-2"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.1989.256.6.E760"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1016\/j.ajpath.2012.09.014"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1016\/S0091-6773(74)90935-3"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.E04-04-0337"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2012050449"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00397.2011"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1001\/archinte.1967.04410010047006"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00965.x"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1210\/endo-116-4-1621"},{"key":"B63","first-page":"1311","volume":"65","author":"Schrier RW","year":"1989","journal-title":"Nihon Naibunpi Gakkai Zasshi"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1124\/mol.54.3.525"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1530\/EJE-09-1057"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-79-5-679"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00075.2004"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00109.2009"},{"key":"B70","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.2.F414"},{"key":"B71","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfs292"},{"key":"B72","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M207525200"},{"key":"B73","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.1984.247.4.E540"},{"key":"B74","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1988.188"},{"key":"B75","doi-asserted-by":"publisher","DOI":"10.1016\/j.amjmed.2007.09.001"},{"key":"B76","doi-asserted-by":"publisher","DOI":"10.1016\/0009-8981(95)06068-O"},{"key":"B77","first-page":"737","volume":"15","author":"Wilson DM","year":"1973","journal-title":"Curr Ther Res Clin Exp"},{"key":"B78","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.272.4.F443"},{"key":"B79","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.me.31.020180.001531"},{"key":"B80","first-page":"iii12","volume":"2","author":"Zietse R","year":"2009","journal-title":"NDT Plus"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00723.2012","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,4,30]],"date-time":"2025-04-30T18:10:02Z","timestamp":1746036602000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00723.2012"}},"issued":{"date-parts":[[2013,12,15]]},"references-count":74,"journal-issue":{"issue":"12","published-print":{"date-parts":[[2013,12,15]]}},"alternative-id":["10.1152\/ajprenal.00723.2012"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00723.2012","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2013,12,15]]}},{"indexed":{"date-parts":[[2025,11,3]],"date-time":"2025-11-03T08:58:06Z","timestamp":1762160286516},"reference-count":171,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2005,4]]},"abstract":"<jats:p>The \u201cprogramming hypothesis\u201d proposes that an adverse perinatal milieu leads to adaptation that translates into cardiovascular disease in adulthood. The balance between nitric oxide (NO) and reactive oxygen species (ROS) is disturbed in cardiovascular diseases, including hypertension. Conceivably, this balance is also disturbed in pregnancy, altering the fetal environment; however, effects of perinatal manipulation of NO and ROS on adult blood pressure (BP) are unknown. In spontaneously hypertensive rats (SHR), NO availability is decreased and ROS are increased compared with normotensive Wistar-Kyoto rats, and, despite the genetic predisposition, the perinatal environment can modulate adult BP. Our hypothesis is that a disturbed NO-ROS balance in the SHR dam persistently affects BP in her offspring. Dietary supplements, which support NO formation and scavenge ROS, administered during pregnancy and lactation resulted in persistently lower BP for up to 48 wk in SHR offspring. The NO donor molsidomine and the superoxide dismutase mimic tempol-induced comparable effects. Specific inhibition of inducible nitric oxide synthase (NOS) reduces BP in adult SHR, suggesting that inducible NOS is predominantly a source of ROS in SHR. Indeed, inducible NOS inhibition in SHR dams persistently reduced BP in adult offspring. Persistent reductions in BP were accompanied by prevention of proteinuria in aged SHR. We propose that in SHR the known increase in ANG II type 1 receptor density during development leads to superoxide production, which enhances inducible NOS activity. The relative shortage of substrate and cofactors leads to uncoupling of inducible NOS, resulting in superoxide production, activating transcription factors that subsequently again increase inducible NOS expression. This vicious circle probably is perpetuated into adult life.<\/jats:p>","DOI":"10.1152\/ajprenal.00314.2004","type":"journal-article","created":{"date-parts":[[2004,11,17]],"date-time":"2004-11-17T03:33:40Z","timestamp":1100662420000},"page":"F626-F636","source":"Crossref","is-referenced-by-count":68,"title":["Programming blood pressure in adult SHR by shifting perinatal balance of NO and reactive oxygen species toward NO: the inverted Barker phenomenon"],"prefix":"10.1152","volume":"288","author":[{"given":"Simona","family":"Racasan","sequence":"first","affiliation":[]},{"given":"Branko","family":"Braam","sequence":"additional","affiliation":[]},{"given":"Hein A.","family":"Koomans","sequence":"additional","affiliation":[]},{"given":"Jaap A.","family":"Joles","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000019781.90630.0F"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00060.2004"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1016\/0002-9378(87)90378-4"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1159\/000052764"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000053448.95913.3D"},{"key":"R6","doi-asserted-by":"crossref","unstructured":"Alvarez Aand Sanz MJ.Reactive oxygen species mediate angiotensin II-induced leukocyte-endothelial cell interactions in vivo.J Leukoc Biol70: 199\u2013206, 2001.","DOI":"10.1189\/jlb.70.2.199"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-002-0941-z"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000118528.00817.8E"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-199104000-00003"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1016\/S1043-2760(02)00689-6"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1136\/bmj.301.6746.259"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1136\/bmj.298.6673.564"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(89)90710-1"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.0600031083.x"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1016\/0895-7061(94)00198-K"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00406.x"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2003.052068"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1016\/j.amjmed.2003.09.034"},{"key":"R19","unstructured":"Bridges AB, Scott NA, Parry GJ, and Belch JJ.Age, sex, cigarette smoking and indices of free radical activity in healthy humans.Eur J Med2: 205\u2013208, 1993."},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.87.10.840"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1161\/hy0202.102815"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1136\/bmj.315.7111.786"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1161\/hy0202.103264"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000054214.10670.4C"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1161\/hc3901.095767"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0704105"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.1.F10"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1136\/bmj.326.7389.571"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1987.253.4.H980"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1093\/ajcn\/78.4.773"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1172\/JCI650"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1995.sp020986"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.68.2.450"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000052949.85257.8E"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0703393"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00653.x"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.35.1.164"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1042\/cs0980137"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1161\/01.ATV.21.6.1017"},{"key":"R40","unstructured":"Dwyer CM, Madgwick AJ, Crook AR, and Stickland NC.The effect of maternal undernutrition on the growth and development of the guinea pig placenta.J Dev Physiol18: 295\u2013302, 1992."},{"key":"R41","doi-asserted-by":"crossref","unstructured":"Eberhardt W, Pluss C, Hummel R, and Pfeilschifter J.Molecular mechanisms of inducible nitric oxide synthase gene expression by IL-1\u03b2 and cAMP in rat mesangial cells.J Immunol160: 4961\u20134969, 1998.","DOI":"10.4049\/jimmunol.160.10.4961"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1159\/000025613"},{"key":"R43","doi-asserted-by":"crossref","unstructured":"Enseleit F, Hurlimann D, and Luscher TF.Vascular protective effects of angiotensin converting enzyme inhibitors and their relation to clinical events.J Cardiovasc Pharmacol37,Suppl1: S21\u2013S30, 2001.","DOI":"10.1097\/00005344-200109011-00004"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2796.2003.01289.x"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.1994.tb02505.x"},{"key":"R46","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.1995.tb01995.x"},{"key":"R47","unstructured":"Esther CR Jr, Howard TE, Marino EM, Goddard JM, Capecchi MR, and Bernstein KE.Mice lacking angiotensin-converting enzyme have low blood pressure, renal pathology, and reduced male fertility.Lab Invest74: 953\u2013965, 1996."},{"key":"R48","doi-asserted-by":"publisher","DOI":"10.1007\/PL00005231"},{"key":"R49","doi-asserted-by":"publisher","DOI":"10.1093\/jn\/134.1.211"},{"key":"R50","doi-asserted-by":"publisher","DOI":"10.1136\/bmj.319.7222.1403"},{"key":"R51","doi-asserted-by":"publisher","DOI":"10.1136\/bmj.315.7112.837"},{"key":"R52","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(96)07631-3"},{"key":"R53","doi-asserted-by":"publisher","DOI":"10.1016\/S0008-6363(03)00461-9"},{"key":"R54","doi-asserted-by":"publisher","DOI":"10.1016\/S0008-6363(02)00508-4"},{"key":"R55","doi-asserted-by":"publisher","DOI":"10.1097\/00005344-200210000-00002"},{"key":"R56","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2004.064055"},{"key":"R57","doi-asserted-by":"crossref","unstructured":"Ghosh SS, Basu AK, Ghosh S, Hagley R, Kramer L, Schuetz J, Grogan WM, Guzelian P, and Watlington CO.Renal and hepatic family 3A cytochromes P450 (CYP3A) in spontaneously hypertensive rats.Biochem Pharmacol50: 49\u201354, 1995.","DOI":"10.1016\/0006-2952(95)00110-L"},{"key":"R58","doi-asserted-by":"publisher","DOI":"10.1126\/science.1095292"},{"key":"R59","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.1998.tb02178.x"},{"key":"R60","doi-asserted-by":"publisher","DOI":"10.1046\/j.1440-1681.2001.03480.x"},{"key":"R61","doi-asserted-by":"publisher","DOI":"10.1016\/S0895-7061(03)00999-3"},{"key":"R62","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.86.5.494"},{"key":"R63","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-200204000-00018"},{"key":"R64","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.1998.tb02182.x"},{"key":"R65","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.2000.279.1.R340"},{"key":"R66","doi-asserted-by":"publisher","DOI":"10.1161\/hy1101.095331"},{"key":"R67","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0703603"},{"key":"R68","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-200018070-00002"},{"key":"R69","doi-asserted-by":"publisher","DOI":"10.1042\/cs1030633"},{"key":"R70","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-199917090-00002"},{"key":"R71","doi-asserted-by":"publisher","DOI":"10.1093\/jn\/118.5.579"},{"key":"R72","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000034745.98129.EC"},{"key":"R73","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-199109010-00003"},{"key":"R74","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1993.1408"},{"key":"R75","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.2001.281.3.H981"},{"key":"R76","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.33.6.1353"},{"key":"R77","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000139843.05436.A0"},{"key":"R78","doi-asserted-by":"publisher","DOI":"10.1042\/cs0910169"},{"key":"R79","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-199917010-00004"},{"key":"R80","unstructured":"Kunes J, Hojna S, Kadlecova M, Dobesova Z, Rauchova H, Vokurkova M, Loukotova J, Pechanova O, and Zicha J.Altered balance of vasoactive systems in experimental hypertension: the role of relative NO deficiency.Physiol Res53,Suppl1: S23\u2013S34, 2004."},{"key":"R81","doi-asserted-by":"publisher","DOI":"10.1016\/S0024-3205(99)00536-6"},{"key":"R82","doi-asserted-by":"publisher","DOI":"10.1161\/01.STR.0000039340.62995.F2"},{"key":"R83","doi-asserted-by":"publisher","DOI":"10.1079\/PNS2001111"},{"key":"R84","doi-asserted-by":"publisher","DOI":"10.1042\/cs0930423"},{"key":"R85","doi-asserted-by":"publisher","DOI":"10.1016\/0300-9629(94)00177-U"},{"key":"R86","doi-asserted-by":"publisher","DOI":"10.1042\/cs0910607"},{"key":"R87","doi-asserted-by":"publisher","DOI":"10.1136\/bmj.306.6869.24"},{"key":"R88","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-199608000-00002"},{"key":"R89","doi-asserted-by":"publisher","DOI":"10.1161\/hc0902.104677"},{"key":"R90","doi-asserted-by":"publisher","DOI":"10.1136\/bmj.312.7028.401"},{"key":"R91","doi-asserted-by":"publisher","DOI":"10.1136\/jcp.48.4.385"},{"key":"R92","doi-asserted-by":"crossref","unstructured":"Lewis RM, Bassett NS, Johnston BM, and Skinner SJ.Fetal and placental glucose and amino acid uptake in the spontaneously hypertensive rat.Placenta19: 403\u2013408, 1998.","DOI":"10.1016\/S0143-4004(98)90080-7"},{"key":"R93","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0705838"},{"key":"R94","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.30.3.307"},{"key":"R95","doi-asserted-by":"publisher","DOI":"10.1079\/BJN2003881"},{"key":"R96","doi-asserted-by":"publisher","DOI":"10.1136\/bmj.312.7028.406"},{"key":"R97","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.25.6.1245"},{"key":"R98","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.2001.280.4.C719"},{"key":"R99","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-200206000-00025"},{"key":"R100","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(96)04257-2"},{"key":"R101","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-199607000-00011"},{"key":"R102","doi-asserted-by":"publisher","DOI":"10.1016\/0031-9384(94)90069-8"},{"key":"R103","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.1995.tb02888.x"},{"key":"R104","unstructured":"McCausland JE, Bertram JF, Ryan GB, and Alcorn D.Glomerular number and size following chronic angiotensin II blockade in the postnatal rat.Exp Nephrol5: 201\u2013209, 1997."},{"key":"R105","doi-asserted-by":"publisher","DOI":"10.1016\/S1051-0443(07)61964-2"},{"key":"R106","doi-asserted-by":"publisher","DOI":"10.1016\/0031-9384(88)90348-4"},{"key":"R107","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.88.22.10045"},{"key":"R108","doi-asserted-by":"publisher","DOI":"10.1016\/0006-291X(91)92027-H"},{"key":"R109","doi-asserted-by":"publisher","DOI":"10.1016\/0006-2952(78)90043-6"},{"key":"R110","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000116220.39793.c9"},{"key":"R111","doi-asserted-by":"publisher","DOI":"10.1172\/JCI116491"},{"key":"R112","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M203749200"},{"key":"R113","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199007053230105"},{"key":"R114","doi-asserted-by":"crossref","unstructured":"Patel HR, Thiara AS, West KP, Lodwick D, and Samani NJ.Increased expression of the SA gene in the kidney of the spontaneously hypertensive rat is localized to the proximal tubule.J Hypertens12: 1347\u20131352, 1994.","DOI":"10.1097\/00004872-199412000-00005"},{"key":"R115","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1992.tb09356.x"},{"key":"R116","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa032292"},{"key":"R117","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.17.2.242"},{"key":"R118","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-200309000-00018"},{"key":"R119","unstructured":"Racasan S, Braam B, Koomans HA, and Joles JA.Brief perinatal inducible NO synthase inhibition and NO supplementation both lead to sustained reduction in blood pressure in SHR (Abstract).J Am Soc Nephrol13: 52A\u201353A, 2002."},{"key":"R120","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000133251.40322.20"},{"key":"R121","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00410.x"},{"key":"R122","doi-asserted-by":"publisher","DOI":"10.1093\/jn\/131.4.1217"},{"key":"R123","doi-asserted-by":"publisher","DOI":"10.1136\/bmj.315.7105.396"},{"key":"R124","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.00536.2002"},{"key":"R125","unstructured":"Robinson JS, Jones CT, and Kingston EJ.Studies on experimental growth retardation in sheep. The effects of maternal hypoxaemia.J Dev Physiol5: 89\u2013100, 1983."},{"key":"R126","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000052833.20759.64"},{"key":"R127","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.33.1.83"},{"key":"R128","doi-asserted-by":"publisher","DOI":"10.1126\/science.2492116"},{"key":"R129","doi-asserted-by":"publisher","DOI":"10.1172\/JCI116616"},{"key":"R130","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.33.1.424"},{"key":"R131","doi-asserted-by":"publisher","DOI":"10.1016\/S0303-7207(01)00633-5"},{"key":"R132","doi-asserted-by":"publisher","DOI":"10.1042\/cs0980269"},{"key":"R133","doi-asserted-by":"publisher","DOI":"10.1042\/cs0940373"},{"key":"R134","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.31.1.373"},{"key":"R135","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.33.1.256"},{"key":"R136","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(96)04547-3"},{"key":"R137","doi-asserted-by":"publisher","DOI":"10.1097\/00041433-200210000-00006"},{"key":"R138","doi-asserted-by":"publisher","DOI":"10.1038\/sj.mn.7800141"},{"key":"R139","doi-asserted-by":"publisher","DOI":"10.3109\/10641969309041642"},{"key":"R140","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.8.4754"},{"key":"R141","doi-asserted-by":"publisher","DOI":"10.1016\/S0890-6238(01)00161-7"},{"key":"R142","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.21.6.929"},{"key":"R143","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118394"},{"key":"R144","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.1.F110"},{"key":"R145","doi-asserted-by":"publisher","DOI":"10.1016\/S0008-6363(03)00424-3"},{"key":"R146","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.31.6.1248"},{"key":"R147","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.36.6.957"},{"key":"R148","doi-asserted-by":"publisher","DOI":"10.1016\/j.ajog.2003.12.030"},{"key":"R149","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00484.x"},{"key":"R150","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-2999(00)00900-6"},{"key":"R151","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9378(98)80007-0"},{"key":"R152","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.99.15.2027"},{"key":"R153","doi-asserted-by":"publisher","DOI":"10.1016\/S0895-7061(99)00103-X"},{"key":"R154","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.1.F130"},{"key":"R155","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0705448"},{"key":"R156","doi-asserted-by":"publisher","DOI":"10.1053\/plac.2002.0860"},{"key":"R157","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00511.x"},{"key":"R158","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.22.2.139"},{"key":"R159","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.23.6.819"},{"key":"R160","doi-asserted-by":"publisher","DOI":"10.1016\/0895-7061(95)00388-6"},{"key":"R161","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00522.2001"},{"key":"R162","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-199816080-00010"},{"key":"R163","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.35.5.1055"},{"key":"R164","doi-asserted-by":"publisher","DOI":"10.1161\/hy1201.099611"},{"key":"R165","doi-asserted-by":"publisher","DOI":"10.1038\/nrd873"},{"key":"R166","doi-asserted-by":"publisher","DOI":"10.1016\/S0008-6363(99)00085-1"},{"key":"R167","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-200410000-00027"},{"key":"R168","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00372.x"},{"key":"R169","doi-asserted-by":"publisher","DOI":"10.3109\/10641969609081779"},{"key":"R170","doi-asserted-by":"publisher","DOI":"10.3109\/10641969609081035"},{"key":"R171","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1999.79.4.1227"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00314.2004","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,4,30]],"date-time":"2023-04-30T08:21:20Z","timestamp":1682842880000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00314.2004"}},"issued":{"date-parts":[[2005,4]]},"references-count":171,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2005,4]]}},"alternative-id":["10.1152\/ajprenal.00314.2004"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00314.2004","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2005,4]]}},{"indexed":{"date-parts":[[2025,11,3]],"date-time":"2025-11-03T08:59:59Z","timestamp":1762160399686},"reference-count":56,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2005,8]]},"abstract":"<jats:p>Podocyte differentiation is required for normal glomerular filtration barrier function and is regulated by the transcription factor WT1. We identified WT1-interacting protein (WTIP) and hypothesized that it functions as both a scaffold for slit diaphragm proteins and a corepressor of WT1 transcriptional activity by shuttling from cell-cell junctions to the nucleus after injury. Endogenous WTIP colocalizes with zonula occludens-1 (ZO-1) in cultured mouse podocyte adherens junctions. To model podocyte injury in vitro, we incubated differentiated podocytes with puromycin aminonucleoside (PAN; 100 \u03bcg\/ml) for 24 h, which disassembled cell-cell contacts, rearranged actin cytoskeleton, and caused process retraction. Podocyte synaptopodin expression diminished after PAN treatment, consistent with podocyte dedifferentiation in some human glomerular diseases. To assess podocyte function, we measured albumin flux across differentiated podocytes cultured on collagen-coated Transwell filters. Albumin transit across PAN-treated cells increased to levels observed with undifferentiated podocytes. Consistent with our hypothesis, WTIP, as well as ZO-1, translocated from podocyte adherens junctions to nuclei in PAN-treated cells. Because WTIP is a transcriptional corepressor for WT1, we examined the effect of PAN on expression of retinoblastoma binding protein Rbbp7 (also known as RbAp46), a WT1 target gene expressed in S-shaped bodies during nephrogenesis. Rbbp7 expression in PAN-treated podocytes was reduced compared with untreated cells. In conclusion, WTIP translocates from cell-cell junctions to the nucleus in PAN-treated podocytes. We suggest that WTIP monitors slit diaphragm protein assembly and shuttles into the nucleus after podocyte injury, translating changes in slit diaphragm structure into altered gene expression and a less differentiated phenotype.<\/jats:p>","DOI":"10.1152\/ajprenal.00389.2004","type":"journal-article","created":{"date-parts":[[2005,3,30]],"date-time":"2005-03-30T01:33:56Z","timestamp":1112146436000},"page":"F431-F441","source":"Crossref","is-referenced-by-count":58,"title":["WT1-interacting protein and ZO-1 translocate into podocyte nuclei after puromycin aminonucleoside treatment"],"prefix":"10.1152","volume":"289","author":[{"given":"Maribel","family":"Rico","sequence":"first","affiliation":[]},{"given":"Amitava","family":"Mukherjee","sequence":"additional","affiliation":[]},{"given":"Martha","family":"Konieczkowski","sequence":"additional","affiliation":[]},{"given":"Leslie A.","family":"Bruggeman","sequence":"additional","affiliation":[]},{"given":"R. Tyler","family":"Miller","sequence":"additional","affiliation":[]},{"given":"Shenaz","family":"Khan","sequence":"additional","affiliation":[]},{"given":"Jeffrey R.","family":"Schelling","sequence":"additional","affiliation":[]},{"given":"John R.","family":"Sedor","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200309159"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1016\/S0925-4773(99)00314-7"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200210020"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/19.9.2024"},{"key":"R5","unstructured":"Barisoni L, Kriz W, Mundel P, and D'Agati V.The dysregulated podocyte phenotype: a novel concept in the pathogenesis of collapsing idiopathic focal segmental glomerulosclerosis and HIV-associated nephropathy.J Am Soc Nephrol10: 51\u201361, 1999."},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00149.x"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1034\/j.1600-0854.2003.00102.x"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200308162"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1016\/S0955-0674(00)00213-1"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1016\/S0168-9525(98)01424-3"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1152\/physiolgenomics.00164.2003"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-5793(01)02487-5"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.6.F999"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.cellbio.15.1.607"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.93.20.10779"},{"key":"R16","doi-asserted-by":"crossref","unstructured":"Gross SSand Levi R.Tetrahydrobiopterin synthesis. An absolute requirement for cytokine-induced nitric oxide generation by vascular smooth muscle.J Biol Chem267: 25722\u201325729, 1992.","DOI":"10.1016\/S0021-9258(18)35667-9"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.42.27047"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/1.5.293"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(03)00642-1"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.C200678200"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1016\/S0888-7543(05)80139-9"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.11.10.3299"},{"key":"R23","unstructured":"Khan S, Cleveland RP, Koch CJ, and Schelling JR.Hypoxia induces renal tubular epithelial cell apoptosis in chronic renal disease.Lab Invest79: 1089\u20131099, 1999."},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1007\/s007090200000"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.060003957.x"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfg375"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1016\/j.ydbio.2004.05.024"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1006\/excr.2000.5131"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.00644"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1038\/nm761"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/15.10.1547"},{"key":"R32","doi-asserted-by":"crossref","unstructured":"Macconi D, Ghilardi M, Bonassi ME, Mohamed EI, Abbate M, Colombi F, Remuzzi G, and Remuzzi A.Effect of angiotensin-converting enzyme inhibition on glomerular basement membrane permeability and distribution of zonula occludens-1 in MWF rats.J Am Soc Nephrol11: 477\u2013489, 2000.","DOI":"10.1681\/ASN.V113477"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1177\/39.8.1856454"},{"key":"R34","doi-asserted-by":"crossref","unstructured":"Mundel P, Reiser J, and Kriz W.Induction of differentiation in cultured rat and human podocytes.J Am Soc Nephrol8: 697\u2013705, 1997.","DOI":"10.1681\/ASN.V85697"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1006\/excr.1997.3739"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/ddh040"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.138.5.1139"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M102820200"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1152\/physiolgenomics.00201.2004"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/ddg240"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.11.1.117"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1186\/1471-2121-6-1"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1002\/jemt.10076"},{"key":"R44","doi-asserted-by":"crossref","unstructured":"Reiser J, Kriz W, Kretzler M, and Mundel P.The glomerular slit diaphragm is a modified adherens junction.J Am Soc Nephrol11: 1\u20138, 2000.","DOI":"10.1681\/ASN.V1111"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1016\/S0378-1119(02)01173-3"},{"key":"R46","doi-asserted-by":"publisher","DOI":"10.1007\/s00418-002-0398-y"},{"key":"R47","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)64421-5"},{"key":"R48","unstructured":"Sasaki T, Hatta H, and Osawa G.Cytokines and podocyte injury: the mechanism of fibroblast growth factor 2-induced podocyte injury.Nephrol Dial Transplant14,Suppl1: 33\u201334, 1999."},{"key":"R49","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/17.15.6419"},{"key":"R50","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0407123101"},{"key":"R51","doi-asserted-by":"publisher","DOI":"10.1002\/jemt.10082"},{"key":"R52","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M314155200"},{"key":"R53","doi-asserted-by":"publisher","DOI":"10.1016\/S0167-4889(02)00349-X"},{"key":"R54","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1827.1995.tb03487.x"},{"key":"R55","doi-asserted-by":"publisher","DOI":"10.1006\/geno.2002.6844"},{"key":"R56","doi-asserted-by":"publisher","DOI":"10.1101\/gad.13.15.1924"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00389.2004","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,7,7]],"date-time":"2021-07-07T14:40:52Z","timestamp":1625668852000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00389.2004"}},"issued":{"date-parts":[[2005,8]]},"references-count":56,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2005,8]]}},"alternative-id":["10.1152\/ajprenal.00389.2004"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00389.2004","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2005,8]]}},{"indexed":{"date-parts":[[2025,11,4]],"date-time":"2025-11-04T22:28:26Z","timestamp":1762295306387},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1987,11,1]]},"abstract":"<jats:p> The present study was performed to quantitate and compare the luminal and the peritubular uptake of 125I-labeled insulin in isolated, perfused, proximal tubules from rabbit kidneys. 125I-insulin was added in physiological concentrations of 3.0-7.0 ng\/ml or 59.0-89.5 ng\/ml (high insulin concentrations) to either the perfusate or the bath fluid for 30 min. The luminal uptake in 30 min averaged 0.76 pg\/mm at physiological concentrations and 18.0 pg\/mm at high insulin concentrations. About 15-41% of the absorbed insulin was digested and less than 5% was transported from the lumen to the peritubular space as intact insulin. The peritubular binding\/uptake of 125I-insulin at physiological and high concentrations in the bath was 0.136 and 0.318 pg, respectively. Addition of excess unlabeled insulin (10(-5) M) to the bath produced significant inhibition of binding (53.7%) at 7.0 ng\/ml, but no inhibition at 89.5 ng\/ml labeled insulin in the bath. This indicates that insulin is bound\/absorbed at the basolateral membranes both by a saturable specific mechanism and a nonspecific, nonsaturable mechanism. The basolateral absorption constituted 15.2 and 1.8% of the total tubular extraction of insulin at physiological and high insulin concentrations, respectively. Electron microscope autoradiography showed that, after luminal as well as basolateral endocytosis, insulin was exclusively accumulated in endocytic vacuoles and lysosomes. <\/jats:p>","DOI":"10.1152\/ajprenal.1987.253.5.f857","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T04:14:24Z","timestamp":1514002464000},"page":"F857-F867","source":"Crossref","is-referenced-by-count":7,"title":["Luminal and basolateral uptake of insulin in isolated, perfused, proximal tubules"],"prefix":"10.1152","volume":"253","author":[{"given":"S.","family":"Nielsen","sequence":"first","affiliation":[{"name":"Department of Cell Biology, University of Aarhus, Denmark."}]},{"given":"J. T.","family":"Nielsen","sequence":"additional","affiliation":[{"name":"Department of Cell Biology, University of Aarhus, Denmark."}]},{"given":"E. I.","family":"Christensen","sequence":"additional","affiliation":[{"name":"Department of Cell Biology, University of Aarhus, Denmark."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1987.253.5.F857","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:54:33Z","timestamp":1567972473000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1987.253.5.F857"}},"issued":{"date-parts":[[1987,11,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1987,11,1]]}},"alternative-id":["10.1152\/ajprenal.1987.253.5.F857"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1987.253.5.f857","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1987,11,1]]}},{"indexed":{"date-parts":[[2025,11,4]],"date-time":"2025-11-04T11:15:49Z","timestamp":1762254949410,"version":"3.37.3"},"reference-count":74,"publisher":"American Physiological Society","issue":"5","funder":[{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK128017"],"award-info":[{"award-number":["DK128017"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK118391"],"award-info":[{"award-number":["DK118391"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK101405"],"award-info":[{"award-number":["DK101405"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000005","name":"U.S. Department of Defense","doi-asserted-by":"publisher","award":["PR221810"],"award-info":[{"award-number":["PR221810"]}],"id":[{"id":"10.13039\/100000005","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2024,11,1]]},"abstract":"<jats:p> Our study shows that a brief harvesting-freezing delay associated with organ collection and freezing can significantly alter the kidney metabolic profile of both male and female wild-type and a genetic model of chronic kidney disease. Importantly, given that the effect of this delay differs among genotypes, it is not safe to assume that equally delaying harvesting-freezing in wild-type and polycystic kidney disease kidneys adequately controls this effect, ultimately leading to false positive and negative results among different renal diseases. <\/jats:p>","DOI":"10.1152\/ajprenal.00131.2024","type":"journal-article","created":{"date-parts":[[2024,8,29]],"date-time":"2024-08-29T08:00:25Z","timestamp":1724918425000},"page":"F697-F711","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["A brief harvesting-freezing delay significantly alters the kidney metabolome and leads to false positive and negative results"],"prefix":"10.1152","volume":"327","author":[{"ORCID":"https:\/\/orcid.org\/0009-0006-1425-0002","authenticated-orcid":false,"given":"Yahya","family":"Alsawaf","sequence":"first","affiliation":[{"name":"Mayo Translational PKD Center, Division of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4379-6884","authenticated-orcid":false,"given":"Igor","family":"Maksimovic","sequence":"additional","affiliation":[{"name":"Mayo Translational PKD Center, Division of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota, United States"}]},{"given":"Jamie","family":"Zheng","sequence":"additional","affiliation":[{"name":"Mayo Translational PKD Center, Division of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota, United States"}]},{"given":"Song","family":"Zhang","sequence":"additional","affiliation":[{"name":"Metabolomics Core, Mayo Clinic, Rochester, Minnesota, United States"},{"name":"Department of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7806-7238","authenticated-orcid":false,"given":"Ivan","family":"Vuckovic","sequence":"additional","affiliation":[{"name":"Metabolomics Core, Mayo Clinic, Rochester, Minnesota, United States"}]},{"given":"Petras","family":"Dzeja","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6054-5163","authenticated-orcid":false,"given":"Slobodan","family":"Macura","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, Mayo Clinic, Rochester, Minnesota, United States"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9904-7778","authenticated-orcid":false,"given":"Maria V.","family":"Irazabal","sequence":"additional","affiliation":[{"name":"Mayo Translational PKD Center, Division of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota, United States"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1979.236.5.F423"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2015030302"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1126\/scisignal.aax9760"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/nature17184"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014121181"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pgen.1003053"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1038\/nm.3092"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/4551054a"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1042\/BA20060221"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1038\/nm.3762"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1172\/jci.insight.86976"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2016.186"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.26355\/eurrev_201807_15419"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1038\/s41467-017-01646-6"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1016\/j.celrep.2019.04.012"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.3389\/fphys.2021.645857"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/j.ebiom.2016.01.027"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00238.2015"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00025.2018"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1038\/s42003-018-0200-x"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1038\/s41467-018-03036-y"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00262.2021"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1016\/S0021-9258(18)51740-3"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1042\/bj1200105"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1016\/bs.mcb.2019.05.009"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1038\/nm935"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004121090"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1053\/j.gastro.2006.12.039"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007060688"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfn527"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00345.2014"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1007\/BF00362995"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1016\/0003-9861(72)90170-1"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-4615-7751-5_7"},{"volume-title":"A User\u2019s Guide to Principal Components","year":"1991","author":"Je J","key":"B35"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfx349"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1038\/s41581-018-0051-1"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1016\/j.molcel.2014.08.018"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2015020132"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1042\/bj1170091"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1042\/bj1030852"},{"key":"B42","first-page":"335","volume-title":"Principles of Fermentation Technology","author":"Stanbury PF","year":"2016"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1016\/0017-9310(66)90112-8"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1016\/S0021-9258(18)57094-0"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1038\/185666a0"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1021\/bi00903a023"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1152\/ajplegacy.1966.211.2.493"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1042\/bj1180221"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2728(70)90158-1"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1016\/S0021-9258(17)40153-0"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1161\/01.res.43.5.808"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2728(88)90119-3"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1979.237.5.H535"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1983.244.2.H281"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1007\/BF01910459"},{"key":"B56","first-page":"S568","volume":"46","author":"Pisarenko O","year":"1987","journal-title":"Biomed Biochim Acta"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1016\/j.ccr.2004.11.022"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1126\/stke.4072007cm8"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1007\/BF00974874"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1117773108"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1038\/nature10642"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1096\/fasebj.9.11.7649415"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1042\/bj2430803"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.3109\/10715769309147501"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1007\/s007010070042"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0705776"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.3390\/ijms21061994"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.1152\/ajplegacy.1965.209.6.1193"},{"key":"B69","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1986.8"},{"key":"B70","doi-asserted-by":"publisher","DOI":"10.1016\/j.molmet.2022.101596"},{"key":"B71","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.me.26.020175.002135"},{"key":"B72","doi-asserted-by":"publisher","DOI":"10.2174\/157488612802715681"},{"key":"B73","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0117232"},{"key":"B74","doi-asserted-by":"publisher","DOI":"10.1002\/bmc.3010"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00131.2024","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,10,14]],"date-time":"2024-10-14T16:59:39Z","timestamp":1728925179000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00131.2024"}},"issued":{"date-parts":[[2024,11,1]]},"references-count":74,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2024,11,1]]}},"alternative-id":["10.1152\/ajprenal.00131.2024"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00131.2024","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2024,11,1]]},"assertion":[{"value":"2024-04-30","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2024-07-25","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2024-08-13","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2024-10-14","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2025,11,6]],"date-time":"2025-11-06T12:16:26Z","timestamp":1762431386044},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1996,7,1]]},"abstract":"<jats:p> These studies were conducted to determine whether the alpha 2-agonists epinephrine and dexmedetomidine inhibit osmotic water permeability (Pf) and urea permeability (Pu) in the rat inner medullary collecting duct (IMCD). Wistar rat IMCD segments were perfused via standard methods, and Pf and Pu were determined in separate studies. The control period was followed by adding 220 pM arginine vasopressin (AVP) or 10(-4) M dibutyryladenosine 3',5'-cyclic monophosphate (DBcAMP) to the bath. Epinephrine or dexmedetomidine, both at 1 microM, was then added to the bath, and this period was followed by adding 1 microM atipamezole, a selective alpha 2-antagonist. The phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine was present in all experiments with DBcAMP. Epinephrine inhibited AVP- and DBcAMP-stimulated Pf by 90% and 80%, respectively. Dexmedetomidine inhibited AVP- and DBcAMP-stimulated Pf by 98% and 97%, respectively. Epinephrine inhibited AVP- and DBcAMP-stimulated Pu by 70% and 60%, respectively. Dexmedetomidine failed to affect Pu. Atipamezole reversed all inhibitory effects. These data confirm an alpha 2-mediated mechanism in the IMCD that modulates Pf and Pu, and they indicate that inhibition occurs via post-cAMP cellular events. <\/jats:p>","DOI":"10.1152\/ajprenal.1996.271.1.f150","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T06:50:32Z","timestamp":1514011832000},"page":"F150-F157","source":"Crossref","is-referenced-by-count":8,"title":["Alpha 2-adrenergic-mediated inhibition of water and urea permeability in the rat IMCD"],"prefix":"10.1152","volume":"271","author":[{"given":"A. J.","family":"Rouch","sequence":"first","affiliation":[{"name":"Oklahoma State University College of Osteopathic Medicine, Tulsa 74107, USA."}]},{"given":"L. H.","family":"Kudo","sequence":"additional","affiliation":[{"name":"Oklahoma State University College of Osteopathic Medicine, Tulsa 74107, USA."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1996.271.1.F150","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:06:59Z","timestamp":1567973219000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1996.271.1.F150"}},"issued":{"date-parts":[[1996,7,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1996,7,1]]}},"alternative-id":["10.1152\/ajprenal.1996.271.1.F150"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1996.271.1.f150","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1996,7,1]]}},{"indexed":{"date-parts":[[2025,11,6]],"date-time":"2025-11-06T19:57:54Z","timestamp":1762459074211},"reference-count":120,"publisher":"American Physiological Society","issue":"9","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,5,1]]},"abstract":"<jats:p>The intrarenal autocrine\/paracrine dopamine (DA) system contributes to natriuresis in response to both acute and chronic Na<jats:sup>+<\/jats:sup>loads. While the acute DA effect is well described, how DA induces natriuresis chronically is not known. We used an animal and a cell culture model to study the chronic effect of DA on a principal renal Na<jats:sup>+<\/jats:sup>transporter, Na<jats:sup>+<\/jats:sup>\/H<jats:sup>+<\/jats:sup>exchanger-3 (NHE3). Intraperitoneal injection of Gludopa in rats for 2 days elevated DA excretion and decreased total renal cortical and apical brush-border NHE3 antigen. Chronic treatment of an opossum renal proximal cell line with DA decreased NHE3 activity, cell surface and total cellular NHE3 antigen, but not NHE3 transcript. The decrease in NHE3 antigen was dose and time dependent with maximal inhibition at 16\u201324 h and half maximal effect at 3 \u00d7 10<jats:sup>\u22127<\/jats:sup>M. This is in contradistinction to the acute effect of DA on NHE3 (half maximal at 2 \u00d7 10<jats:sup>\u22126<\/jats:sup>M), which was not associated with changes in total cellular NHE3 protein. The DA-induced decrease in total NHE3 protein was associated with decrease in NHE3 translation and mediated by cis-sequences in the NHE3 5\u2032-untranslated region. DA also decreased cell surface and total cellular NHE3 protein half-life. The DA-induced decrease in total cellular NHE3 was partially blocked by proteasome inhibition but not by lysosome inhibition, and DA increased ubiquitylation of total and surface NHE3. In summary, chronic DA inhibits NHE3 with mechanisms distinct from its acute action and involves decreased NHE3 translation and increased NHE3 degradation, which are novel mechanisms for NHE3 regulation.<\/jats:p>","DOI":"10.1152\/ajprenal.00630.2012","type":"journal-article","created":{"date-parts":[[2013,2,21]],"date-time":"2013-02-21T06:41:33Z","timestamp":1361428893000},"page":"F1169-F1180","source":"Crossref","is-referenced-by-count":23,"title":["Chronic regulation of the renal Na<sup>+<\/sup>\/H<sup>+<\/sup>exchanger NHE3 by dopamine: translational and posttranslational mechanisms"],"prefix":"10.1152","volume":"304","author":[{"given":"Ming Chang","family":"Hu","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas;"},{"name":"Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, Texas; and"},{"name":"Charles and Jane Pak Center of Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, Texas"}]},{"given":"Francesca","family":"Di Sole","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas;"},{"name":"Charles and Jane Pak Center of Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, Texas"}]},{"given":"Jianning","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas;"}]},{"given":"Paul","family":"McLeroy","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas;"}]},{"given":"Orson W.","family":"Moe","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas;"},{"name":"Department of Physiology, University of Texas Southwestern Medical Center, Dallas, Texas;"},{"name":"Charles and Jane Pak Center of Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, Texas"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118670"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.2000.278.4.R1064"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1242\/jeb.027375"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.4.F917"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1172\/JCI2913"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.404"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1995.269.1.C126"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.252.1.F39"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.62.1.621"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1172\/JCI3685"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00380.2004"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00308.x"},{"key":"B13","doi-asserted-by":"crossref","first-page":"1604","DOI":"10.1681\/ASN.V991604","volume":"9","author":"Baines AD","year":"1998","journal-title":"J Am Soc Nephrol"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2125.1977.tb00681.x"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.270.1.F164"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00879.x"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.267.3.F437"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00156.x"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000198427.96225.36"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1982.242.6.F634"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.259.6.F924"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1988.254.6.F795"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00447.2004"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2006.07.001"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-008-0595-1"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00708.2009"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.3.F629"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1999.276.1.C102"},{"key":"B29","first-page":"17","volume":"199","author":"Chan YL","year":"1976","journal-title":"J Pharmacol Exp Ther"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.19.6.589"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-199917121-00033"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008121255"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.21399"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1242\/jeb.028605"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.4161\/cc.11.2.18699"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.264.6.F1032"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1093\/ajh\/3.6.126S"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.E04-03-0176"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.258.3.F514"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.18.5.614"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00186.2004"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.264.4.F618"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00027.2001"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1042\/cs0760517"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1002\/j.1460-2075.1990.tb07635.x"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-2999(97)01564-1"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-2999(03)01965-4"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-199103000-00010"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00005.2004"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.2170\/jjphysiol.40.351"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1991.30"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.258.1.F28"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200309000-00008"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-003-1066-3"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.13.6.828"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1093\/ajh\/3.6.78S"},{"key":"B57","first-page":"733","volume":"45","author":"Hollenberg NK","year":"1973","journal-title":"Clin Sci Mol Med"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.22-24-10801.2002"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M011338200"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0b013e3282f4e4fd"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1038\/nrm2838"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1016\/0895-7061(95)00351-7"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1016\/S0163-7258(98)00027-8"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1007\/s11906-000-0079-y"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1164\/rccm.200703-347OC"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00365.2001"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000098700.70804.D3"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00082.2004"},{"key":"B69","doi-asserted-by":"publisher","DOI":"10.1007\/s003359900171"},{"key":"B70","first-page":"214","volume":"105","author":"Krishna GG","year":"1985","journal-title":"J Lab Clin Med"},{"key":"B71","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.18.6.709"},{"key":"B72","doi-asserted-by":"crossref","first-page":"975","DOI":"10.1681\/ASN.V96975","volume":"9","author":"Lederer ED","year":"1998","journal-title":"J Am Soc Nephrol"},{"key":"B73","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.281.4.F718"},{"key":"B74","doi-asserted-by":"publisher","DOI":"10.1111\/j.1474-8673.1990.tb00235.x"},{"key":"B75","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.38.3.303"},{"key":"B76","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0409767102"},{"key":"B77","doi-asserted-by":"crossref","first-page":"1560","DOI":"10.1681\/ASN.V991560","volume":"9","author":"Loffing J","year":"1998","journal-title":"J Am Soc Nephrol"},{"key":"B78","doi-asserted-by":"publisher","DOI":"10.1172\/JCI104996"},{"key":"B79","doi-asserted-by":"publisher","DOI":"10.3858\/emm.2010.42.4.032"},{"key":"B80","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115487"},{"key":"B81","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1990.249"},{"key":"B82","doi-asserted-by":"publisher","DOI":"10.1042\/cs0900511"},{"key":"B83","doi-asserted-by":"crossref","first-page":"9331","DOI":"10.1016\/S0021-9258(19)50428-8","volume":"267","author":"Orlowski J","year":"1992","journal-title":"J Biol Chem"},{"key":"B84","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1983.245.2.F247"},{"key":"B85","doi-asserted-by":"publisher","DOI":"10.1042\/bj3120433"},{"key":"B86","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00237.2003"},{"key":"B87","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-006-0321-1"},{"key":"B88","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(94)90462-6"},{"key":"B89","first-page":"61","volume":"36","author":"Romero-Vecchione E","year":"1995","journal-title":"Invest Clin"},{"key":"B90","doi-asserted-by":"publisher","DOI":"10.1038\/969"},{"key":"B91","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M010642200"},{"key":"B92","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.264.4.F737"},{"key":"B93","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M110.115089"},{"key":"B94","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.257.3.F469"},{"key":"B95","doi-asserted-by":"publisher","DOI":"10.1210\/endo-115-6-2085"},{"key":"B96","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/16.21.6325"},{"key":"B97","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00020.2005"},{"key":"B98","doi-asserted-by":"publisher","DOI":"10.1291\/hypres.30.93"},{"key":"B99","doi-asserted-by":"publisher","DOI":"10.3109\/10641969309041614"},{"key":"B100","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.1984.247.3.E285"},{"key":"B101","doi-asserted-by":"publisher","DOI":"10.1007\/BF00374216"},{"key":"B102","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2012.08.063"},{"key":"B103","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(94)90502-9"},{"key":"B104","doi-asserted-by":"publisher","DOI":"10.1016\/0303-7207(82)90061-2"},{"key":"B105","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.29.1.228"},{"key":"B106","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.1992.tb00474.x"},{"key":"B107","doi-asserted-by":"publisher","DOI":"10.1007\/s11906-999-0013-x"},{"key":"B108","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00480.x"},{"key":"B109","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1990.323"},{"key":"B110","doi-asserted-by":"publisher","DOI":"10.1042\/cs0840549"},{"key":"B111","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00418.2002"},{"key":"B112","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.51.32749"},{"key":"B113","doi-asserted-by":"publisher","DOI":"10.1124\/mol.59.3.485"},{"key":"B114","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00434.2005"},{"key":"B115","first-page":"1141","volume":"9","author":"Yoshimura M","year":"1987","journal-title":"Clin Exp Hypertens A"},{"key":"B116","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.01036.2007"},{"key":"B117","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.110.157727"},{"key":"B118","doi-asserted-by":"publisher","DOI":"10.2174\/187152507781058708"},{"key":"B119","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.7.3978"},{"key":"B120","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000057422.75590.D7"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00630.2012","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,2,9]],"date-time":"2022-02-09T04:00:09Z","timestamp":1644379209000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00630.2012"}},"issued":{"date-parts":[[2013,5,1]]},"references-count":120,"journal-issue":{"issue":"9","published-print":{"date-parts":[[2013,5,1]]}},"alternative-id":["10.1152\/ajprenal.00630.2012"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00630.2012","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2013,5,1]]}},{"indexed":{"date-parts":[[2025,11,2]],"date-time":"2025-11-02T16:41:19Z","timestamp":1762101679385},"reference-count":33,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2002,3,1]]},"abstract":"<jats:p> We investigated a possible involvement of the sympathetic nervous system in the parallel increase of renin, cyclooxygenase-2 (COX-2), and neuronal nitric oxide synthase (nNOS) gene expression in the juxtaglomerular apparatus of rat kidneys induced by salt deficiency. Therefore, we determined the effects of renal denervation and the \u03b2-adrenoreceptor antagonist metoprolol (50 mg\/kg body wt po, twice a day) on renocortical expression of renin, COX-2, and nNOS in rats fed a low-salt (0.02% wt\/wt) diet or treated for 1 wk with ramipril (10 mg\/kg body wt) in combination with a low-salt diet. We found that a low-salt diet in combination with ramipril strongly increased renocortical mRNA levels of renin, COX-2, and nNOS 9-, 7-, and 2.5-fold, respectively. Treatment with metoprolol did not change basal expression of the three genes or induction of renin and COX-2 gene expression, while induction of nNOS expression was clearly attenuated. Similarly, unilateral renal denervation attenuated induction of nNOS expression but had no effect on all other parameters. These findings suggest that \u03b2-adrenergic stimulation is not required for stimulation of renin and COX-2 gene expression in the juxtaglomerular apparatus during salt deficiency. However, \u03b2-adrenoreceptor activity or renal nerve activity appears to be required for the full stimulation of nNOS expression by low salt intake or combined with angiotensin-converting enzyme inhibition. <\/jats:p>","DOI":"10.1152\/ajprenal.00209.2001","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:34:32Z","timestamp":1425414872000},"page":"F478-F484","source":"Crossref","is-referenced-by-count":27,"title":["Role of renal nerves in stimulation of renin, COX-2,  and nNOS in rat renal cortex during salt deficiency"],"prefix":"10.1152","volume":"282","author":[{"given":"K.","family":"H\u00f6cherl","sequence":"first","affiliation":[{"name":"Departments of Pharmacology,"}]},{"given":"M.","family":"Kammerl","sequence":"additional","affiliation":[{"name":"Physiology, and"}]},{"given":"F.","family":"Kees","sequence":"additional","affiliation":[{"name":"Departments of Pharmacology,"}]},{"given":"B. K.","family":"Kr\u00e4mer","sequence":"additional","affiliation":[{"name":"Internal Medicine II, University of Regensburg, 93040 Regensburg, Germany"}]},{"given":"H. F.","family":"Grobecker","sequence":"additional","affiliation":[{"name":"Departments of Pharmacology,"}]},{"given":"A.","family":"Kurtz","sequence":"additional","affiliation":[{"name":"Physiology, and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1982.243.3.F276"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.059002515.x"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.6.F793"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1007\/s004240000438"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.1.F122"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1172\/JCI5505"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/0003-2697(87)90021-2"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1997.77.1.75"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/S0378-4347(00)80427-2"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.54.1.1"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1990.70.4.1067"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.29.1.297"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117620"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.31.1.201"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.57.2.278"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1007\/BF00374504"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.266.5.F738"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.3.F659"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.275.6.F849"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1984.246.6.F811"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.2000.279.5.R1641"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.1.F119"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.36.2.276"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1016\/S0009-9236(99)70056-1"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.97.15.8617"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.6.F825"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1007\/s004240050150"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1536\/ihj.36.389"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.34.5.1101"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-199715120-00014"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.34.1.96"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.89.24.11993"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.34.3.503"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00209.2001","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T21:59:13Z","timestamp":1567979953000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00209.2001"}},"issued":{"date-parts":[[2002,3,1]]},"references-count":33,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2002,3,1]]}},"alternative-id":["10.1152\/ajprenal.00209.2001"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00209.2001","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2002,3,1]]}},{"indexed":{"date-parts":[[2025,11,3]],"date-time":"2025-11-03T13:37:21Z","timestamp":1762177041705},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1994,1,1]]},"abstract":"<jats:p> Effects of RU-28362 (glucocorticoid agonist), RU-38486 (glucocorticoid antagonist), and RU-26752 (mineralocorticoid antagonist) on the apical Na<jats:sup>+<\/jats:sup> permeability of toad bladder were measured and correlated with occupancies of cytosolic type I (mineralocorticoid) and type II (glucocorticoid) receptors. Effects of the above steroids were measured in whole bladders, plasma membrane vesicles, and RNA-injected Xenopus oocytes. RU-38486 was found to fully displace aldosterone from type II receptors without affecting type I occupancy. Under these conditions, RU-38486 inhibited approximately 35% of the effect of aldosterone measured in the whole tissue and isolated membranes. Unexpectedly, oocytes injected with RNA from tissue stimulated with aldosterone plus RU-38486 expressed channel activity that was much higher than the sum of activities induced by either steroid alone. RU-28362 and RU-26752 at concentrations sufficient to fully occupy both receptors had only partial agonistic and antagonistic effects, respectively. The results suggest that at least one-third of the natriferic action of aldosterone measured in the amphibian urinary bladder is mediated by the glucocorticoid receptor. However, some of the effects observed cannot be accounted for by a simple receptor occupancy-response scheme. <\/jats:p>","DOI":"10.1152\/ajprenal.1994.266.1.f108","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T05:59:45Z","timestamp":1514008785000},"page":"F108-F116","source":"Crossref","is-referenced-by-count":5,"title":["Effects of corticoid agonists and antagonists on apical Na+ permeability of toad urinary bladder"],"prefix":"10.1152","volume":"266","author":[{"given":"H.","family":"Garty","sequence":"first","affiliation":[{"name":"Department of Membrane Research and Biophysics, Weizmann Institute of Science, Rehovot, Israel."}]},{"given":"K.","family":"Peterson-Yantorno","sequence":"additional","affiliation":[{"name":"Department of Membrane Research and Biophysics, Weizmann Institute of Science, Rehovot, Israel."}]},{"given":"C.","family":"Asher","sequence":"additional","affiliation":[{"name":"Department of Membrane Research and Biophysics, Weizmann Institute of Science, Rehovot, Israel."}]},{"given":"M. M.","family":"Civian","sequence":"additional","affiliation":[{"name":"Department of Membrane Research and Biophysics, Weizmann Institute of Science, Rehovot, Israel."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1994.266.1.F108","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:31:45Z","timestamp":1567960305000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1994.266.1.F108"}},"issued":{"date-parts":[[1994,1,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1994,1,1]]}},"alternative-id":["10.1152\/ajprenal.1994.266.1.F108"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1994.266.1.f108","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1994,1,1]]}},{"indexed":{"date-parts":[[2025,11,3]],"date-time":"2025-11-03T13:32:27Z","timestamp":1762176747433},"reference-count":53,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2014,9,15]]},"abstract":"<jats:p> Acute kidney injury (AKI) increases the risk of morbidity and mortality after major surgery and transplantation. We investigated the effect of PKC-\u03b5 deficiency on AKI and ischemic allograft damage after kidney transplantation. PKC-\u03b5-deficient and wild type (WT) control mice were subjected to 35 min of renal pedicle clamping to induce AKI. PKC-\u03b5 deficiency was associated with a marked improvement in survival and an attenuated loss of kidney function. Furthermore, functional MRI experiments revealed better renal perfusion in PKC-\u03b5-deficient mice than in WT mice one day after IRI. Acute tubular necrosis and neutrophil infiltration were markedly reduced in PKC-\u03b5-deficient mice. To determine whether this resistance to ischemia-reperfusion injury resulted from changes in local renal cells or infiltrating leukocytes, we studied a life-supporting renal transplant model of ischemic graft injury. We transplanted kidneys from H<jats:sup>2b<\/jats:sup> PKC-\u03b5-deficient mice (129\/SV) and their corresponding WT littermates into major histocompatibility complex-incompatible H<jats:sup>2d<\/jats:sup> recipients (BALB\/c) and induced ischemic graft injury by prolonged cold ischemia time. Recipients of WT allografts developed severe renal failure and died within 10 days of transplantation. Recipients of PKC-\u03b5-deficient allografts had better renal function and survival; they had less generation of ROS and upregulation of proinflammatory proteins (i.e., ICAM-1, inducible nitric oxide synthase, and TNF-\u03b1) and showed less tubular epithelial cell apoptosis and inflammation in their allografts. These data suggest that local renal PKC-\u03b5 expression mediates proapoptotic and proinflammatory signaling and that an inhibitor of PKC-\u03b5 signaling could be used to prevent hypoxia-induced AKI. <\/jats:p>","DOI":"10.1152\/ajprenal.00372.2013","type":"journal-article","created":{"date-parts":[[2014,7,24]],"date-time":"2014-07-24T02:48:09Z","timestamp":1406170089000},"page":"F718-F726","source":"Crossref","is-referenced-by-count":31,"title":["Renal PKC-\u03b5 deficiency attenuates acute kidney injury and ischemic allograft injury via TNF-\u03b1-dependent inhibition of apoptosis and inflammation"],"prefix":"10.1152","volume":"307","author":[{"given":"Song","family":"Rong","sequence":"first","affiliation":[{"name":"Department of Nephrology, Hannover Medical School, Hannover, Germany;"},{"name":"The Transplantation Center, Affiliated Hospital, Zunyi Medical College, Zunyi, China;"}]},{"given":"Katja","family":"Hueper","sequence":"additional","affiliation":[{"name":"Institute for Diagnostic and Interventional Radiology, Medical School Hannover, Hannover, Germany;"}]},{"given":"Torsten","family":"Kirsch","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Hannover Medical School, Hannover, Germany;"}]},{"given":"Robert","family":"Greite","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Hannover Medical School, Hannover, Germany;"}]},{"given":"Christian","family":"Klemann","sequence":"additional","affiliation":[{"name":"Centre for Paediatrics and Adolescent Medicine, Department of Pediatric Surgery, Hannover Medical School, Hannover, Germany"}]},{"given":"Michael","family":"Mengel","sequence":"additional","affiliation":[{"name":"Department of Laboratory Medicine and Pathology, University of Alberta, Edmonton, Canada;"}]},{"given":"Matthias","family":"Meier","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Hannover Medical School, Hannover, Germany;"}]},{"given":"Jan","family":"Menne","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Hannover Medical School, Hannover, Germany;"},{"name":"Phenos GmbH, Hannover, Germany;"}]},{"given":"Michael","family":"Leitges","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Hannover Medical School, Hannover, Germany;"},{"name":"The Biotechnology Centre of Oslo, University of Oslo, Oslo, Norway;"}]},{"given":"Nathan","family":"Susnik","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Hannover Medical School, Hannover, Germany;"}]},{"given":"Martin","family":"Meier","sequence":"additional","affiliation":[{"name":"Imaging Center, Institute for Animal Science, Medical School Hannover, Hannover, Germany; and"}]},{"given":"Hermann","family":"Haller","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Hannover Medical School, Hannover, Germany;"}]},{"given":"Nelli","family":"Shushakova","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Hannover Medical School, Hannover, Germany;"},{"name":"Phenos GmbH, Hannover, Germany;"}]},{"given":"Faikah","family":"Gueler","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Hannover Medical School, Hannover, Germany;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/S1357-2725(03)00210-3"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI45161"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/j.phrs.2007.04.005"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1084\/jem.194.9.1231"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.174.3.1686"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1042\/BST0351040"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1006\/jmcc.2001.1518"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajplung.2000.279.3.L429"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.50.32028"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1097\/00005392-199907000-00068"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2000.00390.x"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00026.x"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1111\/1440-1681.12031"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/j.yjmcc.2010.10.020"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1186\/1471-2369-15-23"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0308684101"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007111267"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.181.2.1179"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1098-2752(1999)19:6<272::AID-MICR3>3.0.CO;2-L"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1148\/radiol.13130367"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1097\/RLI.0b013e31824f272d"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.107.109637"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00064.2009"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-5793(97)01357-4"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000161999.86198.1e"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/j.yjmcc.2007.06.003"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1159\/000048904"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.100.9.967"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1007\/s10495-007-0111-7"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/S1053-2498(99)00052-2"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1097\/TP.0b013e318169c29e"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00099.2004"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00275.2003"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00364.2010"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00434.2001"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00012.2005"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.0590051789.x"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1093\/cvr\/cvp001"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1002\/jemt.21000"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1007\/s12038-011-9006-4"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1016\/S0008-6363(02)00325-5"},{"key":"B42","first-page":"883","volume":"36","author":"Shankar E","year":"2010","journal-title":"Int J Oncol"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1038\/onc.2008.39"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1111\/j.1432-2277.2004.tb00428.x"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M704001200"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.1101678"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.5414\/CNP62121"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M710436200"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1111\/j.1442-2042.2004.00910.x"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000138389.22905.62"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1016\/j.jss.2004.10.011"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1007\/s11010-011-0979-y"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0053849"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00372.2013","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T01:02:43Z","timestamp":1567990963000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00372.2013"}},"issued":{"date-parts":[[2014,9,15]]},"references-count":53,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2014,9,15]]}},"alternative-id":["10.1152\/ajprenal.00372.2013"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00372.2013","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2014,9,15]]}},{"indexed":{"date-parts":[[2025,11,7]],"date-time":"2025-11-07T09:20:58Z","timestamp":1762507258112},"reference-count":46,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1998,12,1]]},"abstract":"<jats:p> To determine the effect of physiological hyperinsulinemia on renal and hepatic substrate metabolism, we assessed systemic and renal glucose release and uptake, systemic and renal gluconeogenesis from glutamine, and certain aspects of systemic and renal glutamine and free fatty acid (FFA) metabolism. These were assessed under basal postabsorptive conditions and during 4-h hyperinsulinemic euglycemic clamp experiments in nine normal volunteers using a combination of isotopic techniques and renal balance measurements. Hepatic glucose release (HGR) and glutamine gluconeogenesis were calculated as the difference between systemic and renal measurements. Infusion of insulin suppressed systemic glucose release and glutamine gluconeogenesis by \u223c50% during the last hour of the insulin infusion ( P &lt; 0.001). Renal glucose release and glutamine gluconeogenesis decreased from 2.3 \u00b1 0.4 to 0.9 \u00b1 0.2 ( P &lt; 0.002) and from 0.52 \u00b1 0.07 to 0.14 \u00b1 0.03 \u03bcmol \u22c5 kg<jats:sup>\u22121<\/jats:sup> \u22c5 min<jats:sup>\u22121<\/jats:sup>( P &lt; 0.001), respectively. HGR and glutamine gluconeogenesis decreased from 8.7 \u00b1 0.4 to 4.5 \u00b1 0.5 ( P &lt; 0.001) and from 0.35 \u00b1 0.02 to 0.27 \u00b1 0.03 \u03bcmol \u22c5 kg<jats:sup>\u22121<\/jats:sup> \u22c5 min<jats:sup>\u22121<\/jats:sup>( P &lt; 0.002), respectively. Renal glucose uptake (RGU) increased from 1.61 \u00b1 0.19 to 2.18 \u00b1 0.25 \u03bcmol \u22c5 kg<jats:sup>\u22121<\/jats:sup> \u22c5 min<jats:sup>\u22121<\/jats:sup>( P = 0.029) but accounted for only \u223c5% of systemic glucose disposal (40.6 \u00b1 4.3 \u03bcmol \u22c5 kg<jats:sup>\u22121<\/jats:sup> \u22c5 min<jats:sup>\u22121<\/jats:sup>). Both systemic and renal FFA clearance increased approximately fourfold ( P &lt; 0.001 for both). Nevertheless, renal FFA uptake decreased ( P = 0.024) and was inversely correlated with RGU ( r = \u22120.582, P = 0.011). Finally, insulin increased systemic glutamine release ( P = 0.007), uptake ( P &lt; 0.005), and clearance ( P &lt; 0.001) but left renal glutamine uptake and release unaffected ( P &gt; 0.4 for both). <\/jats:p>","DOI":"10.1152\/ajprenal.1998.275.6.f915","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T11:36:36Z","timestamp":1514028996000},"page":"F915-F921","source":"Crossref","is-referenced-by-count":32,"title":["Effects of physiological hyperinsulinemia on  systemic, renal, and hepatic substrate metabolism"],"prefix":"10.1152","volume":"275","author":[{"given":"Christian","family":"Meyer","sequence":"first","affiliation":[{"name":"Departments of Medicine and"}]},{"given":"Jean","family":"Dostou","sequence":"additional","affiliation":[{"name":"Departments of Medicine and"}]},{"given":"Veena","family":"Nadkarni","sequence":"additional","affiliation":[{"name":"Departments of Medicine and"}]},{"given":"John","family":"Gerich","sequence":"additional","affiliation":[{"name":"Departments of Medicine and"},{"name":"Physiology and Pharmacology, University of Rochester School of Medicine, Rochester, New York 14642"}]}],"member":"24","reference":[{"issue":"21","key":"B1","first-page":"E1020","volume":"258","author":"Ader M.","year":"1990","journal-title":"Am. J. Physiol."},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.2337\/diab.29.8.610"},{"key":"B3","first-page":"955","volume":"37","author":"Brun C.","year":"1951","journal-title":"J. Lab. Clin. Med."},{"issue":"26","key":"B4","first-page":"E1063","volume":"263","author":"Campbell P.","year":"1992","journal-title":"Am. J. Physiol."},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117270"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.2337\/diab.25.4.283"},{"key":"B7","first-page":"229","volume":"36","author":"Chiasson J.","year":"1977","journal-title":"Fed. Proc."},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1016\/0026-0495(92)90148-4"},{"key":"B9","first-page":"445","volume":"19","author":"DeBodo R.","year":"1963","journal-title":"Recent Prog. Horm. Res."},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.2337\/diab.32.1.35"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1002\/dmr.5610030108"},{"issue":"7","key":"B12","first-page":"E517","volume":"244","author":"Ferrannini E.","year":"1983","journal-title":"Am. J. Physiol."},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.2337\/diab.36.8.914"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115005"},{"issue":"17","key":"B15","first-page":"E700","volume":"254","author":"Jensen M.","year":"1988","journal-title":"Am. J. Physiol."},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1172\/JCI114735"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1080\/10826079408013767"},{"issue":"17","key":"B18","first-page":"R391","volume":"248","author":"Katz J.","year":"1985","journal-title":"Am. J. Physiol."},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1172\/JCI109182"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1042\/bj1010242"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1042\/bj0940712"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1210\/endo-67-6-744"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1139\/y84-010"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.2337\/diab.46.7.1111"},{"issue":"36","key":"B26","first-page":"E650","volume":"273","author":"Meyer C.","year":"1997","journal-title":"Am. J. Physiol."},{"issue":"15","key":"B28","first-page":"E431","volume":"252","author":"Miles J.","year":"1987","journal-title":"Am. J. Physiol."},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199201023260104"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/0026-0495(88)90140-0"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1007\/BF00400657"},{"issue":"32","key":"B32","first-page":"E443","volume":"269","author":"Perriello G.","year":"1995","journal-title":"Am. J. Physiol."},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1210\/endo-95-2-521"},{"issue":"8","key":"B34","first-page":"E294","volume":"245","author":"Sacca L.","year":"1983","journal-title":"Am. J. Physiol."},{"key":"B35","first-page":"347","volume":"14","author":"Schoolwerth A.","year":"1988","journal-title":"Miner. Electrolyte Metab."},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1016\/0304-4157(83)90003-5"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118314"},{"issue":"37","key":"B38","first-page":"E817","volume":"274","author":"Stumvoll M.","year":"1998","journal-title":"Am. J. Physiol."},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1016\/0003-9861(54)90358-6"},{"issue":"34","key":"B40","first-page":"E733","volume":"271","author":"Tessari P.","year":"1996","journal-title":"Am. J. Physiol."},{"issue":"22","key":"B41","first-page":"E397","volume":"259","author":"Virkamaki A.","year":"1990","journal-title":"Am. J. Physiol."},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1042\/cs0870697"},{"key":"B43","doi-asserted-by":"crossref","first-page":"449","DOI":"10.1152\/ajplegacy.1966.211.2.449","volume":"211","author":"White L.","year":"1966","journal-title":"Am. J. Physiol."},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.56.1.247"},{"key":"B45","first-page":"203","volume":"9","author":"Wirthensohn G.","year":"1983","journal-title":"Miner. Electrolyte Metab."},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1986.66.2.469"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1016\/0026-0495(90)90133-W"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.2337\/diab.38.6.744"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1998.275.6.F915","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T17:17:48Z","timestamp":1567963068000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1998.275.6.F915"}},"issued":{"date-parts":[[1998,12,1]]},"references-count":46,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1998,12,1]]}},"alternative-id":["10.1152\/ajprenal.1998.275.6.F915"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1998.275.6.f915","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1998,12,1]]}},{"indexed":{"date-parts":[[2025,11,19]],"date-time":"2025-11-19T07:12:29Z","timestamp":1763536349231,"version":"3.40.4"},"reference-count":48,"publisher":"American Physiological Society","issue":"5","funder":[{"DOI":"10.13039\/100000050","name":"HHS | NIH | National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["HL147976"],"award-info":[{"award-number":["HL147976"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK126452"],"award-info":[{"award-number":["DK126452"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100008480","name":"Arkansas Research Alliance","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100008480","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100006108","name":"HHS | NIH | National Center for Advancing Translational Sciences","doi-asserted-by":"publisher","award":["UL1 TR001436"],"award-info":[{"award-number":["UL1 TR001436"]}],"id":[{"id":"10.13039\/100006108","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2025,5,1]]},"abstract":"<jats:p> Acute preincubation with modulator of p66Shc signaling sulfur heteroarotinoid A2 (SHetA2) revealed dose-dependent ability of SHetA2 to restore renal microvascular reactivity in rats with hypertension-induced nephropathy. Moreover, chronic treatment with SHetA2 prevented loss of renal microvascular responses and decline in renal function. Thus, targeting p66Shc with SHetA2 diminishes renal damage and restores renal afferent arteriolar reactivity caused by hypertension. <\/jats:p>","DOI":"10.1152\/ajprenal.00331.2024","type":"journal-article","created":{"date-parts":[[2025,4,2]],"date-time":"2025-04-02T14:31:21Z","timestamp":1743604281000},"page":"F693-F701","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":2,"title":["Prevention of hypertension-induced renal vascular dysfunction through a p66Shc-targeted mechanism"],"prefix":"10.1152","volume":"328","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8206-4766","authenticated-orcid":false,"given":"Bradley","family":"Miller","sequence":"first","affiliation":[{"name":"Medical College of Wisconsin","place":["United States"]}]},{"given":"John D.","family":"Imig","sequence":"additional","affiliation":[{"name":"Medical College of Wisconsin","place":["United States"]},{"name":"University of Arkansas for Medical Sciences","place":["United States"]}]},{"given":"Mengjie","family":"Li","sequence":"additional","affiliation":[{"name":"The State University of New York at Buffalo","place":["United States"]}]},{"given":"Perrin","family":"Schupbach","sequence":"additional","affiliation":[{"name":"Medical College of Wisconsin","place":["United States"]}]},{"given":"Sukyung","family":"Woo","sequence":"additional","affiliation":[{"name":"The State University of New York at Buffalo","place":["United States"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7606-8245","authenticated-orcid":false,"given":"Doris M.","family":"Benbrook","sequence":"additional","affiliation":[{"name":"The University of Oklahoma Health Sciences Center","place":["United States"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5660-0190","authenticated-orcid":false,"given":"Andrey","family":"Sorokin","sequence":"additional","affiliation":[{"name":"Medical College of Wisconsin","place":["United States"]}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.06745.x"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00345.2004"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00286.2012"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.110.168955"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1172\/JCI18499"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1291\/hypres.27.791"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000179584.39937.41"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00042.2012"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M200280200"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00414.2017"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1172\/JCI75079"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1007\/s11302-024-10010-5"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1007\/s10637-005-2901-5"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1231422100"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1016\/j.mrgentox.2012.03.009"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1158\/1940-6207.CAPR-13-0171"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.3109\/01480545.2012.710632"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.3389\/fcell.2022.848682"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1007\/s10637-013-0041-x"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0194046"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1208\/s12248-020-0421-z"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.7243\/2050-120X-6-2"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1111\/bph.13478"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1080\/10739680701456960"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1161\/01.res.71.2.471"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1007\/s10637-017-0550-0"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/s0272-6386(12)70250-0"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000222003.28517.99"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.3390\/ijms241310470"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-139-4-200308190-00006"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-118-2-199301150-00009"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1001\/jama.288.19.2421"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.2337\/db18-0308"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1016\/j.lfs.2021.119661"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.3390\/cancers13102322"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.3389\/fonc.2022.958536"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1002\/ijc.32830"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1158\/0008-5472.CAN-09-0913"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-021-80966-6"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1038\/s41371-024-00917-2"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1186\/s12882-018-0940-3"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.A110.119107"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1096\/fj.12-218875"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1016\/j.scitotenv.2022.158704"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1161\/JAHA.120.020450"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.123.22608"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1093\/ajh\/hpac077"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00517.2012"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00331.2024","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,4,22]],"date-time":"2025-04-22T12:10:56Z","timestamp":1745323856000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00331.2024"}},"issued":{"date-parts":[[2025,5,1]]},"references-count":48,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2025,5,1]]}},"alternative-id":["10.1152\/ajprenal.00331.2024"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00331.2024","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2025,5,1]]},"assertion":[{"value":"2024-11-14","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2024-12-10","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2025-03-27","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2025-04-22","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2025,12,2]],"date-time":"2025-12-02T03:26:06Z","timestamp":1764645966710},"reference-count":42,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2011,1]]},"abstract":"<jats:p>Uremic cardiomyopathy of men and rodents is characterized by lower myocardial capillary supply that in rats could be prevented by central and peripheral blockade of the sympathetic nervous system. The underlying pathomechanisms remain largely unknown. We investigated whether alterations of cardiac vascular endothelial growth factor (VEGF) gene and protein expression were involved. In our long-term experiment, we analyzed whether VEGF gene and protein expression was altered in the heart of male Sprague-Dawley rats with either sham operation (sham, n = 10) or subtotal nephrectomy (SNX, n = 10). In our short-term experiment (17 sham, 24 SNX), the effect of a putative downregulation of sympathetic nervous activity by surgical renal denervation (interruption of renal afferent pathways) on cardiac gene expression of VEGF, flt-1, and flk-1 and on myocardial capillary supply was analyzed. In the long-term study, cardiac capillary supply and vascular endothelial growth factor gene and protein expression were significantly lower in SNX than in sham. In the short-term experiment, cardiac VEGF mRNA expression was significantly lower in untreated SNX (4,258 \u00b1 2,078 units) than in both sham groups (11,709 \u00b1 4,169 and 8,998 \u00b1 4,823 units); this decrease was significantly prevented by renal denervation (8,190 \u00b1 3,889, P &lt; 0.05). We conclude that cardiac VEGF gene and protein expression is reduced in experimental renal failure, and this may be considered as one potential reason for impaired myocardial adaptation under the situation of cardiac hypertrophy. The beneficial effect of sympathetic downregulation on cardiac structure and function in renal failure may be at least in part explained by increased cardiac VEGF gene expression.<\/jats:p>","DOI":"10.1152\/ajprenal.00363.2010","type":"journal-article","created":{"date-parts":[[2010,10,21]],"date-time":"2010-10-21T02:33:02Z","timestamp":1287628382000},"page":"F105-F112","source":"Crossref","is-referenced-by-count":14,"title":["Sympathetic blockade prevents the decrease in cardiac VEGF expression and capillary supply in experimental renal failure"],"prefix":"10.1152","volume":"300","author":[{"given":"K.","family":"Amann","sequence":"first","affiliation":[{"name":"Departments of 1Pathology,"}]},{"given":"G.","family":"Odoni","sequence":"additional","affiliation":[{"name":"Ospedale Civile di Dolo, Venezia, Italia"}]},{"given":"K.","family":"Benz","sequence":"additional","affiliation":[{"name":"Pediatrics, and"}]},{"given":"V.","family":"Campean","sequence":"additional","affiliation":[{"name":"Departments of 1Pathology,"}]},{"given":"J.","family":"Jacobi","sequence":"additional","affiliation":[{"name":"Hypertensiology and Nephrology, University of Erlangen-N\u00fcrnberg, Erlangen-N\u00fcrnberg;"}]},{"given":"K. F.","family":"Hilgers","sequence":"additional","affiliation":[{"name":"Hypertensiology and Nephrology, University of Erlangen-N\u00fcrnberg, Erlangen-N\u00fcrnberg;"}]},{"given":"A.","family":"Hartner","sequence":"additional","affiliation":[{"name":"Pediatrics, and"}]},{"given":"R.","family":"Veelken","sequence":"additional","affiliation":[{"name":"Hypertensiology and Nephrology, University of Erlangen-N\u00fcrnberg, Erlangen-N\u00fcrnberg;"}]},{"given":"S. R.","family":"Orth","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Regensburg, Regensburg;"},{"name":"Dialysis Centre Bad Aibling, Bad Aibling, Germany; and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"crossref","first-page":"1018","DOI":"10.1681\/ASN.V961018","volume":"9","author":"Amann K","year":"1998","journal-title":"J Am Soc Nephrol"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/15.7.964"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1038\/labinvest.3700359"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1007\/s00428-006-0219-0"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1007\/s00428-006-0219-0"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/13.8.1958"},{"key":"B7","doi-asserted-by":"crossref","first-page":"1702","DOI":"10.1681\/ASN.V1191702","volume":"11","author":"Amann K","year":"2000","journal-title":"J Am Soc Nephrol"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(97)90283-3"},{"key":"B9","first-page":"109","volume":"4","author":"Amann K","year":"2001","journal-title":"J Clin Basic Cardiol"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/11.7.1238"},{"key":"B11","first-page":"S81","volume":"60","author":"Amann K","year":"2003","journal-title":"Clin Nephrol"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1992.390"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00320.2007"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.25.4.878"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1016\/0272-6386(95)90456-5"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1007\/s11906-002-0016-3"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1093\/eurjhf\/hfq038"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199212313272704"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009010061"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000130154.42061.C6"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1007\/s00109-009-0498-4"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00154.x"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1007\/s00428-006-0340-0"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1159\/000085881"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000034043.16664.96"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/0026-2862(76)90004-2"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000448"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000098687.01005.A5"},{"key":"B29","doi-asserted-by":"crossref","first-page":"2427","DOI":"10.1681\/ASN.V12112427","volume":"12","author":"Klein IH","year":"2001","journal-title":"J Am Soc Nephrol"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199904293401704"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1097\/HJH.0b013e328307c3d2"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2818.1990.tb03036.x"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00290.x"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00382.x"},{"key":"B35","first-page":"1","volume":"6","author":"Silberberg J","year":"1990","journal-title":"Can J Cardiol"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1989.192"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1016\/S0165-5728(99)00014-4"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.4.4.499"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1016\/0022-2828(89)90714-1"},{"key":"B40","doi-asserted-by":"crossref","first-page":"667","DOI":"10.1681\/ASN.V75667","volume":"7","author":"Tornig J","year":"1996","journal-title":"J Am Soc Nephrol"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002554"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1016\/S0895-7061(98)00030-2"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00363.2010","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,11,12]],"date-time":"2021-11-12T10:09:40Z","timestamp":1636711780000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00363.2010"}},"issued":{"date-parts":[[2011,1]]},"references-count":42,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2011,1]]}},"alternative-id":["10.1152\/ajprenal.00363.2010"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00363.2010","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2011,1]]}},{"indexed":{"date-parts":[[2025,12,1]],"date-time":"2025-12-01T19:38:12Z","timestamp":1764617892543,"version":"3.46.0"},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2025,11,1]]},"DOI":"10.1152\/ajprenal.2025.329.5.eb","type":"journal-article","created":{"date-parts":[[2025,12,1]],"date-time":"2025-12-01T19:15:52Z","timestamp":1764616552000},"page":"i-i","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Editorial Board"],"prefix":"10.1152","volume":"329","member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.2025.329.5.EB","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,12,1]],"date-time":"2025-12-01T19:15:52Z","timestamp":1764616552000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.2025.329.5.EB"}},"issued":{"date-parts":[[2025,11,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2025,11,1]]}},"alternative-id":["10.1152\/ajprenal.2025.329.5.EB"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.2025.329.5.eb","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2025,11,1]]},"assertion":[{"value":"2025-12-01","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2025,12,17]],"date-time":"2025-12-17T22:51:51Z","timestamp":1766011911579},"reference-count":36,"publisher":"American Physiological Society","issue":"9","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2012,5,1]]},"abstract":"<jats:p>The ubiquitous vacuolar H<jats:sup>+<\/jats:sup>-ATPase (V-ATPase), a multisubunit proton pump, is essential for intraorganellar acidification. Here, we hypothesized that V-ATPase is involved in the pathogenesis of kidney tubulointerstitial fibrosis. We first examined its expression in the rat unilateral ureteral obstruction (UUO) model of kidney fibrosis and transforming growth factor (TGF)-\u03b21-mediated epithelial-to-mesenchymal transition (EMT) in rat proximal tubular epithelial cells (NRK52E). Immunofluorescence experiments showed that UUO resulted in significant upregulation of V-ATPase subunits (B2, E, and c) and \u03b1-smooth muscle actin (\u03b1-SMA) in areas of tubulointerstitial injury. We further observed that TGF-\u03b21 (10 ng\/ml) treatment resulted in EMT of NRK52E (upregulation of \u03b1-SMA and downregulation of E-cadherin) in a time-dependent manner and significant upregulation of V-ATPase B2 and c subunits after 48 h and the E subunit after 24 h, by real-time PCR and immunoblot analyses. The ATP hydrolysis activity tested by an ATP\/NADH-coupled assay was increased after 48-h TGF-\u03b21 treatment. Using intracellular pH measurements with the SNARF-4F indicator, Na<jats:sup>+<\/jats:sup>-independent pH recovery was significantly faster after an NH<jats:sub>4<\/jats:sub>Cl pulse in 48-h TGF-\u03b21-treated cells than controls. Furthermore, the V-ATPase inhibitor bafilomycin A1 partially protected the cells from EMT. TGF-\u03b21 induced an increase in the cell surface expression of the B2 subunit, and small interfering RNA-mediated B2 subunit knockdown partially reduced the V-ATPase activity and attenuated EMT induced by TGF-\u03b21. Together, these findings show that V-ATPase may promote EMT and chronic tubulointerstitial fibrosis due to increasing its activity by either overexpression or redistribution of its subunits.<\/jats:p>","DOI":"10.1152\/ajprenal.00278.2011","type":"journal-article","created":{"date-parts":[[2011,12,2]],"date-time":"2011-12-02T09:17:36Z","timestamp":1322817456000},"page":"F1121-F1132","source":"Crossref","is-referenced-by-count":18,"title":["V-ATPase promotes transforming growth factor-\u03b2-induced epithelial-mesenchymal transition of rat proximal tubular epithelial cells"],"prefix":"10.1152","volume":"302","author":[{"given":"Xueqin","family":"Cao","sequence":"first","affiliation":[{"name":"Departments of 1Nephrology and"}]},{"given":"Qiongqiong","family":"Yang","sequence":"additional","affiliation":[{"name":"Departments of 1Nephrology and"}]},{"given":"Jing","family":"Qin","sequence":"additional","affiliation":[{"name":"Departments of 1Nephrology and"}]},{"given":"Shili","family":"Zhao","sequence":"additional","affiliation":[{"name":"Departments of 1Nephrology and"}]},{"given":"Xiaoyan","family":"Li","sequence":"additional","affiliation":[{"name":"Departments of 1Nephrology and"}]},{"given":"Jinjin","family":"Fan","sequence":"additional","affiliation":[{"name":"Departments of 1Nephrology and"}]},{"given":"Wenfang","family":"Chen","sequence":"additional","affiliation":[{"name":"Pathology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China"}]},{"given":"Yi","family":"Zhou","sequence":"additional","affiliation":[{"name":"Departments of 1Nephrology and"}]},{"given":"Haiping","family":"Mao","sequence":"additional","affiliation":[{"name":"Departments of 1Nephrology and"}]},{"given":"Xueqing","family":"Yu","sequence":"additional","affiliation":[{"name":"Departments of 1Nephrology and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00340.2006"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-009-0668-9"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbabio.2008.03.013"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1158\/0008-5472.CAN-06-4095"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1007\/s004670000461"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1038\/nrm2272"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.13.5965"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-007-0382-4"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M004795200"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2010.090517"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1172\/JCI0215518"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0305165101"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M110.123281"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1172\/JCI44595"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200301000-00005"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1007\/BF02903718"},{"key":"B17","first-page":"219","volume":"146","author":"Le TL","year":"1999","journal-title":"J Cell Biol"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.1.174"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1038\/sj.cdd.4401970"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008121226"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00468.2007"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/j.ceb.2008.03.015"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1007\/s00383-008-2229-2"},{"key":"B24","doi-asserted-by":"crossref","first-page":"4598","DOI":"10.1182\/blood.V90.11.4598","volume":"90","author":"Niessen H","year":"1997","journal-title":"Blood"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M601441200"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1158\/1535-7163.MCT-09-0832"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-008-0458-9"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1385\/CBB:40:2:185"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M703627200"},{"key":"B30","doi-asserted-by":"crossref","first-page":"1173","DOI":"10.1681\/ASN.V1261173","volume":"12","author":"Vielhauer V","year":"2001","journal-title":"J Am Soc Nephrol"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00045.2003"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005121277"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1208927"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010060616"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1038\/nm888"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1172\/JCI36183"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00278.2011","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,12,18]],"date-time":"2021-12-18T10:08:39Z","timestamp":1639822119000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00278.2011"}},"issued":{"date-parts":[[2012,5,1]]},"references-count":36,"journal-issue":{"issue":"9","published-print":{"date-parts":[[2012,5,1]]}},"alternative-id":["10.1152\/ajprenal.00278.2011"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00278.2011","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2012,5,1]]}},{"indexed":{"date-parts":[[2025,12,26]],"date-time":"2025-12-26T22:08:59Z","timestamp":1766786939575},"reference-count":49,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2016,10,1]]},"abstract":"<jats:p> Endoplasmic reticulum (ER) stress has been implicated in some types of glomerular and tubular disorders. The objectives of this study were to elucidate the role of ER stress in lithium-induced nephrogenic diabetes insipidus (NDI) and to investigate whether attenuation of ER stress by 4-phenylbutyric acid (4-PBA) improves urinary concentrating defect in lithium-treated rats. Wistar rats received lithium (40 mmol\/kg food), 4-PBA (320 mg\/kg body wt by gavage every day), or no treatment (control) for 2 wk, and they were dehydrated for 24 h before euthanasia. Lithium treatment resulted in increased urine output and decreased urinary osmolality, which was significantly improved by 4-PBA. 4-PBA also prevented reduced protein expression of aquaporin-2 (AQP2), pS256-AQP2, and pS261-AQP2 in the inner medulla of kidneys from lithium-treated rats after 24-h dehydration. Lithium treatment resulted in increased expression of ER stress markers in the inner medulla, which was associated with dilated cisternae and expansion of ER in the inner medullary collecting duct (IMCD) principal cells. Confocal immunofluorescence studies showed colocalization of a molecular chaperone, binding IgG protein (BiP), with AQP2 in principal cells. Immunohistochemistry demonstrated increased intracellular expression of BiP and decreased AQP2 expression in IMCD principal cells of kidneys from lithium-treated rats. 4-PBA attenuated expression of ER stress markers and recovered ER morphology. In IMCD suspensions isolated from lithium-treated rats, 4-PBA incubation was also associated with increased AQP2 expression and ameliorated ER stress. In conclusion, in experimental lithium-induced NDI, 4-PBA improved the urinary concentrating defect and increased AQP2 expression, likely via attenuating ER stress in IMCD principal cells. <\/jats:p>","DOI":"10.1152\/ajprenal.00225.2016","type":"journal-article","created":{"date-parts":[[2016,7,7]],"date-time":"2016-07-07T01:19:35Z","timestamp":1467854375000},"page":"F763-F776","source":"Crossref","is-referenced-by-count":30,"title":["4-PBA improves lithium-induced nephrogenic diabetes insipidus by attenuating ER stress"],"prefix":"10.1152","volume":"311","author":[{"given":"Peili","family":"Zheng","sequence":"first","affiliation":[{"name":"Institute of Hypertension, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China;"}]},{"given":"Yu","family":"Lin","sequence":"additional","affiliation":[{"name":"Institute of Hypertension, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China;"}]},{"given":"Feifei","family":"Wang","sequence":"additional","affiliation":[{"name":"Institute of Hypertension, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China;"}]},{"given":"Renfei","family":"Luo","sequence":"additional","affiliation":[{"name":"Institute of Hypertension, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China;"}]},{"given":"Tiezheng","family":"Zhang","sequence":"additional","affiliation":[{"name":"Institute of Hypertension, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China;"}]},{"given":"Shan","family":"Hu","sequence":"additional","affiliation":[{"name":"Institute of Hypertension, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China;"}]},{"given":"Pinning","family":"Feng","sequence":"additional","affiliation":[{"name":"Department of Clinical Laboratory, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China; and"}]},{"given":"Xinling","family":"Liang","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China"}]},{"given":"Chunling","family":"Li","sequence":"additional","affiliation":[{"name":"Institute of Hypertension, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China;"}]},{"given":"Weidong","family":"Wang","sequence":"additional","affiliation":[{"name":"Institute of Hypertension, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1210\/mend-5-12-1862"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(87)80098-7"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00180.2004"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00690.2009"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0084663"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1111\/j.1432-1033.1997.t01-1-00120.x"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/j.tcb.2013.06.005"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00383.2005"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00266.2003"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1172\/JCI111901"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00464.2004"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M702672200"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1111\/j.1939-165X.1981.tb00797.x"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.23.14800"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1038\/ncb3184"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00284.2006"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00519.2010"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00050.2008"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMc1505505"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/j.biocel.2015.01.015"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbagen.2013.12.002"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00223.2015"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005080884"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00072.2008"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M303619200"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/j.taap.2010.04.005"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.1101531"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2007.06.009"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117863"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1159\/000182993"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00330.2013"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0910683107"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0070410"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0800001105"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90339.2008"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009060672"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00491.2005"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1038\/nrm2199"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbamcr.2013.06.028"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1016\/j.lfs.2005.07.007"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00433.2009"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2014.107"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfs292"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1126\/science.1209038"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00649.2014"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1177\/1470320313507123"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1038\/sj.npp.1300400"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1096\/fj.08-118422"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1021\/pr800894p"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00225.2016","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T21:22:36Z","timestamp":1567977756000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00225.2016"}},"issued":{"date-parts":[[2016,10,1]]},"references-count":49,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2016,10,1]]}},"alternative-id":["10.1152\/ajprenal.00225.2016"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00225.2016","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2016,10,1]]}},{"indexed":{"date-parts":[[2025,12,26]],"date-time":"2025-12-26T22:08:15Z","timestamp":1766786895414},"reference-count":146,"publisher":"American Physiological Society","issue":"10","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,5,15]]},"abstract":"<jats:p>The importance of innate immunity for survival is underscored by its presence at almost every level of the evolutionary tree of life. The task of \u201cdanger\u201d recognition by the innate immune system is carried out by a broad class of pattern recognition receptors. These receptors are expressed in both hematopoietic and nonhematopoietic cells such as renal epithelial cells. Upon activation, pattern recognition receptors induce essentially two types of defensive responses: inflammation and phagocytosis. In this review, we highlight evidence that renal epithelial cells are endowed with such defensive capabilities and as such fully participate in renal innate immune responses.<\/jats:p>","DOI":"10.1152\/ajprenal.00101.2013","type":"journal-article","created":{"date-parts":[[2013,3,21]],"date-time":"2013-03-21T03:49:21Z","timestamp":1363837761000},"page":"F1243-F1251","source":"Crossref","is-referenced-by-count":28,"title":["Sisters in arms: myeloid and tubular epithelial cells shape renal innate immunity"],"prefix":"10.1152","volume":"304","author":[{"given":"Takashi","family":"Hato","sequence":"first","affiliation":[{"name":"Department of Medicine, Indiana University, Indianapolis, Indiana"}]},{"given":"Tarek M.","family":"El-Achkar","sequence":"additional","affiliation":[{"name":"Department of Medicine, Indiana University, Indianapolis, Indiana"}]},{"given":"Pierre C.","family":"Dagher","sequence":"additional","affiliation":[{"name":"Department of Medicine, Indiana University, Indianapolis, Indiana"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI22029"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/j.ajpath.2011.05.037"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010030233"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010080798"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1038\/76048"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1146\/annurev-immunol-020711-075030"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00452.x"},{"key":"B8","doi-asserted-by":"crossref","first-page":"7","DOI":"10.4049\/jimmunol.134.1.7","volume":"134","author":"Benson EM","year":"1985","journal-title":"J Immunol"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2008-07-019307"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1172\/JCI45161"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.4268-04.2005"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1111\/j.1462-5822.2011.01614.x"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1097\/MOT.0b013e32835e2b0d"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20061884"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1038\/nri3087"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.immunol.021908.132629"},{"key":"B17","doi-asserted-by":"crossref","first-page":"1187","DOI":"10.1681\/ASN.V971187","volume":"9","author":"Deckers JG","year":"1998","journal-title":"J Am Soc Nephrol"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.2.F195"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfs444"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1172\/JCI39421"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00502.x"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002132"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2010.03.003"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)61209-6"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1038\/ncpneph0300"},{"key":"B26","author":"El-Achkar TM","journal-title":"Am J Physiol Renal Physiol"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00621.2010"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00217.2007"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2011.10.054"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00083.2008"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2012.207"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.72.6.3171-3178.2004"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1016\/j.it.2007.10.002"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1097\/00007890-198608000-00008"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1172\/JCI57582"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1038\/ni.2419"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1038\/nri2784"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1126\/science.1178331"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2010.16"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1016\/j.biocel.2007.04.025"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00335.2009"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1016\/j.immuni.2010.05.007"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.pharmtox.010909.105600"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007040469"},{"key":"B45","doi-asserted-by":"crossref","first-page":"2324","DOI":"10.4049\/jimmunol.148.8.2324","volume":"148","author":"Hagerty DT","year":"1992","journal-title":"J Immunol"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1016\/j.it.2012.08.006"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M109.067728"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1016\/j.immuni.2011.09.007"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1172\/JCI41563"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1126\/science.3498215"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1172\/JCI38399"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010050548"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1990.38"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.181.9.5829"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1172\/JCI34487"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1016\/j.it.2011.05.001"},{"key":"B57","doi-asserted-by":"crossref","first-page":"1268","DOI":"10.1016\/S0016-5085(77)80025-5","volume":"72","author":"Jacob AI","year":"1977","journal-title":"Gastroenterology"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1016\/j.clim.2008.08.016"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1990.221"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2007.09.008"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfk047"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2012.11.011"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2011020203"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfs136"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1016\/j.immuni.2011.05.006"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1097\/01.TP.0000158355.83327.62"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.70.5.2650-2656.2002"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.1016\/j.cellimm.2010.11.001"},{"key":"B69","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0810169106"},{"key":"B70","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.164.6.3323"},{"key":"B71","doi-asserted-by":"publisher","DOI":"10.1203\/01.PDR.0000081763.37767.6B"},{"key":"B72","doi-asserted-by":"publisher","DOI":"10.1038\/nri3088"},{"key":"B73","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002293"},{"key":"B74","doi-asserted-by":"publisher","DOI":"10.1155\/2012\/951390"},{"key":"B75","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009060615"},{"key":"B76","doi-asserted-by":"publisher","DOI":"10.1172\/JCI22832"},{"key":"B77","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00291.2001"},{"key":"B78","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2010.03.005"},{"key":"B79","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0912228107"},{"key":"B80","doi-asserted-by":"publisher","DOI":"10.1126\/science.1155406"},{"key":"B81","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M112.348243"},{"key":"B82","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-011-2029-0"},{"key":"B83","doi-asserted-by":"publisher","DOI":"10.1002\/hep.1840080207"},{"key":"B84","doi-asserted-by":"publisher","DOI":"10.1210\/er.2009-0030"},{"key":"B85","doi-asserted-by":"crossref","first-page":"2133","DOI":"10.4049\/jimmunol.123.5.2133","volume":"123","author":"Mathison JC","year":"1979","journal-title":"J Immunol"},{"key":"B86","doi-asserted-by":"publisher","DOI":"10.1586\/eci.12.21"},{"key":"B87","doi-asserted-by":"publisher","DOI":"10.1038\/nri2940"},{"key":"B88","doi-asserted-by":"publisher","DOI":"10.1172\/JCI39087"},{"key":"B89","doi-asserted-by":"publisher","DOI":"10.1038\/ni.2370"},{"key":"B90","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00357.2003"},{"key":"B91","doi-asserted-by":"publisher","DOI":"10.1038\/nri2448"},{"key":"B92","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002627"},{"key":"B93","doi-asserted-by":"publisher","DOI":"10.1126\/science.2409603"},{"key":"B94","doi-asserted-by":"publisher","DOI":"10.1038\/nri3073"},{"key":"B95","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5001565"},{"key":"B96","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2011070680"},{"key":"B97","doi-asserted-by":"publisher","DOI":"10.1159\/000064084"},{"key":"B98","doi-asserted-by":"publisher","DOI":"10.1159\/000332032"},{"key":"B99","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M008610200"},{"key":"B100","doi-asserted-by":"publisher","DOI":"10.1038\/nature07830"},{"key":"B101","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00729.x"},{"key":"B102","doi-asserted-by":"publisher","DOI":"10.1097\/MOL.0b013e32835b4431"},{"key":"B103","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009070722"},{"key":"B104","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0003596"},{"key":"B105","doi-asserted-by":"publisher","DOI":"10.1016\/j.ydbio.2007.05.027"},{"key":"B106","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.177.1.322"},{"key":"B107","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2011.134"},{"key":"B108","doi-asserted-by":"publisher","DOI":"10.1172\/JCI36150"},{"key":"B109","doi-asserted-by":"publisher","DOI":"10.1038\/ni1192"},{"key":"B110","doi-asserted-by":"publisher","DOI":"10.1093\/toxsci\/kfl173"},{"key":"B112","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010040430"},{"key":"B113","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-009-1422-4"},{"key":"B114","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.175.7.4408"},{"key":"B115","doi-asserted-by":"publisher","DOI":"10.1172\/JCI200522720"},{"key":"B116","doi-asserted-by":"publisher","DOI":"10.1038\/ni.2467"},{"key":"B117","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0736473100"},{"key":"B118","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007060684"},{"key":"B119","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00045.2009"},{"key":"B120","doi-asserted-by":"publisher","DOI":"10.1016\/S0272-6386(03)00829-1"},{"key":"B121","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.immunol.26.021607.090326"},{"key":"B122","doi-asserted-by":"publisher","DOI":"10.1038\/nri3070"},{"key":"B123","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.178.10.6252"},{"key":"B124","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.0903065"},{"key":"B125","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.1002330"},{"key":"B126","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008010123"},{"key":"B127","doi-asserted-by":"publisher","DOI":"10.1038\/nm.2505"},{"key":"B128","doi-asserted-by":"publisher","DOI":"10.1172\/JCI59643"},{"key":"B129","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5001567"},{"key":"B130","doi-asserted-by":"crossref","first-page":"3449","DOI":"10.4049\/jimmunol.158.7.3449","volume":"158","author":"Su SJ","year":"1997","journal-title":"J Immunol"},{"key":"B131","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009040407"},{"key":"B132","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2011.129"},{"key":"B133","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.169.4.2026"},{"key":"B134","doi-asserted-by":"publisher","DOI":"10.1172\/JCI62139"},{"key":"B135","doi-asserted-by":"publisher","DOI":"10.1128\/CMR.16.3.379-414.2003"},{"key":"B136","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000017901.77985F"},{"key":"B137","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00786.x"},{"key":"B138","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00237.2011"},{"key":"B139","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfh206"},{"key":"B140","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.168.3.1286"},{"key":"B141","doi-asserted-by":"publisher","DOI":"10.1172\/JCI31008"},{"key":"B142","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1990.46"},{"key":"B143","doi-asserted-by":"publisher","DOI":"10.1016\/j.immuni.2012.12.001"},{"key":"B144","doi-asserted-by":"publisher","DOI":"10.1016\/0162-3109(93)90041-N"},{"key":"B145","doi-asserted-by":"publisher","DOI":"10.1177\/0192623308315832"},{"key":"B146","doi-asserted-by":"publisher","DOI":"10.1172\/JCI60363"},{"key":"B147","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2010.175"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00101.2013","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,5,7]],"date-time":"2024-05-07T19:25:15Z","timestamp":1715109915000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00101.2013"}},"issued":{"date-parts":[[2013,5,15]]},"references-count":146,"journal-issue":{"issue":"10","published-print":{"date-parts":[[2013,5,15]]}},"alternative-id":["10.1152\/ajprenal.00101.2013"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00101.2013","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2013,5,15]]}},{"indexed":{"date-parts":[[2025,12,22]],"date-time":"2025-12-22T18:31:47Z","timestamp":1766428307742},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1989,6,1]]},"abstract":"<jats:p> That the adaptation of the kidney to the acid-base status may be controlled by peptide hormones is considered. In the proximal tubule parathyroid hormone (PTH) inhibits reabsorption of both bicarbonate and phosphate. The former effect is compensated for by an increase in bicarbonate absorption in Henle's loop, and the latter effect serves to augment phosphate concentration in the distal tubular fluid, which stimulates proton secretion in collecting ducts, the net effect of PTH administration being an enhancement of urinary acidification. In the thick ascending limb, both antidiuretic hormone (ADH) and glucagon inhibit bicarbonate absorption. In distal and cortical collecting tubules ADH stimulates net bicarbonate absorption and glucagon net bicarbonate secretion, which results in stimulation and inhibition of final urine acidification, respectively. Acute acid loading stimulates endogenous PTH secretion, which, by enhancing urinary acidification, constitutes a homeostatic response of the parathyroid glands. The major effects of ADH on urinary acidification serve at least to counterbalance disturbing consequences on urinary ammonia excretion of physiological variations in the urinary flow rate. The physiological significance of the effects of glucagon is unclear at present. Thus other peptide hormones may add to PTH and corticosteroid hormones to modulate urinary acidification, which leads to the concept of a pluri-hormonal control of acid-base balance. <\/jats:p>","DOI":"10.1152\/ajprenal.1989.256.6.f973","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T20:49:59Z","timestamp":1513975799000},"page":"F973-F985","source":"Crossref","is-referenced-by-count":4,"title":["Peptide hormone effects on urinary acidification and acid-base balance: PTH, ADH, and glucagon"],"prefix":"10.1152","volume":"256","author":[{"given":"M.","family":"Paillard","sequence":"first","affiliation":[{"name":"Laboratoire de Physiologie et Physiopathologie Renale, Hopital LouisMourier, Colombes, France."}]},{"given":"M.","family":"Bichara","sequence":"additional","affiliation":[{"name":"Laboratoire de Physiologie et Physiopathologie Renale, Hopital LouisMourier, Colombes, France."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1989.256.6.F973","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:05:58Z","timestamp":1567969558000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1989.256.6.F973"}},"issued":{"date-parts":[[1989,6,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1989,6,1]]}},"alternative-id":["10.1152\/ajprenal.1989.256.6.F973"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1989.256.6.f973","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1989,6,1]]}},{"indexed":{"date-parts":[[2025,12,12]],"date-time":"2025-12-12T13:21:16Z","timestamp":1765545676267},"reference-count":42,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2011,7]]},"abstract":"<jats:p> Granulocyte colony-stimulating factor (G-CSF) is renoprotective during acute kidney injury (AKI) induced by ischemia and cisplatin nephrotoxicity; however, the underlying mechanism is not entirely clear. Rhabdomyolysis is another important clinical cause of AKI, due to the release of nephrotoxins (e.g., heme) from disrupted muscles. The current study has determined the effects of G-CSF on rhabdomyolysis-associated AKI using in vivo and in vitro models. In C57BL\/6 mice, intramuscular injection of glycerol induced AKI, which was partially prevented by G-CSF pretreatment. Consistently, glycerol-induced renal tissue damage was ameliorated by G-CSF. In addition, animal survival following the glycerol injection was improved from \u223c30 to \u223c70% by G-CSF. In cultured renal tubular cells, hemin-induced apoptosis was also suppressed by G-CSF. Interestingly, G-CSF induced heme oxygenase-1 (HO-1, a critical enzyme for heme\/hemin degradation and detoxification) in both cultured tubular cells and mouse kidneys. Blockade of HO-1 with protoporphyrin IX zinc(II) (ZnPP) could largely diminish the protective effects of G-CSF. Together, these results demonstrated the renoprotective effects of G-CSF in rhabdomyolysis-associated AKI. Notably, G-CSF may directly protect against tubular cell injury under the disease condition by inducing HO-1. <\/jats:p>","DOI":"10.1152\/ajprenal.00438.2010","type":"journal-article","created":{"date-parts":[[2011,4,21]],"date-time":"2011-04-21T02:14:18Z","timestamp":1303352058000},"page":"F162-F170","source":"Crossref","is-referenced-by-count":46,"title":["Heme oxygenase-1 induction contributes to renoprotection by G-CSF during rhabdomyolysis-associated acute kidney injury"],"prefix":"10.1152","volume":"301","author":[{"given":"Qingqing","family":"Wei","sequence":"first","affiliation":[{"name":"Department of Cellular Biology and Anatomy,"}]},{"given":"William D.","family":"Hill","sequence":"additional","affiliation":[{"name":"Department of Cellular Biology and Anatomy,"},{"name":"Medical Research Line, Charlie Norwood Veterans Affairs Medical Center, Augusta, Georgia"}]},{"given":"Yunchao","family":"Su","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology,"}]},{"given":"Shuang","family":"Huang","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, Medical College of Georgia, Georgia Health Sciences University and"}]},{"given":"Zheng","family":"Dong","sequence":"additional","affiliation":[{"name":"Department of Cellular Biology and Anatomy,"},{"name":"Medical Research Line, Charlie Norwood Veterans Affairs Medical Center, Augusta, Georgia"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007020140"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI37829"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1159\/000102090"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)65019-5"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004121089"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1002\/j.1460-2075.1991.tb07835.x"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00300.2003"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/nm1199"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1161\/01.STR.0000014925.09415.C3"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1186\/cc2978"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1016\/j.nephro.2006.12.002"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004010067"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1007\/s11906-009-0011-z"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00505.x"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005091001"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1797.2008.00928.x"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1203\/01.pdr.0000205156.85990.12"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5001565"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115847"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)65024-9"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2004.09.051"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1159\/000094962"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1097\/nen.0b013e3181257176"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M707568200"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00402.2004"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00977.2007"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1097\/00003246-200003000-00033"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.5.F726"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00297.2003"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004080678"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1177\/154405910608500802"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00007.2005"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000123692.01237.0A"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00339.2006"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006080894"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002471"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M313629200"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002256"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00230.2007"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00184.2005"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.48"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00379.2002"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00438.2010","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T00:14:56Z","timestamp":1567988096000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00438.2010"}},"issued":{"date-parts":[[2011,7]]},"references-count":42,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2011,7]]}},"alternative-id":["10.1152\/ajprenal.00438.2010"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00438.2010","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2011,7]]}},{"indexed":{"date-parts":[[2025,12,23]],"date-time":"2025-12-23T10:44:28Z","timestamp":1766486668960,"version":"3.37.3"},"reference-count":30,"publisher":"American Physiological Society","issue":"4","funder":[{"DOI":"10.13039\/100000968","name":"American Heart Association","doi-asserted-by":"publisher","award":["903584"],"award-info":[{"award-number":["903584"]}],"id":[{"id":"10.13039\/100000968","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"HHS | NIH | National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["HL148114"],"award-info":[{"award-number":["HL148114"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK125464"],"award-info":[{"award-number":["DK125464"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2022,10,1]]},"abstract":"<jats:p> Competent statistical analysis is essential to maintain rigor and reproducibility in physiological research. Unfortunately, the benefits offered by statistics are often negated by misuse or inadequate reporting of statistical methods. To address the need for improved quality of statistical analysis in papers, the American Physiological Society released guidelines for reporting statistics in journals published by the society. The guidelines reinforce high standards for the presentation of statistical data in physiology but focus on the conceptual challenges and, thus, may be of limited use to an unprepared reader. Experimental scientists working in the renal field may benefit from putting the existing guidelines in a practical context. This paper discusses the application of widespread hypothesis tests in a confirmatory study. We simulated pharmacological experiments assessing intracellular calcium in cultured renal cells and kidney function at the systemic level to review best practices for data analysis, graphical presentation, and reporting. Such experiments are ubiquitously used in renal physiology and could be easily translated to other practical applications to fit the reader\u2019s specific needs. We provide step-by-step guidelines for using the most common types of t tests and ANOVA and discuss typical mistakes associated with them. We also briefly consider normality tests, exclusion criteria, and identification of technical and experimental replicates. This review is supposed to help the reader analyze, illustrate, and report the findings correctly and will hopefully serve as a gauge for a level of design complexity when it might be time to consult a biostatistician. <\/jats:p>","DOI":"10.1152\/ajprenal.00427.2021","type":"journal-article","created":{"date-parts":[[2022,7,14]],"date-time":"2022-07-14T15:32:09Z","timestamp":1657812729000},"page":"F389-F400","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":13,"title":["Practical notes on popular statistical tests in renal physiology"],"prefix":"10.1152","volume":"323","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8683-0715","authenticated-orcid":false,"given":"Mykola","family":"Mamenko","sequence":"first","affiliation":[{"name":"Department of Physiology, Augusta University, Augusta, Georgia"}]},{"given":"Daria V.","family":"Lysikova","sequence":"additional","affiliation":[{"name":"Department of Physiology, Augusta University, Augusta, Georgia"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0722-2717","authenticated-orcid":false,"given":"Denisha R.","family":"Spires","sequence":"additional","affiliation":[{"name":"Department of Physiology, Augusta University, Augusta, Georgia"}]},{"given":"Sergey S.","family":"Tarima","sequence":"additional","affiliation":[{"name":"Department of Biostatistics, Medical College of Wisconsin, Milwaukee, Wisconsin"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4832-4170","authenticated-orcid":false,"given":"Daria V.","family":"Ilatovskaya","sequence":"additional","affiliation":[{"name":"Department of Physiology, Augusta University, Augusta, Georgia"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1038\/533452a"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00309.2018"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/advan.00019.2004"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1002\/1097-0258(20001215)19:23<3275::aid-sim626>3.0.co;2-m"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1708279115"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.7554\/eLife.21451"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.7554\/eLife.48175"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pbio.2000995"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1001\/jama.1966.03100130097026"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1983.244.1.R3"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/advan.90207.2008"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1258\/jrsm.2008.080062"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/advan.00022.2007"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.5812\/ijem.3505"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.2307\/2682991"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1007\/s10654-016-0149-3"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1046\/j.1442-9993.2001.01070.x"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1186\/s40168-019-0659-9"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1007\/978-3-030-83266-7_15"},{"key":"B20","volume-title":"Randomization in Clinical Trials: Theory and Practice","author":"Rosenberger WL","year":"2015","edition":"2"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.4103\/2229-3485.100662"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1097\/jp9.0000000000000024"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.4097\/kja.d.18.00242"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.1991.tb01468.x"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1093\/cvr\/28.3.303"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.1998.tb02179.x"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/advan.00001.2010"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1136\/bmj.281.6251.1336"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1111\/opo.12399"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1007\/s11336-022-09856-8"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00427.2021","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,9,27]],"date-time":"2022-09-27T13:50:20Z","timestamp":1664286620000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00427.2021"}},"issued":{"date-parts":[[2022,10,1]]},"references-count":30,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2022,10,1]]}},"alternative-id":["10.1152\/ajprenal.00427.2021"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00427.2021","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2022,10,1]]},"assertion":[{"value":"2021-11-29","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2022-06-14","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2022-07-09","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2022-09-14","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2025,12,25]],"date-time":"2025-12-25T07:20:12Z","timestamp":1766647212818,"version":"3.37.3"},"reference-count":41,"publisher":"American Physiological Society","issue":"5","funder":[{"DOI":"10.13039\/100000009","name":"Foundation for the National Institutes of Health","doi-asserted-by":"publisher","award":["R01 DK41707"],"award-info":[{"award-number":["R01 DK41707"]}],"id":[{"id":"10.13039\/100000009","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81570671","81873602"],"award-info":[{"award-number":["81570671","81873602"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81770711"],"award-info":[{"award-number":["81770711"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Program for HUST Academic Frontier Young Team","award":["2017QYTD20"],"award-info":[{"award-number":["2017QYTD20"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2019,11,1]]},"abstract":"<jats:p> Posttranslational modifications are essential for the regulation of urea transporter-A1 (UT-A1), among which ubiquitination is a rather attractive and complex issue. Previously, our group reported that murine double minute 2 (MDM2) is one of the E3 ubiquitin ligases for UT-A1, and, later, we showed that ubiquitination contributes to the subcellular trafficking and stability of UT-A1. In the present study, we discovered that MDM2 interacts with UT-A1 in an AP50 (a component of the clathrin-coated pit)-dependent manner. However, their binding is irrelevant to the phosphorylatory status of UT-A1. Next, our findings indicated that MDM2 decreases the stability of either total or membrane UT-A1. On the cell membrane, MDM2 and ubiquitinated UT-A1 are both distributed in the lipid raft domain, and their linkage is obviously enhanced under forskolin (FSK) stimulation. In line with these results, in the diabetic rat, not only MDM2 but also ubiquitinated UT-A1 are intensified. Also, in vitro high glucose and angiotensin II play similar roles as FSK does on the association of MDM2 with UT-A1. In conclusion, MDM2 binds with UT-A1 and mediates its ubiquitination and degradation in an AP50-dependent manner, and their binding capacity is strengthened under FSK and diabetic milieu. <\/jats:p>","DOI":"10.1152\/ajprenal.00316.2019","type":"journal-article","created":{"date-parts":[[2019,9,11]],"date-time":"2019-09-11T11:56:02Z","timestamp":1568202962000},"page":"F1331-F1341","source":"Crossref","is-referenced-by-count":4,"title":["E3 ligase MDM2 mediates urea transporter-A1 ubiquitination under either constitutive or stimulatory conditions"],"prefix":"10.1152","volume":"317","author":[{"given":"Hua","family":"Su","sequence":"first","affiliation":[{"name":"Department of Nephrology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China"},{"name":"Department of Physiology, Emory University School of Medicine, Atlanta, Georgia"}]},{"given":"Chen","family":"Ye","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9822-0607","authenticated-orcid":false,"given":"Jeff M.","family":"Sands","sequence":"additional","affiliation":[{"name":"Renal Division, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3565-8024","authenticated-orcid":false,"given":"Chun","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China"}]}],"member":"24","reference":[{"doi-asserted-by":"publisher","key":"B1","DOI":"10.1007\/s001250051671"},{"doi-asserted-by":"publisher","key":"B2","DOI":"10.1523\/JNEUROSCI.2388-11.2011"},{"doi-asserted-by":"publisher","key":"B3","DOI":"10.1152\/ajprenal.00102.2008"},{"doi-asserted-by":"publisher","key":"B4","DOI":"10.1152\/ajprenal.00600.2007"},{"doi-asserted-by":"publisher","key":"B5","DOI":"10.1016\/0092-8674(90)90117-W"},{"doi-asserted-by":"publisher","key":"B6","DOI":"10.1074\/jbc.M605525200"},{"doi-asserted-by":"publisher","key":"B7","DOI":"10.1096\/fj.11-185991"},{"doi-asserted-by":"publisher","key":"B8","DOI":"10.1152\/ajprenal.90482.2008"},{"doi-asserted-by":"publisher","key":"B9","DOI":"10.1016\/S0896-6273(03)00687-1"},{"doi-asserted-by":"publisher","key":"B10","DOI":"10.1146\/annurev.biochem.78.101807.093809"},{"doi-asserted-by":"publisher","key":"B11","DOI":"10.1152\/ajpcell.00499.2003"},{"doi-asserted-by":"publisher","key":"B12","DOI":"10.1073\/pnas.1431613100"},{"doi-asserted-by":"publisher","key":"B13","DOI":"10.1038\/387296a0"},{"doi-asserted-by":"publisher","key":"B14","DOI":"10.1152\/ajprenal.00718.2009"},{"doi-asserted-by":"publisher","key":"B15","DOI":"10.1074\/jbc.M509332200"},{"doi-asserted-by":"publisher","key":"B16","DOI":"10.1152\/ajprenal.00438.2002"},{"doi-asserted-by":"publisher","key":"B17","DOI":"10.1016\/j.gde.2010.10.004"},{"doi-asserted-by":"publisher","key":"B18","DOI":"10.1152\/ajprenal.00682.2009"},{"doi-asserted-by":"publisher","key":"B19","DOI":"10.1038\/387299a0"},{"doi-asserted-by":"publisher","key":"B20","DOI":"10.1126\/science.1091362"},{"doi-asserted-by":"publisher","key":"B21","DOI":"10.1371\/journal.pone.0001487"},{"doi-asserted-by":"publisher","key":"B22","DOI":"10.1074\/jbc.M109.008078"},{"doi-asserted-by":"publisher","key":"B23","DOI":"10.1038\/nrc3120"},{"doi-asserted-by":"publisher","key":"B24","DOI":"10.1016\/0092-8674(94)90041-8"},{"doi-asserted-by":"publisher","key":"B25","DOI":"10.2337\/db05-0450"},{"doi-asserted-by":"publisher","key":"B26","DOI":"10.1126\/science.1127085"},{"doi-asserted-by":"publisher","key":"B27","DOI":"10.1016\/j.bbamcr.2004.09.019"},{"doi-asserted-by":"publisher","key":"B28","DOI":"10.1074\/jbc.M403210200"},{"doi-asserted-by":"publisher","key":"B29","DOI":"10.1074\/jbc.M204677200"},{"doi-asserted-by":"publisher","key":"B30","DOI":"10.1007\/s00232-002-1053-1"},{"doi-asserted-by":"publisher","key":"B31","DOI":"10.1126\/science.1063866"},{"doi-asserted-by":"publisher","key":"B32","DOI":"10.1038\/sj.emboj.7600145"},{"doi-asserted-by":"publisher","key":"B33","DOI":"10.1126\/stke.2001.110.pe41"},{"doi-asserted-by":"publisher","key":"B34","DOI":"10.1152\/ajprenal.00248.2012"},{"doi-asserted-by":"publisher","key":"B35","DOI":"10.1152\/ajprenal.00393.2013"},{"doi-asserted-by":"publisher","key":"B36","DOI":"10.1093\/ndt\/gfs260"},{"doi-asserted-by":"publisher","key":"B37","DOI":"10.1016\/j.tcb.2010.01.009"},{"doi-asserted-by":"publisher","key":"B38","DOI":"10.1128\/MCB.00172-06"},{"doi-asserted-by":"publisher","key":"B39","DOI":"10.1038\/sj.onc.1207411"},{"doi-asserted-by":"publisher","key":"B40","DOI":"10.1152\/ajprenal.0054.2001"},{"doi-asserted-by":"publisher","key":"B41","DOI":"10.1016\/S0092-8674(00)81401-4"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00316.2019","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,11,7]],"date-time":"2019-11-07T09:05:44Z","timestamp":1573117544000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00316.2019"}},"issued":{"date-parts":[[2019,11,1]]},"references-count":41,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2019,11,1]]}},"alternative-id":["10.1152\/ajprenal.00316.2019"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00316.2019","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2019,11,1]]}},{"indexed":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T03:50:13Z","timestamp":1772164213985,"version":"3.50.1"},"reference-count":59,"publisher":"American Physiological Society","issue":"1","funder":[{"DOI":"10.13039\/501100002322","name":"Coordena\u00e7\u00e3o de Aperfei\u00e7oamento de Pessoal de N\u00edvel Superior","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100002322","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001807","name":"Funda\u00e7\u00e3o de Amparo \u00e0 Pesquisa do Estado de S\u00e3o Paulo","doi-asserted-by":"publisher","award":["20\/06970-5"],"award-info":[{"award-number":["20\/06970-5"]}],"id":[{"id":"10.13039\/501100001807","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001807","name":"Funda\u00e7\u00e3o de Amparo \u00e0 Pesquisa do Estado de S\u00e3o Paulo","doi-asserted-by":"publisher","award":["13\/07937-8"],"award-info":[{"award-number":["13\/07937-8"]}],"id":[{"id":"10.13039\/501100001807","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100003593","name":"MCTI | Conselho Nacional de Desenvolvimento Cient\u00edfico e Tecnol\u00f3gico","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100003593","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2022,7,1]]},"abstract":"<jats:p>Prevention of obesity through caloric restriction (CR) is well known to protect many tissues but has been poorly studied in kidneys. Here, we determined the effects of long-term CR in rat kidney mitochondria, which are central players in energy metabolism and aging. Surprisingly, we found that the diet increased mitochondrial reactive oxygen production and permeability transition. This suggests that the kidneys respond differently to restricted diets and may be more susceptible under CR.<\/jats:p>","DOI":"10.1152\/ajprenal.00461.2021","type":"journal-article","created":{"date-parts":[[2022,5,2]],"date-time":"2022-05-02T07:46:38Z","timestamp":1651477598000},"page":"F92-F106","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":13,"title":["Regulation of kidney mitochondrial function by caloric restriction"],"prefix":"10.1152","volume":"323","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2285-5769","authenticated-orcid":true,"given":"Julian D. C.","family":"Serna","sequence":"first","affiliation":[{"name":"Departamento de Bioqu\u00edmica, Instituto de Qu\u00edmica, Universidade de S\u00e3o Paulo, S\u00e3o Paulo, Brazil"}]},{"given":"Andressa G.","family":"Amaral","sequence":"additional","affiliation":[{"name":"Departamento de Fisiologia e Biof\u00edsica, Instituto de Ci\u00eancias Biom\u00e9dicas, Universidade de S\u00e3o Paulo, S\u00e3o Paulo, Brazil"}]},{"given":"Camille C.","family":"Caldeira da Silva","sequence":"additional","affiliation":[{"name":"Departamento de Bioqu\u00edmica, Instituto de Qu\u00edmica, Universidade de S\u00e3o Paulo, S\u00e3o Paulo, Brazil"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7484-0518","authenticated-orcid":true,"given":"Ana C.","family":"Munhoz","sequence":"additional","affiliation":[{"name":"Departamento de Bioqu\u00edmica, Instituto de Qu\u00edmica, Universidade de S\u00e3o Paulo, S\u00e3o Paulo, Brazil"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1565-1618","authenticated-orcid":true,"given":"Eloisa A.","family":"Vilas-Boas","sequence":"additional","affiliation":[{"name":"Departamento de Bioqu\u00edmica, Instituto de Qu\u00edmica, Universidade de S\u00e3o Paulo, S\u00e3o Paulo, Brazil"}]},{"given":"Sergio L.","family":"Menezes-Filho","sequence":"additional","affiliation":[{"name":"Departamento de Bioqu\u00edmica, Instituto de Qu\u00edmica, Universidade de S\u00e3o Paulo, S\u00e3o Paulo, Brazil"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3807-2419","authenticated-orcid":true,"given":"Alicia J.","family":"Kowaltowski","sequence":"additional","affiliation":[{"name":"Departamento de Bioqu\u00edmica, Instituto de Qu\u00edmica, Universidade de S\u00e3o Paulo, S\u00e3o Paulo, Brazil"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.me.24.020173.002053"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2017.107"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.2006.04475.x"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.3945\/ajcn.2010.29885"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbamcr.2018.10.016"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1038\/nrm3412"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1038\/s41580-018-0052-8"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1016\/j.freeradbiomed.2018.08.034"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/j.ceca.2020.102322"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1038\/nature10234"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1038\/nature10230"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1126\/science.1242993"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2019.03.050"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1038\/nature09358"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0055785"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/j.molcel.2014.01.013"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2015.08.019"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/j.celrep.2017.02.032"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.2337\/db16-1237"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-018-2162-8"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1126\/scisignal.aat7397"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1172\/JCI45161.4210"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbabio.2009.06.009"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1089\/ars.2012.4729"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0100579"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00932.2010"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.33594\/000000151"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1016\/s0891-5849(97)00444-9"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1111\/acel.12527"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/j.freeradbiomed.2017.06.013"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1007\/s10863-020-09838-4"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1111\/j.1474-9726.2009.00532.x"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1016\/j.arr.2010.05.002"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1016\/j.freeradbiomed.2009.02.008"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1002\/cpmo.21"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(80)80076-7"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(76)80434-6"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M207765200"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1006\/abio.1997.2391"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1038\/nprot.2012.058"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1016\/0022-2836(73)90198-8"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.76.9.4350"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0510452103"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pmed.0040076"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1113\/JP270543"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbabio.2015.05.005"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2008.01.007"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1016\/j.yjmcc.2013.03.012"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1021\/bi00720a020"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1300410110"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbamem.2016.02.022"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M212661200"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1096\/fj.201901136R"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1016\/j.freeradbiomed.2013.05.037"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.3390\/cells10010079"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1016\/j.ymeth.2008.09.012"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1016\/j.ceca.2012.03.003"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1711303114"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1093\/brain\/awx237"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00461.2021","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,6,21]],"date-time":"2022-06-21T11:57:59Z","timestamp":1655812679000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00461.2021"}},"issued":{"date-parts":[[2022,7,1]]},"references-count":59,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2022,7,1]]}},"alternative-id":["10.1152\/ajprenal.00461.2021"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00461.2021","relation":{"has-preprint":[{"id-type":"doi","id":"10.1101\/2021.12.29.474441","asserted-by":"object"}]},"ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2022,7,1]]},"assertion":[{"value":"2022-01-04","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2022-04-19","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2022-04-25","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2022-06-21","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T03:50:23Z","timestamp":1772164223562,"version":"3.50.1"},"reference-count":45,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2005,1]]},"abstract":"<jats:p>\n                    A high-salt diet increases renal endothelin (ET) production and thick ascending limb (THAL) endothelial nitric oxide synthase (eNOS) expression. ET stimulates THAL eNOS expression via ET\n                    <jats:sub>B<\/jats:sub>\n                    receptors. The tonicity of the renal medulla is highly variable, and hyperosmolality stimulates ET-1 synthesis by endothelial cells. We hypothesized that a high-salt diet raises medullary osmolality, increases ET release by the THAL, and thus enhances eNOS expression. Seven days of high salt (1% NaCl in drinking water) increased eNOS expression in THALs by 125 \u00b1 31%. High salt increased outer medullary osmolality from 362 \u00b1 13 to 423 \u00b1 6 mosmol\/kgH\n                    <jats:sub>2<\/jats:sub>\n                    O ( P &lt; 0.05). Bosentan, a dual-ET receptor antagonist, blocked the increase in THAL eNOS expression caused by high salt (2.66 \u00b1 0.44 absorbance units with bosentan vs. 5.15 \u00b1 0.67 for vehicle; P &lt; 0.05). Conscious systolic blood pressure did not differ between the two groups. In primary cultures of medullary THALs, raising osmolality from 300 to 350 and 400 mosmol\/kgH\n                    <jats:sub>2<\/jats:sub>\n                    O using NaCl increased eNOS expression by 39 \u00b1 11% ( P &lt; 0.05) and 71 \u00b1 16%, respectively ( P &lt; 0.05). In primary cultures of THALs, raising osmolality from 300 to 400 mosmol\/kgH\n                    <jats:sub>2<\/jats:sub>\n                    O for 1 h increased ET-1 release from 62 \u00b1 7 to 113 \u00b1 2 pg\/mg protein ( P &lt; 0.05). BQ-788, an ET\n                    <jats:sub>B<\/jats:sub>\n                    receptor antagonist (1 \u03bcM), blocked the stimulatory effect of 400 mosmol\/kgH\n                    <jats:sub>2<\/jats:sub>\n                    O on eNOS expression (70 \u00b1 13% vs. \u22125 \u00b1 10%; paired difference, 74 \u00b1 15%; P &lt; 0.05). BQ-788 alone had no significant effect. We concluded that high salt stimulates THAL eNOS expression by increasing outer medullary osmolality, ET-1 release by the THAL and ET\n                    <jats:sub>B<\/jats:sub>\n                    receptor activation. This may be an important regulatory mechanism of THAL NaCl absorption when dietary salt intake is increased.\n                  <\/jats:p>","DOI":"10.1152\/ajprenal.00209.2004","type":"journal-article","created":{"date-parts":[[2004,9,7]],"date-time":"2004-09-07T21:43:15Z","timestamp":1094593395000},"page":"F58-F64","source":"Crossref","is-referenced-by-count":85,"title":["A high-salt diet stimulates thick ascending limb eNOS expression by raising medullary osmolality and increasing release of endothelin-1"],"prefix":"10.1152","volume":"288","author":[{"given":"Marcela","family":"Herrera","sequence":"first","affiliation":[]},{"given":"Jeffrey L.","family":"Garvin","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"crossref","unstructured":"Baer PG\n                      , Navar LG, and Guyton AC.\n                      Renal autoregulation, filtration rate, and electrolyte excretion during vasodilatation.\n                      Am J Physiol\n                      219\n                      : 619\u2013625, 1970.","DOI":"10.1152\/ajplegacy.1970.219.3.619"},{"key":"R2","unstructured":"Bankir L\n                      .\n                      Urea and the kidney. In:\n                      The Kidney\n                      , edited by Brenner BM and Rector F. Philadelphia, PA: Saunders, 1996, p. 571\u2013606."},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.73.5.808"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.59.1.437"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1046\/j.1440-1681.1999.02991.x"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1998.274.4.H1075"},{"key":"R7","unstructured":"Forgacs I\n                      , Chatel R, and Visy M.\n                      Renal function in water deprivation.\n                      Acta Physiol Acad Sci Hung\n                      33\n                      : 297\u2013304, 1968."},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00980.x"},{"key":"R9","unstructured":"Heller J\n                      .\n                      Electrolyte and urea concentration in rat kidney tissue during water diuresis and water deprivation.\n                      Physiol Bohemoslov\n                      16\n                      : 489\u2013500, 1967."},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00413.2003"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.72"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1016\/S0895-7061(01)02169-0"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1983.245.5.F634"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.261.2.F221"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1172\/JCI116286"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.272.5.F561"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1159\/000063510"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-201x.2000.00632.x"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199508103330607"},{"key":"R20","unstructured":"Masilamani S\n                      , Knepper MA, and Burg BM.\n                      Urine concentration and dilution. In:\n                      The Kidney\n                      , edited by Brenner BM. Philadelphia, PA: Saunders, 2000, p. 595\u2013636."},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.27.3.688"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00346.2001"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1007\/s004240050572"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000047872.07864.20"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.37.2.467"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00334.2001"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.0075.2001"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.32.2.331"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1993.265.5.C1191"},{"key":"R30","doi-asserted-by":"crossref","unstructured":"Plato CF\n                      , Pollock DM, and Garvin JL.\n                      Endothelin inhibits thick ascending limb chloride flux via ET(B) receptor-mediated NO release.\n                      Am J Physiol Renal Physiol\n                      279\n                      : F326\u2013F333, 2000.","DOI":"10.1152\/ajprenal.2000.279.2.F326"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.35.1.319"},{"key":"R32","doi-asserted-by":"crossref","unstructured":"Plato CF\n                      , Stoos BA, Wang D, and Garvin JL.\n                      Endogenous nitric oxide inhibits chloride transport in the thick ascending limb.\n                      Am J Physiol Renal Physiol\n                      276\n                      : F159\u2013F163, 1999.","DOI":"10.1152\/ajprenal.1999.276.1.F159"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.281.1.F144"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.275.1.F46"},{"key":"R35","doi-asserted-by":"crossref","unstructured":"Saikia TC\n                      .\n                      Composition of the renal cortex and medulla of rats during water diuresis and antidiuresis.\n                      Q J Exp Physiol Cogn Med Sci\n                      50\n                      : 146\u2013157, 1965.","DOI":"10.1113\/expphysiol.1965.sp001777"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00086.2002"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-200307000-00023"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00795.x"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.4.F480"},{"key":"R40","doi-asserted-by":"crossref","unstructured":"Stoos BA\n                      , Garcia NH, and Garvin JL.\n                      Nitric oxide inhibits sodium reabsorption in the isolated perfused cortical collecting duct.\n                      J Am Soc Nephrol\n                      6\n                      : 89\u201394, 1995.","DOI":"10.1681\/ASN.V6189"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.34.6.1237"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.4.F560"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.264.4.F684"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000047204.72286.34"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.1999.277.5.G944"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00209.2004","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,6,25]],"date-time":"2021-06-25T10:38:42Z","timestamp":1624617522000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00209.2004"}},"issued":{"date-parts":[[2005,1]]},"references-count":45,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2005,1]]}},"alternative-id":["10.1152\/ajprenal.00209.2004"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00209.2004","relation":{"has-review":[{"id-type":"doi","id":"10.3410\/f.1025453.298969","asserted-by":"object"}]},"ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2005,1]]}},{"indexed":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T03:50:27Z","timestamp":1772164227904,"version":"3.50.1"},"reference-count":43,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2009,11]]},"abstract":"<jats:p>\n                    Reabsorption of water and other molecules is dependent on the corticomedullary sodium concentration gradient in the kidney. During the early course of acute tubular necrosis (ATN), this gradient is altered. Therefore,\n                    <jats:sup>23<\/jats:sup>\n                    Na magnetic resonance imaging (MRI) was used to study the alterations in renal sodium distribution in the rat kidney during ischemia and reperfusion (IR) injury, which induces ATN. In-magnet ischemia was induced for 0 (control), 10, 20, 30 or 50 min in Wistar rats.\n                    <jats:sup>23<\/jats:sup>\n                    Na images were collected every 10 min during baseline, ischemia, and 60-min reperfusion periods. T\n                    <jats:sub>1<\/jats:sub>\n                    and T\n                    <jats:sub>2<\/jats:sub>\n                    relaxation times were measured by both\n                    <jats:sup>23<\/jats:sup>\n                    Na-MRI and -MRS on a separate cohort of animals during ischemia and reperfusion for correction of relaxation-related tissue sodium concentration (TSC). A marked decrease was observed in the medulla and cortex\n                    <jats:sup>23<\/jats:sup>\n                    Na-MRI signal intensity (SI) during the early evolution of ATN caused by IR injury, with the sodium reabsorption function of the kidney being irreversibly damaged after 50 min of ischemia. Sodium relaxation time characteristics were similar in the medulla and cortex of normal kidney, but significantly decreased with IR. The changes in relaxation times in both compartments were identical; thus the medulla-to-cortex sodium SI ratio represents the TSC ratio of both compartments. The extent of IR damage observed with histological examination correlated with the\n                    <jats:sup>23<\/jats:sup>\n                    Na-MRI data.\n                    <jats:sup>23<\/jats:sup>\n                    Na-MRI has great potential for noninvasive, clinical diagnosis of evolving ATN in the setup of acute renal failure and in differentiating ATN from other causes of renal failure where tubular function is maintained.\n                  <\/jats:p>","DOI":"10.1152\/ajprenal.00388.2009","type":"journal-article","created":{"date-parts":[[2009,9,2]],"date-time":"2009-09-02T21:09:05Z","timestamp":1251925745000},"page":"F1288-F1298","source":"Crossref","is-referenced-by-count":26,"title":["Early monitoring of acute tubular necrosis in the rat kidney by\n                    <sup>23<\/sup>\n                    Na-MRI"],"prefix":"10.1152","volume":"297","author":[{"given":"Bharath K.","family":"Atthe","sequence":"first","affiliation":[{"name":"Departments of Radiology,"},{"name":"Biomedical Engineering,"}]},{"given":"Andriy M.","family":"Babsky","sequence":"additional","affiliation":[{"name":"Departments of Radiology,"}]},{"given":"Paige N.","family":"Hopewell","sequence":"additional","affiliation":[{"name":"Departments of Radiology,"},{"name":"Weldon School of Biomedical Engineering, Purdue University, West Lafayette, Indiana"}]},{"given":"Carrie L.","family":"Phillips","sequence":"additional","affiliation":[{"name":"Pathology and Laboratory Medicine, and"}]},{"given":"Bruce A.","family":"Molitoris","sequence":"additional","affiliation":[{"name":"Medicine, Indiana University-Purdue University at Indianapolis, Indianapolis; and"}]},{"given":"Navin","family":"Bansal","sequence":"additional","affiliation":[{"name":"Departments of Radiology,"},{"name":"Biomedical Engineering,"},{"name":"Weldon School of Biomedical Engineering, Purdue University, West Lafayette, Indiana"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1593\/neo.05130"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1021\/bi00072a020"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1002\/jmri.1880050624"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1522-2586(200005)11:5<532::AID-JMRI9>3.0.CO;2-#"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1981.240.2.F147"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(95)92057-9"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199503093321006"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1002\/mrm.1910040307"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1002\/mrm.1910360115"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1002\/mrm.1311"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1002\/mrm.1910300409"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/0006-291X(85)90110-X"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-0463.2004.apm1120305.x"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199406023302207"},{"key":"B15","doi-asserted-by":"crossref","first-page":"303","DOI":"10.1007\/BF02889375","volume":"19","author":"Glaumann B","year":"1975","journal-title":"Virchows Arch B Cell Pathol"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1007\/BF02892416"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1159\/000063700"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.84.12.1401"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1097\/00007890-198602000-00002"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1097\/00007890-198303000-00002"},{"key":"B21","first-page":"2392","volume":"42","author":"Jamison RL","year":"1983","journal-title":"Fed Proceedings"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.5.F1061"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118498"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1002\/mrm.1910160302"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00475.x"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1002\/mrm.20359"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000152"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1002\/mrm.21031"},{"key":"B29","doi-asserted-by":"crossref","first-page":"124","DOI":"10.1152\/ajplegacy.1955.182.1.124","volume":"182","author":"McIntosh BJ","year":"1955","journal-title":"Am J Physiol"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1172\/JCI112214"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.3109\/00365516809076983"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1159\/000090610"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1002\/mrm.1910070103"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1002\/mrm.1910030613"},{"key":"B35","first-page":"38","volume":"25","author":"Slutsky RA","year":"1984","journal-title":"J Nucl Med"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1016\/j.mri.2003.08.007"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1522-2594(199902)41:2<351::AID-MRM20>3.0.CO;2-H"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1978.87"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.2.F413"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.153"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.258.4.F1125"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfh452"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1097\/FJC.0b013e318030c2c9"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00388.2009","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,10,10]],"date-time":"2021-10-10T05:21:25Z","timestamp":1633843285000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00388.2009"}},"issued":{"date-parts":[[2009,11]]},"references-count":43,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2009,11]]}},"alternative-id":["10.1152\/ajprenal.00388.2009"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00388.2009","relation":{"has-review":[{"id-type":"doi","id":"10.3410\/f.1282020.749110","asserted-by":"object"}]},"ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2009,11]]}},{"indexed":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T03:49:37Z","timestamp":1772164177920,"version":"3.50.1"},"reference-count":43,"publisher":"American Physiological Society","issue":"2","funder":[{"DOI":"10.13039\/501100001515","name":"Cure Kids","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100001515","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100009315","name":"Cystinosis Ireland","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100009315","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100005674","name":"Cystinosis Research Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100005674","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100006346","name":"University of Auckland | Faculty of Medical and Health Sciences, University of Auckland","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100006346","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2022,8,1]]},"abstract":"<jats:p>Animal models of disease are essential to perform preclinical testing of new therapies before they can progress to clinical trials. The cystinosis field has been hampered by a lack of suitable animal models that fully recapitulate the disease. Here, we generated a rat model of cystinosis that closely models the human condition in a timeframe that makes them an excellent model for preclinical drug testing as well as being a powerful tool to advance research.<\/jats:p>","DOI":"10.1152\/ajprenal.00277.2021","type":"journal-article","created":{"date-parts":[[2022,6,13]],"date-time":"2022-06-13T07:59:55Z","timestamp":1655107195000},"page":"F156-F170","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":9,"title":["Cystinosin-deficient rats recapitulate the phenotype of nephropathic cystinosis"],"prefix":"10.1152","volume":"323","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1954-107X","authenticated-orcid":true,"given":"Jennifer A.","family":"Hollywood","sequence":"first","affiliation":[{"name":"Department of Molecular Medicine and Pathology, The University of Auckland, Auckland, New Zealand"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2834-6148","authenticated-orcid":true,"given":"Prasanna K.","family":"Kallingappa","sequence":"additional","affiliation":[{"name":"Vernon Jansen Unit, Faculty of Medical and Health Sciences, The University of Auckland, Auckland, New Zealand"}]},{"given":"Pang Yuk","family":"Cheung","sequence":"additional","affiliation":[{"name":"Department of Molecular Medicine and Pathology, The University of Auckland, Auckland, New Zealand"}]},{"given":"Renita M.","family":"Martis","sequence":"additional","affiliation":[{"name":"Department of Physiology, The University of Auckland, Auckland, New Zealand"}]},{"given":"Sree","family":"Sreebhavan","sequence":"additional","affiliation":[{"name":"Auckland Cancer Society Research Centre, The University of Auckland, Auckland, New Zealand"}]},{"given":"Robert D.","family":"\u2018Atiola","sequence":"additional","affiliation":[{"name":"Department of Molecular Medicine and Pathology, The University of Auckland, Auckland, New Zealand"}]},{"given":"Aparajita","family":"Chatterjee","sequence":"additional","affiliation":[{"name":"Department of Molecular Medicine and Pathology, The University of Auckland, Auckland, New Zealand"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9256-5014","authenticated-orcid":true,"given":"Emma J.","family":"Buckels","sequence":"additional","affiliation":[{"name":"Department of Molecular Medicine and Pathology, The University of Auckland, Auckland, New Zealand"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4145-4696","authenticated-orcid":true,"given":"Brya G.","family":"Matthews","sequence":"additional","affiliation":[{"name":"Department of Molecular Medicine and Pathology, The University of Auckland, Auckland, New Zealand"}]},{"given":"Paula M.","family":"Lewis","sequence":"additional","affiliation":[{"name":"Department of Molecular Medicine and Pathology, The University of Auckland, Auckland, New Zealand"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5732-1193","authenticated-orcid":true,"given":"Alan J.","family":"Davidson","sequence":"additional","affiliation":[{"name":"Department of Molecular Medicine and Pathology, The University of Auckland, Auckland, New Zealand"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1186\/s13023-016-0426-y"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra020552"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM198704163161602"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-147-4-200708210-00006"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2011.277"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-014-3018-x"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/j.jpeds.2004.03.056"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.22.21.7622-7632.2002"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfp553"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013060598"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.4103\/0971-4065.78067"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2019040371"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1038\/srep42583"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1007\/s00335-018-9790-3"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1038\/nature02426"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1038\/nbt.2661"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1186\/s13059-017-1220-4"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/gky354"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1038\/mtna.2014.64"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1002\/bmc.4238"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2017.01.002"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1210\/en.2016-1059"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1002\/jbmr.141"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2015.284"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2013.111"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2002.00433.x"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1007\/s00467-012-2227-4"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2019070712"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/s0002-9343(70)80002-x"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/0090-4295(75)90105-3"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2016.182"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013060653"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00591.2014"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1007\/pl00013448"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2019.01.029"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1002\/stem.1835"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0120998"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1016\/j.ajpath.2019.01.015"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1155\/2010\/403272"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.3390\/ijms21010155"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2012.261"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2014111059"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.3390\/cells11010006"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00277.2021","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,7,19]],"date-time":"2022-07-19T09:58:53Z","timestamp":1658224733000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00277.2021"}},"issued":{"date-parts":[[2022,8,1]]},"references-count":43,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2022,8,1]]}},"alternative-id":["10.1152\/ajprenal.00277.2021"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00277.2021","relation":{"has-preprint":[{"id-type":"doi","id":"10.1101\/2021.06.29.450444","asserted-by":"object"}]},"ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2022,8,1]]},"assertion":[{"value":"2021-07-26","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2022-05-04","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2022-06-07","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2022-07-19","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2025,9,27]],"date-time":"2025-09-27T14:00:56Z","timestamp":1758981656531},"reference-count":45,"publisher":"American Physiological Society","issue":"11","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,12,1]]},"abstract":"<jats:p>In peritoneal dialysis (PD) therapy, physical stresses such as exposure to peritoneal dialysate, catheter trauma, and peritonitis may induce peritoneal injury that can prevent continued long-term PD therapy. Therefore, protection of the peritoneum is an important target to enable long-term PD therapy in patients with end-stage renal disease. We previously showed that neutralization of the membrane complement regulators (CRegs) Crry and CD59 in rat peritoneum provokes development of acute peritoneal injury due to uncontrolled complement activation. C5a is a key effecter molecule of the complement system released during acute inflammation. Control of C5a has been proposed as a strategy to suppress inflammatory reactions and, because peritoneal injury is accompanied by inflammation, we hypothesized that C5a targeted therapy might be an effective way to suppress peritoneal injury. In the present study we used an established acute peritonitis model induced by neutralization of CRegs to investigate the effects on acute peritoneal injury of inhibiting C5a. Intravenous administration of an anti-C5a complementary peptide (AcPepA) up to 4 h after induction of injury significantly and dose-dependently prevented accumulation of inflammatory cells and reduced tissue damage in the model, accompanied by decreased C3b deposition. We show that C5a contributed to the development of peritoneal injury. Our results suggest that C5a is a target for preventing or treating peritoneal injury in patients undergoing prolonged PD therapy or with infectious complications.<\/jats:p>","DOI":"10.1152\/ajprenal.00681.2012","type":"journal-article","created":{"date-parts":[[2013,8,1]],"date-time":"2013-08-01T04:10:59Z","timestamp":1375330259000},"page":"F1603-F1616","source":"Crossref","is-referenced-by-count":11,"title":["Anti-C5a complementary peptide ameliorates acute peritoneal injury induced by neutralization of Crry and CD59"],"prefix":"10.1152","volume":"305","author":[{"given":"Tomohiro","family":"Mizuno","sequence":"first","affiliation":[{"name":"Nephrology, Nagoya University Graduate School of Medicine, Nagoya, Japan;"},{"name":"Clinical Sciences and Neuropsychopharmacology, Meijo University Graduate School of Pharmaceutical Sciences, Nagoya, Japan;"}]},{"given":"Masashi","family":"Mizuno","sequence":"additional","affiliation":[{"name":"Nephrology, Nagoya University Graduate School of Medicine, Nagoya, Japan;"},{"name":"Renal Replacement Therapy, Nagoya University Graduate School of Medicine, Nagoya, Japan;"}]},{"given":"Masaki","family":"Imai","sequence":"additional","affiliation":[{"name":"Immunology, Nagoya City University Graduate School of Medicine, Nagoya, Japan; and"}]},{"given":"Yasuhiro","family":"Suzuki","sequence":"additional","affiliation":[{"name":"Nephrology, Nagoya University Graduate School of Medicine, Nagoya, Japan;"},{"name":"Renal Replacement Therapy, Nagoya University Graduate School of Medicine, Nagoya, Japan;"}]},{"given":"Mayu","family":"Kushida","sequence":"additional","affiliation":[{"name":"Nephrology, Nagoya University Graduate School of Medicine, Nagoya, Japan;"},{"name":"Clinical Sciences and Neuropsychopharmacology, Meijo University Graduate School of Pharmaceutical Sciences, Nagoya, Japan;"}]},{"given":"Yukihiro","family":"Noda","sequence":"additional","affiliation":[{"name":"Clinical Sciences and Neuropsychopharmacology, Meijo University Graduate School of Pharmaceutical Sciences, Nagoya, Japan;"}]},{"given":"Shoichi","family":"Maruyama","sequence":"additional","affiliation":[{"name":"Nephrology, Nagoya University Graduate School of Medicine, Nagoya, Japan;"}]},{"given":"Hidechika","family":"Okada","sequence":"additional","affiliation":[{"name":"Immunology, Nagoya City University Graduate School of Medicine, Nagoya, Japan; and"},{"name":"Choju Medical Institute, Fukushimura Hospital, Toyohashi, Japan"}]},{"given":"Noriko","family":"Okada","sequence":"additional","affiliation":[{"name":"Immunology, Nagoya City University Graduate School of Medicine, Nagoya, Japan; and"}]},{"given":"Seiichi","family":"Matsuo","sequence":"additional","affiliation":[{"name":"Nephrology, Nagoya University Graduate School of Medicine, Nagoya, Japan;"}]},{"given":"Yasuhiko","family":"Ito","sequence":"additional","affiliation":[{"name":"Nephrology, Nagoya University Graduate School of Medicine, Nagoya, Japan;"},{"name":"Renal Replacement Therapy, Nagoya University Graduate School of Medicine, Nagoya, Japan;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/j.cca.2006.06.010"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M109.092106"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1093\/brain\/awp322"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/S1081-1206(10)60584-4"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1038\/10512"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1007\/s10875-007-9090-2"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.0901005"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.172.10.6382"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.C500287200"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.2174\/138945011794182737"},{"key":"B11","doi-asserted-by":"crossref","first-page":"2063","DOI":"10.4049\/jimmunol.135.3.2063","volume":"135","author":"Huey R","year":"1985","journal-title":"J Immunol"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1042\/bj2840169"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1007\/s00268-005-7771-7"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2249.2001.01513.x"},{"key":"B15","doi-asserted-by":"crossref","first-page":"4200","DOI":"10.4049\/jimmunol.153.9.4200","volume":"153","author":"Konteatis ZD","year":"1994","journal-title":"J Immunol"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2010-01-264051"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1532\/IJH97.06117"},{"key":"B18","doi-asserted-by":"crossref","first-page":"262","DOI":"10.1177\/089686080902900306","volume":"29","author":"Mactier R","year":"2009","journal-title":"Perit Dial Int"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1007\/s10157-011-0471-8"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1002\/1529-0131(200110)44:10<2425::AID-ART407>3.0.CO;2-4"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.2174\/092986706777441959"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.2174\/1568010043483890"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.2174\/157488511794079031"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.0804245"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfq683"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00652.2011"},{"key":"B27","doi-asserted-by":"crossref","first-page":"5477","DOI":"10.4049\/jimmunol.162.9.5477","volume":"162","author":"Mizuno M","year":"1999","journal-title":"J Immunol"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1517\/13543784.14.7.807"},{"key":"B29","first-page":"2511","volume":"31","author":"Okada H","year":"2011","journal-title":"Anticancer Res"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1111\/j.1348-0421.2007.tb03918.x"},{"key":"B31","doi-asserted-by":"crossref","first-page":"49","DOI":"10.1177\/089686089501500110","volume":"15","author":"Reddingius RE","year":"1995","journal-title":"Perit Dial Int"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1038\/ni.1923"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1038\/nm1753"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20030374"},{"key":"B35","doi-asserted-by":"crossref","first-page":"3032","DOI":"10.4049\/jimmunol.152.6.3032","volume":"152","author":"Takizawa H","year":"1994","journal-title":"J Immunol"},{"key":"B36","doi-asserted-by":"crossref","first-page":"1301","DOI":"10.4049\/jimmunol.153.3.1301","volume":"153","author":"Tamura M","year":"1994","journal-title":"J Immunol"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2249.2004.02407.x"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1097\/TP.0b013e3181ffb9f5"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00318.x"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1002\/art.10449"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.105.086835"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1016\/j.molimm.2011.04.014"},{"key":"B43","first-page":"1372","volume":"8","author":"Young GA","year":"1993","journal-title":"Nephrol Dial Transplant"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1186\/ar3873"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.1000892"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00681.2012","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,7,3]],"date-time":"2023-07-03T15:58:53Z","timestamp":1688399933000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00681.2012"}},"issued":{"date-parts":[[2013,12,1]]},"references-count":45,"journal-issue":{"issue":"11","published-print":{"date-parts":[[2013,12,1]]}},"alternative-id":["10.1152\/ajprenal.00681.2012"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00681.2012","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2013,12,1]]}},{"indexed":{"date-parts":[[2025,6,29]],"date-time":"2025-06-29T05:10:08Z","timestamp":1751173808709,"version":"3.41.0"},"reference-count":34,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1998,1,1]]},"abstract":"<jats:p>The effect of exogenous \u03b1-ketoglutarate (\u03b1KG) and the peritubular Na<jats:sup>+<\/jats:sup>-dicarboxylate (Na-DC) cotransporter on organic anion\/dicarboxylate (OA\/DC) exchange in S2 segments of single, nonperfused rabbit proximal tubules was measured using 1 \u03bcM fluorescein (FL), a model OA, and epifluorescence microscopy. The effect of different transmembrane distributions of 10 \u03bcM \u03b1KG on peritubular FL uptake was measured at 37\u00b0C using bicarbonate-buffered, nutrient-containing buffers, which are conditions similar to those found in vivo. Compared with FL uptake in the absence of exogenous \u03b1KG, preloading tubules with \u03b1KG ( trans-configuration) or acute exposure to \u03b1KG ( cis-configuration) increased FL uptake 62% and 54%, respectively, whereas a cis-trans-configuration of \u03b1KG increased FL uptake by 76%. The cis-stimulation of FL uptake by \u03b1KG was rapid, within 5\u20137 s. This stimulation was blocked 96% by simultaneous exposure to 2 mM Li<jats:sup>+<\/jats:sup>, indicating that stimulation of transport was secondary to the uptake of exogenous \u03b1KG. In the absence of exogenous \u03b1KG, selective inhibition of Na-DC cotransport using 2 mM Li<jats:sup>+<\/jats:sup>or 1 mM methylsuccinate decreased FL uptake by 25% (effects that were reversible but not additive), suggesting that the Na-DC cotransporter recycles endogenous \u03b1KG that has left the cell in exchange for FL and that this activity supports \u223c25% of baseline activity of the OA\/DC exchanger. With recycling of \u03b1KG accounting for \u223c25% of FL uptake and with accumulation of exogenous \u03b1KG accounting for another \u223c75% increase in FL uptake, Na-DC cotransport appears to directly support (25% + 75%)\/175%, or \u223c57%, of total FL transport.<\/jats:p>","DOI":"10.1152\/ajprenal.1998.274.1.f165","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T14:24:43Z","timestamp":1514039083000},"page":"F165-F174","source":"Crossref","is-referenced-by-count":15,"title":["Effect of \u03b1-ketoglutarate on organic anion transport in single rabbit renal proximal tubules"],"prefix":"10.1152","volume":"274","author":[{"given":"John R.","family":"Welborn","sequence":"first","affiliation":[{"name":"Department of Physiology, College of Medicine, University of Arizona, Tucson, Arizona 85724"}]},{"given":"Shlomo","family":"Shpun","sequence":"additional","affiliation":[{"name":"Department of Physiology, College of Medicine, University of Arizona, Tucson, Arizona 85724"}]},{"given":"William H.","family":"Dantzler","sequence":"additional","affiliation":[{"name":"Department of Physiology, College of Medicine, University of Arizona, Tucson, Arizona 85724"}]},{"given":"Stephen H.","family":"Wright","sequence":"additional","affiliation":[{"name":"Department of Physiology, College of Medicine, University of Arizona, Tucson, Arizona 85724"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1007\/BF00582592"},{"issue":"30","key":"B2","first-page":"F858","volume":"261","author":"Chatsudthipong V.","year":"1991","journal-title":"Am. J. Physiol."},{"issue":"32","key":"B3","first-page":"F384","volume":"263","author":"Chatsudthipong V.","year":"1992","journal-title":"Am. J. Physiol."},{"issue":"40","key":"B4","first-page":"F521","volume":"271","author":"Dantzler W. H.","year":"1996","journal-title":"Am. J. Physiol."},{"key":"B5","doi-asserted-by":"crossref","first-page":"663","DOI":"10.1016\/S0022-3565(25)24457-3","volume":"272","author":"Dantzler W. H.","year":"1995","journal-title":"J. Pharmacol. Exp. Ther."},{"issue":"32","key":"B6","first-page":"F342","volume":"263","author":"Dickman K. G.","year":"1992","journal-title":"Am. J. Physiol."},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1007\/BF00581555"},{"issue":"4","key":"B8","first-page":"F137","volume":"235","author":"Kippen I.","year":"1978","journal-title":"Am. J. Physiol."},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1007\/BF02460467"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1007\/BF01872636"},{"key":"B11","doi-asserted-by":"crossref","first-page":"1261","DOI":"10.1016\/S0022-3565(25)38870-1","volume":"269","author":"Masereeuw R.","year":"1994","journal-title":"J. Pharmacol. Exp. Ther."},{"issue":"40","key":"B12","first-page":"F1173","volume":"271","author":"Masereeuw R.","year":"1996","journal-title":"Am. J. Physiol."},{"issue":"30","key":"B13","first-page":"R1470","volume":"261","author":"Miller D. S.","year":"1991","journal-title":"Am. J. Physiol."},{"key":"B14","first-page":"456","volume":"7","author":"Miller D. S.","year":"1993","journal-title":"FASEB J."},{"issue":"26","key":"B15","first-page":"R501","volume":"257","author":"Miller D. S.","year":"1989","journal-title":"Am. J. Physiol."},{"issue":"4","key":"B16","first-page":"F278","volume":"235","author":"Podevin R. A.","year":"1978","journal-title":"Am. J. Physiol."},{"key":"B17","doi-asserted-by":"crossref","first-page":"1278","DOI":"10.1016\/S0022-3565(25)10636-8","volume":"274","author":"Pritchard J. B.","year":"1995","journal-title":"J. Pharmacol. Exp. Ther."},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/0304-4157(87)90015-3"},{"issue":"24","key":"B19","first-page":"F597","volume":"255","author":"Pritchard J. B.","year":"1988","journal-title":"Am. J. Physiol."},{"key":"B20","doi-asserted-by":"crossref","first-page":"969","DOI":"10.1016\/S0022-3565(25)23220-7","volume":"255","author":"Pritchard J. B.","year":"1990","journal-title":"J. Pharmacol. Exp. Ther."},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1993.73.4.765"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.240"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1002\/bms.1200110105"},{"issue":"22","key":"B24","first-page":"F795","volume":"253","author":"Shimada H.","year":"1987","journal-title":"Am. J. Physiol."},{"issue":"37","key":"B25","first-page":"F1109","volume":"268","author":"Shpun S.","year":"1995","journal-title":"Am. J. Physiol."},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1172\/JCI109353"},{"issue":"31","key":"B27","first-page":"F1039","volume":"262","author":"Simpson D. P.","year":"1992","journal-title":"Am. J. Physiol."},{"issue":"27","key":"B28","first-page":"F46","volume":"258","author":"Sullivan L. P.","year":"1990","journal-title":"Am. J. Physiol."},{"key":"B29","doi-asserted-by":"crossref","first-page":"1192","DOI":"10.1681\/ASN.V271192","volume":"2","author":"Sullivan L. P.","year":"1992","journal-title":"J. Am. Soc. Nephrol."},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/0304-4157(94)90018-3"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1007\/BF00581554"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1007\/BF00581838"},{"key":"B34","doi-asserted-by":"crossref","first-page":"582","DOI":"10.1016\/S0022-3565(25)20639-5","volume":"278","author":"Villalobos A. R.","year":"1996","journal-title":"J. Pharmacol. Exp. Ther."},{"issue":"22","key":"B35","first-page":"F126","volume":"253","author":"Welling L. W.","year":"1987","journal-title":"Am. J. Physiol."}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1998.274.1.F165","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,6,29]],"date-time":"2025-06-29T04:38:18Z","timestamp":1751171898000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1998.274.1.F165"}},"issued":{"date-parts":[[1998,1,1]]},"references-count":34,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1998,1,1]]}},"alternative-id":["10.1152\/ajprenal.1998.274.1.F165"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1998.274.1.f165","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[1998,1,1]]}},{"indexed":{"date-parts":[[2025,4,15]],"date-time":"2025-04-15T00:58:35Z","timestamp":1744678715870},"reference-count":54,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2014,9,1]]},"abstract":"<jats:p> The unfolded protein response and endoplasmic reticulum-associated degradation (ERAD) contribute to injury in renal glomerular diseases, including those mediated by complement C5b-9. In the present study, we address the role of protein-tyrosine phosphatase 1B (PTP1B) in complement-mediated glomerular injury and ERAD. In glomerular epithelial cells (GECs)\/podocytes and PTP1B-deficient mouse embryonic fibroblasts exposed to complement, inhibition\/deletion of PTP1B reduced ERAD, as monitored by the ERAD reporter CD3\u03b4. Overexpression of PTP1B produced an effect similar to PTP1B deficiency on ERAD in complement-treated GECs. Complement-mediated cytotoxicity was reduced after PTP1B overexpression and tended to be reduced after PTP1B inhibition. PTP1B enhanced the induction of certain ERAD components via the inositol-requiring-1\u03b1 branch of the unfolded protein response. PTP1B knockout mice with anti-glomerular basement membrane glomerulonephritis had decreased proteinuria and showed less podocyte loss and endoplasmic reticulum dysfunction compared with wild-type littermates. These results imply that endogenous levels of PTP1B are tightly regulated and that both overexpression and inhibition can affect ERAD. The cytoprotective effects of PTP1B deletion in cultured cells and in anti-glomerular basement membrane nephritis suggest that PTP1B may potentially be a therapeutic target in complement-mediated diseases. <\/jats:p>","DOI":"10.1152\/ajprenal.00191.2014","type":"journal-article","created":{"date-parts":[[2014,7,23]],"date-time":"2014-07-23T22:48:09Z","timestamp":1406155689000},"page":"F634-F647","source":"Crossref","is-referenced-by-count":10,"title":["Complement-mediated glomerular injury is reduced by inhibition of protein-tyrosine phosphatase 1B"],"prefix":"10.1152","volume":"307","author":[{"given":"Lisa","family":"Nezvitsky","sequence":"first","affiliation":[{"name":"Department of Medicine and Biochemistry, McGill University Health Centre, McGill University, Montreal, Quebec, Canada"}]},{"given":"Michel L.","family":"Tremblay","sequence":"additional","affiliation":[{"name":"Department of Medicine and Biochemistry, McGill University Health Centre, McGill University, Montreal, Quebec, Canada"}]},{"given":"Tomoko","family":"Takano","sequence":"additional","affiliation":[{"name":"Department of Medicine and Biochemistry, McGill University Health Centre, McGill University, Montreal, Quebec, Canada"}]},{"given":"Joan","family":"Papillon","sequence":"additional","affiliation":[{"name":"Department of Medicine and Biochemistry, McGill University Health Centre, McGill University, Montreal, Quebec, Canada"}]},{"given":"Andrey V.","family":"Cybulsky","sequence":"additional","affiliation":[{"name":"Department of Medicine and Biochemistry, McGill University Health Centre, McGill University, Montreal, Quebec, Canada"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/j.tibs.2009.10.001"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1042\/BJ20110373"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.4161\/cam.22495"},{"key":"B4","author":"Aoudjit L","year":"2011","journal-title":"J Sig Trans"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1101\/cshperspect.a007526"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/j.ceb.2010.10.002"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M110.186148"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0034412"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M004852200"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/j.ceb.2011.05.004"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200809198"},{"key":"B12","first-page":"184","volume":"4","author":"Coers W","year":"1996","journal-title":"Exp Nephrol"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1985.214"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2009.389"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2012.390"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1159\/000313948"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M500729200"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M204694200"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1002\/phy2.86"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1126\/science.283.5407.1544"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M112.396614"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1172\/JCI17423"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.94.5.1680"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(92)90190-N"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.C400261200"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00027.2011"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.biochem.73.011303.073752"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1038\/nrm3270"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/j.molcel.2009.08.021"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200903014"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1016\/j.febslet.2007.10.033"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M310535200"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbamcr.2012.03.001"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M111.311290"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.00088.2010"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M513556200"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.23.21.7448-7459.2003"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1038\/labinvest.3780451"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.E03-11-0851"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1016\/j.febslet.2007.04.070"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1016\/j.molcel.2008.11.017"},{"key":"B42","first-page":"421","volume-title":"Methods Enzymol","author":"Salant DJ","year":"1988"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000410"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2013.08.009"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2011.472"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1038\/nsmb803"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1042\/BJ20110799"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1172\/JCI26373"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1093\/jb\/mvn091"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1084\/jem.187.6.835"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1016\/j.tibs.2010.03.004"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1038\/nature07203"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.25.17806"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1158\/0008-5472.CAN-06-4338"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00191.2014","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T21:02:03Z","timestamp":1567976523000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00191.2014"}},"issued":{"date-parts":[[2014,9,1]]},"references-count":54,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2014,9,1]]}},"alternative-id":["10.1152\/ajprenal.00191.2014"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00191.2014","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2014,9,1]]}},{"indexed":{"date-parts":[[2025,4,12]],"date-time":"2025-04-12T22:14:01Z","timestamp":1744496041876},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1985,2,1]]},"abstract":"<jats:p> The renal responses to changes in perfusion pressure (RPP) were studied in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) to determine whether an abnormality in the pressure-diuresis phenomenon could be involved in the resetting of kidney function in hypertension. Differences in the neural and endocrine background to the kidneys were minimized by denervating the kidney and by holding plasma vasopressin, aldosterone, corticosterone, and norepinephrine levels constant by intravenous infusion. In WKY, increasing renal perfusion pressure 54 mmHg, from 103 to 157 mmHg, produced a ninefold increase in urine flow and sodium excretion with no measurable change in renal blood flow (RBF) or glomerular filtration rate (GFR). In SHR, increasing renal perfusion pressure 54 mmHg, from 133 to 187 mmHg, produced only a fourfold increase in urine flow and sodium excretion. GFR, RBF, and peritubular capillary pressures were well autoregulated and were similar in the SHR and WKY at pressures above 110 mmHg. These results indicate the presence of intrinsic changes in the kidney of SHR that enhance fractional tubular reabsorption and impair the pressure-diuresis response. This blunting of the renal pressure-diuresis phenomenon in SHR may represent the functional resetting of the kidney that is necessary for sustained hypertension. <\/jats:p>","DOI":"10.1152\/ajprenal.1985.248.2.f199","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T19:43:27Z","timestamp":1513971807000},"page":"F199-F205","source":"Crossref","is-referenced-by-count":20,"title":["Abnormal pressure-diuresis-natriuresis response in spontaneously hypertensive rats"],"prefix":"10.1152","volume":"248","author":[{"given":"R. J.","family":"Roman","sequence":"first","affiliation":[]},{"suffix":"Jr","given":"A. W.","family":"Cowley","sequence":"additional","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1985.248.2.F199","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:33:22Z","timestamp":1567956802000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1985.248.2.F199"}},"issued":{"date-parts":[[1985,2,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1985,2,1]]}},"alternative-id":["10.1152\/ajprenal.1985.248.2.F199"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1985.248.2.f199","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[1985,2,1]]}},{"indexed":{"date-parts":[[2025,10,5]],"date-time":"2025-10-05T11:46:54Z","timestamp":1759664814109},"reference-count":29,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2008,11]]},"abstract":"<jats:p>Sgk1 is an aldosterone-induced kinase that regulates epithelial sodium channel (ENaC)-mediated Na<jats:sup>+<\/jats:sup>transport in the collecting duct and connecting tubule of the kidney. The NH<jats:sub>2<\/jats:sub>terminus of Sgk1 contains instability motifs that direct the ubiquitination of Sgk1 resulting in a rapidly degraded protein. By bioinformatic analysis, we identified a 5\u2032 variant alternate transcript of human Sgk1 (Sgk1_v2) that is widely expressed, is conserved from rodent to humans, and is predicted to encode an Sgk1 isoform, Sgk1_i2, with a different NH<jats:sub>2<\/jats:sub>terminus. When expressed in HEK293 cells, Sgk1_i2 was more abundant than Sgk1 because of an increased protein half-life and this correlated with reduced ubiquitination of Sgk1_i2 and enhanced surface expression of ENaC. Immunocytochemical studies demonstrated that in contrast to Sgk1, Sgk1_i2 is preferentially targeted to the plasma membrane. When coexpressed with ENaC subunits in FRT epithelia, Sgk1_i2 had a significantly greater effect on amiloride-sensitive Na<jats:sup>+<\/jats:sup>transport compared with Sgk1. Together, the data demonstrate that a conserved NH<jats:sub>2<\/jats:sub>-terminal variant of Sgk1 shows improved stability, enhanced membrane association, and greater stimulation of epithelial Na<jats:sup>+<\/jats:sup>transport in a heterologous expression system.<\/jats:p>","DOI":"10.1152\/ajprenal.90239.2008","type":"journal-article","created":{"date-parts":[[2008,8,28]],"date-time":"2008-08-28T00:44:32Z","timestamp":1219884272000},"page":"F1440-F1448","source":"Crossref","is-referenced-by-count":22,"title":["An evolutionarily conserved N-terminal Sgk1 variant with enhanced stability and improved function"],"prefix":"10.1152","volume":"295","author":[{"given":"Nandita S.","family":"Raikwar","sequence":"first","affiliation":[]},{"given":"Peter M.","family":"Snyder","sequence":"additional","affiliation":[]},{"given":"Christie P.","family":"Thomas","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2003.042903"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.E06-10-0968"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0800958105"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0604816103"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M002076200"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1042\/BJ20060905"},{"key":"R7","doi-asserted-by":"crossref","unstructured":"Bens M, Vallet V, Cluzeaud F, Pascual-Letallec L, Kahn A, Rafestin-Oblin ME, Rossier BC, Vandewalle A.Corticosteroid-dependent sodium transport in a novel immortalized mouse collecting duct principal cell line.J Am Soc Nephrol10: 923\u2013934, 1999.","DOI":"10.1681\/ASN.V105923"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1111\/j.1742-4658.2006.05304.x"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M207604200"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.11.7253"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/20.24.7052"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M403260200"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00079.2002"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00394.2004"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00050.2005"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M211649200"},{"key":"R17","doi-asserted-by":"crossref","unstructured":"Loffing J, Flores SY, Staub O.Sgk kinases and their role in epithelial transport.Annu Rev Physiol68: 16.11\u201316.30, 2006.","DOI":"10.1146\/annurev.physiol.68.040104.131654"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.4.F675"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.E02-03-0170"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00339.2007"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1159\/000110432"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1172\/JCI7869"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M407858200"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.C100623200"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1007\/s004240050674"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.94.9.4440"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.13.4.2031"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1172\/JCI29850"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M411053200"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.90239.2008","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,9,15]],"date-time":"2021-09-15T16:19:07Z","timestamp":1631722747000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.90239.2008"}},"issued":{"date-parts":[[2008,11]]},"references-count":29,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2008,11]]}},"alternative-id":["10.1152\/ajprenal.90239.2008"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.90239.2008","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2008,11]]}},{"indexed":{"date-parts":[[2025,10,6]],"date-time":"2025-10-06T18:46:19Z","timestamp":1759776379781},"reference-count":47,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2004,3]]},"abstract":"<jats:p>Cytosolic PLA<jats:sub>2<\/jats:sub>-\u03b1 (cPLA<jats:sub>2<\/jats:sub>) and metabolites of arachidonic acid (AA) are key mediators of complement-dependent glomerular epithelial cell (GEC) injury. Assembly of C5b-9 increases cytosolic Ca<jats:sup>2+<\/jats:sup>concentration and results in transactivation of receptor tyrosine kinases and activation of PLC-\u03b31 and the 1,2-diacylglycerol (DAG)-PKC pathway. Ca<jats:sup>2+<\/jats:sup>and PKC are essential for membrane association and increased catalytic activity of cPLA<jats:sub>2<\/jats:sub>. This study addresses the role of the actin cytoskeleton in cPLA<jats:sub>2<\/jats:sub>activation. Depolymerization of F-actin by cytochalasin D or latrunculin B reduced complement-dependent [<jats:sup>3<\/jats:sup>H]AA release, as well as the complement-induced increase in cPLA<jats:sub>2<\/jats:sub>activity. These effects were due to inhibition of [<jats:sup>3<\/jats:sup>H]DAG production and PKC activation, implying interference with PLC. Complement-dependent [<jats:sup>3<\/jats:sup>H]AA release was also reduced by jasplakinolide, a compound that stabilizes F-actin and organizes actin filaments at the cell periphery, and calyculin A, which induces condensation of actin filaments at the plasma membrane. The latter drugs did not affect [<jats:sup>3<\/jats:sup>H]DAG production, suggesting their inhibitory actions were downstream of PKC. Neither cytochalasin D, latrunculin B, nor calyculin A affected association of cPLA<jats:sub>2<\/jats:sub>with microsomal membranes, and cytochalasin D and latrunculin B did not alter the localization of the endoplasmic reticulum. Stable transfection of constitutively active RhoA induced formation of stress fibers, stabilized F-actin, and attenuated the complement-induced increase in [<jats:sup>3<\/jats:sup>H]AA. Thus in GEC, cPLA<jats:sub>2<\/jats:sub>activation is dependent, in part, on actin remodeling. By regulating complement-mediated activation of cPLA<jats:sub>2<\/jats:sub>, the actin cytoskeleton may contribute to the pathophysiology of GEC injury.<\/jats:p>","DOI":"10.1152\/ajprenal.00260.2003","type":"journal-article","created":{"date-parts":[[2004,2,3]],"date-time":"2004-02-03T20:35:42Z","timestamp":1075840542000},"page":"F466-F476","source":"Crossref","is-referenced-by-count":20,"title":["The actin cytoskeleton facilitates complement-mediated activation of cytosolic phospholipase A<sub>2<\/sub>"],"prefix":"10.1152","volume":"286","author":[{"given":"Andrey V.","family":"Cybulsky","sequence":"first","affiliation":[{"name":"Department of Medicine, McGill University Health Centre, McGill University, Montreal, Quebec, Canada H3A 1A1"}]},{"given":"Tomoko","family":"Takano","sequence":"additional","affiliation":[{"name":"Department of Medicine, McGill University Health Centre, McGill University, Montreal, Quebec, Canada H3A 1A1"}]},{"given":"Joan","family":"Papillon","sequence":"additional","affiliation":[{"name":"Department of Medicine, McGill University Health Centre, McGill University, Montreal, Quebec, Canada H3A 1A1"}]},{"given":"Abdelkrim","family":"Khadir","sequence":"additional","affiliation":[{"name":"Department of Medicine, McGill University Health Centre, McGill University, Montreal, Quebec, Canada H3A 1A1"}]},{"given":"Krikor","family":"Bijian","sequence":"additional","affiliation":[{"name":"Department of Medicine, McGill University Health Centre, McGill University, Montreal, Quebec, Canada H3A 1A1"}]},{"given":"Ludmilla","family":"Le Berre","sequence":"additional","affiliation":[{"name":"Department of Medicine, McGill University Health Centre, McGill University, Montreal, Quebec, Canada H3A 1A1"}]}],"member":"24","reference":[{"key":"REF1","doi-asserted-by":"publisher","DOI":"10.1126\/science.287.5458.1604"},{"key":"REF2","doi-asserted-by":"publisher","DOI":"10.1042\/bj3480241"},{"key":"REF3","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.105.4.1473"},{"key":"REF4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.265.4.F551"},{"key":"REF5","unstructured":"Cybulsky AV, Foster MH, Quigg RJ, and Salant DJ.Immunologic mechanisms of glomerular disease. In:TheKidney: Physiology and Pathophysiology(3rd ed.), edited by Seldin DW and Giebisch G. Philadelphia, PA: Lippincott-Raven, 2000, p. 2645-2697."},{"key":"REF6","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00013.x"},{"key":"REF7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.257.5.F826"},{"key":"REF8","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M204694200"},{"key":"REF9","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)65485-5"},{"key":"REF10","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00932.x"},{"key":"REF11","doi-asserted-by":"publisher","DOI":"10.1016\/S1388-1981(00)00108-6"},{"key":"REF12","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.17.9991"},{"key":"REF13","doi-asserted-by":"publisher","DOI":"10.1016\/S1388-1981(00)00115-3"},{"key":"REF14","unstructured":"Huwiler A, Schulze-Lohoff E, Fabbro D, and Pfeilschifter J.Immunocharacterization of protein kinase C isoenzymes in rat kidney glomeruli and cultured glomerular epithelial and mesangial cells.Exp Nephrol1: 19-25, 1993."},{"key":"REF15","doi-asserted-by":"publisher","DOI":"10.1016\/1074-5521(95)90276-7"},{"key":"REF16","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M108297200"},{"key":"REF17","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200203048"},{"key":"REF18","doi-asserted-by":"publisher","DOI":"10.1042\/bj3530079"},{"key":"REF19","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.2000.279.6.C2019"},{"key":"REF20","doi-asserted-by":"crossref","unstructured":"Morgan BP.Effects of the membrane attack complex of complement on nucleated cells.Curr Topics Microbiol Immunol178: 115-140, 1992.","DOI":"10.1007\/978-3-642-77014-2_8"},{"key":"REF21","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.275.2.1161"},{"key":"REF22","doi-asserted-by":"publisher","DOI":"10.1007\/BF02918256"},{"key":"REF23","doi-asserted-by":"crossref","unstructured":"Panesar M, Papillon J, McTavish AJ, and Cybulsky AV.Activation of phospholipase A2by complement C5b-9 in glomerular epithelial cells.J Immunol159: 3584-3594, 1997.","DOI":"10.4049\/jimmunol.159.7.3584"},{"key":"REF24","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00020.2002"},{"key":"REF25","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.169.5.2594"},{"key":"REF26","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)81560-3"},{"key":"REF27","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(92)90163-7"},{"key":"REF28","doi-asserted-by":"publisher","DOI":"10.1096\/fasebj.13.13.1658"},{"key":"REF29","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.275.11.7527"},{"key":"REF30","doi-asserted-by":"publisher","DOI":"10.1002\/1097-0169(200102)48:2<96::AID-CM1001>3.0.CO;2-B"},{"key":"REF31","doi-asserted-by":"publisher","DOI":"10.1034\/j.1600-065X.2001.1800104.x"},{"key":"atypb1","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00560.x"},{"key":"REF33","unstructured":"Shin ML, Rus HG, and Niculescu FI.Membrane attack by complement: assembly and biology of terminal complement complexes. In:Biomembranes, edited by Lee AG. Greenwich, CT: JAI, 1996, p. 119-146."},{"key":"REF34","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)81011-9"},{"key":"REF35","doi-asserted-by":"publisher","DOI":"10.1002\/cm.970130302"},{"key":"REF36","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)65080-8"},{"key":"REF37","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.102.043604"},{"key":"REF38","unstructured":"Tischer CGand Couser WG.Milestones in nephrology. [Heymann W, Hackel DB, Harwood S, Wilson SGF, and Hunter JL. Production of nephrotic syndrome in rats by Freund's adjuvants and rat kidney suspensions.Proc Soc Exp Biol Med180: 660-664, 1951.]J Am Soc Nephrol10: 183-188, 2000."},{"key":"REF39","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00407.x"},{"key":"REF40","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.43.28322"},{"key":"REF41","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.49.34507"},{"key":"REF42","doi-asserted-by":"publisher","DOI":"10.1038\/ncb810"},{"key":"REF43","doi-asserted-by":"publisher","DOI":"10.1042\/bj3630117"},{"key":"REF44","doi-asserted-by":"publisher","DOI":"10.1042\/bj3630657"},{"key":"REF45","doi-asserted-by":"publisher","DOI":"10.1165\/ajrcmb.24.3.3995"},{"key":"REF46","doi-asserted-by":"crossref","unstructured":"Yang LJ, Rhee SG, and Williamson JR.Epidermal growth factor-induced activation and translocation of phospholipase C-\u03b31to the cytoskeleton in rat hepatocytes.J Biol Chem269: 7156-7162, 1994.","DOI":"10.1016\/S0021-9258(17)37261-7"},{"key":"REF47","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.2001.281.3.C932"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00260.2003","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,4,27]],"date-time":"2023-04-27T20:49:40Z","timestamp":1682628580000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00260.2003"}},"issued":{"date-parts":[[2004,3]]},"references-count":47,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2004,3]]}},"alternative-id":["10.1152\/ajprenal.00260.2003"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00260.2003","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2004,3]]}},{"indexed":{"date-parts":[[2025,10,18]],"date-time":"2025-10-18T10:00:25Z","timestamp":1760781625903},"reference-count":48,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2010,7]]},"abstract":"<jats:p> Recently, we demonstrated a chronic neurosteroid-dependent inhibition of activity-dependent spinal reflex potentiation (SRP), but it remains unclear whether neurosteroids acutely modulate SRP induction. This study shows progesterone as well as two of its 3\u03b1,5\u03b1-derivatives, allopregnalonone and 3\u03b1,5\u03b1-tetrahydrodeoxycorticosterone (THDOC), to be capable of producing acute GABA<jats:sub>A<\/jats:sub> receptor (GABA<jats:sub>A<\/jats:sub>R)-dependent inhibition of SRP. When compared with test simulation (1 stimulation\/30 s) of pelvic afferent nerves that evoked a baseline reflex activity in an external urethra sphincter electromyogram, repetitive stimulation (RS; 1 stimulation\/1 s) induced SRP characterized by an increase in the evoked activity. Intrathecal progesterone (3\u201330 \u03bcM, 10 \u03bcl) at 10 min before stimulation onset dose dependently prevented RS induction. Intrathecal allopregnalonone (10 \u03bcM, 10 \u03bcl it) and THDOC (10 \u03bcM, 10 \u03bcl it) also prevented the SRP caused by RS. Pretreatment with the GABA<jats:sub>A<\/jats:sub>R antagonist bicuculline (10 \u03bcM, 10 \u03bcl it) at 1 min before progesterone\/neurosteroid injection attenuated the inhibition of SRP caused by progesterone, allopregnanolone, and THDOC. Results suggest that progesterone and its neurosteroid metabolites may be crucial to the development of pelvic visceral neuropathic\/postinflammatory pain and imply clinical use of neurosteroids, such as allopregnanolone and THDOC, for visceral pain treatment. <\/jats:p>","DOI":"10.1152\/ajprenal.00632.2009","type":"journal-article","created":{"date-parts":[[2010,4,1]],"date-time":"2010-04-01T02:12:19Z","timestamp":1270087939000},"page":"F43-F48","source":"Crossref","is-referenced-by-count":7,"title":["Acute neurosteroids inhibit the spinal reflex potentiation via GABAergic neurotransmission"],"prefix":"10.1152","volume":"299","author":[{"given":"Junn-Liang","family":"Chang","sequence":"first","affiliation":[{"name":"Department of Pathology and Laboratory Medicine Taoyuan Armed Forces General Hospital, Taoyuan;"},{"name":"Department of Biomedical Engineering and"}]},{"given":"Hsien-Yu","family":"Peng","sequence":"additional","affiliation":[{"name":"Department of Urology, China Medical University Hospital, Taichung;"},{"name":"Department of Physiology,"}]},{"given":"Hsi-Chin","family":"Wu","sequence":"additional","affiliation":[{"name":"Department of Urology, China Medical University Hospital, Taichung;"},{"name":"College of Medicine, China Medical University, Taichung; and"}]},{"given":"Hsiao-Ting","family":"Lu","sequence":"additional","affiliation":[{"name":"Department of Biomedical Engineering and"},{"name":"College of Medicine, China Medical University, Taichung; and"}]},{"given":"Shwu-Fen","family":"Pan","sequence":"additional","affiliation":[{"name":"Department of Biotechnology, Ming-Chuan University, Taoyuan;"}]},{"given":"Mei-Jung","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Biomedical Engineering and"}]},{"given":"Tzer-Bin","family":"Lin","sequence":"additional","affiliation":[{"name":"Department of Urology, China Medical University Hospital, Taichung;"},{"name":"Department of Physiology,"},{"name":"Graduate Institute of Biomedical Electronics and Bioinformatics, National Taiwan University, Taipei, Taiwan"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/0960-0760(90)90490-C"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1210\/en.2004-1142"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00135.2007"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00600.2007"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuroscience.2005.10.059"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00256.2006"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90254.2008"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.22.13284"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/j.neulet.2003.12.009"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/j.pbb.2006.06.016"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1037\/0735-7044.118.6.1352"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/j.psyneuen.2004.11.001"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1037\/0735-7044.118.2.306"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/j.brainres.2004.01.020"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1111\/j.1460-9568.2007.05645.x"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/j.pain.2007.10.014"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1002\/cne.20540"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1046\/j.1460-9568.2003.02479.x"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-8993(02)03704-6"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/jn.1999.82.1.143"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.1981-07.2007"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1096\/fj.07-8930com"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1038\/nature06493"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.R300024200"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1016\/S0028-3908(02)00371-4"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.4945-06.2007"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1007\/s00018-007-7403-5"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1016\/j.jsbmb.2008.03.002"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/j.nbd.2007.12.001"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1124\/mol.64.4.857"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.90243.2008"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00126.2008"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuropharm.2007.11.017"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.90289.2008"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00287.2009"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1016\/j.pain.2008.12.023"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.00129.2009"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1016\/j.pain.2008.11.017"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.3841-05.2005"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1152\/jn.00606.2007"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1016\/S0165-0173(01)00123-0"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.4928-07.2008"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuropharm.2005.04.026"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1016\/j.pharmthera.2007.03.008"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1016\/j.euroneuro.2005.09.005"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.00049.2002"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1016\/S0166-4328(03)00067-6"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.5599-07.2008"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00632.2009","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T00:04:28Z","timestamp":1567987468000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00632.2009"}},"issued":{"date-parts":[[2010,7]]},"references-count":48,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2010,7]]}},"alternative-id":["10.1152\/ajprenal.00632.2009"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00632.2009","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2010,7]]}},{"indexed":{"date-parts":[[2025,10,18]],"date-time":"2025-10-18T20:45:15Z","timestamp":1760820315559},"reference-count":30,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2011,7]]},"abstract":"<jats:p>In viral infections, disease manifestations and tissue damage often result primarily from immune cells infiltrating target organs on the basis of an ineffectual viral clearance with persistent antigenemia or an inappropriate immune response. Cell types and mediators defining these inflammatory processes are still inadequately understood. In hepatitis C virus-associated glomerulonephritis, analysis of interferon-\u03b3-inducible protein (IP-10) as a chemokine centrally involved in early antiviral response and TNF-\u03b1 known to balance proinflammatory and immunosuppressive effects in inflammation shows a significant upregulation of both IP-10 and TNF-\u03b1 mediated specifically by the viral receptor Toll-like receptor 3 expressed on mesangial cells. IP-10 induction is further potentiated by TNF-\u03b1 signaling, preferentially via the TNF-\u03b1 receptor subtype 2 selectively increased upon stimulation of viral receptors in the proinflammatory milieu.<\/jats:p>","DOI":"10.1152\/ajprenal.00083.2011","type":"journal-article","created":{"date-parts":[[2011,3,31]],"date-time":"2011-03-31T00:54:44Z","timestamp":1301532884000},"page":"F57-F69","source":"Crossref","is-referenced-by-count":17,"title":["TLR3-dependent regulation of cytokines in human mesangial cells: a novel role for IP-10 and TNF-\u03b1 in hepatitis C-associated glomerulonephritis"],"prefix":"10.1152","volume":"301","author":[{"given":"Monika","family":"Merkle","sequence":"first","affiliation":[{"name":"Nephrology, Klinikum Traunstein, Traunstein; and"}]},{"given":"Andrea","family":"Ribeiro","sequence":"additional","affiliation":[{"name":"Medizinische Poliklinik der LMU, M\u00fcnchen, Germany"}]},{"given":"Markus","family":"W\u00f6rnle","sequence":"additional","affiliation":[{"name":"Medizinische Poliklinik der LMU, M\u00fcnchen, Germany"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1038\/35099560"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1096\/fj.05-3841com"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1111\/j.1572-0241.2008.02040.x"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1093\/rheumatology\/kep270"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.168.9.4301"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2009.142"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1089\/08828240260066215"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1016\/0022-1759(85)90036-5"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.02181205"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2009.08.019"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.78.3.1575-1581.2004"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1089\/1079990041689665"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1002\/eji.200424887"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1159\/000101411"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000343"},{"key":"B16","first-page":"14","volume":"10","author":"Missale G","year":"1995","journal-title":"Ann Ital Med Int"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1006\/cyto.2001.0997"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.21815"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-6143.2004.00525.x"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006101104"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)63152-5"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1111\/j.1752-8062.2008.00053.x"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1172\/JCI200523348"},{"key":"B24","first-page":"20","volume":"384","author":"Vitour D","year":"2007","journal-title":"Sci STKE"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007050556"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfn627"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2006.050491"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1186\/1471-2369-5-8"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/j.jviromet.2007.11.002"},{"key":"B30","doi-asserted-by":"crossref","first-page":"675","DOI":"10.1111\/j.1365-2893.2006.00838.x","volume":"14","author":"Zeremski M","year":"2007","journal-title":"J Viral Hepat"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00083.2011","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,4,5]],"date-time":"2024-04-05T15:49:27Z","timestamp":1712332167000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00083.2011"}},"issued":{"date-parts":[[2011,7]]},"references-count":30,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2011,7]]}},"alternative-id":["10.1152\/ajprenal.00083.2011"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00083.2011","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2011,7]]}},{"indexed":{"date-parts":[[2025,10,31]],"date-time":"2025-10-31T21:40:30Z","timestamp":1761946830107,"version":"3.37.3"},"reference-count":57,"publisher":"American Physiological Society","issue":"5","funder":[{"DOI":"10.13039\/501100003549","name":"OTKA","doi-asserted-by":"crossref","award":["H07-B-74286","K-112964","K-125174"],"award-info":[{"award-number":["H07-B-74286","K-112964","K-125174"]}],"id":[{"id":"10.13039\/501100003549","id-type":"DOI","asserted-by":"crossref"}]},{"name":"NVKP","award":["NVKP_16-1-2016-0042"],"award-info":[{"award-number":["NVKP_16-1-2016-0042"]}]},{"name":"Ministry of Human Capacities, Hungary","award":["EFOP-3.6.3-VEKOP-16-2017-00009"],"award-info":[{"award-number":["EFOP-3.6.3-VEKOP-16-2017-00009"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2019,11,1]]},"abstract":"<jats:p>Tachykinins (TKs) are involved in both the physiological regulation of urinary bladder functions and development of overactive bladder syndrome. The aim of the present study was to investigate the signal transduction pathways of TKs in the detrusor muscle to provide potential pharmacological targets for the treatment of bladder dysfunctions related to enhanced TK production. Contraction force, intracellular Ca<jats:sup>2+<\/jats:sup>concentration, and RhoA activity were measured in the mouse urinary bladder smooth muscle (UBSM). TKs and the NK2 receptor (NK2R)-specific agonist [\u03b2-Ala<jats:sup>8<\/jats:sup>]-NKA(4\u201310) evoked contraction, which was inhibited by the NKR2 antagonist MEN10376. In G\u03b1<jats:sub>q\/11<\/jats:sub>-deficient mice, [\u03b2-Ala<jats:sup>8<\/jats:sup>]-NKA(4\u201310)-induced contraction and the intracellular Ca<jats:sup>2+<\/jats:sup>concentration increase were abolished. Although G<jats:sub>q\/11<\/jats:sub>proteins are linked principally to phospholipase C\u03b2 and inositol trisphosphate-mediated Ca<jats:sup>2+<\/jats:sup>release from intracellular stores, we found that phospholipase C\u03b2 inhibition and sarcoplasmic reticulum Ca<jats:sup>2+<\/jats:sup>depletion failed to have any effect on contraction induced by [\u03b2-Ala<jats:sup>8<\/jats:sup>]-NKA(4\u201310). In contrast, lack of extracellular Ca<jats:sup>2+<\/jats:sup>or blockade of voltage-dependent Ca<jats:sup>2+<\/jats:sup>channels (VDCCs) suppressed contraction. Furthermore, [\u03b2-Ala<jats:sup>8<\/jats:sup>]-NKA(4\u201310) increased RhoA activity in the UBSM in a G<jats:sub>q\/11<\/jats:sub>-dependent manner and inhibition of Rho kinase with Y-27632 decreased contraction force, whereas the combination of Y-27632 with either VDCC blockade or depletion of extracellular Ca<jats:sup>2+<\/jats:sup>resulted in complete inhibition of [\u03b2-Ala<jats:sup>8<\/jats:sup>]-NKA(4\u201310)-induced contractions. In summary, our results indicate that NK2Rs are linked exclusively to G<jats:sub>q\/11<\/jats:sub>proteins in the UBSM and that the intracellular signaling involves the simultaneous activation of VDCC and the RhoA-Rho kinase pathway. These findings may help to identify potential therapeutic targets of bladder dysfunctions related to upregulation of TKs.<\/jats:p>","DOI":"10.1152\/ajprenal.00106.2019","type":"journal-article","created":{"date-parts":[[2019,8,28]],"date-time":"2019-08-28T16:50:59Z","timestamp":1567011059000},"page":"F1154-F1163","source":"Crossref","is-referenced-by-count":6,"title":["NK2 receptor-mediated detrusor muscle contraction involves G<sub>q\/11<\/sub>-dependent activation of voltage-dependent Ca<sup>2+<\/sup>channels and the RhoA-Rho kinase pathway"],"prefix":"10.1152","volume":"317","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0604-8411","authenticated-orcid":false,"given":"B\u00e1lint","family":"D\u00e9r","sequence":"first","affiliation":[{"name":"Institute of Translational Medicine, Semmelweis University, Budapest, Hungary"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2508-2343","authenticated-orcid":false,"given":"P\u00e9ter J\u00f3zsef","family":"Moln\u00e1r","sequence":"additional","affiliation":[{"name":"Institute of Translational Medicine, Semmelweis University, Budapest, Hungary"},{"name":"Department of Urology, Semmelweis University, Budapest, Hungary"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7779-226X","authenticated-orcid":false,"given":"\u00c9va","family":"Ruisanchez","sequence":"additional","affiliation":[{"name":"Institute of Translational Medicine, Semmelweis University, Budapest, Hungary"}]},{"given":"Petra","family":"\u0150rsy","sequence":"additional","affiliation":[{"name":"Institute of Translational Medicine, Semmelweis University, Budapest, Hungary"}]},{"given":"Margit","family":"Ker\u00e9k","sequence":"additional","affiliation":[{"name":"Institute of Translational Medicine, Semmelweis University, Budapest, Hungary"}]},{"given":"Bernadett","family":"Farag\u00f3","sequence":"additional","affiliation":[{"name":"Institute of Translational Medicine, Semmelweis University, Budapest, Hungary"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7037-4919","authenticated-orcid":false,"given":"P\u00e9ter","family":"Nyir\u00e1dy","sequence":"additional","affiliation":[{"name":"Department of Urology, Semmelweis University, Budapest, Hungary"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8676-6805","authenticated-orcid":false,"given":"Stefan","family":"Offermanns","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6015-0359","authenticated-orcid":false,"given":"Zolt\u00e1n","family":"Beny\u00f3","sequence":"additional","affiliation":[{"name":"Institute of Translational Medicine, Semmelweis University, Budapest, Hungary"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1007\/BF00182729"},{"key":"B2","first-page":"1","volume":"85","author":"Abrams P","year":"2000","journal-title":"BJU Int"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1111\/bph.13878"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.3390\/medsci7050067"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1515\/jbcpp-2017-0071"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1007\/978-3-642-16499-6_19"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00378.2002"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1007\/978-3-642-16499-6_18"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(05)68047-0"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/S0165-1838(97)00032-5"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1007\/PL00005270"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1046\/j.1474-8673.2002.00258.x"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1002\/nau.20475"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/j.freeradbiomed.2010.09.027"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.pa.36.040196.002405"},{"key":"B16","first-page":"899","volume":"39","author":"Faustini S","year":"1989","journal-title":"Arzneimittelforschung"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1111\/bph.12502"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.107.125393"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejphar.2009.03.036"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00106.2018"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1007\/s002100000228"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.7554\/eLife.38689"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1161\/ATVBAHA.117.310038"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1096\/fj.09-149856"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/27.22.4324"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.1994.tb16181.x"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(01)67290-2"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1016\/0143-4179(94)90016-7"},{"key":"B29","first-page":"1327","volume":"264","author":"Lecci A","year":"1993","journal-title":"J Pharmacol Exp Ther"},{"key":"B30","first-page":"77","volume":"151","author":"Maggi CA","year":"1990","journal-title":"Ciba Found Symp"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1016\/0306-3623(94)00292-U"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1016\/0301-0082(94)E0017-B"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1016\/0306-4522(88)90140-6"},{"key":"B34","first-page":"1172","volume":"257","author":"Maggi CA","year":"1991","journal-title":"J Pharmacol Exp Ther"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.1991.tb09823.x"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1111\/j.2042-7158.1987.tb03447.x"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1016\/0014-2999(88)90438-4"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejphar.2017.12.017"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1046\/j.1464-410x.2001.02228.x"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1016\/j.tcm.2012.07.007"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/17.15.4304"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1159\/000283067"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M104363200"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1016\/j.lfs.2003.09.039"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1016\/j.tips.2006.07.002"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1111\/j.1464-410X.2004.05017.x"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1038\/bjp.2008.29"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.1989.tb12615.x"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1038\/5007"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00031.2013"},{"key":"B51","doi-asserted-by":"crossref","first-page":"327","DOI":"10.1007\/s00345-002-0301-4","volume":"20","author":"Stewart WF","year":"2003","journal-title":"World J Urol"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.108.139295"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1007\/s002109900204"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1096\/fj.04-1516fje"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0705109"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1038\/nm1666"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(01)67505-0"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00106.2019","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,1,17]],"date-time":"2021-01-17T15:58:54Z","timestamp":1610899134000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00106.2019"}},"issued":{"date-parts":[[2019,11,1]]},"references-count":57,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2019,11,1]]}},"alternative-id":["10.1152\/ajprenal.00106.2019"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00106.2019","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2019,11,1]]}},{"indexed":{"date-parts":[[2025,10,31]],"date-time":"2025-10-31T18:46:04Z","timestamp":1761936364913,"version":"build-2065373602"},"reference-count":37,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2005,4]]},"abstract":"<jats:p> Transient exposure to ANG II results in the development of salt-sensitive hypertension in rats. This study was performed to determine whether a transient hypertensive episode can induce salt-sensitive hypertension in transgenic rats with inducible expression of the mouse Ren2 renin gene [strain name TGR(Cyp1a1-Ren2)]. Systolic blood pressures were measured in conscious male Cyp1a1-Ren2 rats ( n = 6) during control conditions and during dietary administration of indole-3-carbinol (I3C; 0.15%, wt\/wt), for 14 days. Systolic pressure increased from 135 \u00b1 5 to 233 \u00b1 7 mmHg by day 14. I3C administration was terminated and blood pressure returned to normal levels (137 \u00b1 5 mmHg) within 10 days. Subsequently, the rats were placed on a high-salt diet (8% NaCl) for 10 days. Systolic pressure increased by 34 \u00b1 2 mmHg throughout 10 days of the high-salt diet. Neither glomerular filtration rate nor renal plasma flow was altered in Cyp1a1-Ren2 rats with salt-sensitive hypertension. In a separate group of male Cyp1a1-Ren2 rats ( n = 6) transiently induced with 0.15% I3C for 14 days, administration of the superoxide dismutase mimetic tempol (4-hydroxy-2,2,6,6-tetramethyl piperidinoxyl, 2 mM) attenuated the increase in systolic pressure induced by high salt. Systolic pressure increased by only 11 \u00b1 1 mmHg throughout 8 days of a high-salt diet and tempol administration. Thus transient induction of ANG II-dependent hypertension via activation of the Cyp1a1-Ren2 transgene induces salt-sensitive hypertension in these transgenic rats. The attenuation by tempol of the high salt-induced blood pressure elevation indicates that ANG II-induced production of superoxide anion contributes to the development of salt-sensitive hypertension after transient induction of ANG II-dependent hypertension. <\/jats:p>","DOI":"10.1152\/ajprenal.00148.2004","type":"journal-article","created":{"date-parts":[[2004,12,8]],"date-time":"2004-12-08T03:33:34Z","timestamp":1102476814000},"page":"F810-F815","source":"Crossref","is-referenced-by-count":22,"title":["Salt-sensitive hypertension develops after transient induction of ANG II-dependent hypertension in Cyp1a1-Ren2 transgenic rats"],"prefix":"10.1152","volume":"288","author":[{"given":"Laura L.","family":"Howard","sequence":"first","affiliation":[]},{"given":"Matthew E.","family":"Patterson","sequence":"additional","affiliation":[]},{"given":"John J.","family":"Mullins","sequence":"additional","affiliation":[]},{"given":"Kenneth D.","family":"Mitchell","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"doi-asserted-by":"publisher","key":"R1","DOI":"10.1097\/00004872-200204000-00031"},{"doi-asserted-by":"publisher","key":"R2","DOI":"10.1016\/S0895-7061(97)00088-5"},{"doi-asserted-by":"publisher","key":"R3","DOI":"10.1111\/j.1524-6175.2002.00503.x"},{"unstructured":"Campbell SJ, Carlotti F, Hall PA, Clark AJ, and Wolf CR. Regulation of the CYP1A1 promoter in transgenic mice: an exquisitely sensitive on-off system for cell specific gene regulation. J Cell Sci. 109: 2619\u20132625, 1996.","key":"R4"},{"doi-asserted-by":"publisher","key":"R5","DOI":"10.1097\/00004872-200018090-00015"},{"doi-asserted-by":"publisher","key":"R6","DOI":"10.1152\/ajpregu.00476.2002"},{"doi-asserted-by":"publisher","key":"R7","DOI":"10.1042\/bj2810359"},{"doi-asserted-by":"publisher","key":"R8","DOI":"10.1152\/physrev.1980.60.4.1107"},{"doi-asserted-by":"publisher","key":"R9","DOI":"10.1161\/01.HYP.0000047881.15426.DC"},{"doi-asserted-by":"publisher","key":"R10","DOI":"10.1161\/01.HYP.0000052944.54349.7B"},{"doi-asserted-by":"publisher","key":"R11","DOI":"10.1016\/0006-2952(93)90258-X"},{"doi-asserted-by":"publisher","key":"R12","DOI":"10.1074\/jbc.M103296200"},{"doi-asserted-by":"publisher","key":"R13","DOI":"10.1097\/00004872-199816030-00006"},{"doi-asserted-by":"publisher","key":"R14","DOI":"10.1161\/01.HYP.33.4.1013"},{"unstructured":"Loub WD, Wattenberg LW, and Davis DW. Aryl hydrocarbon hydroxylase induction in rat tissues by naturally occurring indoles of cruciferous plants. J Natl Cancer Inst 54: 985\u2013988, 1975.","key":"R15"},{"doi-asserted-by":"publisher","key":"R16","DOI":"10.1161\/01.HYP.0000070028.99408.E8"},{"doi-asserted-by":"publisher","key":"R17","DOI":"10.1152\/ajpregu.00346.2001"},{"doi-asserted-by":"publisher","key":"R18","DOI":"10.1016\/0003-9861(91)90442-L"},{"doi-asserted-by":"publisher","key":"R19","DOI":"10.1021\/bi00463a024"},{"doi-asserted-by":"publisher","key":"R20","DOI":"10.1152\/ajprenal.1995.268.5.F821"},{"unstructured":"Pelkonen O and Nebert DW. Metabolism of polycyclic aromatic hydrocarbons: etiologic role in carcinogenesis. Pharmacol Rev 34: 189\u2013222, 1982.","key":"R21"},{"doi-asserted-by":"publisher","key":"R22","DOI":"10.1172\/JCI118623"},{"doi-asserted-by":"publisher","key":"R23","DOI":"10.1046\/j.1523-1755.2001.00737.x"},{"doi-asserted-by":"publisher","key":"R24","DOI":"10.1021\/bi00216a033"},{"doi-asserted-by":"publisher","key":"R25","DOI":"10.3109\/10715769009145682"},{"doi-asserted-by":"publisher","key":"R26","DOI":"10.1007\/978-1-4684-5730-8_12"},{"doi-asserted-by":"publisher","key":"R27","DOI":"10.3109\/10715769109145785"},{"doi-asserted-by":"publisher","key":"R28","DOI":"10.1172\/JCI115163"},{"doi-asserted-by":"publisher","key":"R29","DOI":"10.1161\/01.HYP.32.1.59"},{"doi-asserted-by":"publisher","key":"R30","DOI":"10.1161\/01.HYP.33.1.424"},{"doi-asserted-by":"publisher","key":"R31","DOI":"10.1073\/pnas.92.25.11926"},{"doi-asserted-by":"publisher","key":"R32","DOI":"10.1161\/01.HYP.30.6.1628"},{"doi-asserted-by":"publisher","key":"R33","DOI":"10.1159\/000066791"},{"unstructured":"Ward RJ, Abiaka C, and Peters TJ. Inflammation and tissue injury: the world of free radicals. J Nephrol 7: 89\u201395, 1994.","key":"R34"},{"doi-asserted-by":"publisher","key":"R35","DOI":"10.1046\/j.1365-201x.2000.00668.x"},{"doi-asserted-by":"publisher","key":"R36","DOI":"10.1161\/01.HYP.0000112304.26158.5c"},{"doi-asserted-by":"publisher","key":"R37","DOI":"10.1161\/01.HYP.0000047877.36743.FA"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00148.2004","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T21:48:56Z","timestamp":1567979336000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00148.2004"}},"issued":{"date-parts":[[2005,4]]},"references-count":37,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2005,4]]}},"alternative-id":["10.1152\/ajprenal.00148.2004"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00148.2004","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2005,4]]}},{"indexed":{"date-parts":[[2025,10,31]],"date-time":"2025-10-31T21:40:21Z","timestamp":1761946821046,"version":"3.37.3"},"reference-count":31,"publisher":"American Physiological Society","issue":"6","funder":[{"DOI":"10.13039\/501100003042","name":"Else-Kr\u00f6ner Fresenius Stiftung","doi-asserted-by":"crossref","award":["2012_A246"],"award-info":[{"award-number":["2012_A246"]}],"id":[{"id":"10.13039\/501100003042","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2018,12,1]]},"abstract":"<jats:p> TMEM16A is a transmembrane protein from a conserved family of calcium-activated proteins that is highly expressed in the kidney. TMEM16A confers calcium-activated chloride channel activity, which is of importance for various cellular functions in secretory epithelia and involved in secretion-dependent renal cyst growth. However, its specific function in renal physiology has remained elusive so far. Therefore, we generated conditional nephron-specific TMEM16A-knockout mice and found that these animals suffered from albuminuria. Kidney histology demonstrated an intact corticomedullary differentiation and absence of cysts. Electron microscopy showed a normal slit diaphragm. However, the total number of glomeruli and total nephron count was decreased in TMEM16A-knockout animals. At the same time, glomerular diameter was increased, presumably as a result of the hyperfiltration in the remaining glomeruli. TUNEL and PCNA stainings showed increased cell death and increased proliferation. Proximal tubular cilia were intact in young animals, but the number of properly ciliated cells was decreased in older, albuminuric animals. Taken together, our data suggest that TMEM16A may be involved in ureteric bud branching and proper nephron endowment. Loss of TMEM16A resulted in reduced nephron number and, subsequently, albuminuria and tubular damage. <\/jats:p>","DOI":"10.1152\/ajprenal.00638.2017","type":"journal-article","created":{"date-parts":[[2018,8,29]],"date-time":"2018-08-29T08:12:00Z","timestamp":1535530320000},"page":"F1777-F1786","source":"Crossref","is-referenced-by-count":17,"title":["Nephron-specific knockout of TMEM16A leads to reduced number of glomeruli and albuminuria"],"prefix":"10.1152","volume":"315","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4677-5181","authenticated-orcid":false,"given":"Laura K.","family":"Schenk","sequence":"first","affiliation":[{"name":"Internal Medicine D University Hospital of Muenster, Muenster Germany"}]},{"given":"Bjoern","family":"Buchholz","sequence":"additional","affiliation":[{"name":"Department of Nephrology and Hypertension, Friedrich-Alexander University of Erlangen-N\u00fcrnberg, Erlangen, Germany"}]},{"given":"Sebastian F.","family":"Henke","sequence":"additional","affiliation":[{"name":"Internal Medicine D University Hospital of Muenster, Muenster Germany"}]},{"given":"Ulf","family":"Michgehl","sequence":"additional","affiliation":[{"name":"Internal Medicine D University Hospital of Muenster, Muenster Germany"}]},{"given":"Christoph","family":"Daniel","sequence":"additional","affiliation":[{"name":"Institute for Nephropathology, Friedrich-Alexander University of Erlangen-N\u00fcrnberg, Erlangen, Germany"}]},{"given":"Kerstin","family":"Amann","sequence":"additional","affiliation":[{"name":"Institute for Nephropathology, Friedrich-Alexander University of Erlangen-N\u00fcrnberg, Erlangen, Germany"}]},{"given":"Karl","family":"Kunzelmann","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Regensburg, Regensburg Germany"}]},{"given":"Hermann","family":"Pavenst\u00e4dt","sequence":"additional","affiliation":[{"name":"Internal Medicine D University Hospital of Muenster, Muenster Germany"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00490.2009"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1217072110"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2013.418"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0000000000000211"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013030209"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.2147\/OTT.S95985"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0066629"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2013.535"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2011040396"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1242\/dev.063594"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.201611686"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1186\/1471-2369-13-11"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00029.2001"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/j.stem.2008.05.020"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-015-1767-4"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007101078"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1016\/j.ydbio.2008.06.009"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1002\/dvdy.21676"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.e13-10-0599"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.7554\/eLife.05875"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1159\/000323998"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2015.214"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1159\/000355716"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1016\/j.trsl.2011.10.004"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.00074.2015"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1312014110"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1126\/science.1260419"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1002\/jobm.19810210824"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1102147108"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1038\/nature07313"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.115.05280"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00638.2017","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T11:31:10Z","timestamp":1567942270000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00638.2017"}},"issued":{"date-parts":[[2018,12,1]]},"references-count":31,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2018,12,1]]}},"alternative-id":["10.1152\/ajprenal.00638.2017"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00638.2017","ISSN":["1931-857X","1522-1466"],"issn-type":[{"type":"print","value":"1931-857X"},{"type":"electronic","value":"1522-1466"}],"published":{"date-parts":[[2018,12,1]]}},{"indexed":{"date-parts":[[2025,10,27]],"date-time":"2025-10-27T10:32:55Z","timestamp":1761561175903},"reference-count":38,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2007,9]]},"abstract":"<jats:p>In rodent models of obstructive nephropathy, exogenous epidermal growth factor (EGF) attenuates tubule cell death in rats and exacerbates cell death in mice. To identify species differences in EGF receptor (EGFR) regulation and signaling, cell lysates were prepared from rat, mouse, and human proximal tubule cells (PTC) and compared by immunoblot analysis for expression and phosphorylation of Src and EGFR. Frozen kidney tissue was also analyzed. Results indicate mouse PTC have constitutive Src- and EGFR-kinase activities not detected in rat or human PTC. Immunoblots of rat, mouse, and human kidney homogenates confirmed this finding in vivo. Src-specific inhibitor PP2 and EGFR kinase inhibitor AG1478 decreased EGF-induced apoptosis in mouse PTC by 74% ( P &lt; 0.001) and 70% ( P &lt; 0.001), respectively. Expression of a constitutive Src mutant cDNA in rat PTC rendered cells susceptible to EGF-induced death. EGF decreased stretch-induced apoptosis by 66% ( P &lt; 0.001) relative to vehicle control in human PTC, similar to rat PTC response. We conclude that elevated Src activity in mouse tubular cells alters downstream EGFR signaling and increases susceptibility to EGF-induced cell death. The unexpected finding that a therapeutic agent (EGF) in rats is detrimental in mice underscores the importance of determining which animal best represents the response of human kidneys to a given agent.<\/jats:p>","DOI":"10.1152\/ajprenal.00227.2007","type":"journal-article","created":{"date-parts":[[2007,7,12]],"date-time":"2007-07-12T01:04:21Z","timestamp":1184202261000},"page":"F895-F903","source":"Crossref","is-referenced-by-count":7,"title":["Species differences in renal Src activity direct EGF receptor regulation in life or death response to EGF"],"prefix":"10.1152","volume":"293","author":[{"given":"Susan C.","family":"Kiley","sequence":"first","affiliation":[]},{"given":"Robert L.","family":"Chevalier","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1158\/0008-5472.CAN-05-3757"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1593\/neo.06172"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0437945100"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1126\/science.1125951"},{"key":"R5","unstructured":"Bellmunt J, Montagut C, Abiol S, Carles J, Maroto P, Orsola A.Present strategies in the treatment of metastatic renal cell carcinoma: an update on molecular targeting agents.BJU Int99: 274\u2013280, 2006."},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.12.8335"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.24.16.7059-7071.2004"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1002\/mc.20138"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1016\/0003-2697(76)90527-3"},{"key":"R10","doi-asserted-by":"crossref","unstructured":"Cachat F, Lange-Sperandio B, Chang AY, Kiley SC, Thornhill BA, Forbes MS, Chevalier RL.Ureteral obstruction in neonatal mice elicits segment-specific tubular cell responses leading to nephron loss.Kidney Int63: 564\u2013575, 2002.","DOI":"10.1046\/j.1523-1755.2003.00775.x"},{"key":"R11","doi-asserted-by":"crossref","unstructured":"Cartier N, Lacave R, Vallet V, Hagege R, Hellio J, Robine S, Pringault E, Cluzeaud F, Briand P, Kahn A, Vandewalle A.Establishment of proximal tubule cell lines by targeted oncogenesis in transgenic mice using thel-pyruvate kinase-SV40 (T) antigen hybrid gene.J Cell Sci104: 695\u2013704, 1993.","DOI":"10.1242\/jcs.104.3.695"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00966.x"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1202700"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.7.4079"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1126\/science.1099314"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1200\/JCO.2003.04.190"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1016\/S0090-4295(97)00101-5"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00706.x"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00428.x"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M207289200"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(87)90756-2"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1038\/227680a0"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.19.10.6845"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1158\/1078-0432.CCR-06-0646"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1201642"},{"key":"R26","doi-asserted-by":"crossref","unstructured":"Ram TG, Hosick HL, Ethier SP.Heregulin-\u03b2 is especially potent in activating phosphatidylinositol 3-kinase in nontransformed human mammary epithelial cells.J Cell Physiol18: 301\u2013313, 2000.","DOI":"10.1002\/(SICI)1097-4652(200006)183:3<301::AID-JCP2>3.0.CO;2-W"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1172\/JCI2071"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.44.27456"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00829.x"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.268.3.F435"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1172\/JCI8315"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.4.1415"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M311655200"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00256.x"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00952.x"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1016\/j.cellsig.2005.12.007"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1016\/S0969-2126(99)80086-0"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1124\/jpet.106.107367"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00227.2007","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,8,19]],"date-time":"2021-08-19T01:56:45Z","timestamp":1629338205000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00227.2007"}},"issued":{"date-parts":[[2007,9]]},"references-count":38,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2007,9]]}},"alternative-id":["10.1152\/ajprenal.00227.2007"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00227.2007","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2007,9]]}},{"indexed":{"date-parts":[[2025,10,27]],"date-time":"2025-10-27T10:42:54Z","timestamp":1761561774933},"reference-count":32,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,9,1]]},"abstract":"<jats:p> Increasing evidence nowadays is showing that obesity by itself, independent of other comorbidities like diabetes and hypertension, is associated with renal functional changes and structural damage. Intentional weight loss demonstrates beneficial reduction in proteinuria and albuminuria in patients with mild to moderate chronic kidney disease, particularly those whose renal damage is likely induced by obesity. The safety of some weight loss interventions, particularly the use of high-protein diets and\/or medications, is questionable in this population due to the lack of well-designed randomized controlled studies reporting on their efficacy or harm. Bariatric surgery showed the most promising results with regards to ameliorating glomerular hyperfiltration and albuminuria albeit with a modest risk of increased perioperative complications with advanced stages of chronic kidney disease (CKD). <\/jats:p>","DOI":"10.1152\/ajprenal.00173.2013","type":"journal-article","created":{"date-parts":[[2013,7,4]],"date-time":"2013-07-04T08:28:15Z","timestamp":1372926495000},"page":"F613-F617","source":"Crossref","is-referenced-by-count":20,"title":["Effects of weight reduction regimens and bariatric surgery on chronic kidney disease in obese patients"],"prefix":"10.1152","volume":"305","author":[{"given":"Rana M.","family":"Abou-Mrad","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, American University of Beirut, Beirut, Lebanon"}]},{"given":"Ali K.","family":"Abu-Alfa","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, American University of Beirut, Beirut, Lebanon"}]},{"given":"Fuad N.","family":"Ziyadeh","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, American University of Beirut, Beirut, Lebanon"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfp640"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfq347"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/j.soard.2008.08.016"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2012.12.003"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/j.jada.2009.12.016"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfm511"},{"key":"B7","first-page":"397","volume":"31","author":"Eknoyan G","year":"2011","journal-title":"Nefrolog\u00eda"},{"key":"B8","author":"Fenske WK","year":"2012","journal-title":"Surg Obesity Relat Diseases"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.11741111"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1177\/019262339302100602"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0b013e3283374c09"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-138-6-200303180-00009"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2008.10.003"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1007\/s10157-008-0034-9"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2012.12.005"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.02250409"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1038\/ijo.2012.7"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/j.soard.2009.01.006"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006080917"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/j.semnephrol.2012.12.002"},{"key":"B21a","doi-asserted-by":"publisher","DOI":"10.1053\/j.jrn.2006.04.017"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/j.urology.2010.01.037"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002796"},{"key":"B24","first-page":"1645","volume":"118","author":"Sharma K","year":"2008","journal-title":"J Clin Invest"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1093\/jn\/131.3.913S"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1097\/HJH.0b013e3283418875"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1111\/j.1755-6686.2010.00176.x"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2011050476"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1017\/S0007114511000730"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1053\/ajkd.2002.29865"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00626.x"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000161831.07637.63"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00173.2013","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T23:44:32Z","timestamp":1567986272000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00173.2013"}},"issued":{"date-parts":[[2013,9,1]]},"references-count":32,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2013,9,1]]}},"alternative-id":["10.1152\/ajprenal.00173.2013"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00173.2013","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2013,9,1]]}},{"indexed":{"date-parts":[[2025,10,31]],"date-time":"2025-10-31T07:10:34Z","timestamp":1761894634522},"reference-count":19,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2008,1]]},"abstract":"<jats:p> Glial cell line-derived neurotrophic growth factor (GDNF), a member of the transforming growth factor family, is necessary for renal organogenesis and exhibits changes in expression in models of renal disease. Nestin is an intermediate filament protein originally believed to be a marker of neuroepithelial stem cells and recently proposed as a marker of mesenchymal stem cells (MSC). Having demonstrated the participation of nestin-expressing cells in renoprotection during acute renal ischemia, we hypothesized that growth factors and transcription factors similar to those operating in the nervous system should be also operant in the kidney and may be induced after noxious stimuli, such as an ischemic episode. Using cultured kidney-derived MSC, which abundantly express nestin, we confirmed expression of GDNF by these cells and demonstrated the GDNF-induced expression of GDNF. The cellular expression of nestin paralleled that of GDNF: serum starvation decreased the expression, whereas application of GDNF resulted in a dose-dependent increase in nestin expression. Immunohistochemical and Western blot analyses of kidneys obtained from control and postischemic mice showed that expression of GDNF was much enhanced in the renal cortex, a pattern similar to the previously reported expression of nestin. Based on the observed GDNF-induced GDNF expression, we next explored the effect of supplemental GDNF administered early after ischemia on renal function postischemia. GDNF-treated mice were protected against acute ischemia. To address potential mechanisms of the observed renoprotection, in vitro studies showed that GDNF accelerated MSC migration in a wound-healing assay. Hypoxia did not accelerate, but rather slightly reduced, the motility of MSC and reduced the expression of GDNF in MSC by approximately twofold. Furthermore, GDNF was cytoprotective against oxidative stress-induced apoptotic death of MSC. Collectively, these data establish 1) an autoregulatory circuit of GDNF-induced GDNF expression in renal MSC; 2) induction of GDNF expression in postischemic kidneys; 3) the ability of exogenous GDNF to ameliorate ischemic renal injury; and 4) a possible contribution of GDNF-induced motility and improved survival of MSC to renoprotection. <\/jats:p>","DOI":"10.1152\/ajprenal.00386.2007","type":"journal-article","created":{"date-parts":[[2007,11,14]],"date-time":"2007-11-14T21:05:26Z","timestamp":1195074326000},"page":"F229-F235","source":"Crossref","is-referenced-by-count":39,"title":["Glial cell line-derived neurotrophic growth factor increases motility and survival of cultured mesenchymal stem cells and ameliorates acute kidney injury"],"prefix":"10.1152","volume":"294","author":[{"given":"Haikun","family":"Shi","sequence":"first","affiliation":[]},{"given":"Daniel","family":"Patschan","sequence":"additional","affiliation":[]},{"given":"Gunnar P. H.","family":"Dietz","sequence":"additional","affiliation":[]},{"given":"Mathias","family":"B\u00e4hr","sequence":"additional","affiliation":[]},{"given":"Matthew","family":"Plotkin","sequence":"additional","affiliation":[]},{"given":"Michael S.","family":"Goligorsky","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI26295"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1006\/dbio.1998.9090"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000050961.70182.56"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1016\/j.brainres.2006.01.083"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1242\/dev.02095"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1038\/nm850"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1016\/j.ajog.2004.10.619"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1038\/382076a0"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1172\/JCI20921"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002102"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1038\/382073a0"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00396.2005"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.00786"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1007\/3-211-30714-1_69"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005080835"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00640.2005"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1007\/s00018-004-4144-6"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1002\/glia.10003"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1016\/j.expneurol.2004.08.012"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00386.2007","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:39:42Z","timestamp":1567967982000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00386.2007"}},"issued":{"date-parts":[[2008,1]]},"references-count":19,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2008,1]]}},"alternative-id":["10.1152\/ajprenal.00386.2007"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00386.2007","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2008,1]]}},{"indexed":{"date-parts":[[2025,11,1]],"date-time":"2025-11-01T05:40:24Z","timestamp":1761975624285},"reference-count":45,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2000,1,1]]},"abstract":"<jats:p>.\u2014Changes in activity or expression of transporters may account for alterations in cell behavior in diabetes. We sought to ascertain if mesangial cells (MC) grown in different glucose concentrations exhibit changes in activity and expression of acid-extruding transporters, the Na<jats:sup>+<\/jats:sup>\/H<jats:sup>+<\/jats:sup>and Na<jats:sup>+<\/jats:sup>-dependent Cl<jats:sup>\u2212<\/jats:sup>\/[Formula: see text]exchanger. pH<jats:sub>i<\/jats:sub>was determined by the use of the fluorescent pH-sensitive dye BCECF. In MCs grown in 5 mM glucose (control), the Na<jats:sup>+<\/jats:sup>\/H<jats:sup>+<\/jats:sup>exchanger was responsible for 31.8 \u00b1 5.1% of steady-state pH<jats:sub>i<\/jats:sub>, whereas Na<jats:sup>+<\/jats:sup>-dependent Cl<jats:sup>\u2212<\/jats:sup>\/[Formula: see text]contributed 62.9 \u00b1 4.0% ( n = 11). In MCs grown in high glucose for 2 wk, Na<jats:sup>+<\/jats:sup>\/H<jats:sup>+<\/jats:sup>exchange contribution to acid-extrusion increased as follows: 42.3 \u00b1 4.6% [ n = 8, 10 mM, not significant (NS)], 51.1 \u00b1 5.1% ( n = 8, 20 mM, P &lt; 0.01), and 64.8 \u00b1 5.5% ( n = 7, 30 mM, P &lt; 0.001). The Na<jats:sup>+<\/jats:sup>-dependent Cl<jats:sup>\u2212<\/jats:sup>\/[Formula: see text]exchanger contributed less [47.0 \u00b1 4.6, 38.6 \u00b1 5.8, and 21.1 \u00b1 3.8%, for 10, 20, and 30 mM glucose, respectively ( n &gt; 7)]. We sought to ascertain if the magnitude of the acute stimulated response to ANG II by the Na<jats:sup>+<\/jats:sup>\/H<jats:sup>+<\/jats:sup>and Na<jats:sup>+<\/jats:sup>-dependent Cl<jats:sup>\u2212<\/jats:sup>\/[Formula: see text]exchanger is changed. Na<jats:sup>+<\/jats:sup>\/H<jats:sup>+<\/jats:sup>exchanger (1.89-fold increase in 30 vs. 5 mM, P &lt; 0.002), but not Na<jats:sup>+<\/jats:sup>-dependent Cl<jats:sup>\u2212<\/jats:sup>\/[Formula: see text]exchange (0.17-fold, NS), exhibited an enhanced response to ANG II (1 \u03bcM). Na<jats:sup>+<\/jats:sup>\/H<jats:sup>+<\/jats:sup>exchange (NHE1) expression was significantly different (1.72-fold) after prolonged exposure to high glucose. These results suggest that the Na<jats:sup>+<\/jats:sup>\/H<jats:sup>+<\/jats:sup>exchanger, but not Na<jats:sup>+<\/jats:sup>-dependent Cl<jats:sup>\u2212<\/jats:sup>\/[Formula: see text]exchanger, may play an early role in the response to hyperglycemia in the diabetic state.<\/jats:p>","DOI":"10.1152\/ajprenal.2000.278.1.f91","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T12:05:07Z","timestamp":1514030707000},"page":"F91-F96","source":"Crossref","is-referenced-by-count":22,"title":["High glucose induces the activity and expression of Na<sup>+<\/sup>\/H<sup>+<\/sup>exchange in glomerular mesangial cells"],"prefix":"10.1152","volume":"278","author":[{"given":"Michael B.","family":"Ganz","sequence":"first","affiliation":[{"name":"Section of Nephrology, Department of Medicine, Case Western Reserve University, Veteran Affairs Medical Center, Cleveland, Ohio 44106; and"}]},{"given":"Karen","family":"Hawkins","sequence":"additional","affiliation":[{"name":"Section of Nephrology, Department of Medicine, Case Western Reserve University, Veteran Affairs Medical Center, Cleveland, Ohio 44106; and"}]},{"given":"Robert F.","family":"Reilly","sequence":"additional","affiliation":[{"name":"Section of Nephrology, Department of Medicine, University of Colorado, Veteran Affairs Medical Center, Denver, Colorado 80262"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.2337\/diab.37.12.1695"},{"key":"B2","first-page":"1131","volume":"151","author":"Abrass C. K.","year":"1997","journal-title":"Am. J. Pathol."},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1172\/JCI62"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.4.F917"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.260.2.F185"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1023\/A:1006821828706"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.4.2551"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1007\/s001250050682"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1007\/BF03168191"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.2337\/diab.45.5.642"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1988.255.6.C844"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1988.255.6.C857"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1991.260.1.C167"},{"key":"B15","first-page":"231","volume":"67","author":"Boyle K. M.","year":"1997","journal-title":"J. Cell Biol."},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.95.4.878"},{"key":"B17","doi-asserted-by":"crossref","first-page":"1600","DOI":"10.1681\/ASN.V581600","volume":"5","author":"Cosio F. G.","year":"1995","journal-title":"J. Am. Soc. Nephrol."},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.2337\/diab.43.1.1"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1988.254.6.F787"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1038\/337648a0"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.259.2.F269"},{"key":"B22","first-page":"1638","volume":"4","author":"Ganz M. B.","year":"1990","journal-title":"Fed. Am. Sci. Exp. Biol. J."},{"key":"B23","doi-asserted-by":"crossref","first-page":"23823","DOI":"10.1016\/S0021-9258(18)35911-8","volume":"267","author":"Grinstein S.","year":"1992","journal-title":"J. Biol. Chem."},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.152"},{"key":"B25","first-page":"246","volume":"46","author":"Haller H.","year":"1996","journal-title":"Clin. Nephrol."},{"key":"B26","first-page":"S91","volume":"51","author":"Heilig C. W.","year":"1997","journal-title":"Kidney Int."},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00119.x"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1159\/000057369"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.6.F1045"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1159\/000044988"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1007\/s109-1998-8101-y"},{"key":"B32","doi-asserted-by":"crossref","first-page":"23544","DOI":"10.1016\/S0021-9258(17)31550-8","volume":"269","author":"Kapus A.","year":"1994","journal-title":"J. Biol. Chem."},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.80.6.853"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.2337\/diab.36.2.244"},{"key":"B35","doi-asserted-by":"crossref","first-page":"3700","DOI":"10.4049\/jimmunol.136.10.3700","volume":"136","author":"Lovett D. H.","year":"1986","journal-title":"J. Immunol."},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1007\/s001250050710"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1172\/JCI113750"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.97.2.195"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1007\/s001250050510"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1055\/s-0029-1211787"},{"key":"B41","first-page":"490","volume":"5","author":"Rutherford P. A.","year":"1997","journal-title":"Exp. Nephrol."},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1055\/s-2007-979817"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.2337\/diab.42.12.1815"},{"key":"B44","doi-asserted-by":"crossref","first-page":"15613","DOI":"10.1016\/S0021-9258(17)40725-3","volume":"269","author":"Soleimani M.","year":"1994","journal-title":"J. Biol. Chem."},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.268.1.F13"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117275"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.2000.278.1.F91","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,8,30]],"date-time":"2023-08-30T05:36:25Z","timestamp":1693373785000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.2000.278.1.F91"}},"issued":{"date-parts":[[2000,1,1]]},"references-count":45,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2000,1,1]]}},"alternative-id":["10.1152\/ajprenal.2000.278.1.F91"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.2000.278.1.f91","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2000,1,1]]}},{"indexed":{"date-parts":[[2025,11,27]],"date-time":"2025-11-27T10:41:18Z","timestamp":1764240078134},"reference-count":86,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2017,10,1]]},"abstract":"<jats:p>The renal collecting duct (CD) contains two major cell types, intercalated (ICs) and principal cells (PCs). A previous report showed that deletion of \u03b21-integrin in the entire renal CD causes defective CD morphogenesis resulting in kidney dysfunction. However, subsequent deletion of \u03b21-integrin specifically in ICs and PCs, respectively, did not cause any morphological defects in the CDs. The discrepancy between these studies prompts us to reinvestigate the role of \u03b21-integrin in CD cells, specifically in the PCs. We conditionally deleted \u03b21-integrin in mouse CD PCs using a specific aquaporin-2 (AQP2) promoter Cre-LoxP system. The resulting mutant mice, \u03b2-1<jats:sup>f\/f<\/jats:sup>AQP2-Cre+, had lower body weight, failed to thrive, and died around 8\u201312 wk. Their CD tubules were dilated, and some of them contained cellular debris. Increased apoptosis and proliferation of PCs were observed in the dilated CDs. Trichrome staining and electron microscopy revealed the presence of peritubular and interstitial fibrosis that is associated with increased production of extracellular matrix proteins including collagen type IV and fibronectin, as detected by immunoblotting. Further analysis revealed a significantly increased expression of transforming growth factor-\u03b2 (TGF-\u03b2)-induced protein, fibronectin, and TGF-\u03b2 receptor-1 mRNAs and concomitantly increased phosphorylation of SMAD-2 that indicates the activation of the TGF-\u03b2 signaling pathway. Therefore, our data reveal that normal expression of \u03b21-integrin in PCs is a critical determinant of CD structural and functional integrity and further support the previously reported critical role of \u03b21-integrin in the development and\/or maintenance of the CD structure and function.<\/jats:p>","DOI":"10.1152\/ajprenal.00038.2017","type":"journal-article","created":{"date-parts":[[2017,7,13]],"date-time":"2017-07-13T00:25:26Z","timestamp":1499905526000},"page":"F1026-F1037","source":"Crossref","is-referenced-by-count":23,"title":["Deletion of \u03b21-integrin in collecting duct principal cells leads to tubular injury and renal medullary fibrosis"],"prefix":"10.1152","volume":"313","author":[{"given":"Fahmy A.","family":"Mamuya","sequence":"first","affiliation":[{"name":"Program in Membrane Biology and Division of Nephrology, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts;"},{"name":"Center for Systems Biology, Massachusetts General Hospital, Boston, Massachusetts;"},{"name":"Harvard Medical School, Boston, Massachusetts;"}]},{"given":"Dongping","family":"Xie","sequence":"additional","affiliation":[{"name":"Program in Membrane Biology and Division of Nephrology, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts;"},{"name":"Center for Systems Biology, Massachusetts General Hospital, Boston, Massachusetts;"},{"name":"Harvard Medical School, Boston, Massachusetts;"},{"name":"Department of Physiology, Tongji University School of Medicine, Shanghai, China; and"}]},{"given":"Lei","family":"Lei","sequence":"additional","affiliation":[{"name":"Program in Membrane Biology and Division of Nephrology, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts;"},{"name":"Center for Systems Biology, Massachusetts General Hospital, Boston, Massachusetts;"},{"name":"Department of Pharmacology, School of Basic Medical Sciences, Peking University, Beijing, China"}]},{"given":"Ming","family":"Huang","sequence":"additional","affiliation":[{"name":"Program in Membrane Biology and Division of Nephrology, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts;"},{"name":"Center for Systems Biology, Massachusetts General Hospital, Boston, Massachusetts;"},{"name":"Department of Pharmacology, School of Basic Medical Sciences, Peking University, Beijing, China"}]},{"given":"Kenji","family":"Tsuji","sequence":"additional","affiliation":[{"name":"Program in Membrane Biology and Division of Nephrology, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts;"},{"name":"Center for Systems Biology, Massachusetts General Hospital, Boston, Massachusetts;"},{"name":"Harvard Medical School, Boston, Massachusetts;"}]},{"given":"Diane E.","family":"Capen","sequence":"additional","affiliation":[{"name":"Program in Membrane Biology and Division of Nephrology, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts;"},{"name":"Center for Systems Biology, Massachusetts General Hospital, Boston, Massachusetts;"}]},{"given":"BaoXue","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, School of Basic Medical Sciences, Peking University, Beijing, China"}]},{"given":"Ralph","family":"Weissleder","sequence":"additional","affiliation":[{"name":"Center for Systems Biology, Massachusetts General Hospital, Boston, Massachusetts;"},{"name":"Harvard Medical School, Boston, Massachusetts;"}]},{"given":"Teodor G.","family":"P\u0103unescu","sequence":"additional","affiliation":[{"name":"Program in Membrane Biology and Division of Nephrology, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts;"},{"name":"Center for Systems Biology, Massachusetts General Hospital, Boston, Massachusetts;"},{"name":"Harvard Medical School, Boston, Massachusetts;"}]},{"given":"Hua A. Jenny","family":"Lu","sequence":"additional","affiliation":[{"name":"Program in Membrane Biology and Division of Nephrology, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts;"},{"name":"Center for Systems Biology, Massachusetts General Hospital, Boston, Massachusetts;"},{"name":"Harvard Medical School, Boston, Massachusetts;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1006\/excr.1999.4424"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1203\/00006450-199806000-00011"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M106176200"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM200005043421807"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2010.120"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.190"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199411103311907"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00387.2002"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00085.2012"},{"key":"B10","first-page":"302","volume-title":"Brenner and Rector\u2019s The Kidney","author":"Brown D","year":"2015"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1007\/BF01463929"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/j.yjmcc.2015.11.010"},{"key":"B13","doi-asserted-by":"crossref","first-page":"SA-PO2112","DOI":"10.1681\/ASN.2009030307","volume":"21","author":"Chen Y","year":"2010","journal-title":"J Am Soc Nephrol"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2012010079"},{"key":"B15","first-page":"219","volume":"60","author":"Clapp WL","year":"1989","journal-title":"Lab Invest"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1159\/000180580"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200205014"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013090988"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1007\/BF02581245"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1097\/CCM.0b013e318225761a"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.3109\/03009748909095403"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.00656.x"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1002\/cphy.c100064"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1010364107"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00432.2004"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/S0898-6568(03)00094-9"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00081.x"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013070764"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.2174\/1871530311006040302"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M110.105700"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbadis.2012.10.005"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1007\/s004240050806"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(02)00971-6"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2008.03.066"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1016\/j.ajpath.2012.08.002"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1097\/TP.0b013e3181cd4abb"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.7150\/ijbs.7.1056"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1111\/1523-1747.ep12607024"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013111179"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00158.x"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2011.149"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00179.2003"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1002\/jemt.1060090206"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1111\/j.1582-4934.2011.01419.x"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1038\/embor.2009.276"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1093\/bja\/aes357"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.00568-12"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1998.275.1.C216"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-199809000-00005"},{"key":"B50","first-page":"136","volume":"15","author":"Nielsen S","year":"2000","journal-title":"News Physiol Sci"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00464.2003"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00622.2012"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1016\/S0934-8832(11)80023-5"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013010012"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.150.5.1149"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1126\/scitranslmed.aaa5094"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.12.10.3126"},{"key":"B58","doi-asserted-by":"crossref","first-page":"4586","DOI":"10.1016\/S0021-9258(18)68822-2","volume":"263","author":"Roberts CJ","year":"1988","journal-title":"J Biol Chem"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0511324103"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006090975"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.2215\/CJN.08880914"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00437.2005"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.2741\/3389"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.266.6.F829"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1016\/j.ydbio.2007.04.004"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1089\/dna.1992.11.511"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1053\/gast.1996.v110.pm8964403"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00116.x"},{"key":"B69","doi-asserted-by":"publisher","DOI":"10.1159\/000330082"},{"key":"B70","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00302.2012"},{"key":"B71","doi-asserted-by":"publisher","DOI":"10.1095\/biolreprod.108.075648"},{"key":"B72","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/13.9.2216"},{"key":"B73","doi-asserted-by":"publisher","DOI":"10.1126\/scisignal.2004751"},{"key":"B74","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00394.2012"},{"key":"B75","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.479"},{"key":"B76","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2013.372"},{"key":"B77","doi-asserted-by":"publisher","DOI":"10.1016\/j.tibs.2010.08.002"},{"key":"B78","doi-asserted-by":"crossref","first-page":"21883","DOI":"10.1016\/S0021-9258(20)80623-1","volume":"268","author":"Wu C","year":"1993","journal-title":"J Biol Chem"},{"key":"B79","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2012080866"},{"key":"B80","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90260.2008"},{"key":"B81","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00494.2005"},{"key":"B82","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.E14-07-1203"},{"key":"B83","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00122.2001"},{"key":"B84","doi-asserted-by":"publisher","DOI":"10.1242\/dev.036269"},{"key":"B85","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.13.6161"},{"key":"B86","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.0224.2001"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00038.2017","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,7,30]],"date-time":"2022-07-30T22:09:45Z","timestamp":1659218985000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00038.2017"}},"issued":{"date-parts":[[2017,10,1]]},"references-count":86,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2017,10,1]]}},"alternative-id":["10.1152\/ajprenal.00038.2017"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00038.2017","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2017,10,1]]}},{"indexed":{"date-parts":[[2025,11,27]],"date-time":"2025-11-27T10:41:30Z","timestamp":1764240090009},"reference-count":42,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1998,6,1]]},"abstract":"<jats:p>Hsp110, Osp94, and Hsp70RY are members of the recently described Hsp110\/SSE subfamily of (heat and osmotic) stress proteins whose members are structurally related to the Hsp70\/BiP gene superfamily. To date, little is known about the response of this gene family to stresses in vitro or in vivo. In this study, an analysis of mRNA expression showed that Hsp110 and Osp94, like Hsp70, are induced in renal murine inner medullary collecting duct (mIMCD3) epithelial cells by heat shock, hyperosmotic NaCl, and cadmium, whereas low pH had a suppressive effect on Osp94. H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>decreased expression of Osp94 while inducing levels of Hsp110 and Hsp70 message. Tunicamycin, hypertonic urea, and tumor necrosis factor-\u03b1 had no effects. Hsp70RY was responsive exclusively to cadmium chloride. Moreover, enhanced expression of Hsp110 and Osp94 was subsequent to induction of Hsp70 and was suppressed by inhibition of protein synthesis by cycloheximide. RT-PCR analysis showed Hsp110, Osp94, and Hsp70RY are ubiquitously expressed in mouse tissues. In murine kidney, there was a corticomedullary gradient of expression of Hsp110, Osp94, Hsp70RY, and Hsp70 but not Hsc70 or BiP. Furthermore, dehydration increased inner medullary expression of Hsp110 and Osp94. An analysis of stress tolerance in mIMCD3 cells showed that heat shock and hyperosmotic NaCl stress are cross-tolerant stresses, suggesting hyperosmolality is a physiological correlate of heat shock in mammalian kidney. Thus Hsp110 and Osp94 behave as heat shock proteins, although they are regulated differently than Hsp70.<\/jats:p>","DOI":"10.1152\/ajprenal.1998.274.6.f1054","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T15:24:19Z","timestamp":1514042659000},"page":"F1054-F1061","source":"Crossref","is-referenced-by-count":22,"title":["Characterization of the Hsp110\/SSE gene family response to hyperosmolality and other stresses"],"prefix":"10.1152","volume":"274","author":[{"given":"Bento C.","family":"Santos","sequence":"first","affiliation":[{"name":"Renal Division, Department of Medicine, Brigham and Women\u2019s Hospital and Harvard Institutes of Medicine, Boston, Massachusetts 02115; and"}]},{"given":"Alejandro","family":"Chevaile","sequence":"additional","affiliation":[{"name":"Renal Division, Department of Medicine, Brigham and Women\u2019s Hospital and Harvard Institutes of Medicine, Boston, Massachusetts 02115; and"}]},{"given":"Ryoji","family":"Kojima","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Faculty of Pharmacy, Meijo University, Nagoya 468, Japan"}]},{"given":"Steven R.","family":"Gullans","sequence":"additional","affiliation":[{"name":"Renal Division, Department of Medicine, Brigham and Women\u2019s Hospital and Harvard Institutes of Medicine, Boston, Massachusetts 02115; and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.13.4.2486"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.117.6.1151"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.117.6.1137"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1126\/science.2188360"},{"issue":"37","key":"B5","first-page":"F983","volume":"268","author":"Burg M. B.","year":"1995","journal-title":"Am. J. Physiol."},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(96)00011-7"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1991.261.4.C594"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1994.2221"},{"key":"B10","doi-asserted-by":"crossref","first-page":"810","DOI":"10.4049\/jimmunol.151.2.810","volume":"151","author":"Fathallah D. M.","year":"1993","journal-title":"J. Immunol."},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1126\/science.8383878"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1038\/370111a0"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1007\/BF01923453"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1007\/BF01923455"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1038\/381571a0"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.1041590107"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.5.2640"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1007\/BF01833521"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.21.12327"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.26.15725"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1099\/13500872-141-3-687"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.109.5.1947"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117655"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.87.10.3748"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.8.11.4736"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1016\/0378-1119(93)90514-4"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1007\/BF02191910"},{"issue":"34","key":"B30","first-page":"F416","volume":"265","author":"Rauchman M. I.","year":"1993","journal-title":"Am. J. Physiol."},{"issue":"42","key":"B31","first-page":"F9","volume":"273","author":"Rauchman M. I.","year":"1997","journal-title":"Am. J. Physiol."},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.13.3.1392"},{"issue":"36","key":"B33","first-page":"F28","volume":"267","author":"Sheikh-Hamad D.","year":"1994","journal-title":"Am. J. Physiol."},{"key":"B34","doi-asserted-by":"crossref","first-page":"323","DOI":"10.1007\/BF00280382","volume":"240","author":"Shirayama M.","year":"1993","journal-title":"Mol. Gen. Genet."},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.97.5.1389"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1038\/356037a0"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.24.15389"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1016\/0167-4781(88)90006-1"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1989.256.3.C614"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1099\/00221287-138-10-2125"},{"key":"B41","doi-asserted-by":"crossref","first-page":"26049","DOI":"10.1016\/S0021-9258(19)74274-4","volume":"268","author":"Wang T.-F.","year":"1993","journal-title":"J. Biol. Chem."},{"issue":"39","key":"B42","first-page":"F1057","volume":"270","author":"Wang Y.-H.","year":"1996","journal-title":"Am. J. Physiol."},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1038\/368032a0"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119619"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.50.29718"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1998.274.6.F1054","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,8,30]],"date-time":"2023-08-30T05:40:13Z","timestamp":1693374013000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1998.274.6.F1054"}},"issued":{"date-parts":[[1998,6,1]]},"references-count":42,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1998,6,1]]}},"alternative-id":["10.1152\/ajprenal.1998.274.6.F1054"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1998.274.6.f1054","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1998,6,1]]}},{"indexed":{"date-parts":[[2026,1,13]],"date-time":"2026-01-13T15:46:48Z","timestamp":1768319208066,"version":"3.49.0"},"reference-count":59,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,3,1]]},"abstract":"<jats:p>Pathways that contribute to TNF production by the kidney are not well defined. Mice given 1% NaCl in the drinking water for 3 days exhibited a 2.5-fold increase in urinary, but not plasma, TNF levels compared with mice given tap water. Since furosemide attenuated the increase in TNF levels, we hypothesized that hypertonic NaCl intake increases renal TNF production by a pathway involving the Na<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-2Cl<jats:sup>\u2212<\/jats:sup>cotransporter (NKCC2). A 2.5-fold increase in NKCC2A mRNA accumulation was observed in medullary thick ascending limb (mTAL) tubules from mice given 1% NaCl; a concomitant 2-fold increase in nuclear factor of activated T cells 5 (NFAT5) mRNA and protein expression was observed in the outer medulla. Urinary TNF levels were reduced in mice given 1% NaCl after an intrarenal injection of a lentivirus construct designed to specifically knockdown NKCC2A (EGFP-N2A-ex4); plasma levels of TNF did not change after injection of EGFP-N2A-ex4. Intrarenal injection of EGFP-N2A-ex4 also inhibited the increase of NFAT5 mRNA abundance in the outer medulla of mice given 1% NaCl. TNF production by primary cultures of mTAL cells increased approximately sixfold in response to an increase in osmolality to 400 mosmol\/kgH<jats:sub>2<\/jats:sub>O produced with NaCl and was inhibited in cells transiently transfected with a dnNFAT5 construct. Transduction of cells with EGFP-N2A-ex4 also prevented increases in TNF mRNA and protein production in response to high NaCl concentration and reduced transcriptional activity of a NFAT5 promoter construct. Since NKCC2A expression is restricted to the TAL, NKCC2A-dependent activation of NFAT5 is part of a pathway by which the TAL produces TNF in response to hypertonic NaCl intake.<\/jats:p>","DOI":"10.1152\/ajprenal.00243.2012","type":"journal-article","created":{"date-parts":[[2012,12,27]],"date-time":"2012-12-27T01:36:42Z","timestamp":1356572202000},"page":"F533-F542","source":"Crossref","is-referenced-by-count":25,"title":["NKCC2A and NFAT5 regulate renal TNF production induced by hypertonic NaCl intake"],"prefix":"10.1152","volume":"304","author":[{"given":"Shoujin","family":"Hao","sequence":"first","affiliation":[{"name":"Department of Pharmacology, New York Medical College, Valhalla, New York"}]},{"given":"Lars","family":"Bellner","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, New York Medical College, Valhalla, New York"}]},{"given":"Nicholas R.","family":"Ferreri","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, New York Medical College, Valhalla, New York"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00223.2005"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00650.2010"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00056.2006"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00106.2008"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.168.11.5817"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/11.5.1475"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.1.F46"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.3.F619"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00466.2007"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00426.2006"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2009.142"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1994.266.6.C1568"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/gki701"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1986.250.1.F176"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1159\/000096320"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00258.2012"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.3.F360"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.1.F148"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00011.2004"},{"key":"B20","doi-asserted-by":"crossref","first-page":"17713","DOI":"10.1016\/S0021-9258(17)32499-7","volume":"269","author":"Gamba G","year":"1994","journal-title":"J Biol Chem"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00153.2006"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90436.2008"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00408.2010"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00600.2010"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1981.241.4.F443"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00209.2004"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00383.2006"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2010.469"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.3.F405"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00502.2006"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.2006.01551.x"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1002\/1521-4141(200007)30:7<2038::AID-IMMU2038>3.0.CO;2-K"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.6.F925"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.108.120881"},{"key":"B35","doi-asserted-by":"crossref","first-page":"1327","DOI":"10.1152\/ajplegacy.1967.212.6.1327","volume":"212","author":"Landwehr DM","year":"1967","journal-title":"Am J Physiol"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00145.2006"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006060664"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1006\/meth.2001.1262"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1016\/S1074-7613(01)00165-0"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1204386"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1994.250"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.5.2538"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.3.F347"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)64445-8"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006040384"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006091070"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00382.2003"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1006\/cyto.1998.0426"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/29.9.e45"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.111.189761"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1046\/j.1440-1681.2003.03810.x"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006050454"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90297.2008"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00611.2009"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.601"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.090091297"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.165.9.4884"},{"key":"B58","first-page":"293","volume":"172","author":"van Lanschot JJ","year":"1991","journal-title":"Surg Gynecol Obstet"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00108.2002"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00243.2012","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,2,4]],"date-time":"2022-02-04T17:14:51Z","timestamp":1643994891000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00243.2012"}},"issued":{"date-parts":[[2013,3,1]]},"references-count":59,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2013,3,1]]}},"alternative-id":["10.1152\/ajprenal.00243.2012"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00243.2012","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2013,3,1]]}},{"indexed":{"date-parts":[[2026,1,13]],"date-time":"2026-01-13T14:16:55Z","timestamp":1768313815073,"version":"3.49.0"},"reference-count":50,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2010,7]]},"abstract":"<jats:p>We have previously reported that Dot1a is located in the cytoplasm and nucleus (Reisenauer MR, Anderson M, Huang L, Zhang Z, Zhou Q, Kone BC, Morris AP, Lesage GD, Dryer SE, Zhang W. J Biol Chem 284: 35659\u201335669, 2009), widely expressed in the kidney as detected by its histone H3K79 methyltransferase activity (Zhang W, Hayashizaki Y, Kone BC. Biochem J 377: 641\u2013651, 2004), and involved in transcriptional control of the epithelial Na<jats:sup>+<\/jats:sup>channel subunit-\u03b1 gene ( \u03b1ENaC) (Zhang W, Xia X, Jalal DI, Kuncewicz T, Xu W, Lesage GD, Kone BC. Am J Physiol Cell Physiol 290: C936\u2013C946, 2006). Aldosterone releases repression of \u03b1ENaC by reducing expression of Dot1a and its partner AF9 (Zhang W, Xia X, Reisenauer MR, Hemenway CS, Kone BC. J Biol Chem 281: 18059\u201318068, 2006) and by impairing Dot1a-AF9 interaction via Sgk1-mediated AF9 phosphorylation (Zhang W, Xia X, Reisenauer MR, Rieg T, Lang F, Kuhl D, Vallon V, Kone BC. J Clin Invest 117: 773\u2013783, 2007). This network also appears to regulate transcription of several other aldosterone target genes. Here, we provide evidence showing that Dot1a contains at least three potential nuclear localization signals (NLSs). Deletion of these NLSs causes green fluorescent protein-fused Dot1a fusions to localize almost exclusively in the cytoplasm of 293T cells as revealed by confocal microscopy. Deletion of NLSs abolished Dot1a-mediated repression of \u03b1ENaC-promoter luciferase construct in M1 cells. AF9 is widely expressed in mouse kidney. Similar to \u03b1ENaC, the mRNA levels of \u03b2ENaC, \u03b3ENaC, and Sgk1 are also downregulated by Dot1a and AF9 overexpression. Small interference RNA-mediated knockdown of Dot1a and AF9 or aldosterone treatment leads to an opposite effect. Using single-cell fluorescence imaging or equivalent short-circuit current in IMCD3 and M1 cells, we show that observed transcriptional alterations correspond to changes in ENaC and Sgk1 protein levels as well as benzamil-sensitive Na<jats:sup>+<\/jats:sup>transport. In brief, Dot1a and AF9 downregulate Na<jats:sup>+<\/jats:sup>transport, most likely by regulating ENaC mRNA and subsequent protein expression and ENaC activity.<\/jats:p>","DOI":"10.1152\/ajprenal.00105.2010","type":"journal-article","created":{"date-parts":[[2010,4,29]],"date-time":"2010-04-29T02:14:22Z","timestamp":1272507262000},"page":"F63-F76","source":"Crossref","is-referenced-by-count":38,"title":["Dot1a contains three nuclear localization signals and regulates the epithelial Na<sup>+<\/sup>channel (ENaC) at multiple levels"],"prefix":"10.1152","volume":"299","author":[{"given":"Mary Rose","family":"Reisenauer","sequence":"first","affiliation":[{"name":"Departments of 1Internal Medicine,"}]},{"given":"Steven W.","family":"Wang","sequence":"additional","affiliation":[{"name":"Ophthalmology and Visual Science,"}]},{"given":"Yang","family":"Xia","sequence":"additional","affiliation":[{"name":"Biochemistry and Molecular Biology, and"},{"name":"Graduate School of Biomedical Sciences, University of Texas Health Science Center at Houston, Houston, Texas"}]},{"given":"Wenzheng","family":"Zhang","sequence":"additional","affiliation":[{"name":"Departments of 1Internal Medicine,"},{"name":"Graduate School of Biomedical Sciences, University of Texas Health Science Center at Houston, Houston, Texas"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2787(73)90374-2"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1186\/1471-2407-9-103"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1038\/onc.2009.16"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1996.271.2.C605"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90248.2008"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfl668"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.5.2514"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/20.24.7052"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1992.sp019053"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1997.272.5.C1482"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1016\/0006-2952(94)90044-2"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1677\/jme.1.02084"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00353.2002"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1172\/JCI36908"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0b013e328332bda4"},{"key":"B16","doi-asserted-by":"crossref","first-page":"19458","DOI":"10.1016\/S0021-9258(19)47322-5","volume":"264","author":"Harootunian AT","year":"1989","journal-title":"J Biol Chem"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00299.2002"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.00257-06"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1111\/j.1442-2050.2008.00907.x"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00216.x"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.R800083200"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/j.virol.2008.09.037"},{"key":"B23","doi-asserted-by":"crossref","first-page":"RE17","DOI":"10.1126\/stke.2001.108.re17","volume":"2001","author":"Lang F","year":"2001","journal-title":"Sci STKE"},{"key":"B24","author":"Lin JJ","journal-title":"J Biol Chem"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.110.6.717"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1172\/JCI7840"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(03)00114-4"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1172\/JCI21454"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1210\/mend.15.7.0659"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1159\/000070245"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000013292.78621.FD"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.265.3.F416"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M109.038448"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1007\/BF00373903"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.051603198"},{"key":"B36","first-page":"307","volume":"449","author":"Sheldon C","year":"2004","journal-title":"Pfl\u00fcgers Arch"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1126\/scisignal.279pe41"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1210\/en.2005-0894"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.259.2.F222"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1999.276.5.C1154"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00320.2001"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1621\/nrs.05012"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1172\/JCI26620"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1016\/j.brainresbull.2007.03.002"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1172\/JCI0215696"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1172\/JCI113663"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1042\/bj20030839"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00431.2005"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M601903200"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1172\/JCI29850"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00105.2010","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,3,26]],"date-time":"2024-03-26T04:38:37Z","timestamp":1711427917000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00105.2010"}},"issued":{"date-parts":[[2010,7]]},"references-count":50,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2010,7]]}},"alternative-id":["10.1152\/ajprenal.00105.2010"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00105.2010","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2010,7]]}},{"indexed":{"date-parts":[[2026,1,9]],"date-time":"2026-01-09T02:56:54Z","timestamp":1767927414450,"version":"3.49.0"},"reference-count":76,"publisher":"American Physiological Society","issue":"10","funder":[{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)","doi-asserted-by":"publisher","award":["DK091623"],"award-info":[{"award-number":["DK091623"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)","doi-asserted-by":"publisher","award":["079312"],"award-info":[{"award-number":["079312"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000738","name":"U.S. Department of Veterans Affairs (VA)","doi-asserted-by":"publisher","award":["Merit"],"award-info":[{"award-number":["Merit"]}],"id":[{"id":"10.13039\/100000738","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2016,5,15]]},"abstract":"<jats:p>Serum albumin is the most abundant plasma protein and has a long half-life due to neonatal Fc receptor (FcRn)-mediated transcytosis by many cell types, including proximal tubule cells of the kidney. Albumin also interacts with, and is modified by, many small and large molecules. Therefore, the focus of the present study was to address the impact of specific known biological albumin modifications on albumin-FcRn binding and cellular handling. Binding at pH 6.0 and 7.4 was performed since FcRn binds albumin strongly at acidic pH and releases it after transcytosis at physiological pH. Equilibrium dissociation constants were measured using microscale thermophoresis. Since studies have shown that glycated albumin is excreted in the urine at a higher rate than unmodified albumin, we studied glucose and methylgloxal modified albumins (21 days). All had reduced affinity to FcRn at pH 6.0, suggesting these albumins would not be returned to the circulation via the transcytotic pathway. To address why modified albumin has reduced affinity, we analyzed the structure of the modified albumins using small-angle X-ray scattering. This analysis showed significant structural changes occurring to albumin with glycation, particularly in the FcRn-binding region, which could explain the reduced affinity to FcRn. These results offer an explanation for enhanced proximal tubule-mediated sorting and clearance of abnormal albumins.<\/jats:p>","DOI":"10.1152\/ajprenal.00605.2015","type":"journal-article","created":{"date-parts":[[2016,2,18]],"date-time":"2016-02-18T04:14:32Z","timestamp":1455768872000},"page":"F1089-F1102","source":"Crossref","is-referenced-by-count":30,"title":["Mechanism of increased clearance of glycated albumin by proximal tubule cells"],"prefix":"10.1152","volume":"310","author":[{"given":"Mark C.","family":"Wagner","sequence":"first","affiliation":[{"name":"Nephrology Division, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana; and"}]},{"given":"Jered","family":"Myslinski","sequence":"additional","affiliation":[{"name":"Nephrology Division, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana; and"}]},{"given":"Shiv","family":"Pratap","sequence":"additional","affiliation":[{"name":"The Council of Scientific and Industrial Research Institute of Microbial Technology, Chandigarh, India"}]},{"given":"Brittany","family":"Flores","sequence":"additional","affiliation":[{"name":"Nephrology Division, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana; and"}]},{"given":"George","family":"Rhodes","sequence":"additional","affiliation":[{"name":"Nephrology Division, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana; and"}]},{"given":"Silvia B.","family":"Campos-Bilderback","sequence":"additional","affiliation":[{"name":"Nephrology Division, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana; and"}]},{"given":"Ruben M.","family":"Sandoval","sequence":"additional","affiliation":[{"name":"Nephrology Division, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana; and"}]},{"given":"Sudhanshu","family":"Kumar","sequence":"additional","affiliation":[{"name":"Nephrology Division, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana; and"}]},{"given":"Monika","family":"Patel","sequence":"additional","affiliation":[{"name":"Nephrology Division, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana; and"}]},{"family":"Ashish","sequence":"additional","affiliation":[{"name":"The Council of Scientific and Industrial Research Institute of Microbial Technology, Chandigarh, India"}]},{"given":"Bruce A.","family":"Molitoris","sequence":"additional","affiliation":[{"name":"Nephrology Division, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana; and"},{"name":"Department of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana;"},{"name":"Roudebush Veterans Affairs Medical Center, Indianapolis, Indiana; and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2010050492"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M113.463000"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M109.081828"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/ncomms1607"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1002\/eji.200636556"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/j.cca.2013.07.013"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000141"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00398.2004"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/0047-6374(93)90065-Y"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1021\/bi052628y"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20021829"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/j.biochi.2006.05.011"},{"key":"B13","doi-asserted-by":"crossref","first-page":"595","DOI":"10.1016\/S0021-9258(17)37845-6","volume":"254","author":"Day JF","year":"1979","journal-title":"J Biol Chem"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013090950"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1093\/intimm\/13.8.993"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.89.2.638"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1984.55"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.E07-02-0101"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.76.9.4258"},{"key":"B20","doi-asserted-by":"crossref","first-page":"632","DOI":"10.1681\/ASN.V114632","volume":"11","author":"Haymann JP","year":"2000","journal-title":"J Am Soc Nephrol"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1038\/nature07255"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1006\/jmbi.1993.1220"},{"key":"B23","doi-asserted-by":"crossref","first-page":"13542","DOI":"10.1016\/S0021-9258(18)67052-8","volume":"261","author":"Iberg N","year":"1986","journal-title":"J Biol Chem"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1016\/j.abb.2012.10.002"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbapap.2007.09.001"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/j.molstruc.2014.03.009"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.00286.2005"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1107\/S0021889803012779"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1084\/jem.166.5.1259"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1016\/0024-3205(92)90335-M"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1016\/0168-8227(96)01296-X"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1016\/j.jasms.2003.11.014"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1001\/jama.2015.0602"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1521-4141(199807)28:07<2092::AID-IMMU2092>3.0.CO;2-E"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.3389\/fphys.2014.00299"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.4161\/mabs.28744"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.172.4.2021"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1093\/intimm\/13.12.1551"},{"key":"B39","volume-title":"All About Albumin Biochemistry, Genetics, and Medical Applications","author":"Peters TJ","year":"1996"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1107\/S0021889812007662"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0700337104"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.1403014"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1002\/hep.20720"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1016\/j.dsx.2014.09.017"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1038\/nature12070"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1016\/j.febslet.2008.04.057"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1016\/j.biochi.2010.12.003"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1159\/000068039"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008050503"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002041"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M114.587675"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.3389\/fimmu.2014.00682"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-59745-178-9_28"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2011070666"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2008090976"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbagen.2007.02.001"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1016\/j.str.2013.08.022"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1186\/1472-6807-12-17"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1016\/j.ymeth.2012.12.005"},{"key":"B61","doi-asserted-by":"crossref","first-page":"3812","DOI":"10.1016\/S0021-9258(17)43168-1","volume":"259","author":"Shaklai N","year":"1984","journal-title":"J Biol Chem"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1023\/A:1015960205409"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M114.563486"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1107\/S0021889895007047"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-3495(01)76260-1"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1107\/S0021889892001663"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-3495(99)77443-6"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013010018"},{"key":"B69","doi-asserted-by":"publisher","DOI":"10.1016\/j.sbi.2010.01.010"},{"key":"B70","doi-asserted-by":"publisher","DOI":"10.1155\/2012\/481520"},{"key":"B71","doi-asserted-by":"publisher","DOI":"10.1007\/s004180100317"},{"key":"B72","doi-asserted-by":"publisher","DOI":"10.1021\/bi970841r"},{"key":"B73","doi-asserted-by":"publisher","DOI":"10.1016\/S0969-2126(98)00008-2"},{"key":"B74","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2736(96)00043-0"},{"key":"B75","doi-asserted-by":"publisher","DOI":"10.1021\/bi000749m"},{"key":"B76","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-2836(03)00952-5"},{"key":"B77","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfu261"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00605.2015","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,6,4]],"date-time":"2022-06-04T12:22:21Z","timestamp":1654345341000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00605.2015"}},"issued":{"date-parts":[[2016,5,15]]},"references-count":76,"journal-issue":{"issue":"10","published-print":{"date-parts":[[2016,5,15]]}},"alternative-id":["10.1152\/ajprenal.00605.2015"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00605.2015","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2016,5,15]]}},{"indexed":{"date-parts":[[2026,1,9]],"date-time":"2026-01-09T13:11:18Z","timestamp":1767964278024,"version":"3.49.0"},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1983,3,1]]},"abstract":"<jats:p> The rate of intracellular metabolism of citrate plays a major role in determining the amount of citrate excreted in the urine. Fractional excretion of citrate can be increased either by increasing intracellular citrate synthesis from precursors or by inhibiting mitochondrial citrate metabolism. Increased excretion secondary to increased synthesis of citrate occurs when citric acid cycle precursors such as malate or succinate are infused. Increased excretion resulting from inhibition of citrate metabolism occurs when malonate, maleate, or fluorocitrate is administered. Systemic acid-base changes cause striking changes in citrate clearance and metabolism. Recent evidence suggests that the effects of acid-base changes are mediated by alteration in the pH gradient across the inner mitochondrial membrane. Metabolic alkalosis causes cytoplasmic pH and bicarbonate to increase, resulting in a decrease in the mitochondrial pH gradient. This change inhibits the tricarboxylate carrier, slowing entry of citrate into the mitochondrial matrix compartment. The level of citrate in the cytoplasm increases, tubular and peritubular citrate uptake are reduced, and citrate clearance increases. Opposite changes occur in acidosis. Change in the mitochondrial pH gradient provides a sensitive mechanism for regulating renal substrate metabolism. <\/jats:p>","DOI":"10.1152\/ajprenal.1983.244.3.f223","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T15:34:14Z","timestamp":1513956854000},"page":"F223-F234","source":"Crossref","is-referenced-by-count":30,"title":["Citrate excretion: a window on renal metabolism"],"prefix":"10.1152","volume":"244","author":[{"given":"D. P.","family":"Simpson","sequence":"first","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1983.244.3.F223","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T18:25:47Z","timestamp":1567967147000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1983.244.3.F223"}},"issued":{"date-parts":[[1983,3,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1983,3,1]]}},"alternative-id":["10.1152\/ajprenal.1983.244.3.F223"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1983.244.3.f223","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1983,3,1]]}},{"indexed":{"date-parts":[[2026,1,8]],"date-time":"2026-01-08T16:58:07Z","timestamp":1767891487709,"version":"3.49.0"},"reference-count":61,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2022,7,1]]},"abstract":"<jats:p> Dysregulation in glomerular hemodynamics favors hyperfiltration in diabetic kidney disease (DKD). Although carnosine supplementation ameliorates features of DKD, its effect on glomerular vasoregulation is not known. We assessed the influence of carnosine and carnosinase-1 (CN1) on afferent glomerular arteriole vasodilation and its association with glomerular size, hypertrophy, and nephrin expression in diabetic BTBR <jats:sup>ob\/ob<\/jats:sup> mice. Our results provide evidence that carnosine feeding and CN1 overexpression likely affect intraglomerular pressure through vasoregulation of the afferent arteriole. <\/jats:p>","DOI":"10.1152\/ajprenal.00232.2021","type":"journal-article","created":{"date-parts":[[2022,5,30]],"date-time":"2022-05-30T11:45:20Z","timestamp":1653911120000},"page":"F69-F80","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":10,"title":["Influence of carnosine and carnosinase-1 on diabetes-induced afferent arteriole vasodilation: implications for glomerular hemodynamics"],"prefix":"10.1152","volume":"323","author":[{"given":"Angelica","family":"Rodriguez-Ni\u00f1o","sequence":"first","affiliation":[{"name":"Department of Nephrology, University Medical Centre Groningen and University of Groningen, Groningen, The Netherlands"},{"name":"Vth Medical Department, University Hospital Mannheim, Heidelberg University, Mannheim, Germany"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5955-7335","authenticated-orcid":true,"given":"Diego O.","family":"Pastene","sequence":"additional","affiliation":[{"name":"Vth Medical Department, University Hospital Mannheim, Heidelberg University, Mannheim, Germany"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8454-5221","authenticated-orcid":true,"given":"Steffen A.","family":"Hettler","sequence":"additional","affiliation":[{"name":"Vth Medical Department, University Hospital Mannheim, Heidelberg University, Mannheim, Germany"}]},{"given":"Jiedong","family":"Qiu","sequence":"additional","affiliation":[{"name":"Vth Medical Department, University Hospital Mannheim, Heidelberg University, Mannheim, Germany"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2234-0909","authenticated-orcid":true,"given":"Thomas","family":"Albrecht","sequence":"additional","affiliation":[{"name":"Vth Medical Department, University Hospital Mannheim, Heidelberg University, Mannheim, Germany"}]},{"given":"Srishti","family":"Vajpayee","sequence":"additional","affiliation":[{"name":"Cyanagen Srl, Bologna, Italy"}]},{"given":"Rossana","family":"Perciaccante","sequence":"additional","affiliation":[{"name":"Cyanagen Srl, Bologna, Italy"}]},{"given":"Norbert","family":"Gretz","sequence":"additional","affiliation":[{"name":"Central Medical Research Facility ZMF, University Hospital Mannheim, Heidelberg University, Mannheim, Germany"}]},{"given":"Stephan J. L.","family":"Bakker","sequence":"additional","affiliation":[{"name":"Department of Nephrology, University Medical Centre Groningen and University of Groningen, Groningen, The Netherlands"}]},{"given":"Bernhard K.","family":"Kr\u00e4mer","sequence":"additional","affiliation":[{"name":"Vth Medical Department, University Hospital Mannheim, Heidelberg University, Mannheim, Germany"},{"name":"European Center for Angioscience, Mannheim, Germany"}]},{"given":"Benito A.","family":"Yard","sequence":"additional","affiliation":[{"name":"Vth Medical Department, University Hospital Mannheim, Heidelberg University, Mannheim, Germany"},{"name":"European Center for Angioscience, Mannheim, Germany"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7883-5361","authenticated-orcid":true,"given":"Jacob","family":"van den Born","sequence":"additional","affiliation":[{"name":"Department of Nephrology, University Medical Centre Groningen and University of Groningen, Groningen, The Netherlands"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/j.diabres.2019.107843"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2014.08.001"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2016060666"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/s41581-020-0256-y"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.4239\/wjd.v3.i1.1"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1007\/s00125-010-1794-9"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1002\/cphy.c100049"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1007\/s00125-009-1268-0"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.2337\/dc11-2189"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1172\/JCI12066"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1080\/10715762.2020.1856830"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00039.2012"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1038\/srep44492"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.2337\/db07-0177"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1111\/j.1582-4934.2010.01101.x"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.3923\/jas.2007.2252.2260"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1159\/000331740"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1007\/s00125-011-2178-5"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfl717"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.54.8.2320"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/j.diabres.2009.06.001"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.2337\/db09-1377"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.2337\/db07-0128"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00329.2019"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1007\/s00109-020-01957-0"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009121290"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.14814\/phy2.13186"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00279.2012"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1007\/s00726-012-1244-8"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-018-36741-1"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2818.2006.01706.x"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1093\/bioinformatics\/btt276"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002408"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1097\/HJH.0000000000002326"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2012.19"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-008-0581-7"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1007\/BF00371101"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.265"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00145.2014"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00415.2016"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00074.2008"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfn379"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.5.F817"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00421.2010"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.V1261211"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000068462.38661.89"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2013.265959"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1222433110"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1007\/s11095-008-9726-9"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1007\/s00232-010-9334-6"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00264.2020"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfg263"},{"key":"B53","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.39.8.989"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1007\/BF00401144"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1007\/BF00252683"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1016\/S0024-3205(01)01090-6"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00457.2007"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00693.2005"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1172\/JCI10963"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-017-13649-w"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1002\/oby.21434"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00232.2021","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,6,21]],"date-time":"2022-06-21T15:57:45Z","timestamp":1655827065000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajprenal.00232.2021"}},"issued":{"date-parts":[[2022,7,1]]},"references-count":61,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2022,7,1]]}},"alternative-id":["10.1152\/ajprenal.00232.2021"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00232.2021","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2022,7,1]]},"assertion":[{"value":"2021-06-15","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2022-05-12","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2022-05-12","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2022-06-21","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]},{"indexed":{"date-parts":[[2026,1,9]],"date-time":"2026-01-09T23:43:55Z","timestamp":1768002235637,"version":"3.49.0"},"reference-count":61,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2002,6,1]]},"abstract":"<jats:p>We previously characterized the prostaglandin (PG) transporter PGT as an exchanger in which [<jats:sup>3<\/jats:sup>H]PGE<jats:sub>2<\/jats:sub>influx is coupled to the efflux of a countersubstrate. Here, we cultured HeLa cells that stably expressed human PGT under conditions known to favor glycolysis (glucose as a carbon source) or oxidative phosphorylation (glutamine as a carbon source) and studied the effect on PGT-mediated [<jats:sup>3<\/jats:sup>H]PGE<jats:sub>2<\/jats:sub>influx. PGT-expressing cells grown in glutamine exhibited a 2- to 4-fold increase in [<jats:sup>3<\/jats:sup>H]PGE<jats:sub>2<\/jats:sub>influx compared with the antisense control, whereas cells grown in glucose exhibited a 14-fold increase. In the presence of 10 vs. 25 mM glucose during the uptake, there was a dose-dependent increment in [<jats:sup>3<\/jats:sup>H]PGE<jats:sub>2<\/jats:sub>influx. Cis inhibition of [<jats:sup>3<\/jats:sup>H]PGE<jats:sub>2<\/jats:sub>influx occurred with lactate at physiological concentrations (apparent K<jats:sub>m<\/jats:sub>= 48 \u00b1 12 mM). Preloading with lactate caused a dose-dependent trans stimulation of PGT-mediated [<jats:sup>3<\/jats:sup>H]PGE<jats:sub>2<\/jats:sub>uptake, and external lactate caused trans stimulation of PGT-mediated [<jats:sup>3<\/jats:sup>H]PGE<jats:sub>2<\/jats:sub>release. Together, these data are consistent with PGT-mediated PG-lactate exchange. Cells engaged in glycolysis would then be poised energetically for prostanoid uptake by means of PGT.<\/jats:p>","DOI":"10.1152\/ajprenal.00151.2001","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:32:23Z","timestamp":1425414743000},"page":"F1097-F1102","source":"Crossref","is-referenced-by-count":62,"title":["Identification of lactate as a driving force for prostanoid transport by prostaglandin transporter PGT"],"prefix":"10.1152","volume":"282","author":[{"given":"Brenda S.","family":"Chan","sequence":"first","affiliation":[{"name":"Department of Medicine, Albert Einstein College of Medicine, Bronx, New York 10461;"}]},{"given":"Shinichi","family":"Endo","sequence":"additional","affiliation":[{"name":"Department of Urology, Yamanashi Medical University, Yamanashi 409-3898; and"}]},{"given":"Naoaki","family":"Kanai","sequence":"additional","affiliation":[{"name":"Department of BioMedical Engineering, Tokai University, Kanagawa 259-11, Japan"}]},{"given":"Victor L.","family":"Schuster","sequence":"additional","affiliation":[{"name":"Department of Medicine, Albert Einstein College of Medicine, Bronx, New York 10461;"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/0090-6980(76)90067-8"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1006\/mgme.1998.2791"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00152.2001"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/0090-6980(81)90203-3"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1995.268.2.H713"},{"key":"B6","first-page":"66","volume":"1","author":"Beamish RE","year":"1985","journal-title":"Can J Cardiol"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1002\/nbm.1940070603"},{"key":"B8","doi-asserted-by":"crossref","first-page":"1580","DOI":"10.1152\/ajplegacy.1975.229.6.1580","volume":"229","author":"Bito LZ","year":"1975","journal-title":"Am J Physiol"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.1041600103"},{"key":"B10","first-page":"326","volume":"12","author":"Brezis M","year":"1986","journal-title":"Miner Electrolyte Metab"},{"key":"B11","first-page":"2924","volume":"45","author":"Brooks GA.","year":"1986","journal-title":"Federation Proc"},{"key":"B12","first-page":"228","volume":"1000","author":"Bucher T.","year":"1989","journal-title":"Biochim Biophys Acta"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.12.6689"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1054\/bjoc.2000.1309"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1007\/978-3-642-69132-4_56"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1977.233.5.H573"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1038\/216868a0"},{"key":"B18","first-page":"55","volume":"33","author":"Floridi A","year":"1989","journal-title":"J Neurosurg Sci"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/S0956-5663(98)00090-6"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1998.274.4.H1239"},{"key":"B21","doi-asserted-by":"crossref","first-page":"6713","DOI":"10.1016\/S0021-9258(19)45905-X","volume":"246","author":"Hamberg M","year":"1971","journal-title":"J Biol Chem"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/0090-6980(77)90195-2"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.1999.277.1.E176"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1126\/science.7754369"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.3109\/10409238709082546"},{"key":"B26","doi-asserted-by":"crossref","first-page":"22007","DOI":"10.1016\/S0021-9258(18)41626-2","volume":"267","author":"Kavanaugh MP","year":"1992","journal-title":"J Biol Chem"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1046\/j.1471-4159.1999.0721907.x"},{"key":"B28","first-page":"E229","volume":"236","author":"Kerr JS","year":"1979","journal-title":"Am J Physiol Endocrinol Metab Gastrointest Physiol"},{"key":"B29","first-page":"359","volume":"2","author":"Kristjansen PE","year":"1996","journal-title":"Clin Cancer Res"},{"key":"B30","doi-asserted-by":"crossref","first-page":"10093","DOI":"10.1016\/S0021-9258(18)61081-6","volume":"262","author":"Lanks KW.","year":"1987","journal-title":"J Biol Chem"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1016\/0014-4827(85)90241-1"},{"key":"B32","doi-asserted-by":"crossref","first-page":"351","DOI":"10.1152\/ajplegacy.1976.231.2.351","volume":"231","author":"Longmore WJ","year":"1976","journal-title":"Am J Physiol"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118897"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1111\/j.1460-9568.1995.tb00704.x"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1984.247.5.C433"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1098\/rstb.1999.0471"},{"key":"B38","doi-asserted-by":"crossref","first-page":"655","DOI":"10.1152\/ajplegacy.1968.215.3.655","volume":"215","author":"Needleman P","year":"1968","journal-title":"Am J Physiol"},{"key":"B39","first-page":"281","volume":"15","author":"Negoescu A.","year":"2000","journal-title":"Histol Histopathol"},{"key":"B40","doi-asserted-by":"crossref","first-page":"867","DOI":"10.1152\/ajplegacy.1974.226.4.867","volume":"226","author":"O'Neil JJ","year":"1974","journal-title":"Am J Physiol"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1097\/00005344-198406002-00006"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.91.22.10625"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1038\/225600a0"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1177\/10454411990100020201"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1999.277.3.R734"},{"key":"B46","doi-asserted-by":"crossref","first-page":"2669","DOI":"10.1016\/S0021-9258(17)30124-2","volume":"254","author":"Reitzer LJ","year":"1979","journal-title":"J Biol Chem"},{"key":"B47","first-page":"E619","volume":"235","author":"Rhoades RA","year":"1978","journal-title":"Am J Physiol Endocrinol Metab Gastrointest Physiol"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.37.6.742"},{"key":"B49","first-page":"1442","volume":"31","author":"Samuelsson B.","year":"1972","journal-title":"Federation Proc"},{"key":"B50","first-page":"63","volume":"48","author":"Schror K","year":"1997","journal-title":"Agents Actions Suppl"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1177\/019262339702500117"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2281.1998.00111.x"},{"key":"B53","first-page":"439","volume":"115","author":"Sinzinger H","year":"1988","journal-title":"Folia Haematol Int Mag Klin Morphol Blutforsch"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1249\/00005768-199809000-00012"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1016\/S0360-3016(00)00411-9"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1042\/bj2590315"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1016\/S0090-6980(79)80002-7"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1152\/jappl.1976.41.5.714"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.3109\/10428199909083376"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1987.253.5.R679"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1038\/383634a0"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.1040950106"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00151.2001","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,5,1]],"date-time":"2022-05-01T09:32:17Z","timestamp":1651397537000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00151.2001"}},"issued":{"date-parts":[[2002,6,1]]},"references-count":61,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2002,6,1]]}},"alternative-id":["10.1152\/ajprenal.00151.2001"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00151.2001","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2002,6,1]]}},{"indexed":{"date-parts":[[2026,1,14]],"date-time":"2026-01-14T23:15:00Z","timestamp":1768432500333,"version":"3.49.0"},"reference-count":40,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2003,2,1]]},"abstract":"<jats:p>The polarized distribution of Na-K-ATPase at the basolateral membranes of renal tubule epithelial cells is maintained via a tethering interaction with the underlying spectrin-ankyrin cytoskeleton. In this study, we have explored the mechanism underlying the loss of Na-K-ATPase polarity after ischemic injury in Madin-Darby canine kidney (MDCK) cells, utilizing a novel antibody raised against a recently described kidney-specific isoform of ankyrin. In control MDCK cells, ankyrin was colocalized with Na-K-ATPase at the basolateral membrane. ATP depletion resulted in a duration-dependent mislocation of Na-K-ATPase and ankyrin throughout the cytoplasm. Colocalization studies showed a partial overlap between the distribution of ankyrin and Na-K-ATPase at all periods after ATP depletion. By immunoprecipitation with anti-ankyrin antibody, the mislocated Na-K-ATPase remained bound to ankyrin at all time points after ATP depletion. However, the interaction between ankyrin and spectrin was markedly diminished within 3 h of ATP depletion and was completely lost after 6 h. In solution binding assays using a fusion peptide of glutathione S-transferase with the ankyrin binding domain of Na-K-ATPase, a complex with ankyrin was detected at all time points after ATP depletion, but spectrin was lost from the complex in a duration-dependent manner. The loss of spectrin binding was not attributable to spectrin degradation but was associated with hyperphosphorylation of ankyrin. The results suggest that a dissociation of the membrane-cytoskeleton complex at the spectrin-ankyrin interface may contribute to the loss of Na-K-ATPase polarity after ischemic injury and reaffirm a critical adapter role for ankyrin in the normal maintenance of Na-K-ATPase polarity.<\/jats:p>","DOI":"10.1152\/ajprenal.00100.2002","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:37:06Z","timestamp":1425415026000},"page":"F358-F364","source":"Crossref","is-referenced-by-count":36,"title":["Dissociation of spectrin-ankyrin complex as a basis for loss of Na-K-ATPase polarity after ischemia"],"prefix":"10.1152","volume":"284","author":[{"given":"Robert","family":"Woroniecki","sequence":"first","affiliation":[{"name":"Division of Pediatric Nephrology, Albert Einstein College of Medicine, New York, New York 10467;"}]},{"given":"Jean R.","family":"Ferdinand","sequence":"additional","affiliation":[{"name":"Division of Pediatric Nephrology, Albert Einstein College of Medicine, New York, New York 10467;"}]},{"given":"Jon S.","family":"Morrow","sequence":"additional","affiliation":[{"name":"Division of Pathology, Yale University School of Medicine, New Haven, Connecticut 06520; and"}]},{"given":"Prasad","family":"Devarajan","sequence":"additional","affiliation":[{"name":"Division of Pediatric Nephrology, Albert Einstein College of Medicine, New York, New York 10467;"},{"name":"Department of Nephrology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio 45229-3039"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.415"},{"key":"B2","doi-asserted-by":"crossref","first-page":"3301","DOI":"10.1242\/jcs.107.12.3301","volume":"107","author":"Bacallao R","year":"1994","journal-title":"J Cell Sci"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1996.270.5.C1263"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.2001.81.3.1353"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/S0955-0674(00)00175-7"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.2.F211"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1002\/jcb.240370305"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1016\/S0955-0674(98)80071-9"},{"key":"B9","doi-asserted-by":"crossref","first-page":"2331","DOI":"10.1242\/jcs.113.13.2331","volume":"113","author":"De Matteis MA","year":"2000","journal-title":"J Cell Sci"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/S0070-2161(08)60386-X"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.91.8.2965"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.133.4.819"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.94.20.10711"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1993.264.4.C1003"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.6.F837"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.12.12.3864"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.10.2.455"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.00102"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1006\/exmp.2001.2377"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.87.8.3009"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1999.055003963.x"},{"key":"B22","doi-asserted-by":"crossref","first-page":"14958","DOI":"10.1016\/S0021-9258(18)95686-3","volume":"260","author":"Lu PW","year":"1985","journal-title":"J Biol Chem"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.10.5659"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.265.5.F693"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.263.3.F488"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.4.F790"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115326"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.1.F1"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.108.2.455"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.130.2.313"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.9.11.3161"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1016\/S1074-7613(02)00396-5"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200007000-00015"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1203\/00006450-199408000-00001"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.256.3.F430"},{"key":"B36","first-page":"490","volume":"18","author":"Sutton TA","year":"1998","journal-title":"Semin Nephrol"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.37.23952"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.26.16133"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1006\/abbi.1993.1580"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.30.18681"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00100.2002","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,5,1]],"date-time":"2022-05-01T09:36:16Z","timestamp":1651397776000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00100.2002"}},"issued":{"date-parts":[[2003,2,1]]},"references-count":40,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2003,2,1]]}},"alternative-id":["10.1152\/ajprenal.00100.2002"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00100.2002","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2003,2,1]]}},{"indexed":{"date-parts":[[2026,1,15]],"date-time":"2026-01-15T02:49:41Z","timestamp":1768445381081,"version":"3.49.0"},"reference-count":47,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2006,6]]},"abstract":"<jats:p>In kidneys subjected to ischemic reperfusion injury (IRI) stathmin, a tubulin-binding protein involved in the regulation of mitosis, is expressed in dedifferentiated and proliferating renal tubule cells during the recovery phase. To ascertain the role of stathmin in the recovery from ischemic kidney injury, stathmin-deficient (OP18\u2212\/\u2212) and wild-type (WT) animals were subjected to experimental IRI. At 3, 7, and 14 days after reperfusion serum samples and kidneys were collected for the examination of parameters of renal function, morphology, and recovery. Our studies indicate that on day 14 after reperfusion OP18\u2212\/\u2212 mice have significant renal failure, whereas the creatinine levels of WT animals have returned to baseline. Compared with WT animals OP18\u2212\/\u2212 mice had more extensive tubular fibrosis. The examination of proliferating cell nuclear antigen expression indicated that OP18\u2212\/\u2212 animals have increased proliferative or DNA repair activity for a more prolonged duration. The OP18\u2212\/\u2212 animals also had an increased number of tubules with apoptotic cells. These results suggest that in stathmin-deficient mice subjected to IRI, the aberrant regulation of cell cycle progression, not observed under normal conditions, impairs or at least delays the process of tubular repair and recovery after acute renal injury.<\/jats:p>","DOI":"10.1152\/ajprenal.00424.2005","type":"journal-article","created":{"date-parts":[[2006,1,25]],"date-time":"2006-01-25T03:08:42Z","timestamp":1138158522000},"page":"F1559-F1567","source":"Crossref","is-referenced-by-count":21,"title":["Stathmin-deficient mice develop fibrosis and show delayed recovery from ischemic-reperfusion injury"],"prefix":"10.1152","volume":"290","author":[{"given":"Kamyar","family":"Zahedi","sequence":"first","affiliation":[]},{"given":"Monica P.","family":"Revelo","sequence":"additional","affiliation":[]},{"given":"Sharon","family":"Barone","sequence":"additional","affiliation":[]},{"given":"Zhaohui","family":"Wang","sequence":"additional","affiliation":[]},{"given":"Kathy","family":"Tehrani","sequence":"additional","affiliation":[]},{"given":"David P.","family":"Citron","sequence":"additional","affiliation":[]},{"given":"John J.","family":"Bissler","sequence":"additional","affiliation":[]},{"given":"Hamid","family":"Rabb","sequence":"additional","affiliation":[]},{"given":"Manoocher","family":"Soleimani","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1097-0215(19971127)73:5<678::AID-IJC11>3.0.CO;2-2"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.0050.2001"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1038\/bjc.1998.565"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1993.163"},{"key":"R5","unstructured":"Brattsand G, Roos G, Marklund U, Ueda H, Landberg G, Nanberg E, Sideras P, and Gullberg M.Quantitative analysis of the expression and regulation of an activation-regulated phosphoprotein (oncoprotein 18) in normal and neoplastic cells.Leukemia7: 569\u2013579, 1993."},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1038\/326515a0"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1002\/gcc.2870020208"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1002\/pros.2990270207"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.12.1.73"},{"key":"R10","doi-asserted-by":"crossref","unstructured":"Hughes J, Brown P, and Shankland SJ.Cyclin kinase inhibitor p21CIP1\/WAF1 limits interstitial cell proliferation following ureteric obstruction.Am J Physiol Renal Physiol277: F948\u2013F956, 1999.","DOI":"10.1152\/ajprenal.1999.277.6.F948"},{"key":"R11","unstructured":"Humes HD, Lake EW, and Liu S.Renal tubule cell repair following acute renal injury.Miner Electrolyte Metab21: 353\u2013365, 1995."},{"key":"R12","doi-asserted-by":"crossref","unstructured":"Iancu C, Mistry SJ, Arkin S, Wallenstein S, and Atweh GF.Effects of stathmin inhibition on the mitotic spindle.J Cell Sci114: 909\u2013916, 2001.","DOI":"10.1242\/jcs.114.5.909"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1126\/science.2897717"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1002\/1097-0215(20001201)88:5<685::AID-IJC1>3.0.CO;2-Z"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(95)00416-7"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000040596.23073.01"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.17.9.5530"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.23.14175"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-5793(97)01519-6"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)64866-3"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1021\/bi00433a034"},{"key":"R22","doi-asserted-by":"crossref","unstructured":"Lovric J, Dammeier S, Kieser A, Mischak H, and Kolch W.Activated raf induces the hyperphosphorylation of stathmin and the reorganization of the microtubule network.J Biol Chem273: 22848\u201322855, 1998.","DOI":"10.1016\/S0021-9258(18)48797-2"},{"key":"R23","doi-asserted-by":"crossref","unstructured":"Luo XN, Mookerjee B, Ferrari A, Mistry S, and Atweh GF.Regulation of phosphoprotein p18 in leukemic cells. Cell cycle regulated phosphorylation by p34cdc2 kinase.J Biol Chem269: 10312\u201310318, 1994.","DOI":"10.1016\/S0021-9258(17)34062-0"},{"key":"R24","doi-asserted-by":"crossref","unstructured":"Marklund U, Brattsand G, Osterman O, Ohlsson PI, and Gullberg M.Multiple signal transduction pathways induce phosphorylation of serines 16, 25, and 38 of oncoprotein 18 in T lymphocytes.J Biol Chem268: 25671\u201325680, 1993.","DOI":"10.1016\/S0021-9258(19)74442-1"},{"key":"R25","doi-asserted-by":"crossref","unstructured":"Marklund U, Brattsand G, Shingler V, and Gullberg M.Serine 25 of oncoprotein 18 is a major cytosolic target for the mitogen-activated protein kinase.J Biol Chem268: 15039\u201315047, 1993.","DOI":"10.1016\/S0021-9258(18)82435-8"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1111\/j.1432-1033.1994.00053.x"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1002\/j.1460-2075.1996.tb00914.x"},{"key":"R28","doi-asserted-by":"crossref","unstructured":"Marklund U, Osterman O, Melander H, Bergh A, and Gullberg M.The phenotype of a \u201cCdc2 kinase target site-deficient\u201d mutant of oncoprotein 18 reveals a role of this protein in cell cycle control.J Biol Chem269: 30626\u201330635, 1994.","DOI":"10.1016\/S0021-9258(18)43860-4"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00078.2002"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00044.x"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.17.6.3459"},{"key":"R32","unstructured":"Mistry SJand Atweh GF.Role of stathmin in the regulation of the mitotic spindle: potential applications in cancer therapy.Mt Sinai J Med69: 299\u2013304, 2002."},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1046\/j.1471-4159.1998.70062386.x"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.01-07-0362"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1111\/j.1432-1033.1997.t01-2-00794.x"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.386"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1159\/000045786"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(88)90493-X"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1038\/326517a0"},{"key":"R40","unstructured":"Rowlands DC, Williams A, Jones NA, Guest SS, Reynolds GM, Barber PC, and Brown G.Stathmin expression is a feature of proliferating cells of most, if not all, cell lineages.Lab Invest72: 100\u2013113, 1995."},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.24.14062"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.2000.278.2.H515"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M005437200"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1204777"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117214"},{"key":"R46","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00432.2003"},{"key":"R47","doi-asserted-by":"crossref","unstructured":"Zweier JL, Duilio C, Kuppusamy P, Santoro G, Elia PP, Tritto I, Cirillo P, Condorelli M, and Chiariello M.A short burst of oxygen radicals at reflow induces sustained release of oxidized glutathione from postischemic hearts.J Biol Chem268: 18532\u201318541, 1993.","DOI":"10.1016\/S0021-9258(17)46660-9"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00424.2005","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,7,23]],"date-time":"2021-07-23T03:04:08Z","timestamp":1627009448000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00424.2005"}},"issued":{"date-parts":[[2006,6]]},"references-count":47,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2006,6]]}},"alternative-id":["10.1152\/ajprenal.00424.2005"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00424.2005","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2006,6]]}},{"indexed":{"date-parts":[[2026,3,24]],"date-time":"2026-03-24T04:04:47Z","timestamp":1774325087277,"version":"3.50.1"},"reference-count":30,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2001,1,1]]},"abstract":"<jats:p>The role of epithelial Na channels in the response of the kidney to short-term Na deprivation was studied in rats. Animals were fed either a control-Na (3.9 g\/kg) or a low-Na ( 3.8 mg\/kg) diet for 15 h. Urinary excretion of Na (\u03bcmol\/min), measured in conscious animals in metabolic cages, was 0.45 \u00b1 0.07 in controls and 0.04 \u00b1 0.01 in Na-deprived animals. Glomerular filtration rate, measured as the clearance of creatinine, was unaffected by the change in diet, suggesting that the reduced Na excretion was the result of increased Na reabsorption. K excretion (\u03bcmol\/min), increased after the 15-h period of Na deprivation from 0.70 \u00b1 0.10 to 1.86 \u00b1 0.19. Thus the decrease in urine Na was compensated for, in terms of electrical charge balance, by an increase in urine K. Plasma aldosterone increased from 0.50 \u00b1 0.08 to 1.22 \u00b1 0.22 nM. Principal cells from cortical collecting tubules isolated from the animals were studied by using the patch-clamp technique. Whole cell amiloride-sensitive currents were negligible in the control group (5 \u00b1 4 pA\/cell) but substantial in the Na-deprived group (140 \u00b1 28 pA\/cell). The abundance of the epithelial Na channel subunits, \u03b1, \u03b2, and \u03b3 in the kidney was estimated by using immunoblots. There was no change in the overall abundance of any of the subunits after the 15-h Na deprivation. However, the apparent molecular mass of a fraction of the \u03b3-subunits decreased as was previously reported for long-term Na deprivation. Calculations of the rate of Na transport mediated by the Na channels indicated that activation of the channels during short-term Na deprivation could account in large part for the increased Na reabsorption under these conditions.<\/jats:p>","DOI":"10.1152\/ajprenal.2001.280.1.f112","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T13:34:15Z","timestamp":1514036055000},"page":"F112-F118","source":"Crossref","is-referenced-by-count":68,"title":["Activation of epithelial Na channels during short-term Na deprivation"],"prefix":"10.1152","volume":"280","author":[{"given":"Gustavo","family":"Frindt","sequence":"first","affiliation":[{"name":"Department of Physiology and Biophysics, Weill Medical College of Cornell University, New York, New York 10021; and"}]},{"given":"Shyama","family":"Masilamani","sequence":"additional","affiliation":[{"name":"Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892"}]},{"given":"Mark A.","family":"Knepper","sequence":"additional","affiliation":[{"name":"Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892"}]},{"given":"Lawrence G.","family":"Palmer","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, Weill Medical College of Cornell University, New York, New York 10021; and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1996.271.2.C605"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1980.238.3.F181"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1210\/endo-88-3-556"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/0889-1605(88)90052-3"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1997.272.5.C1482"},{"key":"B6","doi-asserted-by":"crossref","first-page":"1494","DOI":"10.1093\/clinchem\/29.8.1494","volume":"29","author":"Fossati P","year":"1983","journal-title":"Clin Chem"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.268.3.F480"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1966.sp007954"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1983.245.1.F89"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1992.263.4.C825"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.24.14552"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1977.118"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1172\/JCI7840"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.84.5.1464"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1007\/s004240050462"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.102.1.25"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.102.1.43"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.5.F805"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.1998.151bo.x"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1172\/JCI112433"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1007\/BF00373903"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.258.1.F199"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1007\/BF00584753"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1978.235.6.F576"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1981.241.4.F395"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.2.F414"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1172\/JCI111935"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.253.3.F555"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.3.F319"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.1985.248.1.G124"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.2001.280.1.F112","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2020,10,24]],"date-time":"2020-10-24T20:35:34Z","timestamp":1603571734000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.2001.280.1.F112"}},"issued":{"date-parts":[[2001,1,1]]},"references-count":30,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2001,1,1]]}},"alternative-id":["10.1152\/ajprenal.2001.280.1.F112"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.2001.280.1.f112","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2001,1,1]]}},{"indexed":{"date-parts":[[2026,3,24]],"date-time":"2026-03-24T09:00:58Z","timestamp":1774342858004,"version":"3.50.1"},"reference-count":48,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2001,9,1]]},"abstract":"<jats:p> Puromycin aminonucleoside (PAN) has been suggested to reduce glomerular charge density, to create large glomerular \u201cleaks,\u201d or not to affect the glomerular barrier. Therefore, we analyzed glomerular charge and size selectivity in vivo and in isolated kidneys perfused at 8\u00b0C (cIPK) in control and PAN-treated rats. The fractional clearances (\u03b8) for albumin and Ficoll of similar hydrodynamic size were 0.0017 \u00b1 0.0004 and 0.15 \u00b1 0.02, respectively, in control cIPKs. Two-pore analysis gave similar results in vivo and in vitro, with small- and large-pore radii of 47\u201352 and 85\u2013105 \u00c5, respectively, in controls. Puromycin increased the number of large pores 40\u201350 times, the total pore area over diffusion distance decreased by a factor of 25\u201330, and the small-pore radius increased by 33% ( P &lt; 0.001 for all comparisons of size selectivity and \u03b8). The effect of PAN was less dramatic on the estimated wall charge density, which was 73% of that of controls. We conclude that puromycin effectively destroys the glomerular size barrier with minimal effects on charge density. <\/jats:p>","DOI":"10.1152\/ajprenal.2001.281.3.f503","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T14:12:44Z","timestamp":1514038364000},"page":"F503-F512","source":"Crossref","is-referenced-by-count":21,"title":["Puromycin aminonucleoside damages the glomerular size barrier with minimal effects on charge density"],"prefix":"10.1152","volume":"281","author":[{"given":"Clara","family":"Hjalmarsson","sequence":"first","affiliation":[{"name":"Departments of Physiology and"}]},{"given":"Maria","family":"Ohlson","sequence":"additional","affiliation":[{"name":"Departments of Physiology and"}]},{"given":"B\u00f6rje","family":"Haraldsson","sequence":"additional","affiliation":[{"name":"Departments of Physiology and"},{"name":"Nephrology, G\u00f6teborg University, G\u00f6teborg SE-405 30, Sweden"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1985.153"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.273.3.F430"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1172\/JCI108751"},{"key":"B4","first-page":"503","volume":"40","author":"Caufield JP.","year":"1979","journal-title":"Lab Invest"},{"key":"B5","first-page":"505","volume":"39","author":"Caufield JP","year":"1978","journal-title":"Lab Invest"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1007\/s004249900120"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1985.249.3.F374"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1980.238.2.F126"},{"key":"B9","first-page":"437","volume":"50","author":"Fiegelson EB","year":"1957","journal-title":"J Lab Clin Med"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1007\/BF02890122"},{"key":"B11","doi-asserted-by":"crossref","first-page":"1","DOI":"10.1111\/j.1748-1716.1986.tb07973.x","volume":"128","author":"Haraldsson B.","year":"1986","journal-title":"Acta Physiol Scand"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1254\/jjp.70.25"},{"key":"B13","first-page":"1009","volume":"149","author":"Holth\u00f6fer H","year":"1996","journal-title":"Am J Pathol"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1994.tb09676.x"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1991.310"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1984.65"},{"key":"B17","first-page":"121","volume":"4","author":"Kanwar YS","year":"1981","journal-title":"Renal Physiol"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00044.x"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/S1097-2765(00)80057-X"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1989.140"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1977.2"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-201x.1999.00559.x"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00308.x"},{"key":"B24","first-page":"393","volume":"125","author":"Mahan JD","year":"1986","journal-title":"Am J Pathol"},{"key":"B25","first-page":"660","volume":"103","author":"Malis CD","year":"1984","journal-title":"J Lab Clin Med"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/S0376-7388(00)80439-1"},{"key":"B27","first-page":"30","volume":"117","author":"Nevins TE","year":"1984","journal-title":"Am J Pathol"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.1.F84"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.3.F396"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1159\/000395223"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1987.217"},{"key":"B32","first-page":"271","volume":"44","author":"Olson JL","year":"1981","journal-title":"Lab Invest"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.1.F139"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1797.1996.tb00088.x"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1053\/lc.1999.v133.a94726"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1994.74.1.163"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.14.7962"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1975.105"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1990.88"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.4.F646"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-201x.1998.00315.x"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1979.140"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00797.x"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1992.263.4.F601"},{"key":"B44a","first-page":"50","volume":"7","author":"Waniewski J","year":"1992","journal-title":"Nephrol Dial Transplant"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-201X.1996.552307000.x"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1006\/clin.1996.0073"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00314.x"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.2001.281.3.F503","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:56:27Z","timestamp":1567976187000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.2001.281.3.F503"}},"issued":{"date-parts":[[2001,9,1]]},"references-count":48,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2001,9,1]]}},"alternative-id":["10.1152\/ajprenal.2001.281.3.F503"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.2001.281.3.f503","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2001,9,1]]}},{"indexed":{"date-parts":[[2026,3,24]],"date-time":"2026-03-24T08:54:16Z","timestamp":1774342456942,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1990,4,1]]},"abstract":"<jats:p> These studies were designed to characterize mechanisms leading to decreased plasma osmolality (Posmol) and osmotic thresholds (T) for arginine vasopressin (AVP) release (TAVP) and thirst (Tthirst) in pregnancy. First, the influence of the pregnancy hormone, human chorionic gonadotrophin (hCG), was tested in six nonpregnant women who received hypertonic saline during the luteal phase of the menstrual cycle on two occasions (randomly allocated), once after 15,000 IU of hCG when Posmol, TAVP, and Tthirst decreased 6, 5, and 5 mosmol\/kgH2O, respectively (P less than 0.01). In contrast, hCG pretreatment of males (n = 6) had no significant effect. Next, the role of decreased effective vascular volume (underfilling) was evaluated in seven women undergoing hypertonic saline infusion in the presence and absence of head-out water immersion (randomly allocated) during early and late pregnancy and postpartum. Posmol, TAVP, and Tthirst were not influenced by immersion and remained 10 mosmol\/kgH2O lower in pregnancy (P less than 0.01). Central redistribution of intravascular volume consistently lowered hematocrit and rate of rise of PAVP per unit increment in Posmol (P less than 0.01). Although these data failed to support the hypothesis that the osmoregulatory change in human pregnancy is attributable to decrements in effective central volume (underfill), they do suggest that hCG may play a role. <\/jats:p>","DOI":"10.1152\/ajprenal.1990.258.4.f900","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T23:20:11Z","timestamp":1513984811000},"page":"F900-F907","source":"Crossref","is-referenced-by-count":4,"title":["Influence of humoral and volume factors on altered osmoregulation of normal human pregnancy"],"prefix":"10.1152","volume":"258","author":[{"given":"J. M.","family":"Davison","sequence":"first","affiliation":[{"name":"Medical Research Council Human Reproduction Group, Princess MaryMaternity Hospital, University of Newcastle, Newcastle upon Tyne, UnitedKingdom."}]},{"given":"E. A.","family":"Shiells","sequence":"additional","affiliation":[{"name":"Medical Research Council Human Reproduction Group, Princess MaryMaternity Hospital, University of Newcastle, Newcastle upon Tyne, UnitedKingdom."}]},{"given":"P. R.","family":"Philips","sequence":"additional","affiliation":[{"name":"Medical Research Council Human Reproduction Group, Princess MaryMaternity Hospital, University of Newcastle, Newcastle upon Tyne, UnitedKingdom."}]},{"given":"M. D.","family":"Lindheimer","sequence":"additional","affiliation":[{"name":"Medical Research Council Human Reproduction Group, Princess MaryMaternity Hospital, University of Newcastle, Newcastle upon Tyne, UnitedKingdom."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1990.258.4.F900","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:22:13Z","timestamp":1567970533000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1990.258.4.F900"}},"issued":{"date-parts":[[1990,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1990,4,1]]}},"alternative-id":["10.1152\/ajprenal.1990.258.4.F900"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1990.258.4.f900","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1990,4,1]]}},{"indexed":{"date-parts":[[2026,3,24]],"date-time":"2026-03-24T09:27:21Z","timestamp":1774344441518,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1986,5,1]]},"abstract":"<jats:p> The equations of mass conservation and electroneutrality are used to extend a nonequilibrium thermodynamic model of the rat proximal tubule epithelium to a representation of a 0.5-cm segment of tubule. The output of the tubule model includes the luminal profiles and absolute proximal reabsorption of Na, K, Cl, HCO3, HPO4, H2PO4, glucose, and urea, generated by the epithelial model. Transport rates and permeabilities, chosen in agreement with those of the rat, result in luminal glucose and bicarbonate depletion and a transition from an electronegative to positive lumen. Despite the development of significant transepithelial osmotic driving forces (a transepithelial glucose gradient and Cl-HCO3 asymmetry), intraepithelial solute-solvent coupling remains an important force for water reabsorption along the proximal tubule length. In particular, this means that when osmotic gradients that appear under free-flow conditions are used in the calculation of the epithelial water permeability, a substantial overestimate of this permeability will be obtained. A single first-order differential equation has been derived in conjunction with an approximate nonelectrolyte model of the proximal tubule that represents both coupled and gradient-driven water reabsorption. In the present work, this equation is shown to yield an accurate description of water transport by the comprehensive tubule model. <\/jats:p>","DOI":"10.1152\/ajprenal.1986.250.5.f860","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T20:02:00Z","timestamp":1513972920000},"page":"F860-F873","source":"Crossref","is-referenced-by-count":30,"title":["A mathematical model of the rat proximal tubule"],"prefix":"10.1152","volume":"250","author":[{"given":"A. M.","family":"Weinstein","sequence":"first","affiliation":[]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1986.250.5.F860","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:34:44Z","timestamp":1567956884000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1986.250.5.F860"}},"issued":{"date-parts":[[1986,5,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1986,5,1]]}},"alternative-id":["10.1152\/ajprenal.1986.250.5.F860"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1986.250.5.f860","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1986,5,1]]}},{"indexed":{"date-parts":[[2026,3,18]],"date-time":"2026-03-18T22:34:45Z","timestamp":1773873285368,"version":"3.50.1"},"reference-count":50,"publisher":"American Physiological Society","issue":"12","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2014,6,15]]},"abstract":"<jats:p>\u03b1<jats:sub>v<\/jats:sub>\u03b2<jats:sub>8<\/jats:sub>-Integrin is most abundantly expressed in the kidney, brain, and female reproductive organs, and its cognate ligand is latent transforming growth factor (LTGF)-\u03b2. Kidney \u03b1<jats:sub>v<\/jats:sub>\u03b2<jats:sub>8<\/jats:sub>-integrin localizes to mesangial cells, and global \u03b2<jats:sub>8<\/jats:sub>-integrin gene ( Itgb8) deletion results in embryonic lethality due to impaired placentation and cerebral hemorrhage. To circumvent the lethality and better define kidney \u03b1<jats:sub>v<\/jats:sub>\u03b2<jats:sub>8<\/jats:sub>-integrin function, Cre-lox technology was used to generate mesangial-specific Itgb8-null mice. Platelet-derived growth factor-\u03b2 receptor ( PDGFBR)- Cre mice crossed with a reporter strain revealed functional Cre recombinase activity in a predicted mesangial pattern. However, mating between two different PDGFBR-Cre or Ren1<jats:sup>d<\/jats:sup>-Cre strains with Itgb8<jats:sup>flox\/\u2212<\/jats:sup>mice consistently resulted in incomplete recombination, with no renal phenotype in mosaic offspring. Induction of a renal phenotype with Habu snake venom, a reversible mesangiolytic agent, caused exaggerated glomerular capillary microaneurysms and delayed recovery in Cre<jats:sup>+\/\u2212<\/jats:sup>PDGFRB<jats:sup>flox\/\u2212<\/jats:sup>mice compared with Cre<jats:sup>+\/\u2212<\/jats:sup>PDGFRB<jats:sup>flox\/+<\/jats:sup>control mice. To establish the mechanism, in vitro experiments were conducted in Itgb8-null versus Itgb8-expressing mesangial cells and fibroblasts, which revealed \u03b2<jats:sub>8<\/jats:sub>-integrin-regulated adhesion to Arg-Gly-Asp (RGD) peptides within a mesangial-conditioned matrix as well as \u03b2<jats:sub>8<\/jats:sub>-integrin-dependent migration on RGD-containing LTGF-\u03b2 or vitronectin matrices. We speculate that kidney \u03b1<jats:sub>v<\/jats:sub>\u03b2<jats:sub>8<\/jats:sub>-integrin indirectly controls glomerular capillary integrity through mechanical tension generated by binding RGD peptides in the mesangial matrix, and healing after glomerular injury may be facilitated by mesangial cell migration, which is guided by transient \u03b2<jats:sub>8<\/jats:sub>-integrin interactions with RGD ligands.<\/jats:p>","DOI":"10.1152\/ajprenal.00624.2013","type":"journal-article","created":{"date-parts":[[2014,4,17]],"date-time":"2014-04-17T05:10:16Z","timestamp":1397711416000},"page":"F1400-F1409","source":"Crossref","is-referenced-by-count":15,"title":["Mesangial cell \u03b1<sub>v<\/sub>\u03b2<sub>8<\/sub>-integrin regulates glomerular capillary integrity and repair"],"prefix":"10.1152","volume":"306","author":[{"given":"Sujata","family":"Lakhe-Reddy","sequence":"first","affiliation":[{"name":"Department of Medicine, Case Western Reserve University, Rammelkamp Center for Research, MetroHealth Medical Center, Cleveland, Ohio; and"}]},{"given":"Vincent","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Medicine, Case Western Reserve University, Rammelkamp Center for Research, MetroHealth Medical Center, Cleveland, Ohio; and"}]},{"given":"Thomas D.","family":"Arnold","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, University of California, San Francisco, California"}]},{"given":"Shenaz","family":"Khan","sequence":"additional","affiliation":[{"name":"Department of Medicine, Case Western Reserve University, Rammelkamp Center for Research, MetroHealth Medical Center, Cleveland, Ohio; and"}]},{"given":"Jeffrey R.","family":"Schelling","sequence":"additional","affiliation":[{"name":"Department of Medicine, Case Western Reserve University, Rammelkamp Center for Research, MetroHealth Medical Center, Cleveland, Ohio; and"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M110.212845"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2004.00634.x"},{"key":"B3","first-page":"1366","volume":"143","author":"Barnes JL","year":"1993","journal-title":"Am J Pathol"},{"key":"B4","first-page":"460","volume":"70","author":"Barnes JL","year":"1994","journal-title":"Lab Invest"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/S0960-9822(02)70717-3"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)62497-2"},{"key":"B7","first-page":"7084","volume":"60","author":"Cambier S","year":"2000","journal-title":"Cancer Res"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1002\/dvg.20769"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1002\/dvg.20400"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2005.10.034"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.198"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00204.2005"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000082999.46030.FE"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1042\/BST20120103"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1159\/000110022"},{"key":"B16","first-page":"261","volume-title":"Pathology of the Kidney","author":"Heptinstall RH","year":"1992"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1172\/JCI38399"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119592"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M204901200"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0067839"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5001988"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1016\/j.ajpath.2010.10.031"},{"key":"B23","first-page":"115","volume":"52","author":"Khan S","year":"2006","journal-title":"Cell Mol Biol"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200211121"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M601110200"},{"key":"B26","doi-asserted-by":"crossref","first-page":"753","DOI":"10.1242\/jcs.105.3.753","volume":"105","author":"Langhofer M","year":"1993","journal-title":"J Cell Sci"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1101\/gad.8.16.1875"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1242\/dev.01551"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.22.21.7667-7677.2002"},{"key":"B30","doi-asserted-by":"crossref","first-page":"19650","DOI":"10.1016\/S0021-9258(18)55042-0","volume":"266","author":"Moyle M","year":"1991","journal-title":"J Biol Chem"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200109100"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.3467-05.2005"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.095794"},{"key":"B34","first-page":"813","volume":"78","author":"Schelling JR","year":"1998","journal-title":"Lab Invest"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0001013"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1016\/S1357-2725(99)00005-9"},{"key":"B37","first-page":"470","volume":"124","author":"Sedor JR","year":"1994","journal-title":"J Lab Clin Med"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.99"},{"key":"B39","doi-asserted-by":"crossref","first-page":"19836","DOI":"10.1016\/S0021-9258(17)32096-3","volume":"269","author":"Seiffert D","year":"1994","journal-title":"J Biol Chem"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1016\/S1534-5807(04)00134-0"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1101\/gad.8.16.1888"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M314155200"},{"key":"B43","doi-asserted-by":"crossref","first-page":"S144","DOI":"10.1681\/ASN.V210s144","volume":"2","author":"Stahl RA","year":"1992","journal-title":"J Am Soc Nephrol"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1038\/nature06110"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.6.4.419"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1093\/embo-reports\/kve064"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1007\/s10157-012-0711-6"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1186\/1472-6750-10-75"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.122.1.235"},{"key":"B50","doi-asserted-by":"crossref","first-page":"2891","DOI":"10.1242\/dev.129.12.2891","volume":"129","author":"Zhu JW","year":"2002","journal-title":"Development"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00624.2013","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,4,1]],"date-time":"2022-04-01T20:15:15Z","timestamp":1648844115000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00624.2013"}},"issued":{"date-parts":[[2014,6,15]]},"references-count":50,"journal-issue":{"issue":"12","published-print":{"date-parts":[[2014,6,15]]}},"alternative-id":["10.1152\/ajprenal.00624.2013"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00624.2013","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2014,6,15]]}},{"indexed":{"date-parts":[[2026,3,18]],"date-time":"2026-03-18T23:28:25Z","timestamp":1773876505826,"version":"3.50.1"},"reference-count":43,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2013,9,15]]},"abstract":"<jats:p>Podocyte damage and accumulation of advanced glycation end products (AGEs) are characteristics of diabetic nephropathy (DN). The pathophysiology of AGE-challenged podocytes, such as hypertrophy, apoptosis, and reduced cell migration, is closely related to the induction of the cell cycle inhibitor p27<jats:sup>Kip1<\/jats:sup>and to the inhibition of neuropilin 1 (NRP1). We have previously demonstrated that treatment with erythropoietin is associated with protective effects for podocytes in vitro. db\/ db mice with overt DN aged 15\u201316 wk were treated with either placebo, epoetin-\u03b2, or continuous erythropoietin receptor activator (CERA) for 2 wk. db\/ db mice compared with nondiabetic db\/ m control mice revealed the expected increases in body weight, blood glucose, albumin-to-creatinine ratio, and AGE accumulation. Whereas there were no differences in body weight, hyperglycemia and AGEs were observed among diabetic mice that received epoetin-\u03b2 compared with CERA and placebo treatment, indicating that epoetin-\u03b2\/CERA treatment does not interfere with the development of diabetes in this model. However, the albumin-to-creatinine ratio was significantly lower in db\/ db mice treated with epoetin-\u03b2 or CERA. Furthermore, kidney weights in db\/ db mice were increased compared with db\/ m control mice, indicating renal hypertrophy, whereas the increase in renal weight in epoetin-\u03b2- or CERA-treated db\/ db mice was significantly lower than in placebo-treated control mice. Induction of p27<jats:sup>Kip1<\/jats:sup>and suppression of NRP1 were significantly reduced in the epoetin-\u03b2 treatment group versus the CERA treatment group. Furthermore, erythropoietin treatment diminished the diabetes-induced podocyte loss. Together, independently from hematopoetic effects, epoetin-\u03b2 or CERA treatment was associated with protective changes in DN, especially that NRP1 and p27<jats:sup>Kip1<\/jats:sup>expressions as well as numbers of podocytes returned to normal levels. Our data show, for the first time, that medication of overt DN with erythropoietin for a short time can ameliorate albuminuria and podocyte loss.<\/jats:p>","DOI":"10.1152\/ajprenal.00643.2012","type":"journal-article","created":{"date-parts":[[2013,7,4]],"date-time":"2013-07-04T08:28:15Z","timestamp":1372926495000},"page":"F911-F918","source":"Crossref","is-referenced-by-count":37,"title":["Erythropoietin ameliorates podocyte injury in advanced diabetic nephropathy in the<i>db<\/i>\/<i>db<\/i>mouse"],"prefix":"10.1152","volume":"305","author":[{"given":"Ivonne","family":"Loeffler","sequence":"first","affiliation":[{"name":"Department of Internal Medicine III, University Hospital Jena, Jena, Germany"}]},{"given":"Christiane","family":"R\u00fcster","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine III, University Hospital Jena, Jena, Germany"}]},{"given":"Sybille","family":"Franke","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine III, University Hospital Jena, Jena, Germany"}]},{"given":"Marita","family":"Liebisch","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine III, University Hospital Jena, Jena, Germany"}]},{"given":"Gunter","family":"Wolf","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine III, University Hospital Jena, Jena, Germany"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1742-1241.2006.01259.x"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0b013e3283451901"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1007\/s00125-006-0247-y"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002101"},{"key":"B5","doi-asserted-by":"crossref","first-page":"990","DOI":"10.1681\/ASN.V17990","volume":"1","author":"Bennett WM","year":"1991","journal-title":"J Am Soc Nephrol"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2008.603"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1159\/000227762"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.2337\/diacare.24.3.495"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2362.2010.02317.x"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2011.473"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1159\/000084109"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfr698"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002311"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1038\/sj.cdd.4401450"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.2174\/1573399052952622"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2011.03.033"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5002362"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1016\/j.jdiacomp.2005.08.001"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfs579"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006070699"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfs005"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/15.9.1379"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119163"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.7150\/ijbs.4.161"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1007\/s00125-006-0514-y"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.2337\/db09-1766"},{"key":"B27","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2006.02.170"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfn085"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1159\/000319653"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1159\/000186368"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa1005109"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1100\/tsw.2009.133"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1016\/j.diabres.2009.10.022"},{"key":"B34","doi-asserted-by":"crossref","first-page":"1656","DOI":"10.1681\/ASN.V1191656","volume":"11","author":"Tanji N","year":"2000","journal-title":"J Am Soc Nephrol"},{"key":"B35","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejphar.2009.03.065"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1369\/jhc.2009.953224"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000065100.17349.CA"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.54.6.1626"},{"key":"B39","doi-asserted-by":"publisher","DOI":"10.1159\/000155230"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00570.x"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.1998.00829.x"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1159\/000101797"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1186\/1758-5996-1-10"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00643.2012","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,2,27]],"date-time":"2022-02-27T08:59:33Z","timestamp":1645952373000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00643.2012"}},"issued":{"date-parts":[[2013,9,15]]},"references-count":43,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2013,9,15]]}},"alternative-id":["10.1152\/ajprenal.00643.2012"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00643.2012","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2013,9,15]]}},{"indexed":{"date-parts":[[2026,3,14]],"date-time":"2026-03-14T03:49:33Z","timestamp":1773460173276,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1997,2,1]]},"abstract":"<jats:p> Aquaporin-3 (AQP3) is unique in its structure (lowest homology with other aquaporins) and in its function (significantly conductive to both small nonelectrolytes and water). However, there is a controversy among researchers on its water transport and induction by dehydration. We examined its localization and the effect of dehydration on its expression in the kidney, as well as its water channel activity when expressed in Xenopus oocytes. In vitro translation using reticulocyte lysate revealed that the size of rat AQP3 was 26 kDa, and the band shifted to around 31 kDa with microsomal fraction, which was sensitive to the digestion with N-glycosidase F. In Western blot analysis of rat kidney medulla, AQP3 appeared as a sharp band at 27 kDa and a broad band at 34-40 kDa. In immunohistochemistry, AQP3 was localized to principal cells and absent in intercalated cells in outer medulla. In inner medulla, AQP3 was restricted to inner medullary collecting duct (IMCD) cells. AQP3 was confined to the basolateral membrane of these cells. Although dehydration of rats for 2 days did not change the distribution pattern of AQP3 in IMCD cells, the dehydration increased AQP3 mRNA by twofold with slight increase of its protein level in kidney medulla. Finally, we confirmed its water channel activity when expressed in Xenopus oocytes. The human AQP3 stimulated osmotic water permeability by eightfold, which was inhibited by 0.3 mM mercury chloride by 34% and reversed by beta-mercaptoethanol. Our results indicate that AQP3 is a glycosylated protein and a mercury-sensitive water channel localized at the basolateral membrane of principal cells and IMCD cells, and its expression is induced by dehydration at both protein and mRNA level. <\/jats:p>","DOI":"10.1152\/ajprenal.1997.272.2.f235","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T08:43:57Z","timestamp":1514018637000},"page":"F235-F241","source":"Crossref","is-referenced-by-count":24,"title":["Immunolocalization and effect of dehydration on AQP3, a basolateral water channel of kidney collecting ducts"],"prefix":"10.1152","volume":"272","author":[{"given":"K.","family":"Ishibashi","sequence":"first","affiliation":[{"name":"Second Department of Internal Medicine, Tokyo Medical and DentalUniversity, Japan."}]},{"given":"S.","family":"Sasaki","sequence":"additional","affiliation":[{"name":"Second Department of Internal Medicine, Tokyo Medical and DentalUniversity, Japan."}]},{"given":"K.","family":"Fushimi","sequence":"additional","affiliation":[{"name":"Second Department of Internal Medicine, Tokyo Medical and DentalUniversity, Japan."}]},{"given":"T.","family":"Yamamoto","sequence":"additional","affiliation":[{"name":"Second Department of Internal Medicine, Tokyo Medical and DentalUniversity, Japan."}]},{"given":"M.","family":"Kuwahara","sequence":"additional","affiliation":[{"name":"Second Department of Internal Medicine, Tokyo Medical and DentalUniversity, Japan."}]},{"given":"F.","family":"Marumo","sequence":"additional","affiliation":[{"name":"Second Department of Internal Medicine, Tokyo Medical and DentalUniversity, Japan."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1997.272.2.F235","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:16:29Z","timestamp":1567973789000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1997.272.2.F235"}},"issued":{"date-parts":[[1997,2,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1997,2,1]]}},"alternative-id":["10.1152\/ajprenal.1997.272.2.F235"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1997.272.2.f235","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1997,2,1]]}},{"indexed":{"date-parts":[[2026,3,14]],"date-time":"2026-03-14T03:45:22Z","timestamp":1773459922818,"version":"3.50.1"},"reference-count":76,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2011,5]]},"abstract":"<jats:p>Activation of the renal kallikrein-kinin system results in natriuresis and diuresis, suggesting its possible role in renal tubular sodium transport regulation. Here, we used patch-clamp electrophysiology to directly assess the effects of bradykinin (BK) on the epithelial Na<jats:sup>+<\/jats:sup>channel (ENaC) activity in freshly isolated split-opened murine aldosterone-sensitive distal nephrons (ASDNs). BK acutely inhibits ENaC activity by reducing channel open probability ( P<jats:sub>o<\/jats:sub>) in a dose-dependent and reversible manner. Inhibition of B2 receptors with icatibant (HOE-140) abolished BK actions on ENaC. In contrast, activation of B1 receptors with the selective agonist Lys-des-Arg<jats:sup>9<\/jats:sup>-BK failed to reproduce BK actions on ENaC. This is consistent with B2 receptors playing a critical role in mediating BK signaling to ENaC. BK has little effect on ENaC P<jats:sub>o<\/jats:sub>when G<jats:sub>q\/11<\/jats:sub>was inhibited with Gp antagonist 2A. Moreover, inhibition of phospholipase C (PLC) with U73122, but not saturation of cellular cAMP levels with the membrane-permeable nonhydrolysable cAMP analog 8-cpt-cAMP, prevents BK actions on ENaC activity. This argues that BK stimulates B2 receptors with subsequent activation of G<jats:sub>q\/11<\/jats:sub>-PLC signaling cascade to acutely inhibit ENaC activity. Activation of BK signaling acutely depletes apical PI( 4 , 5 )P<jats:sub>2<\/jats:sub>levels. However, inhibition of Ca<jats:sup>2+<\/jats:sup>pump SERCA of the endoplasmic reticulum with thapsigargin does not prevent BK signaling to ENaC. Furthermore, caffeine, while producing a similar rise in [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>as in response to BK stimulation, fails to recapitulate BK actions on ENaC. Therefore, we concluded that BK acutely inhibits ENaC P<jats:sub>o<\/jats:sub>in mammalian ASDN via stimulation of B2 receptors and following depletion of PI( 4 , 5 )P<jats:sub>2<\/jats:sub>, but not increases in [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>.<\/jats:p>","DOI":"10.1152\/ajprenal.00606.2010","type":"journal-article","created":{"date-parts":[[2011,2,17]],"date-time":"2011-02-17T03:36:01Z","timestamp":1297913761000},"page":"F1105-F1115","source":"Crossref","is-referenced-by-count":44,"title":["Bradykinin acutely inhibits activity of the epithelial Na<sup>+<\/sup>channel in mammalian aldosterone-sensitive distal nephron"],"prefix":"10.1152","volume":"300","author":[{"given":"Oleg","family":"Zaika","sequence":"first","affiliation":[{"name":"Department of Integrative Biology and Pharmacology, The University of Texas Health Science Center at Houston, Houston, Texas"}]},{"given":"Mykola","family":"Mamenko","sequence":"additional","affiliation":[{"name":"Department of Integrative Biology and Pharmacology, The University of Texas Health Science Center at Houston, Houston, Texas"}]},{"given":"Roger G.","family":"O'Neil","sequence":"additional","affiliation":[{"name":"Department of Integrative Biology and Pharmacology, The University of Texas Health Science Center at Houston, Houston, Texas"}]},{"given":"Oleh","family":"Pochynyuk","sequence":"additional","affiliation":[{"name":"Department of Integrative Biology and Pharmacology, The University of Texas Health Science Center at Houston, Houston, Texas"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.29.1.483"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1996.1076"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/S0091-679X(08)60982-6"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1034\/j.1600-0854.2001.21104.x"},{"key":"B5","doi-asserted-by":"crossref","first-page":"1","DOI":"10.1016\/S0031-6997(25)00058-4","volume":"44","author":"Bhoola KD","year":"1992","journal-title":"Pharmacol Rev"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1046\/j.1439-0272.2003.00533.x"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.279.1.F12"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00371.2009"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1590\/S0100-879X2000000600008"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000119190.06968.f1"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1038\/367463a0"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1007\/s00232-001-0098-x"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1177\/43.2.7822771"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1016\/0162-3109(96)00016-1"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M302517200"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1997.77.2.359"},{"key":"B17","first-page":"249","volume":"35","author":"Gavras I","year":"1990","journal-title":"Adv Intern Med"},{"key":"B18","doi-asserted-by":"crossref","first-page":"3440","DOI":"10.1016\/S0021-9258(19)83641-4","volume":"260","author":"Grynkiewicz G","year":"1985","journal-title":"J Biol Chem"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1016\/0163-7258(92)90016-S"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1016\/S0306-3623(96)00174-7"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1038\/ng0995-76"},{"key":"B22","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.25.11495"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1007\/s11906-003-0005-1"},{"key":"B24","doi-asserted-by":"publisher","DOI":"10.1096\/fj.04-2314fje"},{"key":"B25","doi-asserted-by":"publisher","DOI":"10.1016\/S0895-7061(02)03152-7"},{"key":"B26","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(01)00241-0"},{"key":"B27","doi-asserted-by":"crossref","first-page":"414","DOI":"10.1016\/S0022-3565(25)31342-X","volume":"206","author":"Ludens JH","year":"1978","journal-title":"J Pharmacol Exp Ther"},{"key":"B28","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.C100737200"},{"key":"B29","doi-asserted-by":"publisher","DOI":"10.1016\/0378-1119(94)90162-7"},{"key":"B30","doi-asserted-by":"publisher","DOI":"10.1038\/ncpneph0444"},{"key":"B31","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.29.1.471"},{"key":"B32","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.22.5.705"},{"key":"B33","doi-asserted-by":"publisher","DOI":"10.1139\/y97-049"},{"key":"B34","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.30.3.358"},{"key":"B35","volume":"31","author":"Margolius HS","year":"1972","journal-title":"Circ Res"},{"key":"B36","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.35.6.820"},{"key":"B37","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.21.6.961"},{"key":"B38","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00056.2003"},{"key":"B39","first-page":"1","volume":"38","author":"Nolly HL","year":"1992","journal-title":"Agents Actions Suppl"},{"key":"B40","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.253.2.F333"},{"key":"B41","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M807129200"},{"key":"B42","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00403.2007"},{"key":"B43","doi-asserted-by":"publisher","DOI":"10.1096\/fj.09-151506"},{"key":"B44","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.200709800"},{"key":"B45","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2006.127449"},{"key":"B46","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.17.2.242"},{"key":"B47","doi-asserted-by":"publisher","DOI":"10.1016\/j.intimp.2007.09.013"},{"key":"B48","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.24.15045"},{"key":"B49","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0b013e328011a20c"},{"key":"B50","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.265.4.F569"},{"key":"B51","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.6.F1010"},{"key":"B52","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00068.2002"},{"key":"B53","first-page":"395","volume":"17","author":"Schild L","year":"1996","journal-title":"Nephrologie"},{"key":"B54","doi-asserted-by":"publisher","DOI":"10.1007\/s10254-004-0023-7"},{"key":"B55","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-4757-3401-0_20"},{"key":"B56","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00535.2002"},{"key":"B57","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.107.108126"},{"key":"B58","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1986.14"},{"key":"B59","doi-asserted-by":"publisher","DOI":"10.1515\/BC.2006.019"},{"key":"B60","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(94)90250-X"},{"key":"B61","doi-asserted-by":"publisher","DOI":"10.1096\/fj.99-1010fje"},{"key":"B62","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.23.6.1068"},{"key":"B63","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.90225.2008"},{"key":"B64","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007010020"},{"key":"B65","doi-asserted-by":"publisher","DOI":"10.1172\/JCI112268"},{"key":"B66","doi-asserted-by":"publisher","DOI":"10.1172\/JCI111935"},{"key":"B67","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00261.2004"},{"key":"B68","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.86.5.589"},{"key":"B69","doi-asserted-by":"publisher","DOI":"10.1097\/00005344-200204000-00003"},{"key":"B70","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.13.6.658"},{"key":"B71","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.143.2.501"},{"key":"B72","doi-asserted-by":"publisher","DOI":"10.1007\/BF00232796"},{"key":"B73","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.23.2.236"},{"key":"B74","doi-asserted-by":"publisher","DOI":"10.1172\/JCI108655"},{"key":"B75","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00462.2006"},{"key":"B76","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.258.6.F1584"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00606.2010","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,3,2]],"date-time":"2025-03-02T17:44:55Z","timestamp":1740937495000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00606.2010"}},"issued":{"date-parts":[[2011,5]]},"references-count":76,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2011,5]]}},"alternative-id":["10.1152\/ajprenal.00606.2010"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00606.2010","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2011,5]]}},{"indexed":{"date-parts":[[2026,3,14]],"date-time":"2026-03-14T03:45:47Z","timestamp":1773459947994,"version":"3.50.1"},"reference-count":9,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1997,10,1]]},"abstract":"<jats:p>The K-selective channel, TOK1, recently identified in yeast, displays the unusual structural feature of having two putative pore regions, in contrast to all previously cloned K channels. Using the TOK1 pore regions as probes, we identified a human kidney cDNA encoding a 337-amino acid protein (hKCNK1) with four transmembrane segments and two pore regions containing the signature sequence of K channels. Amino acid identity to TOK1 is only 15% overall but 40% at the pores. Northern analysis indicates high expression of a 1.9-kb message in brain &gt; kidney &gt;&gt; heart. Nephron segment localization, carried out in rabbit by reverse transcription-polymerase chain reaction, reveals that KCNK1 is expressed in cortical thick ascending limb, connecting tubule, and cortical collecting duct. It was not detected in the proximal tubule, medullary thick ascending limb, distal convoluted tubule, and glomerulus. We conclude that KCNK1 is a unique, double-pore, mammalian K channel, distantly related to the yeast channel TOK1, that is expressed in distal tubule and is a candidate to participate in renal K homeostasis.<\/jats:p>","DOI":"10.1152\/ajprenal.1997.273.4.f663","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T14:56:01Z","timestamp":1514040961000},"page":"F663-F666","source":"Crossref","is-referenced-by-count":13,"title":["Cloning and localization of a double-pore K channel, KCNK1: exclusive expression in distal nephron segments"],"prefix":"10.1152","volume":"273","author":[{"given":"Marcelo","family":"Orias","sequence":"first","affiliation":[{"name":"Department of Medicine, Yale University School of Medicine and Department of Veterans Affairs Medical Center, New Haven, Connecticut 06510"}]},{"given":"Heino","family":"Vel\u00e1zquez","sequence":"additional","affiliation":[{"name":"Department of Medicine, Yale University School of Medicine and Department of Veterans Affairs Medical Center, New Haven, Connecticut 06510"}]},{"given":"Freeman","family":"Tung","sequence":"additional","affiliation":[{"name":"Department of Medicine, Yale University School of Medicine and Department of Veterans Affairs Medical Center, New Haven, Connecticut 06510"}]},{"given":"George","family":"Lee","sequence":"additional","affiliation":[{"name":"Department of Medicine, Yale University School of Medicine and Department of Veterans Affairs Medical Center, New Haven, Connecticut 06510"}]},{"given":"Gary V.","family":"Desir","sequence":"additional","affiliation":[{"name":"Department of Medicine, Yale University School of Medicine and Department of Veterans Affairs Medical Center, New Haven, Connecticut 06510"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.93.23.13256"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/362031a0"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1038\/376690a0"},{"key":"B4","doi-asserted-by":"crossref","first-page":"19867","DOI":"10.1016\/S0021-9258(18)54860-2","volume":"266","author":"Kozak M.","year":"1991","journal-title":"J. Biol. Chem."},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1038\/364802a0"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1002\/j.1460-2075.1996.tb00437.x"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.8.4183"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/331143a0"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/0028-3908(96)00126-8"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1997.273.4.F663","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,8,11]],"date-time":"2022-08-11T03:47:41Z","timestamp":1660189661000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1997.273.4.F663"}},"issued":{"date-parts":[[1997,10,1]]},"references-count":9,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1997,10,1]]}},"alternative-id":["10.1152\/ajprenal.1997.273.4.F663"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1997.273.4.f663","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1997,10,1]]}},{"indexed":{"date-parts":[[2026,3,14]],"date-time":"2026-03-14T03:48:55Z","timestamp":1773460135975,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1994,12,1]]},"abstract":"<jats:p> Leukocytes, particularly neutrophils, have been implicated in ischemic-reperfusion organ injury (IRI). However, their role in kidney IRI is controversial. Leukocytes express the adhesion molecules CD11\/CD18 on their surface, which mediate many functions that can lead to tissue damage. To determine the role of CD11a and CD11b in IRI in the kidney, uninephrectomized Sprague-Dawley rats were pretreated with monoclonal antibodies (MAbs) directed against CD11a and CD11b or control MAbs. The serum creatinine (SCr), complete blood count, and kidney histopathological damage scores (PDS) (scale: 0-4) were assessed prior to and 24 h after 60 min of ischemia. Mean SCr 24 h after ischemia was significantly decreased in the anti-CD11a- and -CD11b-treated group compared with the control MAb-treated group (2.5 +\/- 0.3 mg\/dl vs. 3.4 +\/- 0.2 mg\/dl, P &lt;0.05). PDS were also reduced in the CD11a and CD11b group compared with controls (2.7 +\/- 0.2 vs. 3.5 +\/- 0.1, P &lt; 0.001). These data show that the CD11\/CD18 leukocyte adhesion pathway plays a role in mediating ischemic acute renal failure in rats. <\/jats:p>","DOI":"10.1152\/ajprenal.1994.267.6.f1052","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T04:54:01Z","timestamp":1514004841000},"page":"F1052-F1058","source":"Crossref","is-referenced-by-count":27,"title":["Role of CD11a and CD11b in ischemic acute renal failure in rats"],"prefix":"10.1152","volume":"267","author":[{"given":"H.","family":"Rabb","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, University of South Florida."}]},{"given":"C. C.","family":"Mendiola","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of South Florida."}]},{"given":"J.","family":"Dietz","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of South Florida."}]},{"given":"S. R.","family":"Saba","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of South Florida."}]},{"given":"T. B.","family":"Issekutz","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of South Florida."}]},{"given":"F.","family":"Abanilla","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of South Florida."}]},{"given":"J. V.","family":"Bonventre","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of South Florida."}]},{"given":"G.","family":"Ramirez","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of South Florida."}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1994.267.6.F1052","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T19:55:49Z","timestamp":1567972549000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1994.267.6.F1052"}},"issued":{"date-parts":[[1994,12,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1994,12,1]]}},"alternative-id":["10.1152\/ajprenal.1994.267.6.F1052"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1994.267.6.f1052","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1994,12,1]]}},{"indexed":{"date-parts":[[2026,3,14]],"date-time":"2026-03-14T03:25:04Z","timestamp":1773458704427,"version":"3.50.1"},"reference-count":68,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2007,12]]},"abstract":"<jats:p>Mice deficient in the ATP6V1B1 (\u201cB1\u201d) subunit of the vacuolar proton-pumping ATPase (V-ATPase) maintain body acid-base homeostasis under normal conditions, but not when exposed to an acid load. Here, compensatory mechanisms involving the alternate ATP6V1B2 (\u201cB2\u201d) isoform were examined to explain the persistence of baseline pH regulation in these animals. By immunocytochemistry, the mean pixel intensity of apical B2 immunostaining in medullary A intercalated cells (A-ICs) was twofold greater in B1\u2212\/\u2212 mice than in B1+\/+ animals, and B2 was colocalized with other V-ATPase subunits. No significant upregulation of B2 mRNA or protein expression was detected in B1\u2212\/\u2212 mice compared with wild-type controls. We conclude that increased apical B2 staining is due to relocalization of B2-containing V-ATPase complexes from the cytosol to the plasma membrane. Recycling of B2-containing holoenzymes between these domains was confirmed by the intracellular accumulation of B1-deficient V-ATPases in response to the microtubule-disrupting drug colchicine. V-ATPase membrane expression is further supported by the presence of \u201crod-shaped\u201d intramembranous particles seen by freeze fracture microscopy in apical membranes of normal and B1-deficient A-ICs. Intracellular pH recovery assays show that significant (28\u201340% of normal) V-ATPase function is preserved in medullary ICs from B1\u2212\/\u2212 mice. We conclude that the activity of apical B2-containing V-ATPase holoenzymes in A-ICs is sufficient to maintain baseline acid-base homeostasis in B1-deficient mice. However, our results show no increase in cell surface V-ATPase activity in response to metabolic acidosis in ICs from these animals, consistent with their inability to appropriately acidify their urine under these conditions.<\/jats:p>","DOI":"10.1152\/ajprenal.00160.2007","type":"journal-article","created":{"date-parts":[[2007,9,27]],"date-time":"2007-09-27T00:35:04Z","timestamp":1190853304000},"page":"F1915-F1926","source":"Crossref","is-referenced-by-count":58,"title":["Compensatory membrane expression of the V-ATPase B2 subunit isoform in renal medullary intercalated cells of B1-deficient mice"],"prefix":"10.1152","volume":"293","author":[{"given":"Teodor G.","family":"P\u0103unescu","sequence":"first","affiliation":[]},{"given":"Leileata M.","family":"Russo","sequence":"additional","affiliation":[]},{"given":"Nicolas","family":"Da Silva","sequence":"additional","affiliation":[]},{"given":"Jana","family":"Kovacikova","sequence":"additional","affiliation":[]},{"given":"Nilufar","family":"Mohebbi","sequence":"additional","affiliation":[]},{"given":"Alfred N.","family":"Van Hoek","sequence":"additional","affiliation":[]},{"given":"Mary","family":"McKee","sequence":"additional","affiliation":[]},{"given":"Carsten A.","family":"Wagner","sequence":"additional","affiliation":[]},{"given":"Sylvie","family":"Breton","sequence":"additional","affiliation":[]},{"given":"Dennis","family":"Brown","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1002\/aja.1001880406"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.86.14.5429"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M109967200"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.3.F437"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115268"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.med.52.1.471"},{"key":"R7","doi-asserted-by":"crossref","unstructured":"Bernasconi P, Rausch T, Struve I, Morgan L, Taiz L.An mRNA from human brain encodes an isoform of the B subunit of the vacuolar H+-ATPase.J Biol Chem265: 17428\u201317431, 1990.","DOI":"10.1016\/S0021-9258(18)38179-1"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1242\/jeb.02014"},{"key":"R9","doi-asserted-by":"crossref","unstructured":"Bowman BJ, Allen R, Wechser MA, Bowman EJ.Isolation of genes encoding theNeurosporavacuolar ATPase. Analysis of vma-2 encoding the 57-kDa polypeptide and comparison to vma-1.J Biol Chem263: 14002\u201314007, 1988.","DOI":"10.1016\/S0021-9258(18)68176-1"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.269.6.F761"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00340.2006"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.5.F717"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M909857199"},{"key":"R14","unstructured":"Brown D, Breton S.H+V-ATPase-dependent luminal acidification in the kidney collecting duct and the epididymis\/vas deferens: vesicle recycling and transcytotic pathways.J Exp Biol203: 137\u2013145, 2000."},{"key":"R15","doi-asserted-by":"crossref","unstructured":"Brown D, Breton S.Mitochondria-rich, proton-secreting epithelial cells.J Exp Biol199: 2345\u20132358, 1996.","DOI":"10.1242\/jeb.199.11.2345"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.105.4.1637"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1038\/331622a0"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1172\/JCI113833"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1007\/BF01463929"},{"key":"R20","unstructured":"Brown D, Sabolic I, Gluck S.Colchicine-induced redistribution of proton pumps in kidney epithelial cells.Kidney Int Suppl33: S79\u2013S83, 1991."},{"key":"R21","doi-asserted-by":"crossref","unstructured":"Brown D, Smith PJ, Breton S.Role of V-ATPase-rich cells in acidification of the male reproductive tract.J Exp Biol200: 257\u2013262, 1997.","DOI":"10.1242\/jeb.200.2.257"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1996.76.1.245"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00596.2006"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1016\/S0378-5955(03)00108-4"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0506769102"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1016\/S0378-1119(03)00790-X"},{"key":"R27","doi-asserted-by":"crossref","unstructured":"Futai M, Oka T, Sun-Wada G, Moriyama Y, Kanazawa H, Wada Y.Luminal acidification of diverse organelles by V-ATPase in animal cells.J Exp Biol203: 107\u2013116, 2000.","DOI":"10.1242\/jeb.203.1.107"},{"key":"R28","doi-asserted-by":"crossref","unstructured":"Gruber G, Wieczorek H, Harvey WR, Muller V.Structure-function relationships of A- F- and V-ATPases.J Exp Biol204: 2597\u20132605, 2001.","DOI":"10.1242\/jeb.204.15.2597"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5320(75)80018-9"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1038\/ncb1348"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1016\/S0378-1119(02)00542-5"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00374.2001"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004110935"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1038\/5022"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.11.6337"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-5793(03)00396-X"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1996.270.1.C382"},{"key":"R38","doi-asserted-by":"crossref","unstructured":"Manolson MF, Ouellette BF, Filion M, Poole RJ.cDNA sequence and homologies of the \u201c57-kDa\u201d nucleotide-binding subunit of the vacuolar ATPase fromArabidopsis.J Biol Chem263: 17987\u201317994, 1988.","DOI":"10.1016\/S0021-9258(19)81313-3"},{"key":"R39","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00084.2004"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1999.79.2.361"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.89.8.3541"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1038\/nrm729"},{"key":"R43","doi-asserted-by":"publisher","DOI":"10.1016\/S0074-7696(08)61289-9"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M309543200"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00464.2003"},{"key":"R46","doi-asserted-by":"publisher","DOI":"10.1095\/biolreprod.105.043752"},{"key":"R47","doi-asserted-by":"crossref","unstructured":"Puopolo K, Kumamoto C, Adachi I, Magner R, Forgac M.Differential expression of the \u201cB\u201d subunit of the vacuolar H+-ATPase in bovine tissues.J Biol Chem267: 3696\u20133706, 1992.","DOI":"10.1016\/S0021-9258(19)50581-6"},{"key":"R48","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006070753"},{"key":"R49","doi-asserted-by":"publisher","DOI":"10.1172\/JCI111871"},{"key":"R50","doi-asserted-by":"publisher","DOI":"10.1038\/318368a0"},{"key":"R51","doi-asserted-by":"crossref","unstructured":"Silberstein C, Bouley R, Huang Y, Fang P, Pastor-Soler N, Brown D, Van Hoek AN.Membrane organization and function of M1 and M23 isoforms of aquaporin-4 in epithelial cells.Am J Physiol Renal Physiol287: F501\u2013F511, 2004.","DOI":"10.1152\/ajprenal.00439.2003"},{"key":"R52","doi-asserted-by":"publisher","DOI":"10.1016\/S0378-1119(02)00884-3"},{"key":"R53","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M107267200"},{"key":"R54","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004090761"},{"key":"R55","doi-asserted-by":"publisher","DOI":"10.1038\/79208"},{"key":"R56","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1980.6"},{"key":"R57","doi-asserted-by":"publisher","DOI":"10.1136\/jmg.39.11.796"},{"key":"R58","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.86.16.6067"},{"key":"R59","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M307197200"},{"key":"R60","doi-asserted-by":"publisher","DOI":"10.1016\/S0378-1119(02)01099-5"},{"key":"R61","doi-asserted-by":"publisher","DOI":"10.1021\/bi00578a012"},{"key":"R62","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.2.F310"},{"key":"R63","doi-asserted-by":"publisher","DOI":"10.1007\/s002329900438"},{"key":"R64","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00045.2003"},{"key":"R65","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-003-1082-3"},{"key":"R66","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0307321101"},{"key":"R67","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005121277"},{"key":"R68","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.26.15494"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00160.2007","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,8,24]],"date-time":"2021-08-24T09:44:08Z","timestamp":1629798248000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00160.2007"}},"issued":{"date-parts":[[2007,12]]},"references-count":68,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2007,12]]}},"alternative-id":["10.1152\/ajprenal.00160.2007"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00160.2007","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2007,12]]}},{"indexed":{"date-parts":[[2026,3,14]],"date-time":"2026-03-14T03:11:53Z","timestamp":1773457913760,"version":"3.50.1"},"reference-count":55,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2007,7]]},"abstract":"<jats:p>An electroneutral organic cation (OC)\/proton exchanger in the apical membrane of proximal tubules mediates the final step of renal OC excretion. Two members of the multidrug and toxin extrusion family, MATE1 and MATE2-K, were recently identified in human and rodent kidney and proposed to be the molecular basis of renal OC\/H<jats:sup>+<\/jats:sup>exchange. To take advantage of the comparative value of the large database on the kinetic and selectivity characteristics of OC\/H<jats:sup>+<\/jats:sup>exchange that exists for rabbit kidney, we cloned rbMATE1 and rbMATE2-K. The rabbit homologs have 75% (MATE1) and 74% (MATE2-K) amino acid identity to their human counterparts (and 51% identity with each other). rbMATE1 and rbMATE2-K exhibited H<jats:sup>+<\/jats:sup>gradient-dependent uptake and efflux of tetraethylammonium (TEA) when expressed in Chinese hamster ovary cells. Both transporters displayed similar affinities for selected compounds [IC<jats:sub>50<\/jats:sub>values within 2-fold for TEA, 1-methyl-4-phenylpyridinium, and quinidine] and very different affinities for others (IC<jats:sub>50<\/jats:sub>values differing by 8- to 80-fold for choline and cimetidine, respectively). These results indicate that rbMATE1 and rbMATE2-K are multispecific OC\/H<jats:sup>+<\/jats:sup>exchangers with similar, but distinct, functional characteristics. Overall, the selectivity of MATE1 and MATE2-K correlated closely with that observed in rabbit renal brush-border membrane vesicles.<\/jats:p>","DOI":"10.1152\/ajprenal.00102.2007","type":"journal-article","created":{"date-parts":[[2007,4,19]],"date-time":"2007-04-19T00:38:47Z","timestamp":1176943127000},"page":"F360-F370","source":"Crossref","is-referenced-by-count":43,"title":["Molecular identification and functional characterization of rabbit MATE1 and MATE2-K"],"prefix":"10.1152","volume":"293","author":[{"given":"Xiaohong","family":"Zhang","sequence":"first","affiliation":[]},{"given":"Nathan J.","family":"Cherrington","sequence":"additional","affiliation":[]},{"given":"Stephen H.","family":"Wright","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/gkh380"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1023\/A:1012164203648"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1007\/BF00550869"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1124\/mol.105.016832"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.266.3.F450"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0408624102"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1038\/372549a0"},{"key":"R8","doi-asserted-by":"crossref","unstructured":"Hartley DP, Klaassen CD.Detection of chemical-induced differential expression of rat hepatic cytochrome P450 mRNA transcripts using branched DNA signal amplification technology.Drug Metab Dispos28: 608\u2013616, 2000.","DOI":"10.1016\/S0090-9556(24)15107-0"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1007\/s00424-003-1192-y"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00090.2006"},{"key":"R11","unstructured":"Holohan PD, Ross CR.Mechanisms of organic cation transport in kidney plasma membrane vesicles: 1. Countertransport studies.J Pharmacol Exp Ther215: 191\u2013197, 1980."},{"key":"R12","unstructured":"Holohan PD, Ross CR.Mechanisms of organic cation transport in kidney plasma membrane vesicles: 2. \u0394pH studies.J Pharmacol Exp Ther216: 294\u2013298, 1981."},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1046\/j.1432-1033.2003.03418.x"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.23.21.7902-7908.2003"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.2000.279.2.H679"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.26.15971"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1016\/j.tips.2004.05.005"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1006\/jmbi.2000.4315"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1990.258.3.F597"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1007\/BF01872636"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2006030205"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.252.3.F525"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.256.4.F540"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1989.257.2.F243"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2736(87)90102-7"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.1992.263.5.G775"},{"key":"R27","doi-asserted-by":"crossref","unstructured":"Motohashi H, Sakurai Y, Saito H, Masuda S, Urakami Y, Goto M, Fukatsu A, Ogawa O, Inui KI.Gene expression levels and immunolocalization of organic anion transporters in the human kidney.J Am Soc Nephrol13: 866\u2013874, 2002.","DOI":"10.1681\/ASN.V134866"},{"key":"R28","doi-asserted-by":"crossref","unstructured":"Ohta KY, Inoue K, Hayashi Y, Yuasa H.Molecular identification and functional characterization of rat MATE1 as an organic cation\/H+antiporter in the kidney.Drug Metab Dispos(34: 1868\u20131874), 2006.","DOI":"10.1124\/dmd.106.010876"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1996.1056"},{"key":"R30","doi-asserted-by":"publisher","DOI":"10.1016\/j.tips.2006.09.001"},{"key":"R31","doi-asserted-by":"crossref","unstructured":"Otsuka M, Matsumoto T, Morimoto R, Arioka S, Omote H, Moriyama Y.A human transporter protein that mediates the final excretion step for toxic organic cations.Proc Natl Acad Sci USA102:17923\u201317928, 2005.","DOI":"10.1073\/pnas.0506483102"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1991.261.3.F443"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1993.73.4.765"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1983.245.2.F238"},{"key":"R35","unstructured":"Sonnhammer EL, von Heijne G, Krogh A.A hidden Markov model for predicting transmembrane helices in protein sequences.Proc Int Conf Intell Syst Mol Biol6: 175\u2013182, 1998."},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2736(84)90556-X"},{"key":"R37","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-5793(97)01441-5"},{"key":"R38","doi-asserted-by":"publisher","DOI":"10.1007\/s11095-006-9016-3"},{"key":"R39","doi-asserted-by":"crossref","unstructured":"Tsuda M, Terada T, Asaka JI, Katsura T, Inui KI.Oppositely-directed H+gradient functions as a driving force of rat H+\/organic cation antiporter MATE1.Am J Physiol Renal Physiol292: F593\u2013F598, 2007.","DOI":"10.1152\/ajprenal.00312.2006"},{"key":"R40","doi-asserted-by":"publisher","DOI":"10.1093\/bioinformatics\/17.9.849"},{"key":"R41","doi-asserted-by":"publisher","DOI":"10.1007\/s002329900247"},{"key":"R42","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1995.269.5.R1050"},{"key":"R43","doi-asserted-by":"crossref","unstructured":"Villalobos AR, Braun EJ.Substrate specificity of organic cation\/H+ exchange in avian renal brush-border membranes.J Pharmacol Exp Ther287: 944\u2013951, 1998.","DOI":"10.1016\/S0022-3565(24)37885-1"},{"key":"R44","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00040.2003"},{"key":"R45","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00115.2004"},{"key":"R46","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1987.253.5.F1040"},{"key":"R47","doi-asserted-by":"crossref","unstructured":"Wright SH, Wunz TM.Mechanism ofcis-andtrans-substrate interactions at the tetraethylammonium\/H+exchanger of rabbit renal brush-border membrane vesicles.J Biol Chem263: 19494\u201319497, 1988.","DOI":"10.1016\/S0021-9258(19)77661-3"},{"key":"R48","doi-asserted-by":"publisher","DOI":"10.1007\/s004240050658"},{"key":"R49","doi-asserted-by":"publisher","DOI":"10.1007\/s004240050823"},{"key":"R50","doi-asserted-by":"publisher","DOI":"10.1007\/BF00233460"},{"key":"R51","doi-asserted-by":"publisher","DOI":"10.1007\/BF00374145"},{"key":"R52","doi-asserted-by":"publisher","DOI":"10.1016\/j.compbiolchem.2003.11.002"},{"key":"R53","doi-asserted-by":"crossref","unstructured":"Yabuuchi H, Tamai I, Nezu JI, Sakamoto K, Oku A, Shimane M, Sai Y, Tsuji A.Novel membrane transporter OCTN1 mediates multispecific, bidirectional, and pH-dependent transport of organic cations.J Pharmacol Exp Ther289: 768\u2013773, 1999.","DOI":"10.1016\/S0022-3565(24)38199-6"},{"key":"R54","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.00004.2001"},{"key":"R55","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00156.2004"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00102.2007","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,1,15]],"date-time":"2025-01-15T20:57:52Z","timestamp":1736974672000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00102.2007"}},"issued":{"date-parts":[[2007,7]]},"references-count":55,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2007,7]]}},"alternative-id":["10.1152\/ajprenal.00102.2007"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00102.2007","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2007,7]]}},{"indexed":{"date-parts":[[2026,3,16]],"date-time":"2026-03-16T10:48:51Z","timestamp":1773658131929,"version":"3.50.1"},"reference-count":36,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2007,5]]},"abstract":"<jats:p>MAK-V\/Hunk is an SNF1-related serine\/threonine kinase which was previously shown to be highly expressed in the mammary gland and central nervous system. In this study, we found MAK-V\/Hunk is abundantly and specifically expressed in the thick ascending limbs and distal convoluted tubules (DCT) of the kidney from the embryonic stage to the adult stage. We demonstrated that dietary salt depletion significantly enhances renal MAK-V\/Hunk mRNA levels compared with a normal-salt diet. To analyze the possible renal cellular function of this kinase, we employed mouse distal convoluted tubule (mDCT) cells. The results of reverse transcriptase-polymerase chain reaction and Western blot analysis revealed that MAK-V\/Hunk is expressed endogenously in mDCT cells. Overexpression of MAK-V\/Hunk by adenoviral gene transfer significantly inhibited the ANG II-induced stimulation of c- fos gene transcription and suppressed the ANG II-mediated increases in transforming growth factor-\u03b2 production into the medium. This phenomenon was accompanied by inhibition of ANG II-induced activation of BrdU incorporation. On the other hand, the MAK-V\/Hunk knockdown by siRNA activated the ANG II-induced c- fos gene expression. In the consecutive sections stained for MAK-V\/Hunk and AT<jats:sub>1<\/jats:sub>receptor, MAK-V\/Hunk-immunopositive distal tubules expressed the AT<jats:sub>1<\/jats:sub>receptor. This is the first report on the intrarenal localization of MAK-V\/Hunk and its cellular function in renal tubular cells.<\/jats:p>","DOI":"10.1152\/ajprenal.00451.2006","type":"journal-article","created":{"date-parts":[[2007,2,14]],"date-time":"2007-02-14T02:59:49Z","timestamp":1171421989000},"page":"F1526-F1536","source":"Crossref","is-referenced-by-count":20,"title":["Expression of MAK-V\/Hunk in renal distal tubules and its possible involvement in proliferative suppression"],"prefix":"10.1152","volume":"292","author":[{"given":"Masashi","family":"Sakai","sequence":"first","affiliation":[]},{"given":"Kouichi","family":"Tamura","sequence":"additional","affiliation":[]},{"given":"Yuko","family":"Tsurumi","sequence":"additional","affiliation":[]},{"given":"Yutaka","family":"Tanaka","sequence":"additional","affiliation":[]},{"given":"Yuichi","family":"Koide","sequence":"additional","affiliation":[]},{"given":"Miyuki","family":"Matsuda","sequence":"additional","affiliation":[]},{"given":"Tomoaki","family":"Ishigami","sequence":"additional","affiliation":[]},{"given":"Machiko","family":"Yabana","sequence":"additional","affiliation":[]},{"given":"Yasuo","family":"Tokita","sequence":"additional","affiliation":[]},{"given":"Yukio","family":"Hiroi","sequence":"additional","affiliation":[]},{"given":"Issei","family":"Komuro","sequence":"additional","affiliation":[]},{"given":"Satoshi","family":"Umemura","sequence":"additional","affiliation":[]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1432-1033.1996.00736.x"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1006\/dbio.2000.9614"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00190.2004"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.432"},{"key":"R5","doi-asserted-by":"crossref","unstructured":"Gardner HP, Belka GK, Wertheim GB, Hartman JL, Ha SI, Gimotty PA, Marquis ST, Chodosh LA.Developmental role of the SNF1-related kinase Hunk in pregnancy-induced changes in the mammary gland.Development127: 4493\u20134509, 2000.","DOI":"10.1242\/dev.127.20.4493"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1006\/geno.1999.6078"},{"key":"R7","doi-asserted-by":"publisher","DOI":"10.1006\/jmcc.1996.0334"},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.268.1.F89"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00070.2003"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00068.x"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(95)90082-9"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M500296200"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1016\/j.febslet.2004.11.093"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.4.F599"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00321.2001"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00600.2004"},{"key":"R17","doi-asserted-by":"crossref","unstructured":"Kihara M, Umemura S, Yabana M, Sumida Y, Nyui N, Tamura K, Kadota T, Kishida R, Murakami K, Fukamizu A, Ishii M.Dietary salt loading decreases the expressions of neuronal-type nitric oxide synthase and renin in the juxtaglomerular apparatus of angiotensinogen gene-knockout mice.J Am Soc Nephrol9: 355\u2013362, 1998.","DOI":"10.1681\/ASN.V93355"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1007\/s004380000293"},{"key":"R19","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2005060659"},{"key":"R20","doi-asserted-by":"publisher","DOI":"10.1007\/BF02630961"},{"key":"R21","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfi265"},{"key":"R22","doi-asserted-by":"publisher","DOI":"10.1007\/s00427-004-0381-9"},{"key":"R23","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.73.3.424"},{"key":"R24","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.29.4.923"},{"key":"R25","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.28.3.403"},{"key":"R26","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.100519097"},{"key":"R27","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M004421200"},{"key":"R28","doi-asserted-by":"publisher","DOI":"10.1016\/j.febslet.2005.01.068"},{"key":"R29","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M101614200"},{"key":"R30","doi-asserted-by":"crossref","unstructured":"Thompson-Jaeger S, Francois J, Gaughran JP, Tatchell K.Deletion of SNF1 affects the nutrient response of yeast and resembles mutations which activate the adenylate cyclase pathway.Genetics129: 697\u2013706, 1991.","DOI":"10.1093\/genetics\/129.3.697"},{"key":"R31","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5000130"},{"key":"R32","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00151.2005"},{"key":"R33","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.4.F587"},{"key":"R34","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.268.5.F940"},{"key":"R35","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00076.x"},{"key":"R36","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5001846"}],"container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00451.2006","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,8,8]],"date-time":"2021-08-08T18:39:08Z","timestamp":1628447948000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00451.2006"}},"issued":{"date-parts":[[2007,5]]},"references-count":36,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2007,5]]}},"alternative-id":["10.1152\/ajprenal.00451.2006"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00451.2006","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[2007,5]]}},{"indexed":{"date-parts":[[2026,3,16]],"date-time":"2026-03-16T11:50:03Z","timestamp":1773661803976,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[1988,4,1]]},"abstract":"<jats:p> To determine whether angiotensinogen (Ao) and renin are synthesized by the immature kidney and to assess the changes in intrarenal renin distribution that occur with maturation, the kidneys from 24 newborn and 12 adult Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR) were processed for renin immunocytochemistry using a highly specific anti-rat renin antibody. Kidney renin and Ao relative mRNA levels (mRNA\/total RNA) were detected by Northern and dot blot techniques, using full-length rat renin and Ao cDNAs. Renal renin concentration (RRC) was measured by radioimmunoassay of angiotensin I (ANG I) and expressed as ng ANG I.h-1.mg protein-1 in the incubation media. RRC was higher in newborn than in adult SHR (979 +\/- 164 vs. 206 +\/- 47) and WKY (573 +\/- 69 vs. 297 +\/- 74) (P less than 0.05). In the newborn kidneys of both rat strains, renin was distributed throughout the entire length of the afferent arterioles and interlobular arteries, whereas in the adult kidneys renin was confined to the classical juxtaglomerular position. With maturation, there was a decrease in the proportion of immunoreactive juxtaglomerular apparatuses and arterial segments that contained renin. Kidney renin mRNA levels were 7.9-fold higher in the newborn than in the adult animal. Ao mRNA was detected in the newborn and adult kidneys of both rat strains. This study demonstrates conclusively that both renin and Ao genes are expressed in the newborn kidney, providing evidence for a local renin-angiotensin system that is subjected to developmental changes. <\/jats:p>","DOI":"10.1152\/ajprenal.1988.254.4.f582","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T22:22:12Z","timestamp":1513981332000},"page":"F582-F587","source":"Crossref","is-referenced-by-count":22,"title":["Renin and angiotensinogen gene expression in maturing rat kidney"],"prefix":"10.1152","volume":"254","author":[{"given":"R. A.","family":"Gomez","sequence":"first","affiliation":[{"name":"Department of Pediatrics, School of Medicine, University of Virginia, Charlottesville 22908"}]},{"given":"K. R.","family":"Lynch","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, School of Medicine, University of Virginia, Charlottesville 22908"}]},{"given":"R. L.","family":"Chevalier","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, School of Medicine, University of Virginia, Charlottesville 22908"}]},{"given":"N.","family":"Wilfong","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, School of Medicine, University of Virginia, Charlottesville 22908"}]},{"given":"A.","family":"Everett","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, School of Medicine, University of Virginia, Charlottesville 22908"}]},{"given":"R. M.","family":"Carey","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, School of Medicine, University of Virginia, Charlottesville 22908"}]},{"given":"M. J.","family":"Peach","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, School of Medicine, University of Virginia, Charlottesville 22908"}]}],"member":"24","container-title":["American Journal of Physiology-Renal Physiology"],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.1988.254.4.F582","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T15:50:10Z","timestamp":1567957810000},"score":0.0,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.1988.254.4.F582"}},"issued":{"date-parts":[[1988,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1988,4,1]]}},"alternative-id":["10.1152\/ajprenal.1988.254.4.F582"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.1988.254.4.f582","ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"published":{"date-parts":[[1988,4,1]]}}],"items-per-page":1000,"query":{"start-index":1000,"search-terms":null}}}